FLUORIDATION OF PUBLIC WATER SUPPLY SYSTEM
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Interoffice Correspondence Sheet
To:
Garry Brumback, Assistant City Manager
Mahshid Arasteh, Public Works Administrator
From:
Andrew Neff, Public Utilities Director
CC:
Todd Petrie, Assistant Public Utilities Director
Lou Badami, Water Superintendent
Date:
August 20, 2003
RE:
<li.Fl~~iiCftf:~i'fW.rliupply Syst~m
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Fluoridation of the public drinking water supply is a controversial issue. Fluoridation seems to
ignite a great deal of emotion on either side of the debate when addressed. The following
information is intended to outline both the pros and cons for you and provide some background info
to allow you to gain a better understanding of the issues involved. The introduction of fluoride into
a public drinking water system is optional-there is no requirement at this time to do so.
Fluoride prevents tooth decay by reestablishing mineralization of enamel that is under attack and
slows production of acid formed by bacteria. A side effect of too much fluoride being ingested is
called fluorosis-a condition marked by mottling and/or discoloring of tooth enamel and in more
extreme cases causes teeth to become brittle. Fluorosis can also occur in bones.
Regardless of the decision being considered now by Pinellas County, the City of Clearwater will
have to make a decision on fluoridating our locally produced water. If we do nothing, then our
locally produced water will blend with artificially fluoridated water from the county, likely rendering
the final product below what is considered optimal and may have reduced effect. The other option is
to fluoridate our fraction locally produced to match water received from the county (assuming
approval from the County Commission on the use of fluoride in the drinking water supply).
The Surgeon General, the Centers for Disease Control, the Public Health Service, our local Health
Department and many dentists support fluoridation. However, there are also reports indicating that
fluoridation has little effect on reduction of tooth decay and that the risks associated with
fluoridation outweigh benefits.
At the August lzth Pinellas County Commission work session on this subject, I presented the city's
position of waiting until the National Research Council's report (on behalf of the EP A) on the health
effects of fluoride in public water systems. The County Commission felt that since this study was
centered on determining the appropriate maximum contaminate level (now at 4 mg/l), there waslittle
concern for dosing fluoride at lower (about 0.8 mg/l) levels to assist in the prevention of tooth decay.
The information compiled by Pinellas County and provided to the County Commission on the
support and beneficial use of fluoride in drinking water is available in the Commission Library. I am
providing this information to you so that you have the benefit of what your counterparts are
reviewing in their decision process.
In sum, this info supports the concept of adding fluoride to the public drinking water supply with
statements from the Centers for Disease Control (CDC) and the Surgeon General. The essential
argument is that fluoride is safe and effective for preventing tooth decay.
Information in this portion of the material includes:
· Recommendations for Using Fluoride to Prevent and Control Dental Caries in the United
States
· Health Effects oflngested Fluoride (this is the 1993 National Research Council report being
updated)
· Toxicologic Risk of Fluoride in Drinking Water
· Surgeon Generals Statement on Community Water Fluoridation
· Populations Receiving Optimally Fluoridated Public Drinking Water-United States, 2000
I am also proving some additional information to you outlining research and data discussing the
negligible effect of fluoridation on tooth decay and it's risks vs. benefits. Key issues discussed
include little difference between fluoridated communities and those that are not (supported by
cessation studies), concern about the health effects of ingested fluoride, concern about the
effectiveness of ingested fluoride v. topical application and concern about the total daily intake of
fluoride for people. This information includes:
· Water Fluoridation and Tooth Decay: Results from the 1986-87 National Survey of
Schoolchildren (no statistically significant differences were found between fluoridated
communities and non-fluoridated)
· Abstracts from cessation studies for Durham NC and Kuopio, Finland. (stopping the
addition of fluoride had little effect)
· Fluoridation of Water-Questions about health risks and benefits remain after 40 years
· Risk Factors for Dental Fluorosis: A review of Recent Literature (potential for
fluorosis/many reports had differing results)
· New Evidence on Fluoridation (harmful to bone, no reliable benefits)
· Dental Caries (tooth decay) and dental fluorisis at varying water fluoride concentrations
(fluorosis seen starting at 0.7 ppm-at the optimal level)
· Why I Changed my Mind about Water Fluoridation
· A summary of the Town ofNatick, MA, Report-Should Natick Fluoridate? (panel review
of question-didn't fluoridate based on little positive effect, fluorisis risk, and health effects)
· The case for eliminating the use of dietary fluoride supplements for young children (children
intake fluoride from many sources-strong risk of fluorosis)
· Effects of Fluoride on the immune system (believed to be safe, now some doubts)
I should also note that outside the United States, particularly in Europe, fluoride is not added to most
public water systems. These countries tend to think that fluoride is a medication-best left to people
and their physicians.
These reports and studies suggest fluoridation of drinking water has limited benefits and may have
some increased risk factors associated with this practice-notably for the elderly, kidney patients
and debate continues over its effects concerning cancer.
When I conveyed the information about the results of the County Commission worksession on
fluoridation, I indicated I was leaning towards supporting the County's trend towards approving use
in drinking water supplies here. Based on additional research, I came upon the above info that I
believe indicates we should take a cautious approach.
The 1993 National Research Council report "Health Effects of Ingested Fluoride" indicates the
current maximum contaminate level of 4 mg/l is appropriate as an interim standard. The
subcommittee working on this report found inconsistencies in fluoride toxicity data base and gaps in
knowledge. They recommended further research concerning fluoride intake, dental fluorosis, bone
strength, fractures and carcinogenicity. They recommend the EPA's interim standard of 4 mg/l be
reviewed when the new information is available and revised if needed.
My recommendation at this point is to make a decision as to whether or not to fluoridate our water
supply after the NRC completes their report, titled ''Toxicologic Risk of Fluoride in Drinking
Water", to learn more about the health effects of ingested fluoride. This review compares literature
on fluoridating drinking water since 1993 and brings the database up to date while providing a
recommendation to EP A on the maximum contaminate level. This study will look at ingestion of
fluoride from all sources.
If you have any questions on this report, please contact me at 562-4960, ext. 7222.
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No Fluoridation
Table of Contents
· Three reasons why those who Supported the use of Fluoride say NO to Fluoridation today
· Citizens for Safe Drinking Water, Request for Due Diligence
· United States Code, 1994 Edition; Title 42 - The Public Health and Welfare
· Drinking Water Public Health Goal of the Office of Environmental Health Hazard Assessment
· Fluoride is already in our food and beverages
· Food and Beverage Sources of Fluoride Exposure
· Letter re Environmental Assessment for Proposed Water Fluoridation, Fort Detrick, MD and
supporting charts
· Fluorides, Hydrogen Fluoride and Fluorine
· Dental Fluorosis Classification
· American Academy of Pediatrics, Fluoride Supplementation for Children: Interim Policy
Recommendations
· Dental Fluorosis Prevalence . . .
· Dental Caries and Dental Fluorosis at Varying Water Fluoride Concentrations
· Journal of American Dental Association, Ingested fluoride does not reduce tooth decay, action is
topical, July 2000
· Article from Journal of American Dental Association, the Science and Practice of Caries
Prevention
· CDC Morbidity and Mortality Weeldy Report, Recommendations for using fluoride to prevent and
control dental caries in the US
· Letter from Dept of Health and Human Services to Ken Calvert of Subcommittee on Energy and
Environment re FDA
· Letter to Citizens for safe Drinking Water from National Federation of Federal Employees re:
support of petition to prohibit fluoridation
· Letter to George Glasser from Tudor Davies, US EP A Office of Science and Technology re:
research on fluorosilicic acid
Pinellas County Citizens for Safe Drinking Water
Angela Schrader 727 772.9236
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· American Water Works Assn Committee Personnel (paul Maasen, Secretary, Kaiser Aluminum
and Chemical Corp, Wentzville MO)
· Q&A re EP A removal of endorsement of water fluoridation
· Letter from US Environmental Protection Agency to Ken Calvert, Subcommittee on Energy
and Environment re EP A regulation
· Letter from F James Sensenbrenner, US House ofRep, Committee on Science re questions to EPA
· Letter from Jeffrey Koplan, Dir ofDept of Health & Human Services, to Kenneth Calvert, Sub-
committee on Energy & Environment, House ofRep, re CDC responses to fluoridation
· Congressman Calvert Inquiry May 8, 2002, Response to Questions
· Letter from Melinda Plaisier, Assoc Commissioner for Legislation to Ken Calvert, Chairman,
Subcommittee on Energy and Environment, Committee on Science
· Letter from Robert Thurnau, Treatment Technology Evaluation Branch, Water Supply and
Water Resources Division re: health effects of fluoride compounds
· Letter from Sally Gutierrez, Director, Water Supply & Water Resources Division from US
EP A re EP A endorsement and ORD research into fluoridation
. · Treatment Chemicals Contribute to Arsenic Levels
· Association of Silicofluoride Treated Water with Elevated Blood Lead
· Letter from Kathy Kranzfelder, NID National Institute of Diabetes and Digestive and Kidney
Disease, recommending consumption of bottled water to avoid high fluoride levels
· Municipality Utility District Section 12814, Addition of fluorine or fluorine compounds to
public water supplies; approval of voters.
· Ordinance enacted by the voters of the City ofWatsonville CA - Nov 5,2002
· City ofEscondido CA, Defendant; Reply to opposition of Plaintiff' s to the Demurrer. . .
· Superior Court, San Diego County, State of California, rulings of January 9 and March 27,2003,
and August 22, 2002
· City ofEscondido, CA: Review of the California Oral Health Needs Assessment 1993-94
· Statement of Dr William Hirzy before Subcommittee on Wildlife, Fisheries and Drinking
Water, U.S. Senate, June 29,2000
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· Esteemed voices have, for 50 years, warned the American public that water fluoridation has
dangerous long-term consequences to health
· Fluoride, What is it? by Robert and Kerry Broe
· An article from the Mesa Arizona Tribune, Dec 5, 1999
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Three Reasons Why Those Who Supported the
Use of Fluoride Say No to Fluoridation Today
1 Total fluoride exposure. The fluoridation goal of delivering 1 mg
(mllligram) of fluoride to a chlld per day has already been reached,
and exceeded, even in non fluoridated communities.
The total dosage goal of 1 mg of free-fluoride ion/day for a child was adopted in the
early 1940's when there was little or no other source of exposure.
The 1 mg of free-fluoride ion was to be placed in 1 liter of water, as that was the
amount that a child was assumed to drink per day (The very reason for using the
public water was the assumption that it would be the child's only access to fluoride).
Placing 1 mg into a liter created an equivalent concentration of 1 ppm (part per
million). Promoters have since incorrectly identified the 1 ppm concentration as the
goal, rather than the 1 mg dosage.
Two mg per day was considered by all, induding promoters, to be excessive, as it
caused an unacceptable risk for dental fluorosis (the visible display of fluoride
poisoning the specialized cells that make the enamel, resulting in white opaque spots,
brown stains, mottling and fracture-prone teeth); thus many scientists protested
that there was not an adequate margin of safety. Despite their protests, 1 mg/L
was chosen as the "optimal" concentration, and a temperature adjusted 2 mglL,
or 2 ppm, was chosen for the Maximum Contaminant Level for fluoride
concentration in the water.
US. Public Health Service
documents show that even
in 1991, non-fluoridated
communities were
already receiving equal
to and more than the
targeted fluoride dosage
of 1 mg per day.
Independent laboratory analysis now shows that fluoride is in most cola and
fruit juices at concentrations of 1 ppm and up; in well known cereals at 2 to 10
times the concentration intended for our water; in products using white grape
juice as sweetener or in children's juices at 3 to 1 ppm; and, because of
fluoride-based pesticide residue, on lettuce at 180 ppm and raisins (that we
know no child is going to scrub) at 55 ppm.
U.S. Public Health Service documents show that even in 1991, non-fluoridated
communities were already receiving equal to and more than the targeted fluoride
dosage of 1 mg per day. Fluoridated communities were receiving an estimated 3 to 1
times the "optimal" goal.
Result: in 1986-81,66.4% of all children in so-called" optimally" fluoridated communities
displayed the permanent visible signs that they have been overdosed (dental fluorosis).
(1986-81 survey, National Institute of Dental Research)
2 Adding fluoride to the water to achieve the so-called "optimal"
concentration mass medicates at a higher level than any doctor in the
country following the current recommendations for care can prescribe.
Although promoters of fluoridation often insinuate that children are deficient in
fluoride, 98% of Europe and our own continent's professional associations have seen
that adverse effects have gotten out of hand and have advised their professionals to
adjust for uncontrolled exposure.
In 1994, the American Dental Association Council on Scientific Mfairs and the American
Academy of Pediatrics, while segments of these same trade associations simultaneously
continued to lobby for fluoridation, created new policy recommendations for
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controlled-dose supplementation. which are intended to be the substitute for
fluoridated water in non fluoridated communities.
The new schedules indicate that mass medication, at the claimed "optimal" level of
fluoridation, grossly exceeds the dosage that a qualified professional could prescribe,
even after the professional's individual evaluation of a child for growth and
development, weight, total exposure to fluoride from all sources, and
individual susceptibility.
The.new schedules indicate
that mass medication, at the
claimed "optimal" level of
fluoridation, grossly exceeds
the dosage that a. qualified
professional could prescribe,
According to these new recommendations infants are to receive no
additional fluoride, no matter what the fluoride level in the water; and it is
not until a child reaches the age of 6 that the new prescription
recommendations ever reach the excessive dosage that is thrust upon a
child that consumes fluoridated tap water.
The Canadian Dental Association went even further, stating that fluoride's
effect on caries is topical, rather than systemic, and recommended that if a child
brushes his/her teeth twice a day with fluoridated toothpaste that they should have no
further exposure to fluoride even in a non fluoridated community.
"The level of fluoride incorporated into dental mineral by systemic ingestion is
insufficient to playa significant role in caries prevention." (Featherstone JD. Prevention
and reversal of dental caries: role of low level fluoride. Community Dent Oral Epidemiol
1999;27:31-40.
3 The hazardous waste substances used in 90% of fluoridation have never
been tested, either alone in distilled water. or in combination with other
chemicals and contaminants found in tap water.
The most common substances
now used for fluoridation are
hydrofluosilicic acid and sodium
silicofluoride, which are waste
products that are captured in
scrubber systems of the
phosphate fertilizer industry.
The most common substances now used for
fluoridation are hydrofluosilicic acid and sodium
silicofluoride, which are waste products that are
captured in scrubber systems of the phosphate
fertilizer industry. The resulting toxic waste can
not be diluted by 1 million or even 3 million or
10 million to 1 and dumped in the ocean or river
or landfill, nor allowed to escape into the air
because it would kill all the plants and animals
and people. And it can't be given away because it
would still be classified as a Class I toxic waste and have to be neutralized at the
highest rated hazardous waste facility at a cost of $1.40 per gallon, or more depending
on how much cadmium, lead, uranium, and arsenic are also present.
But, if destined for a water district that will pay $0.35 to $0.45 per gallon for
transportation, the 23% solution in industrial waste water is magically pronounced
benign and shipped. untreated. to be mixed into our water.
If it was not a hazardous waste, it could have been added to salt or some other
universally accessible food source, just like iodine is. more than fifty years ago. Each of
us would then be free to choose for ourselves.
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Citizens for Safe Drinking Water
1010 University Avenue # 52, San Diego, CA 92103
(800) 728-3833
greenieff@cox.net www.Keepers-of-the-Well.org
Request for Due Dilig~Dce -- Fluoridation 2003
For more than fifty years, decision makers charged with the responsibility of protecting the water
supply for entire communities have been confronted by advocates of fluoridation with assurances
that the public policy of mass medicating citizens with a substance that can not be removed by
simple filtration has been fully reviewed and all questions of safety and effectiveness resolved.
Once again we hear that poor children are not swallowing enough fluoride that promoters claim
would otherwise eliminate tooth decay, completely ignoring that fluoride is already present in
higher concentrations than fluoridated water in sodas, fruit juices, cereals, teas, and, because of
fluoride-based pesticide residues, on such produce as tomatoes, lettuce, potatoes, cabbage, and
raisins. In 1991, government documents reported that non-fluoridated communities already
receive the original goal of 1 milligram of fluoride a day, with fluoridated communities receiving
3 to 7 milligrams a day _ far exceeding the margin of safety, and causing permanent scarring of
the enamel of at least one tooth of 66.4% of children in fluoridated communities.
What the fluoride promoters will not reveal to their targeted legislators and City Council
Members, or even their unsuspecting well-intended supporters:
. The July 2000 peer-reviewed cover story of the Journal of the American Dental
Association (JADA) clarified for every dentist in America that ingestion of fluoride does not
provide any significant reduction in the incidence of tooth decay - that any beneficial dental
effect is as a result of topical application directly to the tooth;
. The August 17,2001 MMWR (CDC) report, despite its touting of fluoridation, included:
"The prevalence o( dental caries in a population is not inversely related to the concentration of
fluoride in enamel, and a higher concentration of enamel fluoride is not necessarily more
efficacious in preventing dental caries."
. The American Dental Association and American Academy of Pediatrics have revised
their recommendations for controlled-dose fluoride which restricts a doctor from prescribing
fluoride to a child of 6 months to 3 years of age to the amount found in one cup of fluoridated
water _ none to an infant _ meaning that, as a public policy, fluoridation mass medicates at
a higher expected dosage than a doCtor in a non-fluoridated community can prescribe;
. In a Congressional investigation by the House Committee on Science, the Environmental
Protection Agency, Center for Disease Control, National Sanitation. Foundation, and the Food
and Drug Administration, all replied that they have no scientific studies on the actual fluorlne-
bearing substances used in 90% of the nation's fluoridation programs.
The FDA states that fluoride is a regulated drug when used for the treatment or prevention of
disease, and that no fluoride substance intended to be ingested for the purpose of reducing tooth
decay has ever been approved for safety and effectiveness.
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~. On June 29, 2000, at the U.S. Senate Congressional Hearing on Arsenic, Radon, and
.. Fluoride, held by the subcommittee on Fisheries, Wildlife, and Water, J. William HiIZy, Ph.D.
testified on behalf of the union (that consists of and represents all of the toxicologists, biologists,
chemists, physicians, statisticians, epidemiologists, attorneys, engineers, scientists, and other
professionals at the U.S. Environmental Protection Agency, Washington, D.C.), calling for a
moratorium on all fluoridation. . ..
In his testimony to Congress, Hirzy cited scientific evidence the union of scientists have in their
possession, and court findings in three different states, whose conclusions have never been
overturned on the merits, that. found with reasonable certainty (Le. beyond speculation and guess)
and by preponderance of the evidence, including the testimony of experts learned in the field,
that fluoride in public water supplies causes or contributes to the cause of cancer, genetic
d8mage, intolerant reactions, chronic toxicity, dental fluorosis~ bone pathology and neurological
injury in humans, and that fluoride in public water supplies aggravates malnutrition, iodine
deficiencies, and other existing illnesses;
. Under duress from the Inspector General, in June 2001, an Environmental Assessment for
Proposed Water Fluoridation was redesigned by Pacific Western Technologies for Fort Detrick,
MD, home of the U.S. Army Medical Research and Materiel Command for the entire Army.
The revised Assessment evaluated the variable range in total exposure to fluoride from all food
sources; combined with the variable range of fluoride concentrations in water, and compared it to
the already-established EPA Reference Dose for Fluoride ofO.06mg1kg body weight/per day.
The Environmental Assessment concluded that, in the scenario with exposure to 0.7 parts per
million fluoride in the drinking water, combined with calculable other-than-water sources of
fluoride, significant percentages of children's age group 7 to 9 will receive a total dosage that
exceeds the U.S. EPA's Reference Dose (the point at which known risks increase); and describes
the problem for children aged 1 to ~ to be even more acute.
. Studies published in 1998, 1999, and 2000, illustrate why it is crucial that focus be placed
on the actual substances used for fluoridation. One study. reported that exposure to low levels of
aluminum fluoride delivered twice the amount of aluminum to the brain than concentrations of
aluminum fluoride 100 times the lower levels. At the same levels used to fluoridate our drinking
water, sodium fluoride caused excessive kidney dalJ1age and lesions in the brain similar to those
found in humans with Alzheimer's and other forms of dementia. Aluminum compounds are
commonly used as clarifying agents in tap water.
. A study sampling 280,000 children in Massachusetts, and another sampling 151,000
children in New York, reported a doubling of the risk of lead levels in children's blood rising
above the danger level of 10 micrograms per deciliter when the hazardous wastes from the
phosphate fertilizer industry are used for fluoridation, rather than sodium fluoride or no fluoride
at all.
The correlation with blood lead levels is especially serious because lead poisoning is associated
with higher rates of learning disabilities, hyperactivity, substance abuse, and crime.
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Once again citizens will have to rally to remind decision-makers of the precious nature of our
drinking water and ask that they perform the due diligence worthy of the modem day Keepers-
of-the- Well.
Documentation for all statements made he~iD can be aecessed at: Keepen-of-the-WelLorg
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UNITED STATES CODE
1994 EDITION
CON~AlNING THE GENERAL AND PERMANENT LAWS
OF THE UNITED STATES, IN FORCE
ON JANUARY 4, 1995
Prepared and publiahed UDder authority of Title 2, U.S. Code, SectioD 285b,
by the Office of the Law Rcmaicm COUD8tll of the HoUBtl of. RepreBeDtaUveB . .,
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VOLUME NINETEEN
TITLE 42-THE PUBLIC HEALTH AND WELFARE
111-300bbb
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UNITED STATES
GOVERNMENT PRINTlNG OFFICE
W ABHlNGTON : 1995
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Page 651
TITLE 42-THE PUBLIC HEALTH AND WELFARE
.
(10) National primary drinking water regula-
tions promulgated under this subsection (and
amendments thereto) shall take effect eighteen
months after the date of their promulgation.
Regulations under subsection (a) of this section
shall be superseded by regulations under this
$ubsectlon to the extent provldedby the regula-
tions under this subsection.
(1UNo national primary drinking water regu-
lation may require the addition of any sub-
stance for preventive health care purposes un-
related to contamination of drinking water.
(c) Secondary regulations; publication of propolletl
reaulatlons; promulgation; amendments
The Admlnlstrator shall publish proposed na-
tional .... secondary drlnklng water regulations
within 2'10 days after December 16, 19'14.
Within 90 days after publication of any such
regulation, he shall promulgate such regulation
with such modifications as he deems appropri-
ate. Regulations under this subsection may be
amended from time to time.
(d) ReaulatioDB;publlc hearinp; adminiltratlve con.
sultatloDB
Regulations under thlssection shall. be pre-
Icribed In accordance with section 553 of title 5
(relating to rulemA.1rlng), except that the Ad-
ministrator shall provide opportunity for public
hearing prior to promulgation of such regula-
tions. In proposing and promulgating regula-
tions under this section, the Administrator
shall consult with the Secretary and the Na-
tional Drlnldng Water Advisory Council.
(e) Science Adriaory Board comments
The Administrator shall request comments
from the Science Advisory Board (established
under the Environmental Research, Develop-
ment, and Demonstration Act of U~'I8)prior to
proposal of a maximum contaminant level goal
and national primary drinking water regula-
tion. The Board shall respond, as it deems ap-
propriate, within the time period applicable for
promulgation of the national. primary drinking
water standard concerned. This subsection
shall, under no circumstances, be used to delay
final promulgation of any national primary
drinking water standard.
(July I, 1944, ch. 3'13, title XIV, 11412, as added
Dec. 16, 19'14, Pub. L. 93-523, 12(a), 88 Stat.
1662; amended Nov. 16, 19'1'1, Pub. L. 95-190,
II 3(c), 12(a), 91 Stat. 1394, 1398; June 19, 1986,
Pub. L. 99-339, title I, 1101<aHc)(l), (d), (e),
100 Stat. 642-646.)
R_m:s m TExT
The Federal Insecticide. Fungicide, and Rodenticide
Act, referred to in subsec. (b)(3)(B). is act June 25,
1947. ch. 125, as amended generally by Pub. L. 92-516,
Oct. 21, 1972. 86 stat; 973, which is classified generally
to subehapter II <1138 et leq.) of chapter 8 of Title 7,
Agriculture. For. complete classification of this Act to
the Code, lee Short Title note set out under section
138 of Title '1 and Tablel.
The Environmental Research, Development, and
Demonstration Act of 1978, referred to in 8ubsec. (e),
probably means the Environmental Research, Devel-
opment, and Demonstration Authorization Act of 1978
which Is Pub. L. 95-155. Nov. 8,1977, 91 Stat. 1257. as
amended. Provisions of the Act eltablish1n&' the Sci-
ence Advisory Board are classified to section 4385 of
13_-1
this title. For complete cla.ssiflcatlon of. this Act to the
Code. Bee Tables.
AJlDDIIDft
1988-Subsec. (a). Pub. L. ~.9, 1101<a), amended
subsec. (a) generally. PrIor to amendment, aub8ec. (a)
read as follows: .
"(1) The Administrator 8hall publl8b proposed na-
tional interim pJ1mary ~ water I'eIUlatlcms
within 90 dQB after December 18, 197". WitbiD 180
days after December 18, 19'1", he 8haIl promulpte
such regulations with auch modifications .. he deema
appropriate. RelUlatlODl under this paragraph m&7 be
amended from time to time.
"(2) National interbnprlmarJ'~ water repJa-
tlons promulgated under paragraph (1) 8haIl protect
health to the .extent feasible, uaIDg tecbnolOU, treat-
ment technlqUell, and other meaDS, which .the Admin.
istrator determinell are generallJ available (~
costs Into consideration) on December 18, 19'1"-
"(3) Tbelnterlm pJ1mary regulatlODl tint promul-
gated under paragraph (1) IIball tate effect elahteen
months after the date of their promulgation."
Subsec. (bX1). Pub. L. 99-339, 1101Cb), aubetltuted
provllllons establ18hlng Btandard aettlna 8chedu1ee and
deadllnell for provIIIIODIrelatlDc to estabUsbment of
maximum cont.Alntnant levu. and a list of contami-
nants with advene effect but of undetermined 1eveJa.
Subsec. (bX2). Pub. L. ~39, 1101<b), aubetltuted
provllllons authorizing the AdmInIstrator to 8Ubstltute
contsnnlnants for those referred to In par. (1) and to
supply a list of the cont.amtn....ts propoeed for aubetl-
tutlon, with the decl8lon of the AdmInIstrator to I'eIU-
late such cont......ln....t not subject to JudleIaI review,
for provlBlons which authorized. the Adm1niatrator to
publish in the Federal Relister. propoeed revi8ecI .....
tlonal Interim primary drIDldDc water I'eI'UlatlODl and
180 daYII after the date of such proposed I'eIUlatlODl
to promulgate 8uch reviaed relUlatlons with mocUflca..
tlon as deemed appropriate.
Sub8ec. (bX3). Pub. L. 99-339, 1101<b), substituted
provllllons directing the Adm1DI8trator to publish max-
imum contaminant level goaJs and promulgate nation-
al primary drInldnI water relUlatlons for contaml"
nants. other than specified In par, (1) or (2), whlch.
may have an adverse. effect on health and are mown
orantlclpated to occur In public water 8)'1ltem8, to __
tablish an a.dvisor7 working croup to aid In establl8b-
Inc a list of such cont.unln....ts. and to publiab, within
a specified. time, both proposed and final IIoala and
regulations for Provl81OD1 which required that reviled
national primary dr1nkInC water relUlatlons specIf, .
maximum contaminant level or requlretbe use of
treatment technlquell for each CODt.arnln....t, which
level or technique W8B to be B8 clOle to the. recom-
mended level or technique as feB8lble, and defined the
term "feB8lble".
Sublec. (b)(4) to (11). Pub. L. 99-339, 1101<b), (cX1),
(d). added pars. (4) to (8), redesignated former pars.
(4) to (8) as pars. (9) to (11), rellpectlvel1. In par. (9)
subltltuted "National" for "Revised National" and In-
serted provision that review include anal,1la, and pub-
lication in Federal Recister. of innovations In technol-
ogy, treatment technlquell or other actIvitletl 0CCIU'I'Inc
during previouS three years and their feas1bWty, and
in par. (10). lubltltuted "National" for "RevIsed Na-
tional".
Subsec. (e). Pub. L. 99-339, 1101(e), amended sub8ec.
(e) generally,8ubstltutlng provisions which relate to
the requelt by the AdmU1Istrator of comments by the
Science Advisory Board prior to proposal ofa muI-
mum contaminant level coal and national primary
drlnkinc water regulation for provl81ons which related
to study by the National Academy of Sclenca to de-
termine the maximum contaminant levu, report to
Congress, and fund1ng therefor.
1977-Bubsec. (e)(2). Pub. L. 95,-190 Inserted provi-
sions relating to revisions of the required report and
cl. (0).
.
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PREFACE
Drinking Water Public Health Goal of the
Office of Environmental Health H8zard.Assessment
This Public HcaIth GoaJ (pHG) technical support document provides iDfoimatiou on health effects
from cootaminants in drinking water. The PHG dcscn"bcs concentrations of cootaminants. at which
adverse health effects would DOt be expccu:d to occur, even over a lifetime of exposIR. PHOs arc
devdoped for cbcmical contaminants based on the best available toxicological data in thescieotific
'literature. These documents and the analyses contained in them provide estimates of the levels of ' ,
cootaminants in drinking water that would pose DO significant health risk to individuals consumiDg,
the water on a daily.basis over a lifetime.
The California Safe Drinking Water Act of 1996 (amended Health and Safety Code, Section
116365) requires the Office of Environmental HeaI~ Hazard Assessment (OEHHA) to adopt
PHGs for cootaminants in drinking water based exclusively on public health considerations. The
Act requires OEHHA to adopt PHGs that meet the following criteria:
1. PHGs for acutcJytoxic substances shall be set at Jevels at which scientific evidence indicates
that DO known or anticipated adverse effects on health will occur, pJus an adequate margin-of-
safety.
2. PHGs for carcinogens or other substances which can cause chronic dis~e shall be based
soleJy on health effects without regard to cost impacts and sha)) be set at Jevels which OEHHA
has dctennincd do not pose any significant risk to health.
3. To the extent the information is availabJe, OEImA sha)) consider possibJe synergistic effects
resulting from exposure to two Or more contaminants.
4. OEHHA sha)) consider the existence of groups in the population that arc more susceptibJeto
adverse effects of the contaminants than a DOnna) healthy adult.
S. OEHHA shall consider the contaminant exposure and body burden. Jevels that alter
physiological function or structure in a manner that may significantly increase the risk of
illness.
6. In cases of scientific ambiguity,OEHHA shall use criteria most protective of pubJic health and
shall incorporate uncertainty factors of noncarcinogenic substances for which scientific
research indicates a safe dose-response threshoJd.
7. Incases where scientific evidence demonstrates that a safe dose-response threshold for a
contaminant exists, then the PHG should be set at that threshold.
8. The PHG may be set at zero if necessary to satisfy the requirements listed above.
9. OEHHA shall consider exposure to contaminants in media other than drinking water, including
food and air and the resulting body burden.
10. PHGs adopted by OEHHA shaU be reviewed periodicalJy and revised as neef'9saty based on
the availability of DeW ~f!nt1fic data.
, ,\
PHGs adopted by OEHHAarc for use by the California Department ofHca1th Services (DHS) in
establishing primary drinking watersrandards (State Maximwn ContaininantLevels, or MCLs).
Whereas. PHGs are to be based solely on scientific and public health considerations without regard
to economic cost considerations, drinking water standards adopted by.DHS are to consider
economic &c:tors and technical feasibility. For this reason PHGs are only one part,ofthe
Fluoride in Drinking Water iii December 1997
California Public Health Goal (PHG)
~ '
information used by DHS for establishing drinking water standards. PHGs cstablishedby
OEIDiA exert no regulatory burden and represent only non-mandatory Soals. By federal Jaw,
MCLs established by DHS must be at least as stringent as the federal MCL if one exists.
PHG docume:ntsare developed for technical assistance toDHS, but may also benefit fedcla1, state
and local public health officials. While the PHGs are calculated for sinsle chemicals only, they
may, iftbc infonnation is.available, address hazards associated with the interactions of
contaminants in mixtures. Further,PHGs are derived for drinking water ODIyand are ..aOt to be
utilized astarSet levels for the contamination of enviromnental water$ where additional ccmcems of
bioaccumulation in. fish and .shellfish may pertain. Often environmental water c:ontamiDaDt criteria
are more strinsent than drinking water PHGs, to account for human exposures to a sinsle chemical
in multiple environmental media 8nd frombioconcentration by plants aud animals in the food
chain.
F:1uoride in Drinkinl Water
California Public Health Goal (pHG)
iv
December 1997
~
.
4.
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.
Fluoride is already in our food and beverages.
Intended goal of fluoridation: Delivery of 1 milligram (mg) fluoride per day
Intended range of concentration in fluoridated water: 0.7 to 1.2 ppm
{Note: 1 mg (milligram)fLiter = Ippm (parts per million)}
Fluoride Concentration, by specific
independent analysis:
(Individual samples will vary)
Maximum allowable pesticide
residue levels:
Cryolite (sodium aluminum fluoride)
Coca Cola Classic..........................0.98 ppm
, \
Diet Coke .......................,..............1.12 ppm
Sprite....,..................................... ....0.72 ppm
Lucerne 2% Milk ...........................0.72 ,ppm
Minute Maid orange juice ............0.98 ppm
Gerber Graduate Berry Juice .........3.0 ppm
Gerber White Grape Juice.............6.8 ppm
Welch's White Grape Juice
(concentrate).. ..... ...................... ......1.8 ppm
Hawaiian Punch...... .............. ....... .0.85 ppm
Fruit Loops.......... .... ......... .... ;.... ..... .2.1 ppm
General Mill's Wheaties................l0.1 ppm
Kellogg's Shredded Wheat.............9.4 ppm
Post's GrapeNuts cereal.................6.4 ppm
Cabbage............................ .......... .45.00 ppm
Citrus fruits ..................................95.00 ppm
Collards................................ ....... .35.00 ppm
Eggplant........ ..... .............. .......... ..30.00 ppm
Lettuce, head.............................180.00 ppm
Lettuce, leaf..... ........................ ....40.00 ppm
Peaches..... ..... ........ ......... ............ .10.00 ppm
Potatoes, intemal..........................2.00 ppm
Potatoes, wastes and skin ..........22.00 ppm
Raisins............................. ........... ..55.00ppm
Tomatoes.. ................... ............ ....30.00 ppm
Tomato paste. .... ......................... .45.00 ppm
A bowl of Wheaties, a glass of milk,
and a Coke or orange juice delivers
twice the fluoride salesman's
daily goal of fluoridation.
ITEM flUORIDE PPM DOSE (MG)
12 oz. Coke .98 .353
8 oz. 2% Milk .72 .173
Wheaties 10 1.80
TOTAL DOSE 2.326
Exceeds 2330/0
1.0 mg. 1.0
Fluoridation Goal
There is no deficiency of exposure to fluoride for any segment of our population.
. Citizens fur Safe Drinking Water · Jeff Green, Director · 1.800.728.3833
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. Food and Beverage Sources of Fluoride Exposure - Compiled by
Maureen Jones and David C Kennedy, DDS, Past President International Academy of Ora!
Medicine and Toxicology. 3243'Madrid St., San Diego, CA 92110. (800) 728-3833.
, '
Stannard JG et al. Fluoride levels and fluorides contamination of fruit juices. Journal of
Clinical Pediatric Dentistry; 16:38-40, 1991. Forty-three ready-to-drink fruit juices were examined
for fluoride ion concentration. The fluoride levels of the juices ranged from 0.15 to 6.80 (Gerber
White Grape juice). It was found that 42% of the samples had more than 1 ppm of fluoride. Given
that increasing numbers of people are consuming beverages instead of water, fluoride
supplementation should not be based solely upon the concentration of the drinking water, but
should also consider the amount of different beverages consumed and their fluoride content.
Kiritsy, MC et al. Assessing fluoride concentrations of juices and juice-flavored drinks. Journal
AmericanDental Association; 127: 895-901, 1996. 'In this study, the authors analyzed 532 juices
and juice drinks for p,uoride. Fluoride ion concentration ranged from 0.02 to 2.,80 parts per
million. Children's ingestion of fluoride from juices and juice-flavored drinks can be substantial
and a factor in the development of fluorosis. '
Beilman, JR el aI. Fluoride concentrations of infant foods. Journal American Dental Association;
128: 857-63, 1997. In this study, the authors analyzed the fluoride conCentration of238
commercially available infant foods. Fluoride concentrations ranged from 0.01 to 8.38 micrograms
of fluoride per gram, (ppm) with the highest fluoride concentrations found in infant foods
containing chicken.
Beilman, JR el 81. Assessing fluoride levels of carbonated soft drinks. Journal American Dental
Association;, 130: 1593-99, 1999. The authors examined the fluoride concentrations of332 soft
drinks. The fluoride levels of the products ranged from 0.02 to 1.28 ppm, with a mean level of
0.72. Fluoride levels exceeded 0.60 ppm for 71 percent of the products.
Burgstahler, A Wet at Fluoride in California wines and raisins. 'Fluoride; 30: 142-146, 1997.
The water-extractable F content offive brands of California raisins varied from 0.83 to 5.20 ppm
(mean 2.71 ppm). Elevated F levels inthese wines and raisins appear to result from pesticide use of
cryolite (Na3AlF6) in the vineyards. '
Sequoia Analytical, Redwood City, CA, May 1998.
Dole Pineapple juice . . . . ... . . . . . .. 0.78 ppm
Lucerne 2% milk. . .'. . . . . . . . . . . . .. 0.72
Snapple . . . . . . . . . . . . . . . . . . . . . . . . . 0.29
Coka Cola Classic. . . . . . . . . . . . . ; .. 0.82
Hansens Soda. . . . . . . . . . . . . . . . . '. . . .0.45
Minute Maid juice. . . . . . . .. . . . . . . . . 1.20
Capri Sun juice. . . . . . . . . . . . . . . . . . . 0.37
Gerber Strawbeny juice. . . . . . . . . . . . .1.80
Horizon milk (organic). . . . . . . . . . . . .0.22
Sunny Delight. . . . . . . . . . . . . . . . . . . . .0.31
Pepsi. ., . . . . . . . . . . . . . . . . . . . . . . . . .0.37
oKnudson Recharge. . . . . . . . . . . . . . . . . 0.28'
Gerber White Grape. . . . . . . . . . . . . .. 3.50
. '
Expert Chemical Analysis, Inc., San Diego CA, June, 1998.
Gerber Graduates Berry Punch. . . . . .. 3.00 ppm
Coca Cola Classic. . . . . . . . . . . . . . . . .. 0.98
Minute Maid Premium Orange juice. .. 0.98
Kellogs Fruit Loops cereal. . . . . . .. . . . 2.1 mglkilogram
.
Jupiter Environmental Laboratories, Inc., Jupiter, FI, June, 1998.
Gerber White Grape Juice. . . . . . . . . . . . .3.50 ppm
Gatorade Punch Concentrate. . . . . . . . .. 0.44
Diet Coke. . . . . . . . . . . . . . . . . . . . . . . . . 1.12
Lipton Ice Tea . . . . . . ... . . . . . . . . . . . . .0.56
Sprite. . . . . . . . . . . . . . . . . . . . . . . . . . . . ,0.73
Hawaiian Punch. . . . . . . . . . . . . . . . . . .. .0.85
Publix Orange Juice. . . . . . . . . .. . . . . . . .0.79
Analytica Alaska Inc., Juneau, AK. September, 1998.
Welch'sWhite Grape Juice (conc.). .. . . .1.80 ppm
Coca Cola Classic .. . . : . . . . . . . . . . . . .. 0.82
Northwest Testing Laboratories, Portland, OR, July 1960.
Post's Grape Nuts cereal. . . . . . . . . . . .. .6.40 ppm
Kellogg's Shredded Wheat. . . . . . . . .'. . . 9.40
General Mill's Wbeaties. . . . . . . . . . . . . 10.10
.
Environmental Protection Agency (EPA) Pesticide Tolerance for residues of the insecticidal
fluorine compounds cryolite and/or syn~hetic cryolite (sodium aluminum fluoride). Effective
Dec. 5, 1997 to Nov. 21,2001.
Potatoes, on or in. . . . . . . . . . . . . . . . . . . . . 2.00 ppm
Processed potato waste for animal feed. . .22.00
Aug. 1997, proposed tolerances for residues of cryolite and/or synthetic cryolite:
Cabbage. . . . . . . . . . . . . . . . . . . . . . . . . . ,45.00 ppm
Citrus fruits. . . . . . . . . . . . . . . . . . . . . . . .95.00
Collards. . . . . . . . . . . . . . . . . . . . . . . . . . .35.00
Eggplant. . . . . . . . . . . . . . . . . . . . . . . . . . 30.00
Lettuce, head. . . . . . . . . . . . . . . . . . . . . . 180.00
Lettuce, leaf. . . . . . . . . . . . .. . . . . . . . .'. . 40.00
Peaches. . . . . . . . . . . . . . . . . . . . . . . . . . . .10.00
'Raisins. . . . . . . . . . . . . . . . . . . . . . . , . . . . 55.00
Tomatoes. . . . . . . . .. . . . . . . . . . . . . . . . . 30.00
Tomato paste. . .. . . . . . . . . . . . . . . . . .. . 45.00
.
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Pacific Western Technologies, Ltd
8610 N. New Braunfels, Suite 600
San Antonio, TX 78217-6359
June 1,2001
Mr. Gilbert Gonzalez
U.S. Anny Medical Command
ATTN: MCFA-ElBldg 2792
. 2050 Worth Rd., Suite 22
Fort Sam Houston, TX 78234-6022
REF: Environmental Assessment for Proposed Water Fluoridation - Fort Detrick, MD
Dear Mr. Gonzalez:
As we near completion of the draft EA regarding the proposed water fluoridation for Fort Detrick we
have considered possible control settings for the fluoridation equipment. The analysis by Dr. John Beaver
consists 'of an accounting of fluoride intake by residents from food, beverages, and dental hygiene
practices, in addition to fluorides in the drinking water for various scenarios. His calculations included
the "halo effect" of dietary fluoride intake from imported food and beverage items, prepared (outside
Fort Detrick) using water from a fluoridated public water supply.
In order to protect the resident soldier population, the proposed fluoridation equipment at Fort Detrick
should be set for a concentration of approximately 0.7 mgIL. This concentration is well within the. US
EPA's 4.0 mg/L Maximum Contaminant Level Goal (MCLG) and 2.0 mgIL Secondary Maximum
Contaminant Level for fluorides in drinking water supplies. The calculations indicate that the 0.7 mgIL
setting would result in total fluoride intakes for the soldier population (age groups 16-19 and 20-60) that
will be well within the US EPA's Reference Dose (RID) of 60 micrograms of fluorides per kilogram of
body weight per day (ug/kg-day) for all but a few individuals with exceptionally high fluoride intakes.
The RID represents a threshold, below which no adverse effects (in this case, dental fluorosis) have been
observed.
However, findings from the research s~ggest that using this set point at Fort Detrick may result in
problems for younger members of the Fort Detrick resident population. John's calculations for fluoride
intake by age group 7-9 shows 40 percent of this age group exceeding the RID. The problem would be
even more acute for age group 1-3.
I have' attached the supporting infonnation regarding the impact of the "halo effect" for the various age
groups. I am asking for your review and direction with respect to addressing the impact of the
fluoridation levels relating to the lower age groups. Please contact either me or Dr. John Beaver at (216)
751-1326 with any questions regarding the attached materials. Upon resolution of this issue we are
prepared to quickly wrap-up the revisions to the EA and issue a draft for your final review.
Sincerely,
George P. Rasmussen
George P. Rasmussen, P.E.
Vice President
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Scenario 1
0.9 mg F/L tapwater
Median Fluoride Intake, ug Flkg body wt. - day
Age group 1 - 3 yrs 7 - 10 yrs 16-19 yrs
Food 14 10 9
Dental Hygiene 27 15 10
Tapwater 41 24 15
Imported beverages 12 9 5
Total 95 58 39
e~
5% Fluoride Intake, ug Flkg body wt. - day
Age group 1 - 3 yrs 7 - 10 yrs
Food 14 10
Dental Hygiene 15 7
Tapwater 12 7
Imported beverages 7 5
Total 48 28
25% Fluorid~ Intake, ug F/kg body wt. - day
Age group
Food
Dental Hygiene
Tapwater
Imported beverages
Total
1 - 3 yrs
14
21
27
10
72
7 - 10 yrs
10
11
16
7
44
20-64 yrs
8
10
18
3
40
16 - 19 yrs 20-64 yrs
9 8
3 3
4 6
2 2
19 19
16 -19 yrs 20-64 yrs
9 8
7 6
10 12
4 3
29 30
75% Fluoride Intake, ug Flkg body wt. - day
Age group 1 - 3 yrs 7 -10 yrs 1e - 19 yrs 20-64 yrs
Food 14 10 9 8
Dental Hygiene 35 21 14 13
T apwater 60 36 22 25
Imported beverages 16 12 6 4
Total 125 79 50 51
e~
95% Fluoride Intake, ug F/kg body wt. - day
Age group 1 - 3 yrs 7 -10 yrs 16 - 19 yrs 20-64 yrs
Food 14 10 9 8
Dental Hygiene 42 29 17 16
T apwater 102 55 36 40
Imported beverages 23 18 8 6
Total 181 112 70 71
Total Fluoride Intake, ug F/kg body wt. - day 0.9
1 - 3 yrs 7 - 10 yrs 16 - 19 yrs 20-64 yrs Ref. Dose
5% 48 28 19 19
25% 72 44 29 30
50% 95 58 39 40
75% 125 79 50 51
95% 181 112 70 71
~ 00
100% 60
et
.
.200
180
~ 160
"1i'
~ 140
In
C)
~ 120
--
LL
cj'
:1 100
..
CD
.1 ~
S 80
c
-
CD 60
"C
.-
~
0
:1 40
-
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.~
Scenario 1
0.9 mg F/L
20
o
0%
200/0
400/0
60010
800/0
1000/0
Population subgroup
-+- 1 - 3 yrs --- 7 - 10 yrs
---''-- 20-64 yrs -Ref.Dose
16 - 19 yrs
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'Scenario 2
0.7 mg FIL tapwater
Median Fluoride Intake, ug Flkg body wt. - day
Age group 1- 3 yrs 7 -10yrs 16-19 yrs
Food 14 10 9
Dental Hygiene 27 15 10
Tapwater 32 19 12
Imported beverages 12 9 5
Total 86 53 36
'.
5% Fluoride Intake, ug Flkg body wt. . day
Age group 1 - 3 yrs 7 -10 yrs 16 -19 yrs
Food 14 10 9
Dental Hygiene 15 7 3
Tapwater 9 6 3
Imported beverages 7 5 2
Total 45 27 18
25% Fluoride Intake, ug Flkg body wt. - day
Age group 1 - 3 yrs 7 -10 yrs 16 - 19 yrs
Food 14 10 9
Dental Hygiene 21 11 7
Tapwater 21 12 8
Imported beverages 10 7 4
Total 66 40 27
75% Fluoride Intake, ug Flkg body wt. - day
Age group 1- 3 yrs 7 -10 yrs
Food 14 10
Dental Hygiene 35 21
Tapwater 47 28
Imported beverages 16 12
Total 112 71
16- 19 yrs
9
14
17
6
45
95% Fluoride Intake, ug Flkg body wt. - day
Age group 1 - 3 yrs 7 -10 yrs 16 - 19 yrs
Food 14 10 9
Dental Hygiene 42 29 17
Tapwater 79 43 28
Imported beverages 23 18 8
Total 158 100 62
Total Fluoride Intake, ug Flkg body wt. - day
1 - 3 yrs 7 - 10 yrs 16 - 19 yrs
45 27 18
66 40 27
86 53 36
112 71 45
158 100 62
5%
25%
50%
75%
95%
0%
100%
20-64 yrs
8
10
14
3
36
20-64 yrs
8
3
5
2
18
20-64 yrs
8
6
10
3
27
20-64 yrs
8
13
20
4
45
20-64 yrs
8
16
31
6
62
0.7
20-64 yrs Ref.Dose
18
27
36
45
62
60
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0.7 mg F/L
20
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400/0
600/0
800/0
1000/0
Population subgroup
-+- 1 - 3 yrs --- 7 - 10 yrs
~~ 20-64 yrs -Ref.Dose
16 - 19 yrs
Scenario 3
. . 0.5 mg F/L tapwater
.~ Median Fluoride Intake, ug Flkg body wt. -day
Age group 1 - 3 yrs 7 - 10 yrs 16-19 yrs 20-64 yrs
Food 14 10 9 8
Dental Hygiene 27 15 10 10
T apwater 23 13 9 10
Imported beverages 12 9 5 3
Total 76 47 32 31
5% Fluoride Intake, ug Flkg body wt. - day
Age group 1 - 3 yrs 7 - 10 yrs 16-19yrs 20-64 yrs
Food 14 10 9 8
Dental Hygiene 15 7 3 3
T apwater 7 4 2 3
Imported beverages 7 5 2 2
Total 43 25 17 16
25% Fluoride Intake, ug F/kg body wt. - day
Age group 1 - 3 yrs 7-10yrs 16-19yrs 20-64 yrs
Food 14 10 9 8
Dental Hygiene 21 11 7 6
T apwater 15 9 5 7
Imported beverages 10 7 4 3
Total 60 36 25 24
.1 75% Fluoride Intake, ug F/kg bodywt. - day
Age group 1-3yrs 7-10yrs 16-19yrs 20-64 yrs
Food 14 10 9 8
Dental Hygiene 35 21 14 13
T apwater 34 20 12 14
Imported beverages 16 12 6 4
Total 98 63 40 40
95% Fluoride Intake, ug F/kg body wt. - day
Age group 1 - 3 yrs 7-10yrs 16-19yrs 20-64 yrs
Food 14 10 9 8
Dental Hygiene 42 29 17 16
T apwater 56 31 20 22
Imported beverages 23 18 8 6
Total 136 88 54 53
Total Fluoride Intake, ug F/kg body wt - day 0.5
Percentile/Age Group 1-3yrs 7-10yrs 16-19yrs 20-64 yrs Ref. Dose
5% 43 25 17 16
25% 60 36 25 24
50% 76 47 32 31
75% 98 63 40 40
. 95% 136 88 54 53
0% 60
100% 60
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---,~~ 20-64 yrs - Ref. Dose
16-19yrs
.
Fluoride Intake,
mg F/kg BW-day
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. .
..~ FLUORIDES, HYDROGEN FLUORIDE, AND FLUORINE
.~
.~
A Toxicological Profile by the U.S. Dept. of Health and Human Services, Public Health
Service, Agency for Toxic Substances and Disease Registry (ATSDR) TP - 91/17, Pages
3-4, Section 1.2, Paragraph 7 (Public Health Statement), April 1993.
HOW MIGHT I BE EXPOSED TO FLUORINE. HYDROGEN FLUORIDE. OR
FLUORIDES?
To prevent dental decay (caries), fluorides are sometimes added to drinking water to
achieve levels of about 1 ppm. You may also come in contact with fluorides from using
household items. Most of these are dental products, such as toothpastes, fluoride gels,
and fluoride rinses. If you swallow the treated water, or these products, you will be
exposed to fluoride. Swallowing toothpaste can account for a large percentage of the
fluoride to which a small child might be exposed. Certain medicines used to treat some
skin diseases and cancer contain fluorides, and using them also increases exposure.
Skin contact with products such as lubricants and oils containing fluorides or
hydrofluoric acid may also increase your exposure. The average daily fluoride intake
from food and water is estimated to be about 1 milligram (mg) if you have water that is
not artificially fluoridated, and about 2.7 mg if you have fluoridated water.
.
.~
.~
. .
DENTAL FLUOROSIS CLASSIFICATION BY H.T. DEAN. 1942a
CLASSIFICA T10N
CRITERIA
Normal
The enamel represents the usual tranSlucent semivitrifonn type of strUcture. The
surface is smooth, glossy, and usually of a pale cr.eamy while color.
Very Mild
Small, opaque. paper while areas scanered irregularly over the tooth but not '
involving as much as 25 percent of the tooth surface. Frequently included in this ."
classification are teeth showing no more than about 1-2 mm of white opacity at
the tip of the s~mmit of the cusps of the bicuspids or second molars. '
Mild
The white opaque aieas in the ,enamel of the teeth are more extensive but do not
involve as much as SO percent of the tooth.
Moderate
All enamel surfaces of the teeth are affected. and the surfaces subject to attrition
show wear. Brown stain is frequently a disfiguring feature.
Severe
All enamel surfaces are affected and hypoplasia is so marked that the general
fonn of the looth may be affected. TIle major diagnostic sign of this
classification is discrete or confluent pining. . Brown stains are widespread and"
tee.th often present a corroded-like appeBJ:ance.
"Dean H.T. 1942. The Investigation of physiological effects by ,\he epidemiological melhod. In: MoullOll FR. ed. Auorine and
denw health. WashinglOn. DC: American Association for &he Advancement of Science. PubUcaDon No. 19. pp.13-31.
REVIEW OF FLUORIDE BENEFITS AND RISKS
PUBUC HEAL1H SERVICE
DEPARTMENT OF HEAL11l AND HUMAN SERVICES
FEBRUARY 1991
B-2
Dental Fluorosis
Diagnosis and Classification: .
No fluorosis assessment is made for deciduous teeth, permanent teeth not in full eruption, or teeth in which
more than one-half of the visible swface is obscured by a restoration, caries, or an orthodontic appliance.
These tooth spaces will be excluded.
ClassiflcatioD and Scoring:
The most commonly used system for clinically classifying and scoring dental fluorosis is the system
described by Dean in 1942. In Dean's system, each tooth is examined and assigned to one of six categories
according to its degree of fluorosis.' Qassification of a person is based on the two teeth most affected by
fluorosis. lfthe two teeth are not equally affected, theclassificatioD given is that of the less involved tooth.
Oral Health of United StOles Children. National and Regional Findings.
The National Survey of Dental Caries in U.S. School Children: 1986-87.
U.S. Department of Health and Human Services.
. .
INTERVENTION: flUORIDE SUPPLEMENTATION
.
INDICATIONS: Children 6 months to 16 years of age living in areas with lEissthan
optimally fluoridated water, for example, home or "primary" water supply
is fluoride deficient. , ,
ADA Council on Scientific Affairs Recommendations, new dosage schedule approved April 1994:
AGE
FLUORIDE ION LEVEL IN DRINKING WATER (pprn)*
<0.3 ppm
0.3-0.6 ppm
>0.6 ppm
Birth-
6 months
None
None
None
6 months-
3 years
None
None
3-6 years
0.50 mg/day
0.25 mg/day
None
6-16 years
1.0 mg/day
0.50 mg/day
None
· 1.0 ppm = 1 mglliter
t 2.2 mg sodium fluoride contains 1 .mg fluoride ion.
ADVANTAGES: Permits early exposure, which maximizes protection. Fluoride supplements are
sold in two forms: drops for infants age 6 months and 'up, and chewable tablets for
children and adolescents. Systemic and topical benefits when chewed, swished
and swallowed. Caries protection from 6 months of age when used as
recommended.
.
LIMITATIONS: All sources of fluoride must be evaluated with a thorough fluoride history. If
fluoride level is unknown, drinking water must be tested for fluoride content
before supplements are prescribed. For testing of fluoride content, contact the
local or state health department. Requires long-term compliance on a daily basis.
Ingestion of higher than recommended levels of fluoride by children has been
associated with an increase in mild dental fluorosis in developing, uneropted
teeth. Patient exposure to multiple water sources can make proper prescribing
complex.
CONSIDERATIONS:
TOOTH: Caries reduction benefits must be balanced with risk for mild and very mild
fluorosis.
PATIENT: Home water filtration systems may remove fluoride. therefore. treated water
should be tested. Other sources of fluoride need to be determined, including
fluoride prescribed by a physician. (Refer to Figure 5.)
REFERENCES: American Dental Association, Council on Scientific Affairs, Association Report on
Dietary Fluoride Supplements. JADA 1995 (In press).
.
JADA. \'o\. l:lti. June 1995 1908
.~
.~
.~
. .
AMERICAN ACADEMY OF PEDIATRICS
Fl\loride Supplementation for Children: Interim Policy Recommendations '
Committee on Nutrition
The Committee on Nutrition of the American
Academy of Pediatrics (AAP) last issued a statement
in. 1986 on the topic of fluoride supplementation for
children. The recommendations made at that time
recently have been r~as~ssed because of what s~n,u;
to be an increased mCldence of dental fluoroslS m
children living in the United States. Dental fluorosis
appears durin9 to?th f~rmatio~ and is caused by
excessive fluonde lIlgestion, which leads to enamel
protein retention, hypomineralization of the dental
enamel and dentin, and disruption of crystal forma-
tion. The effect is cosmetic only, ranging from barely
perceptible white striations or specks. to confluent
areas of pitting or brownish gray staining. Teeth
affected by fluorosis seem to continue to be resistant
to dental carieS.
The main sources of fluoride include fluoridated ,
water foods or drinks reconstituted or prepared
with fluoridated water, dentifrices, and fluoride sup-
plements. Water is not fluoridated toa uniform level
throughout the United States, and young children
ingest significant but variable amounts of fluoride
while brushing their teeth with fluoride-containing
toothpaste. Because both of these sources.of fluoride
are difficult to control, attention has been directed
again at the dosage of fluoride supplements to
attempt to prevent dental fluorosis.
In January 1994, a Dietary Fluoride Workshop
sponsored by the American Dental Ass~ciation was
convened to address the issue of dental fluorosis.
Although children can receive su~t:W amounts
of fluoride from beverages and .dentifrices, the ex-
perts at this workshop thought the only Source of
fluoride that could be easily altered was the supple-
ment prescribed by physicians and dentists. The par-
ticipants at the workshop recommended the sched-
ule for fluoride supplementation given in the Table.
These recoJIlIIlendations for fluoride supplemen-
The recoD'\ll1endations in this statement do not indicate an exduslw c:oune
of treabnent ,or procedllR to be followed. Variations, taking into account
individual c:in:uJnstaIICI, IIIlIY be appropriate.
PEDIATRlCS (ISSN 003] 4lllIS). Cop)'ri8ht e ]995 by the'American Acad-
t!DIY of Pediatricl.
TABLE. Fluoride Supplementation"
Age Water Fluoride Content (in ppm)
<0.3 0.3-0.6 >0.6
Birth..{i mo 0 0 0
6 m0-3 y 025 0 0
~ Y 0.50 0.25 0
6-16 Y 1.00 0.50 0
. Fluoride dally doses are given in milligrams.
tation represent a modification of those adopted in
19791 and reaffirmed in 1986.2 Fluoride supplemen-
tation is no longer recommended from birth, and'
doses have been decreased during the first 6 years of
life. The level of water fluoride content when sup-
plements are not needed has been lowered from 0.7
to 0.6 ppm. Recently the American Dental Associa-
tion Council on Dental Therapeutics affirmed the
recommendations adopted at the workshop. A coun-
cil report of the workshop will appear in a future
issue of the ]ounuzl of tht American Dentlll Association,
and the proceedings will be published in the ]ounuzl
of Public Health Dentistry. The AAP concurs with
these dosage recommendations, and its Committee
on Nutrition is proceeding with a'complete revision
of the 1986 AAP policy statement entitled "Fluoride
Supplementation." These recommendations super-
sede those contained in the 1986 statement and
republished in the 1993 AAP Peditltric Nutrition
Handbook.
COMMITI'EE ON NtTl'JUTJON, 199410 1995
William J. Klish, MD, Chairperson
Susan S. Balcer, MD
Carlos A. Flores, MD
Michael J<. Georgieff, MD
Alan M. Lake,MD
Rudolph 1.. 1...eJ."be1, MD
John N. Udall, MD
REFERENCES
1. American Acadt!DIY of Pediatrics, Committee on Nubition. Fluoride
supplementation: revised dosage 1IChedule. P.itatrit:s. 1979;63:150-152
2. American Academy of Pediatrics, Committee on Nubition. Fluoride
supp1ementation. P.itltrits. 1~:7S8-761
e'
e~
e~
. .
.,
Dental Fluorosis Prevalence in
15,500D.S. schoolchildren aged 7~17
with lifetime residence in
fluoridated area:
One tooth effected.............. .36.5%
Two teeth or more effected.....29.9%
Total with fluorosis..... .66.4%
, .
Journal of Public Health Dentistry
Vol. 57; No.3, Summer 1997.
.
.
.
136
Journal of Public Health Dentistry
Dental Caries and Dental Fluorosis at Varying Water
Fluoride Concentrations
Keith E. Heller, DDS, DrPH; Stephen A. Eklund, DDS, MHSA, DrPH; Brian A. Burt, MPH, PhD
Abstract
. Objectives: The purpose of this study was to investigate the relationships
between caries experience and dental fluorosis at different fluoride concentrations
in. drinking water. The impact of other fluoride products also was assessed.
Methods: This.stud'( uSl3ddata from the 1986-87 National SuNev of US SchoOl
Children. Fluoride levels of school water were used as an indicator of the children's
water fluoride exposure. The use of fluoride drops, tablets, professional fluoride
treatments, and school fluoride rifl~es w'!re ascertained from caregiver question-
n~ires.On/v childrert with, a sinq/,! continYousresid,!nce (n= 18,755) were includec
kLthis analysis. Results: the sharpest deClines in dfs and DMFS were associat-
ed with increases in water fluoride levels between 0 and 0.7 ppm F, with little,
additional decline between 0.7 and 1.2 ppm F. Fluorosis prevalence was 13.5
percent 21.7 percent, 29.9 percent, and 41.4 percent for children who consumed
<0.3, 0.3 to <0.7, 0.7 to, 1.2 and> 1.2 ppm F water. In addition to fluoridated water,
the use of fluoride supplements was associated with both lower caries and
increased fluorosis. Conclusions: A suitable trade-off between caries and
fluorosis appears to occur around 0.7 ppm F. Data from this study suggest that a
reconsideration of the policies concerning the most appropriate concentrations
for water fluoridation might be appropriate for the United States. [J Public Health
Dent 1997;57(3):136-43J
Key Words: dental caries, caries prevention, dental fluorosis, epidemiology,
fluoride, water fluoridation.
Fifty years ago, when fluoride was
first added to public water supplies for
the purpose of controlling dental de-
cay, fluoride-containing drinking
water was the only significant source
of fluoride exposure. Today, about 56
percent of the US population con-
sumes fluoridated water (1) and there
is. widespread use of fluoride drops,
tablets, gels, mouthrinses, and tooth-
pastes. Furthermore, processed bever-
ages and foods, which are distributed
widely in fluoridated and nonfluori-
dated communities, now can contain
substantial amounts of fluoride due to
the use of fluoridated water in their
production (2,3).
Numerous local and national stud-
ies have demonstrated a substantial
decline in caries prevalence in the
United States over the past several
decades (4-8). Fluoride is considered
to have played a major role in these
reductions. At the same time, the
prevalence of dental fluorosis, which
is caused by excess fluoride intake
during the period of preeruptive tooth
formation, also has increased over the
decades since the start of water fluori-
dation (9-12).
Public policy on the most appropri-
ate concentrations for water fluorida-
tion depends upon the trade-off be-
tween caries control and the undesir-
able side effect of dental fluorosis. The
data on which current policy is based
were collected 40-60 years ago. Be-
cause fluoride exposure in the United
States has changed so much since then,
the data are now of limited use. The
purpose of this project was to analyze
national data to further investigate the
trade-offs between caries experience
and fluorosis from the use of water
fluoridation and other fluoride prod-
ucts.
Methods
This study uses data from the
1986-87 National Survey of Oral
Health of US Schoolchildren con-
ducted by the National Institute of
Dental Research (NIDR). This survey
is unique in that it is the only national
oral health survey in the United States
to collect detailed information on fluo-
ride exposures and dental fluorosis.
Data were obtained from a public use
data tape provided by the NIDR.
The design and conduct of this sur-
vey have been described previously
(6,7,13). Briefly, oral examinations
were completed for 40,693 . children
aged 4-22 years, which is 78 percent of
all sampled students. These examina-
tions included a visual and tactile as-
sessment of dental caries and restora-
tions using the diagnostic criteria of
Radike (14). No radiographs were
taken. Children in grade 2 and higher
were examined for dental fluorosis. A
classification system based on Dean's
Fluorosis Index (15) was used to eval-
uate all erupted permanent teeth. Arti-
ficiallight was used and the teeth were
not air-dried before scoring. Fourteen
field examiners were used in this sur-
vey. Repeated interrater comparisons
during the survey found that the level
of disagreement on diagnosing caries
was extremely small. For exact
fluorosis diagnosis agreement be-
tween examiners, paired T-test P-val-
ues of .05 or less were found for seven
of 28 sets of replicate exams. When the
criterion for agreement was relaxed to
within one point on the fluorosis scale,
no P-values less than .05 were found.
To reduce any effects of examiner bias,
at least five examiners were used in
each of the 14 sampling strata, with
two strata per geographic region (6).
Send correspondence and reprint requests to Dr. Heller, Program in Dental Public Health, School of Public Health, University of Michigan, Ann
Arbor, MI 48109-2029. Internet: kheller@umich.edu. The views expressed in this paper are the authors' and do not necessarily represent those of
the National Institute of Dental research. This research was supported by National Research Service Award 1'32 DE-07157 from the National Institute
of Dental Research. Manuscript received: 9110/96; returned to authors for revision: 10/29/96; accepted for publication: 1/21/97.
Vol. 57: No.3 Summer 1997
.
fect of fluoride tablets varies with
water fluoride level. The observed
effect was that the decrease in DMFS
attributable to fluoride supplements
diminished as water fluoride level
increased. As was found with the pri-
mary dentition, the reported use of
professional fluoride treatments was
significantly associated with higher
DMFS levels.
Dental F1uorosis.The distributions
of fluorosis severity scores for chil-
dren in the four categories of water
fluoride level are presented in Table 5.
All values in this table were derived
using age-and sex-standardization for
all children aged 7 to 17 years with a
l1i~toryofa single residence. Fluorosis
Qrevalence was ietermined by
~.hether or not the child had at least
[w() teeth scored with fluorosis of
Dean's score 1 (very mild) or greater.
Overall, 23.5 percent of the children
had at least very mild fluorosis, and
this percentage increased with increas-
ing water fluoride level. Only 5.7
percent of the children exhibited
fluorosis higher than the very mild
level.
An overall fluorosis severity score
~as calculated for each child, this
5Carebemg . the smaller of the tw()
bi$est, tooth. fluorosis scores amon~
all the scored teeth for the cbild. The
m~anfiuorosis scores for theseanaly-
ses were calculated in a manner simi-
lar to Dean's Community Fluorosis In-
dex (CFI) scores (15). Overall mean
fluorosis severity was 0.47 (Table 5).
Mean fluorosis severity in the current
study increased with increasing water
fluoride level, ranging from 0.30 for
the <0.3 ppm F group, to 0.80 for the
>1.2 ppm F group. Using T-tests for
TABLE 4
Linear Regression Model of DMFS.
Regression
Variable Coefficient SE T-test P-value
Intercept -5.01 0.21 -24.01 <.001
Sex (female) 0.44 0.09 4.94 <.001
. Age (years) 0.69 0.02 31.54 <.001
ppmF -0.59 0.19 3.01 .004
Fluoride drops 0.13 0.18 0.72 .475
Fluoride tablets -0.52 0.22 2.31 ,026
Professional fluoride 0.34 0.09 3.77 <.001
treatment
School fluoride Rinses -0.01 0.17 -0.08 .936
ppm F fluoride tablets 0.94 0.30 3.19 .003
.
"US schoolchildren aged 5-17 years with a history of a single residence (n=18.165).1f=O.258.
comparisons of the means, the mean
fluorosis severity scores. for the chil-
dren in the <0.3 ppm F group were
significantly less than that for the 0.7-
1.2 ppm F group (T-test, P<.OOl) and
the> 1.2 ppm F group (T-test, P<.OO 1).
The mean fluorosis severity score of
the > 1.2 ppm F group was also signif-
icantly greater than that for the 0.3 -
<0.7 ppm F group (T- test, P=.007)
and the 0.7 - 1.2 ppm F group (T-test,
P=.045). Other comparisons of fluo-
rosis severity were not significant at
P<.05.
Figure 2 presents age- and sex-
standardized fluorosis prevalence
(percent fluorosis) and mean fluorosis
severity scores by water fluoride lev-
els. Fluorosis prevalence patterns are .
similar to those for fluorosis severity,
and a pattern of increasing fluorosis
prevalence and severity with increas-
ing water fluoride level is evident. A
similar graph limited to children who
reported no history of fluoride drops
or tablet use (not shown) was almost
identical to Figure 2.
Fluorosis prevalence and severity
generally decreased with increasing
age, as shown in Figure 3. Fluorosis
prevalence ranged. from 27.2 percent
in 8-year-old children to 17.7 percent
in the 16-year-old children. Similarly,
fluorosis severity ranged from 0.53. in
the 8-year-old children to 0.36 in the
17-year-old children.
Logistic regression was used to
model the association between fluoro-
sis prevalence outcome (at the very
mild or greater level) and demo-
graphic and fluoride exposure predic-
tor variables. Variables for sex,
urban/rural status, and race/ethnicity
TABLE 5
Distribution and Mean of Fluorosis Severity Scores, and Fluorosis Prevalence, by Water Fluoridation Status*
Fluorosis Severity (%)
Mean Severitycy % Fluorosis~
nt N%:l: 0 O.~ 1 2 3 4 (SE) (SE)
-- ----
<0.3 ppm F 6,239 35.2 59.8 26.5 10.7 2.4 0.4 0.1 0.30 (0.03) 13.5 (1.9)
0.3 - <O.7ppm F 1,793 10.4 47.4 31.0 17.3 3.1 1.2 0.0 0.43 (0.08) 21.7 (6.0)
O]-1.2ppmF 6,728 51.1 33.6 36.5 22.5 5.8 1.3 0.0 0.58 (0.04) 29.9 (3.4~
>1.2 ppm F 772 3.3 28.1 30.5 27.2 7.0 5.3 2.0 0.80 (0.10) 41.4 (4.4)
All 15,532 100 44.1 32.3 17.9 4.3 1.1 0.3 0.47 (0.04) 23.5 (2.6)
'Scores are standardized to the age and sex distribution of US schoolchildren al!Cd 7-17 year. who had a history of a single residence.
tSample size.
*Weighted population percentage.
~Detennined as Dean's CFI (Dean, 1942).
fHaving at least two teeth with Dean's fluorosis score I (very mild) or greater.
139
Journal of Public Health Dentistry
Vol. 57; No.3 Summer 1997
.
.
.
Citizens for Safe
Drinking Water
1010 University Avenue # 52
San Diego, CA 92103
Conta,ct Jeff Green
(BOO) 728-3833
greenieff@cox.net
JOURNAL OF THE AMERICAN DENTAL ASSOCIATION:
Ingested fluoride does not reduce
tooth decay, action is topical
The featured Cover Story of the July 2000 Journal of the American Dental
Association QADA) is a 13 page article authored by John Featherstone, M.Sc.,
Ph.D., Professor and Chair, Department of Preventive and Restorative Dental
Sciences and Department of Dental Public Health and Hygiene, University of California,
San Francisco.
If that sounds like a mouthful, it is. And that is exactly what Dr. Featherstone delivers.
Following in the footsteps of 16 other dted articles that he has either authored or
co-authored, Featherstone reminds the reader (in this case the dues-paying members
of the American Dental Association) that fluoride's preventive action is topical rather
than systemic.
Before you begin jumping up and down in delight or horror, depending on whether you
are an avid promoter of using the public water for mass medication or a modem-day
Keeper-of-the-Well, hold your horses.
Featherstone continues to give water fluoridation credit for helping reduce tooth decay
- not because it is ingested - but because, he states, fluoridated water and other
fluoride-containing beverages, foods, and oral care products contribute to the daily
topical application of fluoride by bathing the teeth.
In his article, The Science and Practice of Caries Prevention, Featherstone concludes
that fluoride is a key agent in battling caries, but that it is. accomplished by three
prindpal topical mechanisms of action: inhibition of demineralization,
enhancement of remineralization, and inhibition of bacterial enzymes.
He notes that remineralization of early lesions also requires caldum and
phosphate, which are derived primarily from saliva and plaque fluid.
Featherstone makes it clear,
as he has in other publications,
that fluoride incorporated
during tooth development is
insufficient to play a significant
role in caries protection.
Featherstone makes it clear, as he has in other publications, that fluoride
incorporated during tooth development is insufficient to playa significant
role in caries protection. He cites, as an example of the weak pre-eruptive
effects of fluoride, a study of two groups of Okinawa nursing students
which showed that there was no difference in caries status between those
who had received fluoridated water only until about 5 to 8 years of age (and none
thereafter). and those who had never received fluoridated drinking water.
"Importantly. this means that fluoride incorporated during tooth mineral development
at normalleve1s of20 to 100 ppm (even in areas that have fluoridated drinking water
or with the use of fluoride supplements) does not measurably alter the solubility of the
mineral," writes Featherstone. 'Even when the outer enamel has hi~er fluoride levels,
such. as 1 ()()() ppm, it does not measurably withstand acid- .nduced dissolution an)
better than enamel with lower levels of fluoride. "
This is not new information to those who have thoroughly researched the issue, nor is it
new for Dr. Featherstone to write or lecture on this and many other findings with the
same results. Dr. Featherstone was a featured speaker at the 1997 Cansdilln conference
on controlled-dose fluoride supplements at which he reminded representatives of
Canada's dental and medical stakeholders of the reports given at their 1992 conference
on the same subject. These reports indicated that ingested fluoride cannot raise the
fluoride concentration in the glanular saliva suffident to meet the bacterial challenge
present in the oral cavity.
.
.
.
Ingested fluoride does not reduce tooth decay, cont.
As a consequence of that conference, the Canadian Dental Association no longer
recommends fluoride supplements if a child brushes his teeth twice a day with
fluoridated toothpaste, and if individual practitioners are determined to increase
fluoride exposure for high caries-risk patients in non fluoridated regions, CDA
recommends that supplements be used as topical lozenges rather than swallowed.
With a tide as all-inclusive-sounding as The Science and Practice of Caries
Prevention, it is all too easy to erroneously dismiss its importance by pointing to
what was not covered, such as irrigation devices, baby bottle tooth decay, and
early childhood exposure to oral infections from primary care givers; yet many
readers may be surprised at the introduction of other topics that may warrant their
further exploration.
Other detractors may be angered by the avoidance of any mention about what
constantly bathing the teeth with fluoride will do for total fluoride exposure and the
consequences to every other organ and systemic function; but alas the dental industry
has no responsibilities in other health arenas, so this publication may never be seen as
the appropriate venue for that discussion.
And yes, one topic that is glaring by its omission in a dental discussion is the
incidence of dental fluorosis, which has risen to include 66.5% of our
children in fluoridated communities, displaying the visible signs of fluoride
overdose on at least one tooth.
Once again the Journal of
the American Dental
Association has confirmed
that the dental community
is not all of one mind...
So why is this article so important? Contrary to promotional brochures
printed by the dental trade organizations touting the safety and effectiveness
of fluoride at virtually any exposure level, previous articles published by JADA
warned of high concentrations of fluoride in chicken and other baby foods, and
advised dentists to warn parents to restrict children's consumption of fruit juices
because of fluoride pesticide residues. Once again the Journal of the American Dental
Association has confirmed that the dental community is not all of one mind, that the
portrayal of the oral ingestion of fluoride as magically-effective but never-unsafe can
now be corrected by the dental association membership.
It matters not whether Featherstone. does or does not have the proof for his contention
that 1 ppm in the water flowing past the teeth plays any significant role in caries
reduction compared to the 1000 ppm in fluoridated tooth paste. The true question
remains:
Will an infonned public, a deliberative body such as a water board or city
council, or health professional with no other axe to grind than the overall
well-being of their patient, con1inue to support the forced everyday
ingestion of a substance 1hat is fuoctional ooly as a topical applicatioo?
.
COVER
STORY
HHTlCH 1
THE SCIENCE AND PRACTICE
OF CARIES PREVENTION
JOHN D.B. FEATHERSTONE, M.5C, PH.D.
A B S T RAe T
.
Background and Overview. Dental
caries is a bacterially based disease. When
it progresses, acid produced by bacterial
action on dietary fermentable carbohy-
drates diffuses into the tooth and dis-
solves the carbonated hydroxyapatite min-
eral-a process called demineralization.
Pathological factors including acidogenic
bacteria (mutans streptococci.and lacto-
bacilli), salivary dysfunction, and dietary
carbohydrates are related to caries pr0-
gression. Protective factors-which
include salivary calciUJD. phosphate and
proteins, salivary flow, fluoride in saliva,
and antibacterial components or agents-
can balance, prevent or reverse dental
caries.
Conclusions. Caries progression or
reversal is determined by the balance
between protective and pathological fac-
tors'flJ.\J.<.lIi,~~..the key agent in battling
~es!~9!]{s .primarilvvia .toJ>ical mech-
,anisms: inhibition of demineralization,
enhancement of remineralization and
inhibition of bacterial enzymes.
Clinical Implications. Fluoride in drink-
ing water and in fluoride-containing
products reduces caries via these topical
mechanisms. Antibacterial therapy must
be used to combat a high bacterial chal-
lenge. For practical caries management
and prevention or reversal of dental
caries, the sum of the preventive factors
must outweigh the pathological factors.
.
lthough the prevaleuce of dental
caries in children has declined
markedly over the last 20 years in
most countries in the Western world,
the disease continues to be a major problem for both adults
and children everywhere.
The trends in caries in U.S. children during the last 30
years were recently summarizedl on the basis of results of
four national surveys.2-6 By the late 1980s, although
approximately 75 percent of children aged 5 to 11 years
were caries-free, about 70 percent of the 12- to 17-year-olds
still had caries. Approximately 25 percent of children and
adolescents in the 5- to 17 -year age range accounted for 80
percent of the caries in permanent teeth. By age 17 years,
however, 40 percent of the population accounted for 80 per
cent of the caries.l-6 These findings illustrate the need for
management of caries by individual risk assessment and
for measures more specifically directed to high-risk people
and populations.
Although these prevalence rates still leave much to be
desired, the overall caries prevalence in children has
indeed declined in the United States. Smaller epidemiolog-
ic studies in recent years indicate, however, that the
decline in caries has not continued during the 1990s and
that it may have plateaued.6
JADA, Vol. 131, July 2000 887
COYU STORY
.
The reasons for the reduc-
tions in caries prevalence dur-
ing the last 20 years are diffi-
cult to pinpoint. Strong evi-
dence exists, however, that the
near universal use of fluoride
containing products such as
dentifrice, mouthrinses and top-
ical gels applied in the dental
office have been major contribu-
tors.7,8 Earlier caries reductions
of 40 to 70 percent (before the
1970s) had resulted from the
fluoridation of public water sup-
plies in many communities.9.12
Dental caries in adults also
continues to be a major prob-
lem, as illustrated by a recent
U.S. surveyP The survey
reported that 94 percent of all
dentate adults (aged 18 years
or older) had evidence of treat
ed or untreated coronal caries.
Caries obviously still is a
major problem in adults, as
well as children, and we need
an improved approach to pre-
vention and therapy. Thisarti-
cle reviews and summarizes the
scientific basis for and practice
of successful intervention in
the caries process.
.
THE CARIES PROCESS
Bacterial plaque and acid
production. The caries process
is now well-understood; much of
it has been described extensively
in the dental literature. Some
details of the caries process
remain to be unraveled, but, in
general, we understand the
process well enough to initiate
better-targeted methods of caries
prevention and intervention.
The mechanism of dental
caries formation is essentially
straightforward. I Plaque on the
surface of the tooth consists of a
bacterial film that produces
acids as a byproduct of its
metabolism.14.ls To be specific,
certain bacteria within the
.
888 JADA. Vol. 131, July 2000
plaque are acidogenic-that is,
they produce acids when they
metabolize fermentable carbo-
hydrates. 12.14.15 These acids can
dissolve the calcium phosphate
mineral of the tooth enamel or
dentin in a process known as
demineralization.'6-'8 If this
process is not halted or re-
versed via remineralization-
the redeposition of mineral via
saliva-it eventually becomes a
frank cavity.
Dental caries of the enamel
typically is first observed clini-
cally as a so-called "white-spot
lesion." This is a small area of
subsurface demineralization
beneath the dental plaque. The
The mutans
streptoeocciand
the lactobacilli,
either separately
or together, are
the primary
causative agents .of
dental. caries.
body of the subsurface lesion
may have lost as much as 50
percent of its original mineral
content and often is covered by
an "apparently intact surface
layer.''' 19 The surface layer forms
by remineralization. The
process of demineralization con-
tinues each time there is carbo-
hydrate taken into the mouth
that is metabolized by the bac-
teria. The saliva has numerous
roles, including buffering (neu-
tralizing) the acid and reminer-
alization by providing minerals
that can replace those dissolved
from the tooth during deminer-
alization. 1,20,2 I
Any fermentable carbohy-
drate (such as glucose, sucrose,
fructose or cooked starch) can
be metabolized by the acido-
genic bacteria and create the
aforementioned organic acids as
byproducts.22 The acids diffuse
through the plaque and into the
porous subsurface enamel (or
dentin, if exposed), dissociating
to produce hydrogen ions as
they travel. 17,23 The hydrogen
ions readily dissolve the miner-
al, freeing calcium and phos-
phate into solution, which can
diffuse out of the tooth. Most
importantly, lactic acid dissoci-
ates more readily than the
other acids, producing hydrogen
ions that rapidly lower the pH
in the plaque.'7 As the pH is
lowered, acids diffuse rapidly
into the underlying enamel or
dentin.
The two most important
groups of bacteria that predom-
inantly produce lactic acid are
the mutans streptococci and the
lactobacilli.'4 Each group con-
tains several species, each of
which is cariogenic. Mutans
streptococci include Strep-
tococcus mutans and S. sobri
nus. The lactobacilli species
also are prolific producers of
lactic acid and appear in plaque
before caries is clinically
observed.242S These two groups
of bacteria, either separately or
together, are the primary
causative agents of dental
caries.
HOW FLUORIDE
COMBATS THE
CARIES PROCESS
The ability of fluoride to pre-
vent and arrest caries has been
researched extensively. fluo-
ride has three principal topical
mechanisms of action:
- inhibiting bacterial metabo-
lism after diffusing into the
.
bacteria as the hydrogen fluo-
ride, or HF, molecule when the
plaque is acidified;
- inhibiting demineralization
when fluoride is present at the
crystal surfaces during an acid
challenge;
- enhancing remineralization
and thereby forming a low-
solubility veneer similar to the
acid-resistant mineral fluorap-
atite, or PAP, on the remineral
ized crystals.
Inhibiting bacterial
metabolism. Several investiga-
tors have studied the possible
effects of fluoride on oral bacte-
ria.26-28 The most significant
finding reported is that the ion
ized form of fluoride, or P-, can
not cross the cell wall and
membrane but can rapidly trav-
el into the cariogenic bacterial
cells in the unchanged form as
HF. 26-28
When the pH in the plaque
falls as the bacteria produce
acids, a portion of the fluoride
present in the plaque fluid then
combines with hydrogen ions to
form HP and rapidly diffuses
into the cell, effectively drawing
more HF from the outside.I,26-28
Once inside the cell, the HF dis-
sociates, acidifying the cell and
releasing fluoride ions that
interfere with enzyme activity
in the bacterium. Por example,
fluoride inhibits enolase, an
enzyme necessary for the bacte-
ria to metabolize carbohydrates.
As fluoride is trapped in the
cell, the process becomes cumu-
lative.
In summary, fluoride from
topical sources is converted par-
tially to HF by the acid that the
bacteria produce and diffuses
into the cell, thereby inhibiting
essential enzyme activity.
Inhibiting demineraliza-
tion. The mineral of our teeth
(enamel, cementum, dentin)
.
.
COVIR STORY
Flgu... t. HIgh-....olutlon 01__ ml_o 1....._ (m..nlllo81l_
.....1'0............ )(2,000.000) 01 1-........1 _eI oryst.I.. The ....ok
I..... .... __ at 0.101_ ._. WbIch .... v1_I....d "1' .... tech
nl.._. A. Honnal .......1 orystal --.... white -,ch_ (.rrows).
which .... calc....o4Ietlc..nt _ 0.......--..... dat_ ....'-.
B. DeIn.............. orystal .... _ __ at . .........1 ca..... lesion
_1_ .......... _...._1 ....... coIftC1d1ng wit.. t_ .......1.. detect
...'-- _ III _I _. (Adapted troon Fellt_r__ _ col.
1o_.30,3t)
and bones is a carbonated
hydroxyapatite29 that can be
approximately represented by
this simplified formula:
Call1..(Na ).(P04 )6.y(C03)z
(OH)2..(F).
The substitutions in the
hydroxyapatite crystal lattice
(the arrangement of atoms and
ions in the crystal) occur as the
mineral is first laid down dur-
ing tooth development, with the
carbonate (C03) ion in particu-
lar causing major disturbances
in the regular array of ions in
the crystallattice.3D,31 During
demineralization, the carbonate
is lost, and during remineral-
ization it is excluded from the
newly formed mineral. The cal-
cium-deficient, carbonate-rich
regions of the crystal are espe-
JADA, Vol. 131, July 2000 889
COYfn STOny
.
.
Figure 2. Typical pH curve. for nonnal .-"oots with no......1 .allvary
flow and for .-1- with x.rostoonJa ._n for.ach g_J aft.r
lng_Ion ... .ue........ A _rve for In.-Ion ... a ___........ .w_.n.d
product I. .hown f_ _arl.on. .....produced f_ F.attaers1one'
with p.nnl.....n of _ publla_r. CopJrrIght Cl 1_. _..._ard.J
.
cially susceptible to attack by
the acid hydrogen ions during
demineralization, as has been
shown by several investiga
tors.21,29-33 High-resolution lat-
tice imaging, which images
crystals almost to atomic reso-
lution (viewed at about
xl,OOO,OOO magnification), was
used to illustrate the appear-
ance of hexagonal holes in the
early stages of enamel crystal
dissolution in dental caries
(Figure 1), which coincided with
the calcium-deficient, carbon-
ate-substituted regions of the
crystal.3()'33
The carbonated hydroxyap-
atite, or CAP, of our teeth is
much more soluble in acid than
hydroxyapatite, or HAP
(HAP = CaJO(P04)f(OH)2), and
that in turn is much more solu-
ble than fluorapatite, or FAP
(FAP = CaIO(PO')6F2),21 in which
890 JADA, VoL 131, July 2000
the OH- ion in pure hydroxyap-
atite is completely replaced by
an F- ion. The resulting mineral
FAP is highly resistant to disso-
lution by acid.
Fluoride inhibits demineral-
ization. Sound enamel, except
in its outer few micrometers,
generally contains fluoride at
levels of about 20 to 100 parts
per million, or ppm, depending
on the fluoride ingestion during
tooth development.34 Teeth in
children who lived in areas
with fluoridated drinking water
during tooth development have
fluoride content toward the
higher end of this range. The
outer few micrometers of en-
amel can have fluoride levels of
1,000 to 2,000 ppm.34
Fluoride in the solution sur-
rounding CAP crystals has been
shown to be much more effec-
tive in inhibiting demineraliza-
tion than fluoride incorporated
into the crystals at the levels
found in enameI.2I,35 Ten Cate,21
Nelson and colleagues35 and
Featherstone and colleagues35,37
found no measurable reduction
in the acid solubility of synthet-
ic CAP (3 percent C03 by
weight, comparable to that of
dental enamel mineral) with
about 1,000 ppm fluoride incor-
porated. Importantly, this
means that fluoride incorporat ~
eddurin~ tooth mineral devel.
opmentat normal levels of 20
to 100 ppm (even in areas thaI
have fluoridated drinkin~ water
or with the use of fluoride sup~
plements) does not measurably
alter the acid solubility of the
mineral. Even when'the outer
enamel has hi~herfluori<le le~:
els,such as 1,000 ppm, itdoes
notm~asurably withstand acid-
induced dissolution any better
than enamel with lower levels
of fluoride. Only when fluoride
is concentrated into a new crys-
tal surface during remineraliza~
lion is it sufficient to beneficial~
ly alter enamel.solubility.The
fluoride incorporated develop"
mentally-that is, systemically
into the normal tooth mineral-
is insufficient to have a measur-
able effect on acid solubility.l'.38
In contrast to the lack of
effect of fluoride incorporated
into the CAP crystals of tooth
mineral developmentally, as lit-
tle as 1 ppm in the acid solution
reduced the dissolution rate of
CAP to a rate equivalent to
that of HAP.36 Further increas-
es in fluoride in the acid solu-
tion in contact with the CAP
mineral surface decreased the
solubility rate logarithmically.
These results indicate that if
fluoride is present in the aque-
ous solution surrounding the
crystals, it is adsorbed strongly
to the surface of CAP carbonat-
.
ed apatite (enamel mineral)
crystals and thus acts as a
potent protection mechanism
against acid dissolution of the
crystal surface in the tooth's
subsurface region. If fluoride is
in the plaque fluid at the time
that the bacteria generate acid,
it will travel with the acid into
the subsurface of the tooth and,
therefore, adsorb to the crystal
surface and protect it against
being dissolved.
msummM~flooridepre~m
in the water phase at low levels
among the enamel or dentin
crystals adsorbs to the~ crystal
surfaces and can markedly
inhibit dissolution of tooth min-
eral by acid.21,36 Fluoride that
acts in this way comes from the
plaque fluid via topical sources
such as drinking water and
fluoride products. Fluoride
incorporated during tooth
development is insufficient to'
playa significant role in caries
protection. Fluoride is needed
regulMly throughout life to pro-
tect teeth against caries.
Enhancing remineraliza-
tion. As the saliva flows over
the plaque and its components
neutralize the acid, raising the
pH (Figure 2), demineralization
is stopped and rever~d. The
saliva is. supersaturated with
calcium and phosphate, which
can drive mineral back into the
tooth.21,39 The partially deminer-
alized crystal surfaces within
the lesion act as "nucleators,"
and new surfaces grow on the
crystals (Figure 3). These
proces~s constitute remineral-
ization-the replacement of
mineral in the partially de-
mineralized regions of the cari-
ous lesion of enamel or dentin
(including the tooth root).2Il,21
Fluoride enhances remineral-
ization by adsorbing to the crys-
tal surface and attracting calci-
.
.
COY[R STORY
Fl.- 3.. HIg_solutlon .Iectron on'- I_g_ (on.gnltleetl_
_.........eIy ..2,,000.000) of .....1_1 _I crystal. _t vlsu.11ze
.....Inenonz.alon at _ .to....c 18_1. Tbe .......k 11_ .... row. of OIIlcl-
_ __. wIIIch .... vI_II..d "1' ..... tecbaI_.. A.. No......1 ....on.1
crystal d...-ed trona _ m-r ....Ion of _I. _Ing "'on.ll-
willi. 1Nd- of OIIlc.....-...lektnt, ...__rtch ....10.... B. Cry.tel
_ wlllch . ...............11...... .urt.c. _r .... ...... grown .fter t....t-
_ with ____. _Ie..... __ p-.phate. (Ad__ troon
F.__ ~ col18__. 1_1.-)
um ions, followed by phosphate
ions, leading to new mineral
formation. The newly formed
"veneer" excludes carbonate
and has a composition some-
where between HAP and FAP
as described above (Figure 4).
FAP contains approximately
30,000 ppm F and has a very
low solubility in acid. The new
JADA, Vol. 131, July 2000 891
COYU STORY
.
Figure 4. Soh_lc repre_ntatlan of ......'-rallzatlon 'ollow.d "y
......In.rallzatlon In the carl.s' process. If ......____Ion Is succ_aful.
tho final result Is a crystal with a surface _I' of "'fIuorapatltellk.-
IIII...ral of low s_..IIIty. (R_roduced _ F_r_.' with _Is-
sian of the pu..II....r. Copyright 01.... _Icsgaa"".)
.
Figure' 5. TII. carl.s "'Iance: a ~ ellagralll of the ...__
...tw.en _thol_lcal a_ protective .__ In the ca..... proce_.
(R_raduced ........ Feathorst_' with _nnlsaion of the ......11_1'.
Copyright 01999. MlUlksgaa"".)
.
remineralized crystal now will
behave like low-solubility FAP
rather than the highly soluble
CAP of the original crystal
surface.36
In summary, fluoride in solu-
tion from topical sources en-
hances remineralization by
speeding up the growth of a
new surface on the partially
demineralized subsurface crys-
tals in the caries lesion. The
new crystal surface veneer is
FAP-like, with much lower sol-
ubility than the original CAP
tooth mineral. Subsequent acid
challenges must be quite strong
and prolonged to dissolve the
reminera1ized enamel.
Saliva and caries. Saliva has
a critical role in the prevention
or reversal of the caries process;
it provides calcium, phosphate,
proteins that maintain super-
saturation of calcium in the
plaque fluid. proteins and lipids
that form a protective pellicle
on the surface of the tooth, anti-
892 JADA, Vol. 131, July 2000
bacterial substances and
buffers.40 The saliva compo-
nents neutralize the acids pro-
duced by bacterial metabolism
in the plaque, raise the pfI and
,reverse the diffusion gradient
for calcium and phosphate.
Thereby, they return calcium
and phosphate to the subsur-
face lesion, where these ions
can regrow new surfaces on the
crystal remnants that were pro-
duced by demineralization.
These so-called "remineralized"
crystals have a veneer of much
less soluble mineral. Saliva also
clears carbohydrates and'acids
from the plaque.
In the case of salivary dys-
function,41 all of the above bene-
fits of saliva are reduced or
eliminated (as is illustrated
partially in Figure 2 by the pH
prof11e of the subjects with
xerostomia).
THE CARIES BALANCE
Fluoride's three extensively
studied and documented princi~
pal mechanisms of action rely
on the presence of fluoride in
saliva, in the plaque at the
tooth surface and in the fluid
among the crystals in the sub-
surface of the enamel or dentin.
The clinical effects of fluoride,
therefore, can be optimized by
using delivery methods that
bring fluoride to the surface of
the tooth and into the plaque
rather than incorporating fluo-
ride into the tooth mineral crys-
tals during tooth development.
These topical delivery methods
are equally applicable to adults
and children and include fluo-
ride in beverages and foods,
dental products and drinking
water. The benefits of continu-
ally providing low levels of fluo-
ride in the saliva and plaque
from the aforementioned topical
sources are described more fully
.
in a recent review article.'
Pathological and protec-
tive factors in the caries bal-
ance. Caries progression, as
opposed to reversal, consists of
a delicate balance between the
aforementioned factors-name-
ly, a bacterially generated acid
challenge and a combination of
demineralization inhibition and
reversal by remineralizationY2
The balance between pathologi-
cal factors (such as bacteria and
carbohydrates) and protective
factors (such as saliva, calcium,
phosphate and fluoride) isa
delicate one that swings either
way several times daily in most
people (Figure 5).
Protective factors. Saliva is
essential for the protection of
the tooth against dental caries
and provides many natural pro-
tective factors summarized ear-
lier,40.41 including calcium, phos-
phate, antibacterial components
and other proteins with various
functions. Extrinsic antibacteri-
al agents such as chlorhexidine
also can be considered as pro-
tective factors in this balance,
as can fluoride from external
sources. The mechanisms of
action of fluoride described in
this article apply primarily to
fluoride from topical sources;
systemically incorporated fluo-
ride has only a minor role in
protecting against dental caries.
'Ibis conclusion is supported not
only by laboratory data as
described previously, but also
by epidemiologic studies. For
example, a four-year study in
England found a 27 percent
lower caries incidence among
children who were 12 years old
when water fluoridation began
in their communities, relative
to the incidence in control sub-
jects of the same age in nonfluo-
ridated areas.43 This was a well-
conducted study, and it clearly
.
.
showed the posteruptive (topi-
cal) effects of fluoride in the
drinking water. Other studies
have illustrated the weak pre-
eruptive effects of fluoride. For
example, in two groups of
Okinawa nursing students aged
18 to 22 years, there was no dif-
ference in caries status between
those who had received fluori-
dated water only until about 5
to 8 years of age (and none
thereafter) and those who had
never received fluoridated
drinking. water.44
The cariostatic effects of fluo-
ride are, in part. related to the
sustained presence of low con-
centrations of ionic fluoride in
the oral environment, 1.21,38
}I:t,afl';~ihereh;;~'}
,~tn4-7~~:': ,._', - '_ : '- '._ :__~~-'" 'oi';':'
'M,;l\:~ldaken. beli~~ '
~~r}that ..driUing<<)~,,\,
~i:. c'a caries lesion
~~;{;:.): ::,'
(,and placing a
,:'""restoration
,'(,
}' .elinlinates the
"r;~<,"-;
bacteria and
'.:,',therebystops
caries
derived from foods and bever-
ages, drinking water and fluo-
ride-containing dental products
such as toothpaste. Prolonged
and slightly elevated low con-
centrations of fluoride in the
saliva and plaque fluid decrease
the rate of enamel demineral-
ization and enhance the rate of
remineralization.21,36,38,4S-48 For
example, fluoride at 0.04 ppm
in saliva can enhance reminer-
alization. Remineralization of
early lesions also requires calci-
COYfR STORY
um and phosphate, which are
derived primarily from saliva
and plaque fluid.
Pathological factors. Patho-
logical factors obviously include
cariogenic bacteria and the fre-
quency of ingestion of ferment-
able carbohydrates that sustain
these bacteria. The importance
of mutans streptococci (which
includes S. mutans and S.
sobrinus) in the development of
dental caries has been reviewed
extensively.I2,14,15,49.50 Numerous
cross-sectional studies in
humans have shown that great-
er numbers of mutans strep-
tococci and lactobacilli in saliva
or plaque are associated with
high caries rates.IS.25,49,SI-54
Longitudinal studies have
shown that an increase over
time in numbers of both of
these bacterial groups is
associated with caries onset
and progression.24,5S,56
CARIES INTERVENTION
The methods of caries interven-
tion can be summarized by join-
ing the principal components of
the caries process with the
interventional possibilities
(Table).
Cariogenic bacteria and
high bacterial chaUenge.
Dental caries isa transmissible,
bacterially generated disease.
There is the mistaken belief
that drilling out a caries lesion
and placing a restoration elimi-
nates the bacteria and thereby
stops caries progression. Al-
though traditional restorative
work may eliminate the bacte-
ria at the site of the restoration,
the remainder of the mouth is
left untouched, caries continues
unchecked in the remainder of
the mouth and recolonization
commences rapidly at the
margins.s7
It is logical, therefore, to use
JADA, Vol. 131, July 2000 893
.
.
.
COY(R STORY
TABLE
FeI'D1entable Carbohydrates
<>r~lUal~ACidS..PJYd~~~...'...bY
. O~.Jla.~teIi,a .
Antibacterial therapy such as treatment 'With
chlorhexidine gluconate (see text.)
Malee the miner,al less soluble by transforming
it to other crystalline forms such as hydroxy-
apatite 'Without carbonate (future caries-
preventative treatments by specific laser irradia-
tion 'Will enable lhis to be done....'7O)
Reduce the frequency of ingestion; substitute
'With noncariogenic s'Weeteners (this method is
'Well-accepted and used in patient education.
Recommend use of sugar-free che'Wing gum.
'Which reduces frequency of fermentable carbo-
hydrate ingestion and also enhances remineral-
ization
Neutralize the acid by providing extra buffer-
ing or enhancing saliva; sugar-free gum assists
in this as 'Well
Enhance the saliva flo'W and function
Exploit its. kno'Wneffects on bacteria.. inhibi-
tion of demineralization and enhancement of
remineraliz,ation by using "topical"" fluoride
delivery by means of dental products. drinking
'Water. beverages and foods
antibacterial therapy-such as
treatment with chlorhexidine
gluconate rinse-as a caries-
preventive measure. Although
this has been proposed for
many years58-60 and used in sev-
eral European countries, an
antibacterial approach almost
never is used in the United
States for the prevention of the
progression of dental caries.
One of the difficulties in per-
suading clinicians to use the
antibacterial approach is that
there have not been rapid and
accurate methods of determin-
ing the levels of cariogenic bac-
teria in the mouth. Further-
more, although numerous
studies have indicated that
mutans streptococci and lacto-
bacilli definitely are risk factors
for dental caries, there is no
one-to-one direct correlation
between levels of these bacteria
and caries progression.24,49
However, it now is well-estab-
lished that high levels of
mutans streptococci, high levels
of lactobacilli or both constitute
a "high bacterial challenge."24
This bacterial challenge can be
balanced by the protective fac-
tors described earlier, which
include salivary components-
especially calcium, phosphate
and fluoride-and the amount
of saliva present.42
Figure 5 illustrates the bal-
ance between pathological fac-
tors (including cariogenic bacte-
ria, reduced salivary function
and frequency of use of fer-
mentable carbohydrates) and
protective factors. If these
pathological and protective fac-
894 JADA, Vol. 131, July 2000
tors are in balance, caries does
not progress. If they are out of
balance, caries either progresses
or reverses.
Antibacterial therapy for
caries control. Currently, the
most successful antibacterial
therapy against cariogenic bac-
teria is treatment by chlorhexi-
dine gluconate rinse or ge1.47.61
Chlorhexidine is available by
prescription in the United
States. Studies have shown that
a daily dose of chlorhexidine
rinse for two weeks can
markedly reduce the cariogenic
bacteria in the mouth and that,
as a result, recolonization takes
place in three to six months
rather than immediately. 58 In
patients with high levels of bac-
teria, therefore, chlorhexidine
treatments at three-month
.
intervals are indicated.
, The problem faced by clini-
cians is how to determine. in a
timely fashion. whether the
bacterial challenge is high,
medium or low. For many
years. commercial "dip slides"
have been available in Europe,
and they recently became
available in the United
StateS.58 A saliva sample is
taken from the patient and
incubated on the dip slide; two
days later, a result is provided
of the levels of S. mutans and
lactobacilli bacteria in the
mouth. 58 Although these slides
are a major advance in conven-
ience and are the best tools
available at the time of this
writing. it has been shown
that this technology is not
well-correlated with tradition-
al bacterial plating. It is antic-
ipated that methods of rapid
chairside assessment of bacter-
ial challenge, based on molecu-
lar biology. will be available in
the future.
Several investigators have
explored the possibility of
using modem molecular biolo-
gy for better and more rapid
methods of bacterial assess-
ment, 62 but they were unable
to overcome a number of com-
plications. An exciting devel-
opment is work by Shi and col-
leagues,63 who recently pub-
lished a method using species-
specific JPonoclonal antibodies
that recognize the surface of
cariogenic bacteria. With this
technology. it is not necessary
to split open the bacterial cells
to assess the internal DNA or
RNA. These probes can be
tagged either with a fluo-
rescent molecule or with a
marker that can be measured
quantitatively in a simple
spectrophotometer.
It is anticipated that these
.
.
probes will be available com-
mercially in the near future.
and that clinicians will be able
to use them chairside and
obtain results within a few
minutes. This will enable clini-
cians to determine the quanti-
tative levels of bacteria in a
patient's mouth while he or
she is in the operatory and to
factor these numbers into an
overall risk assessment of
caries for that patient. It is
envisaged that computer pro-
grams will be available that
will include the assay num-
bers, as well as other data.
The practitioner will receive
guidance as to the level of
;;;;!C..';'\'(1i~th0d8of(;)"';'
~~iii!X:._.:.',i..."..',...a".'..'pid..'. ' c' L_~~-,I.d"."..'.'.'e.". '..'.:;>:'
-~'~~j-i'? ',A.. ,~
';:.b
i', assessment or.'
"""f
'F bacterial
challenge, based
on molecular
.,.,.'. biology, will~'
;..;....~ailable.. int.h~
-~;,., -
.,.-,"" ~.'
;i,f";'" '" ~ 'lU.mre,~
F~~:\-~1_:.u~r1i+L. :'i,~
caries risk and what regimen
or regimens to use to prevent
further caries and to reduce
the bacterial challenge. With
the new monoclonal antibody
probes, the levels of bacteria
and success of the intervention
could readily be followed over
time. 1bis is an exciting, inno-
vative tool that may become
widely used and accepted
within a few years.
CARIES RISK
ASSESSMENT
Several studies have attempt-
ed to determine risk factors
that can be reliably used to
COY(R STORY
;"~: '-":
assess the level of risk of
caries progression in individ-
ual patients. Studies still are
under way, and there is no
definitive formula yet avail-
able. The status of risk assess-
ment was summarized, how-
ever, by the authors of a spe-
cial supplement to The
Journal of the American
Dental Association in 1995;
this publication can be used as
a guide until more definitive
information is available.64
Figure 5 represents a basis for
determining caries risk with
the information currently
available.
It has been established that
high-risk patients include
those who have a high bacteri-
al challenge, which may con-
sist of a combination of high
numbers of mutans streptococ-
ci, lactobacilli or both.
Although fluoride has excel-
lent properties in terms of bal-
ancing caries challenge, if the
challenge is too high, then
fluoride-even at increased
concentrations. with increased
use or both-cannot balance
that challenge. Therefore, in
the case of high bacterial chal-
lenge, the bacterial infection
must be dealt with, typically
with a chlorhexidine rinse, as
well as the enhancement of
salivary action by topical
delivery of fluoride. These
principles apply equally well
to adults and children.
Accurate detection of early
caries can increase the relia-
bility of caries risk assess-
ment, particularly if those
measurements are made at
three- or six-month intervals
and caries progression can be
measured. In the case of caries
progression, obviously, inter-
vention is needed either anti-
bacterially. with fluoride Or
JADA, Vol. 131, July 2000 895
CoYEn STOny
.
Flqure 6. ScheInaltc dlagraon showing the pDtenffal _ ... speclftc
la_rs tor precl_ ......oval ... _"'- __I _d lIlCIdIfIcIotIon ... the
surrounding a...onel for prev_1on of ......... carles ........_..... .....r
.....toratlon. The la_r would be set first to relllO_ . ..In......... ... _rl.
ous tlss... Then t_ walls...... __ at the c_1ty p_.-tIon __ be
treated with t_ laser to Inhibit ~ _rles __..........
(R_roduoed front F__rstone" wtlh .. _nna_..... at .. ...........r.
C_yrlght C2000 Indiana University ~I at -1stIy.J
.
with other techniques, some of
which are described in the fol-
lowing material.
Caries management by
risk assessment. As the
caries risk assessment
methodologies are refined, we
will have more definitive bio-
logical and chemical risk
assessment measures to guide
clinical decision making.
These measures form the
basis for assessing the direc-
tion in which the caries bal-
ance is likely to move for a
particular patient. Early
caries detection, especially in
occlusal surfaces, is an essen-
tial part of caries management
by risk assessment.
Caries management by risk
assessment now is receiving
considerable attention, and
software programs are being
developed that will aid practi-
tioners in assessing risk and
lead them to the use of cur-
rent and new technologies by
specifying treatments recom-
mended for the various risk
categories.S9,60 As we move into
the future, tooth restorations
.
8% JADA, Vol. 131, July 2000
will become less and less
desirable as a treatment and
will be used only as a final
resort when new intervention
measures have failed or when
people have not participated
in caries intervention pro-
grams such as those indicated
previously.
CARIES MANAGEMENT
TOOLS FOR THE FUTURE
Several technological advance-
ments are currently close to
clinical reality and will be
embraced if they are proven
successful.
Assessment of bacterial
challenge by chairside
molecular probes. The use
of chairside bacterial probes
for assessing a patient's cario-
genic bacterial challenge will
be an essential component of
caries management by risk
assessment.
Caries immunization. In
a program of caries manage-
ment by risk assessment, it is
logical that all available tools
should be used. One such tool
that has been investigated for
many years is an immuniza-
tion against caries. There are
many obstacles to the success
of immunization, as caries is
not a systemic infection that
can be dealt with simply by
administering a specific anti-
biotic. The infection must be
dealt with in the mouth, where
the internal body fluids do not
pass and, therefore, the normal
iDllllune response is not rele-
vant. However, IgA that is pro-
duced by the saliva naturally
can interfere with the coloniza-
tion of the surface of the tooth
by specific bacteria.
Recent studies by Ma and
colleagues65,66 have illustrated
the effectiveness of specific IgA
in the inhibition of recoloniza-
tion of mutans streptococci.
The next logical step is to use
this technology as one of the
tools for caries intervention. It
is possible to use genetically
engineered plants, such as
tobacco or alfalfa, to produce
immunoglobulins.66.67 A study is
in progress at the University of
California, San Francisco, to
test IgA that has been pro-
duced using genetically engi-
neered tobacco plants. At press
time, the results were not
known, but if the trial is suc-
cessful, this IgA can be applied
to the teeth after chlorhexidine
treatment has removed the car-
iogenic bacteria, with the aim
of inhibiting future recoloniza-
tion by mutans streptococci.
Early caries detection
and intervention. Successful
use of the innovative methods
described here for caries inter-
vention will require accurate
methods for the early detection
of dental caries in enamel
and dentin. Early-detection
methods such as fluorescence,
optical coherence tomography,
electrical impedance and
.
ultrasonography are likely to
become available for use by cli-
nicians in the near future.68 It
will be possible to detect
lesions in the occlusal surface
and to determine whether they
have progressed into the dentin
and, if so, how far. This is not
possible with current radio-
graphic technology.
Once new methods are intro-
duced for the early detection of
caries, they can be used in two
opposing fashions. Clinicians
with traditional training are
likely to use these methods to
intervene physically at an ear-
lier stage with carious
lesions-drilling, filling and
placing restomtions. This out-
come is of concern, as many
more restorations would be
placed than may be necessary,
which weakens the tooth struc-
ture. Early detection and inter-
vention by placing a restoration
also does not take advantage of
the body's natural protective
mechanisms of inhibition of
demineralization and enhance-
ment of remineralization via
saliva.
Alternatively, early detection
of caries can be used as an
opportunity to promote re-
mineralization via salivary
enhancement, use of topical
fluoride and chlorhexidine and
meticulous oral hygiene. In
addition, as innovative meth-
ods for early caries interven-
tion are introduced, the need
for restorations may be elimi-
nated for many patients, there-
by preserving the tooth struc-
ture and halting or reversing
progression of dental caries.
Caries prevention by
laser treatment. In May 1997,
the U.S. Food and Drug
Administration approved the
use of an erbium:yttrium-
aluminum-garnet, or Er:YAG,
.
.
laser for use on teeth. This was
the first approval for laser use
on dental hard tissues. This
approval by the FDA was for
this particular laser to be used
for the removal of dental caries
and the cutting of sound tissue
before the placement of restora-
tions. This event has ushered
in a new era for lasers in den~
tistry. Since then., other lasers
have been approved for the
same purpose, and additional
hard-tissue uses are likely to
be approved in the future,
including the use of lasers for
the inhibition of progression of
dental caries by altering the
composition of surface enamel
'Z'itmoVllti."J'.'
methods. for
l{~. early caries:i::t~i
~.......,.. interventioll.',\,;,';
are introduced,. ' .
the need for ..
:;~~storations . ma'i:
tiot,. ...1" ...ted I"',"
~helIl11na. ...191"....,
~y..PAti~n~..;.
or dentin mineral.
Kantorowitz and colleagues69
and Featherstone and col-
leagues7U have studied the
effects of lasers on hard tissues
for almost 20 years. The overall
objective of these studies is to
establish the scientific basis for
the choice of laser parameters
that can be used clinically for
the prevention., removal or
treatment of caries lesions.
Their studies have demonstrat-
ed that specific pulsed carbon
dioxide, or CO2, laser treat-
ment of dental enamel can
inhibit subsequent carieslike
progression in a severe de-
coy(n STOny
mineralization-remineraliza-
tion model in the labomtory by
up to 85 percent. They have
demonstrated that carbonate is
lost from the CAP mineral of
the tooth during specific laser
irradiation, making the miner-
al highly resistant to dissolu-
tion by acid. Although they
have demonstrated in the labo-
mtory, using pH cycling mod-
els, that as little as 20 pulses of
100 microseconds each can pro-
duce a preventive effect similar
to daily use of fluoride denti-
frice, these promising and
exciting results have not yet
been tested in human mouths.70
For pmctical purposes, it
would be desirable to develop a
laser that can remove carious
tissue and subsequently be
used to treat the walls of the
area from which carious tissue
is removed to make them
resistant to subsequent caries
challenge71 (Figure 6). Fried
and colleaguesn recently pub-
lished a report on a new C02
laser that efficiently removes
carious tissue. After caries and
a minimal amount of surround-
ing tissue are removed, it will
be possible to change the laser
parameters to perform caries-
preventive treatment on the
same area. This would be fol-
lowed by placement of a resin-
based composite restoration,
thereby inhibiting subsequent
caries around that restoration.
For example, if an early oc-
clusallesion was detected (by
the new methods described pre-
viously) that was deemed to be
beyond hope of remineraliza-
tion., this lesion could be con-
servatively removed with an
appropriate laser. Then the
surrounding cavity preparation
walls could be treated for caries
prevention by the laser and a
small conservative restoration
JADA, Vol. 131, July 2000 897
COYfR STORY
.
placed. The cavity walls will be
highly resistant to acid attack
and therefore resistant to sec-
ondary caries. Providing bacter-
ial, intervention via chlorhexi-
dine rinse was also part of the
treatment in the same patient,
future caries would be unlikely.
.
SUMMARY AND
CONCLUSIONS
The mechanism of dental caries
is well-established to the point
where new approaches are
being made for caries preven-
tion based ona scientific under-
standing of the processes
involved. Several existing
methodologies are available to
enable successful management
of dental caries by risk assess-
ment. Understanding the bal-
ance between pathological fac-
tors and protective factors is
the key. Beyond the well-
established and currently used
methods, some innovative and
exciting techniques have shown
early research successes that
most likely will be used for
early caries intervention in the
future. These methods include
fluoride therapy for inhibition of
demineralization and enhance-
ment of remineralization, mole-
cular probes for the quantita-
tive detection of cariogenic bac-
teria at chairside, computerized
caries risk assessment pro-
grams, genetically engineered
IgA for inhibition of recoloniza-
tion of cariogenic bacteria, spe-
cific lasers for conservative
removal of carious tissue and
specific lasers for the preven-
tion of caries progression.
The use of these technologies
will require extensive retraining
of clinical dentists. But it will
dramatically alter the way in
which dentists diagnose, inter-
vene, treat and manage caries,
with major benefits to the oral
.
898 JADA, Vol. 131, July 2000
health of their patients. _
Dr. Fealberstone is a professor and the
chair, Department of Pre\oentive and
ReSloralive Dental Sciences and Department
of Dental Public Health and Hygiene,
Uniwrsity of California, San Francisco, 707
Pamassus Ave.. Box 0758. San Francisco,
Calif. 94143, e-mail "jdbf@itsa.ucsf.edu".
Address reprint requests to Dr.
Fealberstone.
The author sincerely acknowledges contri-
butions from numerous colleagues over many
years'ln much of the work reviewed here.
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20. ten Cale 1M, Duijsters PP. Influence of
fluoride in solution on tooth demineralization.
U. Microradiographic data. Caries Res 1983;
17(6):513-9.
21. ten Cate 1M, Featherstone JD.
Mechanistic aspects of the interactions
bdween fluoride and dental enamel. Crit Rev
Oral Bioi Med 1991 ;2(3):283-96.
22. Geddes DA. Acids produced by human
dental plaque metabolism in sibJ. Caries Res
1975;9(2):98-109.
23. Fealberstone JD. Diffusion phenomena
and enamel caries development. In:
Guggenheim B, ed. Proceedings of the
Cariology Today International Congress,
September 1983. Zurich, Switzerland. Basel
Switzerland: Karger; 1984:269-68.
24. Leverett DM, Proskin HM, Featherstone.
JD, et aI. Caries risk assessment in a longihl-
dinal discrimination sbJdy. I Dent Res
1993;72(2):53843.
25. Leverett DM, Featherstone JD, Proskin
HM et aI. Caries risk a~sessment by a cross-
sectional discrimination model. I Dent Res
1993;72(2):529-37.
26. Hamilton IR, Bowden GH. Fluoride
effects on oral bacteria In: Fejerskov 0,
Ekstrand I, Burt BA, eds. Fluoride in den-
tisti)'. Copenhagen. Denmark: Munksgaard
1996:230-51.
27. Whitford GM, Schuster GS. Pa~hley
DM, Venkateswarlu P. Fluoride uprake by
SlreplOCOCCUS mutans 6715. Infecllmmunol
1977;18(3):680-7.
28. Van Louveren C. The antimicrobial
action of fluoride and il~ role in caries inhibi-
tion. I Dent Res 1990;69:676-81.
29. LeGeros RZ. Calcium phosphates in oral
biology and medicine. In: Myers HM, ed.
Monographs in oral science. Basel
- Switzerland: Karger, 1991:1-201.
30. Featherstone ill, Nelson 00, McLean
JD. An eleclron microscope SbJdy of modifica-
tions to defect regions in dental enamel and
synthetic apatites. Caries Res 1981.15(4):
278-88.
31. Featherstone ill, Goodman P, McLean
ill. Electron microscope SbJdy of defect zones
in dental enamel. I Ullraslruc Res 1979;67:
117-23.
32. Nelson 00, McLean JD. High-resolution
elecuon microscopy of octacalcium phosphate
and its hydrolysis products. Calcif TIssue Int
1984;36(2):219-32.
33 Nelson 00, McLean JD. Direct observa-
tion of near-atomic details in synthetic and
biological apatite crysralliles. In: Feamhead
RW, Suga S. ed. Tooth enarnelIV:
Proceedings of the Fourth International
Symposium on the Composition, Properties,
and Fundamental SlrUcmre of Tooth Enamel.
.
Amsterdam, Ne!berlands: Elsevier Science
Publishers; 1984:47-51.
34. Robinson C, Kirkham J, Wearberell JA.
Fluoride in teeth and bone. In: Fejer5kov 0,
Ekslr8nd J, Burt BA, eds. Fluoride in den-
tislIy. Copenhagen. Denmark: Munksgaard;
1996:69 87
35. Nelson 00, Fea!berslOlle ill, Duncan
IF, Cutress Tw. Effect of carlIooate and flu0-
ride on the dissolution behaviour of synthetic
apatites. Caries Res 1983; 17(3):200-11.
36. Featherstone ill, Glena R, Sbariali M,
Shields CP. Dependence of in vilro deminer-
alization of apatite and remineralization of
dental enamel on fluoride concentmtioo. J
Dent Res 1990;69:620-5.
37. Featherstone ill, Shields CP,
Khademazad B, Oldershaw MD. Acid reactiv-
ity of carbonated apatites with sb'Ontium and
fluoride substitutions. J Dent Res 1983;
62(10):1049-53.
38. Fejerskov O. ThylsllUp A, Larsen MI.
Rational use of fluorides in caries prevention.
A concept based on possible carioslatic mech-
anisms. Acta Odont Scand 1981 ;39(4):241-9.
39. Moreno EC, Kresak M, Zahradnick RT.
Physicochemical a~pects of fiuoride-apatite
systems relevant to !be study of dental
caries. Caries Res 1977;11:142-71.
40. Lamkin MS, Oppenheim ro. SlrUctural
features of salivary function. Crit Rev Oral
Bioi Med 1993;4:251-9.
41. Mandel 10. Relation of saliva and
plaque to carie.~. J Dent Res 1974;53(2):
246-66.
42. Fea!berstone JD. Clinical implications:
New strategies for caries prevention. In:
Stookey GK, ed. Indiana Conference 1996:
Early Detection of Dental Caries. indianapo-
lis: Indiana University School of DentislIy.
1996:287-95. '
43. Harwick JL, Teasdale J. Bloodworth G.
Caries increments over 4 years in children
aged 12 at !be start of water fluroridation. Br
Dent J 1982; 153:217-22.
44. KDbayashi S, Kawasaki K, Takagi 0, et
al. Caries experience in subjects 18-22 years
of age after 13 years' discontinued water
fluoridation in Okinawa. Community Dent
Oral Epidemioll992;20:81-3.
45. ten Cate 1M, Mundortf-Shrestha SA.
Working group report: laboratory models for
caries (in vilro and animal models). Adv Dent
Res 1995,9:332-4.
46. Zero DT. In situ caries models. Adv
Dent Res 1995;9:214-30.
47. Featherstone JD, Zero DT. Laboratory
and human stodies to elucidate !be mecha-
nism of action of fluoride-containing denti-
.
.
trices. In: Embery G, Rolla R, eds. (Clinical
and biological aspects of dentitrices. Oxford,
England: Oxford Univer.;ity Press; 1992:
41-50.
48. Arends J, Nelson 00. Dijkman AG,
Jongebloed WL. Effect of various fluorides on
eIIlIJDel strucIIIre and cbemislIy. In:
GuggeDheim B, ed. Proceedings of the
Cariology Today Intemational Congress,
Septembea' 1983, Zurich, Switzerland. Basel.
Switzerland: Karger. 1984:245-58.
49. Krasse B. Biological factors as indica-
Illn of future ames. Int Dent J 1988;38(4):
219-25.
SO. ElIeo RP. Microbiological assays for
dental caries and periodontal disease suscep-
tibility. Oral Sci Rev 1976;(8):3-23.
,51. Alalnusua S, KIeemola-Kujala E,
Nystrom M, Evalahti M, Gronroos L. Caries
in the primlIIy teeth and salivmy Strep-
tococcus mutans and lactobacillus levels a~
indicators of caries in permanent teeth.
Pediab' Pent 1987;9(2):126-30.
52. Klock B, Krasse B. Microbial and sali-
vary conditions in 9- to 12-year-old children.
Scand J Dent Res 1977,85(1):56-63.
53. Klock B, Emilsoo CO, Lind SO,
Gusravsdotter M, OIhede-Weslerlund AM.
Prediction of caries activity in children with
today's low caries incidence. Community Dent
Oral Epidemiol 1989;17(6):285-8.
54. Seppa L, Hausen H. Frequency of initial
caries lesions as predictor of future caries
increment in children. Scand J Dent Res
1988;96(1):9-13.
55. Loesche WJ, Eklund S, Earnest R, Burt
B. Longitudinal imlestigation of bacteriology
of human fissure decay: epidemiological stud-
ies in molars shoJ1Iy llf'ter eruption. Infect
lmmunoI1984;46(3):765-72.
56. Kingman A, Liale W. Gomez I, et al.
Salivary levels of Sb~'Us molans and
lactobacilli and dental caries experiences in a
U.S. adolescent popuiation. Community Dent
Oral Epidemiol 1988.16(2):98-103.
57. Wright IT, Cuttec OR, Dasanayake AP,
Stiles HM. Caufield PW. Effect of convention-
al dental restorative treabI1ent on bacteria in
saliva Community Dent Oral Epidemiol
1992;20(3): 138-43.
58. Anderson MR, Bales OJ, Omnell KA.
Modern management of dental caries: the
cutting edge is DOt !be dental bur. JADA
1993;124(6):37-44.
59. Anusavice 10. Treatment regimens in
preventive and restorative dentislIy. JADA
1995;126(6):727-43.
60. Anusavice 10. Effcacy of nonsurgical
management of the initial caries lesion. J
COYfH STORY
Dent Educ 1997;61 (11 ):895-905.
61. Lagerlof F Oliveby A. Clinical implica-
tions: new Slrategies for caries treabnent. In:
Stookey GH, Beiswanger B, eds. Indiana
Conference 1996: Early DetectiOD of Dental
Caries. Indianapolis: Indiana University
School of DentislIy; 1996.
62. Cangelosi GA, Iversen 1M, Zuo Y
Oswald TK, Lamont RJ. Oligonucleotide
probes for mUlans streptococci. Mol Cell
Probes 1994;8(1):73-80.
63. Shi W, Jewett A. Hume WR. Rapid and
qnantitative detection of Streptococcus
mukuIs with species-specific monoclonal anti-
bodies. Hybridoma 1998;17(4):365-71.
64. Caries diagnosis and risk assessment: a
review of preventive strategies and manage-
ment. JADA 1995,I26(suppl):I"24S.
65. Ma JK, Hunjan M, Smith R, Lehner T.
Specificity of monoclonal antibodies in local
passive immunization against Streptococcus
mukuIs. Clin Exp Immunol 1989;77(3):331-7.
66. Ma JK, Hikmat BY, Wycott K, et al.
OIaracterization of a recombinant plant mon-
oclonal secretory antibody and preventive
immunotherapy in humans. Nat Med
1998;4(5):601-6.
67. Ma JK, Lehner T, Srabila P, Fux CI
Hiatt A. Assembly of monoclonal antibodies
with IgG 1 and IgA heavy chain domains in
ttansgenic tobacco plants. Eur J Immunol
1994;24(1):131-8.
68. Stookey GK. Practical applications of
early caries detection methods. In: Stookey
GK, ed. Early detection of dental caries D:
1999. Indianapolis: Indiana University School
of Dentistry (in press).
69. Kantorowitz Z. Featherstone JD, Fried
D. Caries prevention by co, laser treatment:
dependency on the number of pulses used.
JADA 1998;129:585-91.
70. Featherstone JD. Barrett- Vespone NA
Fried D, KanloroWitz Z. Seka W. CO2 laser
inhibitor of artificial caries-like lesion pro-
gJession in dental enamel. J Dent Res 1998;
77(6):1397-403.
71. Featherstone JD. Innovative methods
for early caries intervention. In: Stookey GK
ed. Early detection of dental caries D: 1999
Indianapolis: Indiana University School of
DentislIy (in press).
72 Fried D, Murray MW, Feathentone JD
et al. Dental hard tissue modification and
removal using sealed TEA lasers operating at
= 9.6 and 10.6 jJIIl. Proceedings of Lasers in
DentislIy V: Jan. 24-25, 1999, San Jose,
Calif. Bellingham. Wash.: SPIE Press;
1999:1~203.
JADA, Vol. 131, July 2000 899
.1
CDC
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August 17, 2001/Vol. 50/ No. RR-14
MMWR~
MORBIDITY/AND MORTALITY
WEEKLY REPORT
Recommendations '
and
~eports
.~
.~
Recommendations for Using ~Iuoride
to Prevent and Control Dental Caries
in the United States
U.s. DEPARTMENT OF HEALTH AND HUMAN SERVICES
Centers for Disease Control and Prevention (CDC)
Atlanta, GA 30333
r~"
l~
Vol. 50 I No. RR-14
MMWR
3
The safety of fluoride, which has been documented comprehensively by other scientific
and public health organizations (e.g., PHS [81, National Research Council (9], World
Health Organization [101, and In~itute of Medicine (11]) is not addressed.
HOW ,FLUORIDE PREVENTS AND CONTROLS DENTAL CARIES
Dental caries is an infectious, transmissible disease in whieh bacterial by-products
(Le., acids) dissolve the hard surfaces of teeth. Unchecked, the bacteria can penetrate the
dissolved surface, attack the underlying dentin, and reach the soft pulp tissue. Dental
caries can result in loss of tooth structure, pain, and tooth loss andean progress to acute
systemic infection.
, Cariogenic bacteria (i.e., bacteria t~at cause dental caries) reside in dental plaque, a
sticky organic matrix of bacteria, food debris, dead m'ucosal cells, and salivary compo-
nents that adheres to tooth enamel. Plaque also contains minerals, primarily calcium and
phosphorus, as well as proteins, polysaccharides, carbohydrates, and lipids. Cariogenic
bacteria colonize on tooth surfaces and produce polysaccharides that enh.ance adher-
ence of the plaque to enamel. left undisturbed, plaque will grow an~ harbor increasin~
numbers of cariogenic bacteria. An initial step in the formation of a carious lesion takes
place when cariogenic bacteria in dental. plaque metabolize a substrate from the diet
(e.g., sugars and other fermentable carbohydrates) and the acid produced as ~ metabolic
by-product demineralizes (i.e., begins to dissolve) the adjacent enamel crystal surface
(Figure 1). Demin.eralization involves the loss of calcium, phosphate, and carbonate.'
These minerals can be captured by surrounding plaque and be available for reuptake by
the enamel surface. Fluoride, when present in the mouth, is also retained and concen-
trated in plaque.
Fluoride works to control early dental caries in several ways. Fluoride concentrated
in plaque and saliva inhibits the demineralization of sound enamel and enhances the
remineralization (I.e., recovery) of demineralized enamel (12,13). As cariogenic bacteria
metabolize carbohydrates and produce acid, fluoride is released from dental plaque in
response to lowered pH atthetooth-plaque interface (14). The released fluoride andthe
fluoride present in saliva are then taken up, along with calcium and phosphate, by de-
mineralized enamel to establish an improved enamel crystal structure. This improved
structure is more acid resistant and contains more fluoride and less carbonate (12,15-
19) (Figure 1). Fluoride is more readily taken up by demineralized enamel than by sound
enamel (20 ). Cycles of demineralization and remineralization continue throughout the
lifetime of the tooth.
Fluoride also inhibits dental caries by affecting the activity of cariogenic bacteria. As
fluoride concentrates in dental plaque, it inhibits the process by which cariogenic bacte-
ria metabolize carbohydrates to produce acid and affects bacterial production of adhe-
sive polysaccharides (21 ).In laboratory studies, when a low concentration of fluoride is
constantly present, one type of cariogenic bacteria, Streptococcus mutans, produces
less acid (22-25). Whether this reduced acid production reduces the cariogenicity of
these bacteria in humans is unclear (26).
Saliva is a major carrier of topical fluoride. The concentration of fluoride in ductal
saliva, as it is secreted from salivary glands, is low - approximately 0.016 parts p,e.r
million (ppm) in areas where drinking water is fluoridated and 0.006 ppm in nonfluoridated
areas (27). This concentration of fluoride is not likely to affect cariogenic activity. How-
ever, drinking fluoridated water, brushing with fluoride toothpaste, or using other fluoride
"
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--
August 17, 2001/Vol. SOl No. RR-14
MMWR~
MORBIDITy'AND MORTALITY
WEEKLY REPORT
Recommendations
and
~eports
\l" .
Recommendations for Using ~Iuoride
to Prevent and Control Dental" Caries ",
in the United States
u.s. DEPARTMENT OF HEALTH AND HUMAN SERVICES
Centers for Disease Control and Prevention (CDC)
Atlanta, GA 30333
r~.'
l~
4
MMWR
August 17, 2001
FIGURE 1. The demineralization and remineralizationprocesses lead to remineralized
enamel crystals with surfaces rich in fluoride and lower in solubility
Demineralization
MId
__--- ~ CKtIn
/EnInlIl~-~ /___
"'~....... /, ~ ~
~
Remineralization / ___ ~
~.::;-..:-
~
Source: Adapted from Featherstone JDB. Prevention and reversal of dental caries: role of low
level fluoride. Community Dent Oral Epidemiol 1999;27:31-40. Reprinted with permission
from Munksgaard International Publishers Ltd., Copenhagen, Denmark.
, dental products can raise the concentration of fluoride in saliva present in the mouth ,00-
to 1 ,OOo-fold. The concentration returns to previous levels within 1-2 hours but, during
this time, saliva serves as an important source of fluoride for concentration in plaque and
for tooth remineralization (28 ).
Applying fluoride gel or other products containing a high concentration of fluoride to
the teeth leaves a temporary layer of calcium fluoride-like material on the enamel sur-
face. The fluoride in this material is released when the pH drops in the mouth in response
to acid production and is available to remineralize enamel (29).
In the earliest days of fluoride research, investigators hypothesized that fluoride af-
fects enamel and inhibits dental caries only when incorporated into developing dental
enamel (Le., preeruptively, before the tooth erupts into the mouth) (30,31 ). Evidence
supports this hypothesis (32-34), but distinguishing a true preeruptive effect after teeth
erupt into a mouth where topical fluoride exposu re occurs regularly is difficult. However,
a high fluoride concentration in sound enamel cannot alone explain the marked reduction
in dental caries that fluoride produces (35,36). The prevalence of dental caries in a
population is not inversely related to the concentration of fluoride in enamel (37), and a
higher concentration of enamel fluoride is not necessarily more efficacious in preventing
dental caries (38).
The laboratory and epidemiologic research that has led to the better understanding
of how fluoride prevents dental caries indicates that fluoride's predominant effect is
posteruptive and topical and that the effect depends on fluoride being in the right amount
in the right place at the right time. Fluoride works primarily after teeth have erupted,
especially when small amounts are maintained constantly in the mouth, specifically in
dental plaque and saliva (37). Thus, adults also benefit from fluoride, rather than only
children, as was previously assumed.
(reference on reverse)
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. DEPARTMENT OF HEALTH &. HUMAN SERVICES
Public Health Service
Food and Drug Administration
Rockville MD 20857
DEe 2 I (U)J
The Honorable Ken Calvert
Chairman
Subcommittee on Energy and Environment
Committee on Science
House of Representatives
Washington, D.C. 20515-6301
Dear Mr. Chairman:
Thank you for the letter of May 8, 2000, to Dr. Jane E.
Henney, Commissioner of Food and Drugs, regarding the
use of fluoride in drinking water and drug products.
We apologize for the delay in responding to you.
We have restated each of your questions, followed by our
response.
1.
If health claims are made for fluoride-containing
products (e.g. that they reduce dental caries incidence
or reduce pathology from osteoporosis), do such claims
mandate that the fluoride-containing product be
considered a drug, and thus subject the product to
applicable regulatory controls?
Fluoride, when used in the diagnosis, cure, mitigation,
treatment, or prevention of disease in man or animal, is a
drug that is subject to Food and Drug Administration (FDA)
regulation. FDA published a final rule on October 6, 1995,
foranticaries drug products for over-the-counter (OTe) human
use (~opy enclosed). This rule establishes the conditions
under which OTC anticaries drug products are generally
recognized as safe and effective and not misbranded. The rule
has provisions for active ingredients, packaging conditions,
labeling, and testing procedures that are required by
manufacturers in order to market anticaries products. A new
drug application (NDA) may be filed for a product containing
fluoride that does not meet the provisions stated in the final
rule. As you know, the Environmental Protection Agency
regulates fluoride in the water supply.
.'"
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Page 2 - 'The Honorable Ken Calvert
2.
Are there any New Drug Applications (NDA) on file, that
have been approved, or that have been rejected, that
involve a fluoride-containing product (including
fluoride-containing vitamin products) intended for
ingestion with the stated aim of reducing dental caries?
If any such NDA's have been rejected, on what grounds
were they r~jected? If any such NDA have been approved,
please provide the data on safety and efficacy that FDA
found persuasive.
No NDAs have been approved or rejected for fluoride drugs
meant for ingestion. Several NDAs have been approved for
fluoride topical products such as denti~rices and gels.
Fluoride products in the form of liquid and tablets meant for
ingestion were in use prior to enactment of the Kefauver-
Harris Amendments (Drug Amendments of 1962) to the Food, Drug~
and Cosmetic Act in which efficacy became a requirement, in
addition to safety, for drugs marketed in the United States
(U~S.). Drugs in use prior to 1962 are being reviewed under a
process known as the drug efficacy study implementation
(DESI). The DESI review of fluoride-containing products has
not been completed.
3.
Does FDA consider dental fluorosis a sign of over
exposure to fluoride?
Dental fluorosis is indicative of greater than optimal
ingestion of fluoride. In 1988, the U.S. Surgeon General
reported that dental fluorosis, while not a desirable
condition, should be considered a cosmetic effect rather than
an adverse health effect. Surgeon General M. Joycelyn Elders
reaffirmed this position in 1994.
4. Does FDA have any action-level or other regulatory
restriction or policy statement on fluoride exposure
aimed at minimizing chronic toxicity in adults or
children?
The monograph for OTC anticaries drug products sets acceptable
concentrations for fluoride dentifrices, gels and rinses (all
for topical use only). This monograph also describes the
acceptable dosing regimens and labeling including warnings and
directions for use. FDA's principal safety concern regarding
fluoride in OTe drugs is the incidence of fluorosis in
el
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Page 3 - 'The Honorable Ken Calvert
children. Children under two years of age do not have control
'of their swallowing reflex and do not have the skills to
expectorate toothpaste properly. Young children are most
susceptible to mild fluorosis as a result of improper use and
swallowing of a fluoride toothpaste. These concerns are
addressed in the monograph by mandating maximum
concentrations, labeling that specifies directions for use' and
age restrictions, and package size limits.
.,.
Thanks again for,contacting us concerning this matter. If you
have further questions, please let us know.
..&~
Melinda K. Pla~sier
Associate Commissioner
"for Legislation
. "
Enclosure
"Final Rule/Federal Register - October 6, 1995
Over,..the-Counter Anticaries Drug Products"
.
.
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~.'"
~
National Federation of Federal Employees
P.o. Box 76082, Washington, DC 20013
202-260-238300 202-401-3139(F)
Local 2050
July 2, 1997
Mr. Jeff Green
Citizens for Safe Drinking Water
3243 Madrid Street
San Diego, CA 92110
Dear Mr. Green:
I am pleased to report that our union, Local 2050, National Federation of Federal Employees, has
voted to co-sponsor the California Citizens' petition to prohibit fluoridation of which your organization is
the sponsor. Our union represents, and is comprised of, the scientists, lawyers, engineers and other
professionals at the headquarters of the U.S. Environmental Protection Agency here in Washington, D.C.
A vote of the membership was taken at a meeting during which Professor Paul Connett and Dr.
Robert Carton made presentations, respectively, on the recent toxicological and epidemiological evidence
developed on fluoride and past actions (and their bases) of Local 2050 with respect to fluoride in drinking
water. The membership vote was unanimous in favor of co-sponsorship.
It is our hope that our co-sponsorship will have a beneficial effect on the health and welfare of all
Californians by helping to keep their drinking water free of a chemical substance for which there is
substantial evidence of adverse health effects and. contrary to public perception, virtually no evidence of
significant benefits.
These judgements are based, in part. on animal studies of the toxicity of fluoride coupled with the
human epidemiology studies which corroborate them. and the studies of rates of decayed, missing and
filled teeth in the United States (fluoridated and non-fluoridated communities) versus non-fluoridated
European countries.
Our members review of the body of evidence over the last eleven years, including animal and
human epidemiology studies, indicate a causal link between fluoride/fluoridation and cancer, genetic
damage. neurological impairment and bone pathology. Of particular concern are recent epidemiology
studies linking fluoride exposures to lower I.Q. in children.
As professionals who are charged with assessing the safety of drinking water. we conclude that the
health and welfare of the public is not served by the addition of this substance to the public water supply.
Best wishes to you and your organization for success in keeping what would otherwise be a
hazardous waste of the fertilizer industry from being disposed of in California's drinking water supplies.
Sincerely,
~y,~7if
Senior Vice-President
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UNITED STATES ENVIRPNMENTAL PROTECTION AGENCY
WASHiNGTCN. D.C. 20460
APR 2 /998
OFFICE OF
wATEI
George C. Glasser
301623rd Street N.
St. Petersburg, FL 33713
Dear Mr. Glasser:
Your March 4, 1998,lener to Carol Browner regarding the need for research on
tluorosilicic acid was forwarded to the Health and Ecological Criteria Division (HECD) of Office
of Science and Technology (OST) at the Office of Water (0'\\<). The Environmental Protection
Agency (EP A) appreci:1tes your interest in this matter.
In the United States, there are no Federal safety standards which are applic:1ble to
drinking water additives, including'those intended for use in fluoridating water. In the past, the
EPA assisted the States and public water systems through the issuance of advisory opinions on
:1cceptability of many additive chemicnls. However, the Federal advisory progr.un was
tenninated on October 4; 1988, and, EPA assisted in cstablishmcnt of voluntary product standards
at ~SF Intem:llional (NSF) in Ann Arbor, MichigiUl. American Nalional Slandards /nslitllle .
fANS/)INSF Slandard 60: Drinking Waler Treatmenr Chemicals - Health Effecrs was de"cloped
:1t ='lSF by a consonium ofrepresentatives from utilities. govcrnment. manuf:1cturers iUld the
public hC:llth community. The first 'edition of the StiUldard was issued in 1988. .Standard 60
applics to all direct addith.c chemic:11s for potable water including sodium fluoride.
hvdrofluosilicic acid :lI1d sodium tluosilic:lle. At the present time, both :"lSF and Underwriter.s
Labor:ltorics (Ul..) e"aluate additive products against Slanuani 60 criteria and publish a listing of
those products that meet the requirements of the StiUldard. You C:lI1 contact NSF or UL for
infonn:1tion on specific tluosilic:1te products.
, EP A does receive many requests for information on the tluosilic:1te :1dditives.
..~ccordingly, EPA is in the process of conducting :1 Jiter:lture se:u:ch and review of the data
a\':lilable on the he:llth effects :md chemistry of these materi:lls. This project should also identify
rese:lrch necds. It is :lI1ticip:lled th:1t the review of the :1v:lil:lble d:1la \vill be completed by this
coming Fall. EPA pliUls to use the d:1ta collected to prepare :l fact sheet that em be sent to
citizens, like yourself, who request infonnation on the fluosilicate additives used in fluoridation.
EP A will also share the information collected with the Chemical Manager for Fluoride at
A TSDR and with NSF international
If you have any funher question on this matter, please feel free to contact Dr.
Joyce Donohue at 202-260-1318.
Sin~
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(,- Office of Science and Technology
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Committee Personnel
The AWWA Standards Committee on Fluorides, which reviewed and approved
this standard, had the following personnel at the time of approval:
Thomas G. Reeves, Chair
James A. McKinzey, Vice-Chair
COMumer Memben
Shahin Rezania, Minneapolis Water Works, Minneap'olis, Minn.
Joseph Studgeon, Complex Administration - Bureau of Water,
Atlanta, Ga. '
J.S. Trotter, City of Bloomington Utilities, Bloomington, Ind.
Gerurallnterest Members
Frederick B'arker, Massachusetts Department of Public Health,
Boston, Mass. ' '
E.E. Baruth,* Standards Engineer Liaison, AWWA, Denver, Colo. '
G.L. Hoffman~ * Council Liaison, Finkbeiner, Pettis & Strout,
Akron, Ohio
R.M. Kril1, Bureau of Water Supply, Madison, Wis.
M.L. Magnant, Department of Public Health, Des Moines, Iowa
T.G. Reeve5', , Centers for Di~ease Control, Atlanta, Ga.
D.H. San'ders,t Centers for Disease Control, Atlanta, Ga.
R.R. Smith, City of Atlanta Water Department, Austell, Ga.
J.U. Tamburini, Rothberg, Tamburini & Winsor Inc., Denver, Colo.
M.L. Wentink, Nebraska Department of Health, North Platte, Neb.
Producer Members
Chuck Kl'epshaw, Cargill Fertilizer'In.., Riverview, Fla.
M.E. Looney, Chemtech Products Inc., St. Louis, Mo.
en ,
J.A McKinzey,LCI Ltd., Ponte Vedra Beach, Fla.
*Liaison, nonvoting
tAltemate
1998 American Water Works Association
, iii
(A WW A)
(AWWA)
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(AWWA)
(A WWA)
(A WW A)
(AWW A)
(A WWA)
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ENa.oSURE
Question 1
I understand that EPA does not endorse water fluoridation. Has the agency taken any steps
to have EP A removed from the list of endorserS of water fluoridation published by the" - ~ .', '
American Dental Association? If you have, have they complied?
, Response
EPA lacks the authority to require the addition of any material to drinking water for
preveiuive health care purposes unrelated to contamination [SDWA Section 1412 (b)(lI)].
For this reaSon, in 1997 when we became aware that we were listed on their web page, EP A
requested that the.American Dental Association remove EPA from the list of organizations
endorsing the fluoridation program. A copy of the letter to the American Dental
Association is enclosed. The American Dental Assodatio'it worked with EPA to insure that'
the reference to EPA on their web page accurately reflects our position relative to
fluoridation.
Question 2
What chronic toxicity test data are there on sodium fluorosilicate?
Onhydrofluorosilidc acid?
Response
Sodium fluorosilicate and hydrofluorosilicicadd are two of the Chemicals used in the
fluoridation of water supplies. In 1998, the Office of Water (OW) at EPA initiated the
development of a fact sheet to provide information on both of these chemicals for interested
citizens. A draft of that fact sheet has been completed and is presendy under review before
being finalized. In collecting the data for the fact sheet, EPA was not able to identify
chronic srudies for these chemicals. However, data from Crosby (1'969) [copy included]
indicate that both chemicals dissociate almost completely at the concentrations added to '
potable water forming hydrogen or sodium ions, fluoride ions, silicon dioxide and water.
Thus, the data from du'onic studies of sodium fluoride carcinogenicity by the National
Toxicology Program (NTP, 1990) and Proctor and Gamble (Mauercr al., 1990) are
applicable to sodium fluorosilicate and hydrofluorosilicic acid.
EPA does not regulate drinking water treatment chemicals. When a member of the public
contactS EPA regarding fluoridation chemicals, EPA refers that person to the agencies that
ceitilY drinking water treatment chemicals, NSF International and Underwriter's
Laboratories, for additional information. A copy of the enclosed. Regulatory Fact Sheet is
sent to the citizen with our response. When the enclosed draft fluorosilicate fact sheet is
finalized it will also be sent to those making inquires. .
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Response
Table 1 below summarizes those populations that the ATSDR Toxicological Profile (1993;
Section 2.7) identifies as sensitive and includes data on the prevalence in the United States of the
underlying physiological, nutritional, or age-related condition. It is important to note that the
population values in Table 1 are numbers of individuals that fall in each category. There are no
data to suggest that these individuals as a group are, or would be, sensitive to fl,uoride at the
levels found in the environment.
The demographic information for cardiovascular disease and renal disorders in Table 1 was
collected by the Office of Water as a component of an effort to identify sensitive populations in
the United States that might be senSitive to specific chemicals by virtue of their chronic disease
state (O'Dey et a!., 1998). Demographic data for the elderly come from a recently completed
study of water intakes by the Office of Water (Jacobs et a!., 2000). Prevalence values have been
rounded to the nearest million and were extrapolated from the survey population to the U.S.
, population. Data on nutrient deficiencies are from the U.S. Department of Agriculture 1994-
1996 Continuing Survey of Food Intake by Individuals (USDA, 1998). The values given are the
percent of the population consuming less than 75% of the Recommended Dietary Allowance for
the nutrient in question.
Table 1
Sensitive Populations
Sensitive Population Group (ATSDR, 1991) Estimated Population
Elderly 52,000,000 (>55 years)
Cardiovascular disease 22,000,000
Renal disorders 2,000,000
Vitamin C deficiency 27%
Magnesium deficiency 37%
Calcium deficiency 44%
Individuals that fall' in ,each of the categories listed in Table 1 have a number of specific risk
factors that impact their health status such as body weight, diet, and life style (e.g. smoking,
alcohol consumption). Advice on beneficial life style changes for each condition is best provided
by the medical community.
EP A is in the process of developing medical fact sheets to provide medical practitioners (doctors,
nurses, dietitians, etc.) with health data relative to drinking water contaminants that can be then
used in counseling patients. This work has just begun, and will initially focus on the elderly,
12
[reference on reverse)
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"Q\:~tion 2. Under ~neral Requirements 3.2.1. fonnulation submission and
reyiew. A NSIINSF 60 .]999. are manufacturers ofhydronuosilicic acid and
silicofluorides required to "submit for each product. when available. a list of
published and unpublished toxicolo2icaJ studies relevant to the treatment
chemical and the chemicals and.impurities present in tbe treatment chemical?"
The standard requires that the manufacturer of a product submitted for certification
provide toxicological information, if available. NSF requires that manufacturers seeking
certification to the standard submit this infonnation as pmt of their formulation or
ingredient supplier submission.
Has your document. General Requirements 3.2.1. Fonnulation submission and
reyiew. A NSIINSF 60 . 1999. been peer reviewed for accuracy? If so. please
provide the names. af1Uiations and contact infonnation for the peer reviewers.
The document (ANSIINSF Standard 60) bas been peer reviewed for accuracy. Joint
Committee and CPHC members and contact information are contained in Attachments
3, 7, and 8.
Please Drovide:
All lists complying with the above requirement submitted by manufacturers of
hydrofluosilicic acid and siliconuorides. '
NSFhas based its certification on the product use not exceeding the EPA's MCL for
fluoride. Separately, NSF has developed an MAL for silicates of 16 mg/L that supports
the silicate portion of the products in question. In addition, potential contaminants are
also limited by the standard. The supporting rationale for the silicate MAL is enclosed
in Attachment 15.
e,
The complete record of aU tests of each nuorine-bearln2 additive 85m2 ion
chrom8tOl~.raphv. atomic absorption spectroscopy. and scintillation coontinl-
NSF toxicology review and testing of fluorosilicate compounds looks for potential trace
contaminants such as heavy metals andradionuclides. Tbe fonnulation review step
examines notoDly the product formulation, but also considers potential contaminants
from the ingredients, processing. aids, and any other factors impacting contaminants in'
the finished drinking water. Contaminants in the finished drinking water are not
pennitted to exceed one-tenth of the EPA's regulated MCL (Maximum Contaminant
Level) when the product is added to drinking water at its Maximum Use Level, unless it
can be documented that a limited number of sources of the contaminant occur in
drinking water.
NSF has reviewed its tiles and has compiled a summary of our findings (Table 1) in
lieu of complete test reports. Individual test reports, as well as formulation infonnation
are protected by nondisclosure agreements with certification clients. '
NSF searched its files to deternUne the level of contaminants found in these
fluoridation products, when the product is dosed to water at the MaximUJll Use Level
(MUL). The exact number of laboratory tests perfonned is not readily available
e~
Page 6 of 10
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~ 'rue and complete copy of an tests ,that identify the full composition of eaCh
nuorine-bearine additive. inclu,dim! an attendant onanic substanceS. radioJluclides
and other chemicals.' ,
Compositional analyses are not required bytbe NSF standard. ~e verification of
composition is perfonned during the annual unannounced plant inspection by NSF auditors
who verify sources and ratios of labeled ingredients. Separately, there are industry
standards fromAWWA (American Wat~ Works Association) (ANSIIAWWA B702-99 for
Sodium Fluorosilicate and ANSIIAWWA B703a-97 for Auosilicic Acid) ,that provide for
compositional requirements.
..,. .
Copies of any and a)) tests or studies of each of the nuorine-bearin~, additives that,
consider or indicate dep-ee of dissociation.
The standard requires testing for contaminants that are likely to be present in the product. A
study by N.T. Crosby,published in1969 in, the Journal of Applied Olemistry (Volume 19),
establishes dissociation of fluotosilicates at. 99%, for 1 ppm fluoride concentrations in
drinking water.
Copies of anv and allstudies that have been perfonned on laboratory animals usinl
bydronuosilieic aei'" or siliconuorides.
NSF does not perform aniinal testing, although these may be required under Standard 60 if
hazardlrisk based action'levels are exceeded. NSF toxicologists may review animal studieS
during the. toxicology evaluation step of the product certification process.
',;
.
Copies of anY risk assessment documents in NSF JDternationalliles that pertaiD to
fluorine-bearin, pesticides. SOdl as c~olite;, .
Fluorine-containing pesticides such as, cryolite are not required analyses ullder the standard,
unless it is detennined to be part of the fonnulation, or a potential cOntaminant. NSF would
test for this or any'other contaminants if indicated duringtbe fonnulation ~ew step.
Question 3. Have any studies on hydroOuosiUeic aeidor siliconoorid~ been
~ubmitted to NSF under claimed Confidential Business Infonnation protection?
There have not been any studies on hydrofluosilicic acid or silicofluondes submitted to
NSF under claimed Confidential Business Information protection.
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Page 8 of 10
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UNITED STATES ENVIRONMENTAL PROTECTION AGENCY
WASHINGTON, D.C. '20460
JUN 2 3 1999
OFFICE OF
WATER
The Honorable Ken Calvert
Chainnan
Subcommittee on Energy and The Environment
Comminee on Science
House of Representatives
Washington, DC 20515-6310
Dear Mr. Chainnan:
Thank you for your May 10, 1999, letter to Carol M. Browner, Administrator of the
United States Environmental P(otection Agency (EPA) regarding fluoride and fluoridation.
Fluoride in drinking water is a subject about which EPA continues to receive a steady series of
questions from a number of concerned stakeholders. We have responded to each of your
questions in the enclosure to this letter.
.
Fluoride in drinking .water is regulated by EPA under Section 1412 ofthe Safe Drinking
Water Act (SD\VA). On April 2, 1986. EPA set a revised MCL at 4 mgIL to protect against
crippling skeletal fluorosis. an adverse health effect. In August 1993. the National Research
Council (NRC) completed a review of fluoride toxicity and exposure for EPA. The findings of
the NRC were published as. hHealth Effects oflngested Fluoride", National Research Council,
National Academy Press, Washington, D.C. 1993. The NRC concluded that the current 4 mgIL
standard is '.appropriate as an interim standard" to protect the public health. In addition, EP A set
a nonenforceable Secondary Maximum Contaminant Level of 2 mgIL to protect against
objectionable dental fluorosis (tooth discoloration).
The SOW A prohibits EP A from requiring the addition of any substance (including
fluoride) to drinking water for preventative health care purposes unrelated.co contamination
[Section 1412 (b)( 11)]. As a consequence. State or local authorities determine whether or not to
fluoridate their water supply. Depending on local 'Conditions, fluoridation in this country is
practiced at a Icvel of about 1 mg/L, which is well below the current 4 mg/L SDW A Federal
standard.
The Centers for Disease Control (CDC) is the principal Federal agency involved in
rcsearch on fluoridation in this count!)'. Some of the questions you have asked pertain to
.tluoridation rather than the EPA MCLlMCLG. For more detailed answers to those questions you
ma)' wish to contaCt:
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'In18m.' Address (URL) . hap:llwww.epa.goV
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ENCLOSURE"
Question 1
I understand that EP A does not endorse water fluoridation. Has the agency taken any steps to
have EP A removed from the listor endorsers of water fluoridation published by the American
Dental Association? If you have, have they complied?
Response
EP A lacks the authority to require the addition of any material to drinking water for preventive
health care purposes unrelated to contamination [SDW A Section 1412 (b)(11)]. For this reason,
in 1997 when we became aware that we were listed on their web page, EP A requested that the
American Dental Association remove EP A from the list of organizations endorsing the
fluoridation program. A copy of the letter to the American Dental Associati9n is enclosed. The
American Dental Association worked with EPA to insure that the reference to EPA on their web
page accurately reflects our position relative to fluoridation.
Question 2
What chronic toxicity test data .are there on sodium fluorosilicate? On hydrofluorosilicic acid?
Response'
Sodium fluorosilicate and hydrofluorosilicic acid are two of the chemicals used in the
fluoridation of water supplies. In 1998, the Office of Water (OW) at EP A initiated the
development of a fact sheet to provide information on both of these chemicals for interested
citizens. A draft of that fact sheet has been completed and is presently under review before being
finalized. In collecting the data for the fact shee~ EP A was not able to identify chronic studies
for these chemicals. However, data from Crosby (1969) [copy included] indicate that both
chemicals dissociate almost completely at the concentrations added to potable water forming
hydrogen or sodium ions, fluoride ions, silicon dioxide and water. Thus, the data from chronic
studies of sodium fluoride carcinogenicity by the National Toxicology Program (NTP, 1990) and
Proctor and Gamble (Mauer er aI., 1990) are applicable to sodium fluorosilicate and
hydrofluorosilicic acid.
EPA does not regulate drinking water treatment chemicals. When a member of the public
contacts EP A regarding fluoridation chemicals, EP A refers that person to the agencies that
certify drinking water treatment chemicals. NSF International and Underwriter's Laboratories,
for additional information. A copy of the enclosed Regulatory Fact Sheet is sent to the citizen
with our response. When the enclosed draft fluorosilicate fact sheet is finalized it will also be
. sent to those making inquires.
1
.
- ,<,.,
Dr. Gene Sterritt
Oral Health Program
Program Services Branch
NCCDHP/CDC
Mail Stop FI0
Davidson Building
2858 Woodcock Boulevard
Chamblee, Georgia 3034 I
-2-
Thank you for your thoughts and concerns; If you have any additional questions, please
feel free to contact me or have your stafT call Dr. Joyce Donohue, Toxicologist in the Office of
Water, at (202) 260-1318.
Enclosures
J. Charles Fox
Assistant Administrator
. ""
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and'EPA will publish and seek public comment on its findings as required by the SDWA Section
.. 1412 (b) (3) (C) (i) (V).
Question 5
.
.
Is the Agency satisfied with fluoride doses delivered to the public via drinking water under an
MCL(G) of 4 milligrams /liter (mglL) when added to the fluoride intake from dental products,
pesticide residues, food and'beverages will not cause an adverse health effect?
Response
EP A realizes that the use of fluoride in dental products has increased since fluoride was regulated
in 1986. In 1998, we commissioned an evaluation of the exposure data for fluoride i~cluding
data on amounts in foods and dental products. We found that the data published in the peer
reviewed literature were limited but did not differ substantially from the data available when
fluoride was regulated. A copy of the draft exposure report is included for your records. When
fluoride is selected for reevaluation of its MCUMCLG, the agency will again examine at relative
sources of exposure.
Question 6
What is the margin of safety for infants who consume drinkir:'g water containing 4 mgIL
fluoride?
Response
The agency does not recommend that infants consume water containing 4 mgIL fluoride. The
Agency requires that all families who receive water from a system with greater than 2 mgIL
fluoride receive a public notification recommending that alternate sources of water be used for
infants and children in that family [4OCFR 143.5]. A copy ofthe public notification statement is
enclosed for your records. The Agency believes that the 2 mg/L SMCL protects children against
dental fluorosis as well as adverse health effects. The Agency acknowledges that the MCL of 4
mgIL does not protect infants and children against dental fluorosis, a cosmetic effect rather than
an adverse health effect.
Question 7
What is the margin of safety for person's receiving kidney dialysis treatment, diabetes, or those
who have a hypersensitivity or allergy to fluoride who consume drinking water containing 4
mgIL fluoride?
3
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Question 3
What steps have.you taken to address questions related to the EPA's Maximum Contaminant
Level Goal (MCL[G]) for fluoride in drinking water? If you have not taken steps to address
these questions, why not? If not, when will you take such steps? When do estimate that the work
involved in addressing these questions will be complete?
.
Response
As required by the SDWA [Section 1412 (b) (B) (9)]. EPA is in the process of reviewing all
established MCLlMCLG values to detennine which chemicals require reevaluation due to recent
developments in our knowledge of their health effects. The chemicals that presently have
MCUMCLG values will be screened to select those needing reevaluation. Fluoride will be
considered in the review process. EPA has started the review of new data on the regulated
chemicals and intends to solicit stakeholder input regarding the review process at a meeting
tentatively scheduled for sometime in the fall of 1999.
In August 1993, the National Research Council (NRC) completed a review of fluoride toxicity
and exposure for EPA. The findings of the NRC were published as, "Health Effects ofIngested
Fluoride", National Research Council, National Academy Press, Washington. D.C. 1993. The
NRC concluded that the current 4 mglL standard is "appropriate as an interim standard" to
protect the public health.
.
Question 4
Do you interpret Section 101 (b) (4) of the Safe Drinking Water Act of 1996 as requiring EPA to
set its MCL(G) at a level that protects all person's including sensitive populations, such as
infants, children, people who drink 4 or more liters of water per day, people with allergies or
hypersensitivity to fluoride and.people with renal disease?
Response
The published Safe Drinking Water Act of 1996 does not have a Section 101 (b) (4). Section'
1412 (b) (4) (a) states that "Each maximum contaminant goal established under this subsection
shall be set at the level at which no known or anticipated adverse effects on the heath effects of
person's occur and which allows an adequate margin of safety."
As required by the SDW A [Section 1458 (a) (I )], EPA is working on collecting information to
identify groups within the general population with increased sensitivity to contaminants such as
infants, children. the elderly, persons with allergies or hypersensitivity to chemicals. When the
MCUMCLG for fluoride is selected for review, data on sensitive populations will be collected
2
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Qu'estioD 9
. ,
What steps has the agency taken to address the hazards identified with fluoride in the following
publications that appeared since EP A reaffinned it's drinking water standard for fluoride?
(Seven references are cited.)
Response
OW has reviewed each of the seven references listed and participated in discussions with the
EP A Office of Research and Development (ORD) regarding the strengths and weaknesses of
each study. (See the enclosed memorandum from William Marcus dated 5/22/98 and the 6/3198
response from Hugh Tilson ofORD.)The data presented in these publications will be utilized in
the review of the MCL values for presently regulated compounds discussed in the response to
Question 3 above.
5
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Response
Agency regulations for potable water do not apply to water used in dialysis. We suggest that you
contact the American Association for Medical Instruments (AAMI) for the standards that apply
to dialysis waters. The address for a contact at AAMI is as follows.
.
Dr. Ronald H Abrahams
American Association of Medical Instruments
Renal Disease and Detoxification Committee
Suite 3330 Washington Boulevard
Arlington, VA 22201-4598
703(525-4890)
The 1993 NRC report on the health effects of ingested fluoride addressed the concern for fluoride
retention in persons with impaired renal function, a group which includes individuals with
diabetes. They concluded that additional research was needed to adequately assess the risk. EP A
is not aware of new data on the health effects of fluoride in persons with impaired renal
clearance. Neither the NRC (1993) report nor the ATSDR (1993) Toxicological Profile on
fluoride provide data that identify any individuals with a fluoride-specific hypersensitivity or
allergy.
Question 8
Does the incidence of dental fluorosis among at least 22% of American children indicate that, at
least among these children, an overdosing is occuning?
.-
Response
The National Survey of Dental Caries in US school children (1986-1987) reported a prevalence
of dental fluorosis of22.3%. Nearly all of the cases were mild to very mild. These data reflect
exposures that occurred before the EP A MCUMCLG was implemented. Data from a
comparable study would have to be available for a time period before and after this survey in
order to determine if the prevalence of dental fluorosis in the population is actually changing.
The National Survey of Dental Caries data were considered by the NAS in their 1993 review of
fluoride. They concluded that the most Ueffective approach to stabilizing the prevalence and
severity of dental fluorosis without jeopardizing the benefits to human health, is likely to come
,from the more judicious control of fluoride in foods, processed beverages, and dental products,
rather than a reduction in the recommendation for fluoride in drinking water." NAS encouraged
the EP A to reevaluate the MCLlMCLG as more data on the factors contributing the severity of
fluorosis became available.
4
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(202) 225-6371
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http://www...-.gcr./8cIencto.welcome.htm
December 13, 1999
Maureen Jones
1205 Sierra Avenue
San Jose, CA 95126
Dear Ms. Jones:
Thank you for your letter on water fluoridation. I also greatly appreciate the reading
materials you sent.
.
Currently, the Committee on Science is investigating this very important issue. As you
may know, Ken Calvert, Chairman of the Subcommittee on Energy and Environment,
sent a set of questions to EP A Administrator Carol Browner in an attempt to better
understand EPA's position on this issue. I am sorry to say that EPA's answers were
extremely insufficient, and as such, the investigation will continue.
As Chairman of the House Science Committee, I have always fought to see that the very
best science is used in making regulatory decisions. Specifically in this case, many
questions still remain concerning the effects different kinds of fluoride might have on the
human body. I believe that the science is still out on this issue and I want to assure you
that I will continue fighting. .
Thank you again for keeping me informed on this very important issue. I hope you will
fee! free to contact me with any. further comments or concerns.
Sin~erely,
~
F. JAMES S
Chairman
FJS/jrd
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The Honorable Ken Calvert
. June 13,2000
Page 2
preclinical or Stage I skeletal fluorosis increases. Stage I rather than Stage III was used
as the adverse effect upon which the UL was based. Stage I skeletal fluorosis is
characterized by occasional stiffuess or pain in joints and some osteosclerosis of the
pelvis and vertebrae; bone ash fluoride concentrations are usually in the range of 6,000-
7,000 ppm (p. 307 of the DRl report). The severely debilitating condition called
crippling skeletal fluorosis is Stage III, in which bone ash fluoride concentrations exceed
9,000 ppm. The DRl report did not assert that crippling Stage III skeletal fluorosis would
occur at intakes greater than 10 ~g/day. As stated on page 307 of the report, evidence of
crippling fluorosis "was not seen in communities in the United States where water
supplies contained up to 20 ppm." In such communities daily fluoride intakes of 20
mg/day would not be uncommon.
Question la: Does NAS/IOM consider it acceptable for a person to begin intakes of 10
mg/day at age 9 years (let along previous intake of this cumulative agent at earlier stages)
and. then by age 19 be at risk of crippling skeletal fluorosis? '
Response: Based upon the response to question 1, there is no scientific evidence
indicating that fluoride intakes of 10 mg/day or less for 10 or more years would increase
the risk of developing Stage I skeletal fluorosis in humans aged 9 years and older. Thus,
a 19-year-old person would certainly not be at risk of Stage III crippling skeletal
fluorosis.
. During the last 35 years, only 5 cases of crippling skeletal fluorosis have been
reported in the United States as stated on page 308 of the DRI report. Only two of those
cases have reported an accurate fluoride intake (pp. S~O ofNRC, 1993). These
individuals consumed up to 6 liters of water per day with fluoride contents of2.4-3.5
,mg/L in the first case and 4.0-7.8 mgIL in the other. The fluoride intake for these
individuals was estimated at 15-20 mg per day for 20 years (pp. 59-60 ofNRC, 1993).
Question lb: Does the NAS/IOM consider it acceptable for a person to acquire Stage I
or Stage II skeletal fluorosis at any time in life? (Or are these considered "cosmetic"
effects?)
Response: The NAS/IOM does not consider it acceptable for a person to acquire Stage I
or Stage II skeletal fluorosis. All stages of skeletal fluorosis are adverse functional
, effects and are not considered cosmetic effects.
Question lc: What does the NAS/IOM consider the minimum dose at which Stage I ..-
skeletal fluorosis wiJ1 appear?
NATIONAL ACADEMY OF SCIENCES
- ~
OFFICE OF THE PRESIDENT
.
.
June 13, 2000
The Honorable Ken Calvert
Chairman
Subcommittee on Energy and Environment
Committee on Science
Suite 2230 Rayburn House Office Building
Washington, D.C. 20515-4410
Dear Mr. Chairman:
Thank you for your May 8, 2000 letter to the National Academies concerning
fluoride and National Academy of Sciences' reports on the topic. The most recent
NASnOM discussion of the role offl].loride in health is found in the 1997 10M report,
Dietary Reference intakes/or Calcium, Phosphorus, Magnesium, Vitamin D, and
Fluoride (DR! report). Enclosed is a copy of the report for your review, along with a
copy of the 1993 National Research Council report, Health Effects 0/ ingested Fluoride
(NRC,1993).
I hope the following comments in response to the questions posed in your letter .
regarding fluoride will be of use to you and other members of the House Committee on
Science: .
Comment 1: NAS/IOM's Dietary Reference Intakes (DR!) publication establishes 10
mglday as a tolerable upper intake level for those aged 9 years or older. The document
also asserts that crippling skeletal fluorosis (defined as Stage III skeletal fluorosis by
Roholm) can occur with intakes of 10 mg or greater per day for 10 or.more years.
Response: The tolerable upper intake level(UL)is defined as the highest level of total
chronic daily nutrient intake that is likely to pose no risk of adverse health effects in
almost all indiViduals in the specified life stage group. As intake increases above the UL,
the risk of adverse effects increases. The term tolerable intake was chosen to avoid
implying a possible beneficial effect. Instead, the term is intended to connote a level of
intake that can, with high probability, be tolerated biologically.
The UL for fluoride for children aged 9 years or older and for adults was '
established at 10 mglday. As explained in the DR! report on page 310, at intakes greater
than 10 mg/day for 10 or more years, the risk of skeletal changes consistent with
THE NATIOf'IAL ACADEMIES
.
Nalional Academy 01 Sciences Nalional Academy 01 Engineering Inslilut. 01 Meclicille Nalional Alsearell Council
2101 ConslilutionAvenue. NW. Washington. DC 20418 Phone: 202 334 2101 Internet: noliono\.ocodemiea.ClI9
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The Honorable Ken Calvert
. June 13,2000
Page 4
induced unscheduled DNA synthesis in human keratinocytes in culture, but doses of 8-
500 Jlg/mL did not induce unscheduled DNA synthesis in hwnan fibroblasts. These
results show a lowest effective dose inhumans of 100 J.lglmL (sodium fluoride at 100 Jlg
is equivalent to fluoride ion at 4S J.lg). This means that the concentration at which
, enzyme inhibition was observed in cell culture is 45 J.lglmL.This level is over 1000
times the highest steady-state concentration of fluoride ion (0.02-0.04 J.lg/mL) observed
in human plasma in two children, one 10-year-old and one 14-year-old, living in a
community where drinking water contained 9.6 mg/Loffluoride (Ekstrand, J. Caries
Res. 12: 123-127, 1979). In this community daily fluoride intakes of 10 mg/day or more
would be expected, assuming total local water intake of more than 1 liter per day.
(Although the weights of these two children were not given, it can be assumed, based on
anthropometric data collected from the 1988-1994 Third National Health and Nutrition
Examination Survey [NHANES III] in the United States, that the 10-year-old weighed
around 4S kg.) If the sensitivity of DNA synthesis in human keratinocyte~ in culture
fairly represents cellular sensitivity in the intact human and if a true threshold does exist
(pp. 100-101 ofNRC, 1993), then clearly a large margin of safety exists between fluoride
concentrations in human plasma at intakes of 10 mg and concentrations that may affect
DNA synthesis.
Request: Please provide the Committee with copies of any NAS publications, studies,
reports" memos, or any correspondence relating to fluoride and water fluoridation.
Response: Enclosed are copies of the two reports previously mentioned, letters received,
and responses sent since the release of the J?RI report.
Thank you again for your interest in the reports of the NASIIOM. If you have any
additional questions, please feel free to contact me or Allison Yates, Director of the Food
and Nutrition Board, at 202-334-1732.
Sincerely,
~~
ce Alberts; Ph.D.
President, National Academy of Sciences
-.
The Honorable Ken Calvert
June 13~ 2000
Page 3
. /I.
It
Response: As stated in the DRl report on page 310, at fluoride intakes greater than 10
mg/day for 10 or more years, the risk of skeletal changes consistent with preclinical or
Stage 1 skeletal fluorosis increases.
Question 2: Please provide a list of publications and curriculwn vitae for all members of
the NAS/I OM responsible for producing the section on fluoride of the DR!.
Response: Attached are biographical sketches of the members of the Standing
Committee on the Scientific Evaluation of Dietary Reference Intakes, the Panel on
Calcium and Related Nutrients, and the Subcommittee on Upper Reference Levels of
Nutrients. All three groups were responsible for the Dietary Reference Intakes for
Calcium, Phosphorus, Magnesium, Vitamin D, and Fluoride.
Question 3: Fluoride is well recognized' as a general enzyme poison (arising from its
powerful hydrogen-bonding propensity thatdisrupts protein [and DNNRNA] stnlctures)
and it displays high acute toxicity (around 5 mg/kg as threshold lethal dose), ranking as
an acute toxicant lying between lead and arsenic. A host of chronic toxic effects oflead
and arsenic are acknowledged by the science community (e.g., hematopoietic effects,
cardiovascular effects, neurologic effects, carcinogenicity, etc.). NAS/IOM's view of ~'
fluoride toxicity appears to be that ingested fluoride strengthens teeth, or will kil~ or will
inflict skeletal fluorosis, but it has no other chronic toxic effects as arsenic and lead do.
How does NAS/IOM explain this unique toxicological behavior of fluoride, especially in
light of its known effect on enzymes?
Response: Although fluoride has been reported to induce unscheduled DNA synthesis in
in vitro cells in humans and animals, other investigators have failed to show any such
effect (pp. 98-99 ofNRC, 1993). This unscheduled DNA synthesis was in mammalian-
cell culture enzymes that lack any possible protective effects of the whole organism. It is
not known how excess fluoride will affect enzymes in the intact human. In addition,
these effects on-'enzymes are based on acute doses of fluoride being added to cultured
cells at levels much higher than those observed in human diets. As stated in the response
to question I, the UL is defined as the highest level of chronic daily intake in humans and
thus acute effects occurring at levels above demonstrated chronic effects were not
considered in determining the UL.
Question 4: What is the minimwn concentration of fluoride ion at which enzyme
inhibition occurs? How does this concentration compare with serum levels of fluoride in
individuals of around 45 kg weight who ingest 10 mg/day of fluoride?
, Response: The latest NAS report to discuss enzyme inhibition effects was the 1993 .
National Research Council report, Health Effects of Ingested Fluoride (NRC, 1993). In r
this report as discussed on page 99, sodium fluoride at conceptrations of 100-300 flglmL
. . Fluorosilicate products are comprised of a fluoride entity as well as a silicate entity.
B~ed on previously published studies, there is'virtually complete dissociation of the
.. fluoride and silicate entities in dilute solutions. A$ such. the toxiCological evaluation of
fluorosilicate products is conducted through the evaluation of each entity separately.
ANSI/NSF Standard 60 requires, when available, that the U$. EPA regulated Maximum
Contaminant Level (MCL) be used to detennine the acceptable level for a contaminanL
The MCL for fluoride is 4 mgIL of drinking. water. As such. NSF has not independently
developed toxicology data to support this level of human exposure. The Maximum
AlIowable Level (MAL) for fluoride ion in drinking water from NSF Certified treatment
chemicals is 1.2 mgIL,.or less than one-third the EPA's MCL. The product Maximum Use
Level (MUL) certified by NSF ranges from 4 - 6.6 mgIL. ,
There is no EPA MCL for silicate in drinking water. When an MCL does not exist for a
contaminant. ANSINSF Standard 60 provides criteria to conduct a toxicological risk
assessment of the contaminant and the development of a Maximum Drinking Water Level
(MDWL). NSF bas established a Maximum Drinking Water Level of silicate at 16 mgIL.
A fluorosilicate product MUL of 4-6.6 mg/L results in silicate drinking water levels
substantially below the 16 mgIL MAL established by NSF for silicates. Attachment 1S
outlines the derivation of the NSF MAL for silicates.
.
In general. NSF Certified fluoridation products have been tested and found to comply
with the requirements of ANSIINSF Standard 60 for 12 additional inorganic chemicals.
Additional testing of these products for radionuclides has resulted in no measurements
above the detection limits. The specific answers below provide additional detail.
If there is any more infonnation that you need. please do not hesita~ to contact me.
Stan Hazan
General Manager
Drinking Water Additives Certification Program
734-769-5105
hvan @nsf.orIL
.
cc:
Dr. Joe CottUvo, NSF
Dr. Lori BesterVelt, NSF
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Page 2 of 10
CD
NSF International
ADD Arbor, MI . SacrameDto~ CA . Washington, D.C. . Brussels, B~ium
. .
July 7, 2000
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The Honorable Ken Calvert
Chainnan Subcommittee on Energy and the Environment
Committee OD Science
U. S. House of Representatives
Suite 2320, Rayburn House Office Building
WashingtOD, DC 20515-6301
Dear Mr. Chainnan:
Thank you. for your letter of May 8, 2000 to Dr. Joseph Cotruvo wherein you request
information from NSF International (NSF) on fluoride containing compounds. We
appreciate baving received an extension in order to allow NSF staff sufficient time to
provide a comprehensive response to your requesL
This response is comprised of a general infonnation section entitled Background on NSF
and the Drinking Water Additives Program and a.section that answers the 8 questions in
your letter. I have attached additional documents that will also assist in answering your
questions.
It is important to note that your questions relate to -two separate issues, and departments,
within NSF ..,. standards and product certification. First, ANSIINSF Standard 60 - the
American National Standard developed. by NSF and a consortium of major stakeholders
consisting of the American Water Works Association (AWWA), the AWWA Research
Foundation (AWWARF),the Association of State Drinking Water Administrators
(ASDWA), and the now inactive Conference of State Health and Environmental Managers
(COSHEM) was developed from 1985 to 1987. Second, NSF operates a separate product
testing, certification and listing program based on the requirements of the standard.
.
The health based principles of Standard 60 were originally developed by the NSF Health
Advisory Board (HAB) which is a panel of non-NSF health science experts. This group
continues its role in an advisory and oversight function to NSF and its Toxicology. staff to
assme that ANSIINSF Standards are consistent with current public health principles.
The standard and the certification program are reCognized and utilized by AWWA and its
member utilities, and adopted in most state regulations. More than 43 states have
regulations in place requiring product compliance with ANSIINSF Standard 60. (See
Attachment 14). The program provides a product quality and safety assurance that aims to
p~vent addition of hannfullevels of contaminants from treatment chemicals.
P.O. Box 1301'40 Ann Arbor. Michi,ao 48113..0140 USA
734-769-8010 1-800-NSF-MARK Fax 734-769-0109
E-Mail: iDfo@DSf.org Web:http://www.osf.cq
Page 1 of 10
'.
. .Back~OUDd on NSF and the Drinkine Water Additives Proeram.
NSF International was established in 1944, as an independent, not-for-profit,third party
.' organization dedicated to the protection of public health and safety. NSF bas more than
300 employees consisting of engineers, chemists and toxicologists wbodevelop U.S.
national standards and provide independent product testing and certification services for
products that impact food, air, water and the environment NSF is a World Health
Organization (WHO) Collaborating Center on Drinking Water Safety and Treatment, as
well as for Food Safety.
.
.
NSFinvolvement in the evaluation of drinking water chemicals, including fluoride-based
chemicals, began in 1985, when the U.S. EPA granted an NSF-led consortium of
stakehold~ the responsibility to develop consensus, health-based, quality specifications
for drinking water treatment chemicals and drinking water system components
(Attachment 1). EPA also requested development of a product testing and certification
program that would allow for independent product evaluations for use by states, cities,
and water utilities, as a basis for product acceptance and use.
The original goal of the standard. and certification program was to develop a preventative
mechanism for selecting treatment chemicals that would not contribute hannfullevels of
contaminants to drinking water. The standards and the certification program were
designed to be dynamic, to change as regulations change, and to constantly be tied to the
. requirements of the Safe Drinking Water Act and its drinking water quality regulations. In
1988, EPA tenninated its informal chemical additives advisory program upon completion
of the NSF standards and successful launch of the NSF product certification program
(Attachment 2). We believe that the NSF standards and certification program have
succeeded in achieving the goals of the original mandate. .
The NSF Certification program consists of seven steps for initial product certification, and
4 steps on an annual basis. (See Attachment 13).
Today, NSF provides testing and certification services for thousands of products from
more than 30 countries. NSF publishes its listings on its web site at www.nsf:mw as weB
as in hardcoPY (Attachment 12). In addition, attached is a copy of the NSF Certification
Policies for Drinking Water Treatment Olemicals (Attachment 9). This document outlines
the rules that govern the product certification program, over and above the requirements
of the standard.
Page 4 of 10
List of Attachments
Attachment
1
2
3
4
5
6
7
8
9
10
11
12
13
14
IS
, 4
Descri tion
FR Notice 5/17/84 - Dis osition of the Federal OWA Adviso Pro
FR Notice 7n188 - Termination of the Federal OWA Pro ,Notice
ANSlINSF Standard 60 - OW Treatment Chemica1s- Health Effects
ANSlINSF Standard 61 - OW S stem Com nents- Health Effects
NSF Standards Oevelo ment and Maintenance Policies
Standards U date -Flowchart of the Standards Devel ment Process
1987 NSF OWA Joint Committee MemQers . List
1987 NSF Council of Public Health Consultants list .
NSF Certification Policies for DW Treatment Chemicals - Standard 60
Toxicolo Data Review Submission Fonn - Part A
Toxicolo Data Review Submission Form - Part B
NSF DWA Listin Book
NSF DWA Certification Process -7 St
ASDWA State Surve of Ado tion of ANSIINSF Standards 60 and 61
NSF MAL perivation for Silicates in Drinkin Wata
,
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Page 30f 10
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. . Q.uestion 2. Under General Requirements 3.2.1. formulation submission and
review ANS~SF 60 -1999. are manufacturers orb roO ili ic acid and
.. ~jliCon~orid',' requiml 10 ''1;ubmil for eoch product. lfheJI 0..00*. o list 0(
published and unpublished toxicolol!ical studies relevant to tbe treatment
chemic I and the che i sa' ' .. e' nt cbemi .",
The standard requires that the manufactUrer of a product submitted for certification
provide toxicological information, if available. NSF requires that manufacturers seeking
certification to the standard submit this information as part of their fonnulation or
in~ent supplier submission.
)Iss.your docuQ)ent. General Requirements 3.2.1. Formulation submission and
:vlew AN..,I!l'!SF 60 - ] . been e r nviewecU r c:cu 11 so
. rovid~ the names. afTiliations and contact information for the peer reviewers.
The document (ANSIINSF Standard 60) has been peer reviewed for accuracy. Joint
Conunittee and CPHC members and contact information are contained in Attachments
3, 7, and 8.
.
Please nTO.Vi:e: . ' ,
~lIlists com lyi~ with the above requirement submitted by manufacturers or
bydrofluosilicic acid and silicofluorides. . '
NSF bas based its certification on the product use not exceeding the EPA's MCL for
fluoride. Separately, NSF has developed an MAL for silicates of 16 mg/L that supports
the silicate portion of the products in question. In addition, potential contaminants are
also limited by the standard. The supporting rationale for the,silicate MAL is enclosed
in Attachment 15.
The cOll\Plete record of aU tests of each fluorine-bearin, additive usine ion
chro to ra h at m.c a 0 ti n s co a d .n.na on coon .
NSF toxicology review and testing of fluorosilicate compounds looks for potential traee
contaminants such as heavy metals and radionuclides. The fonnulation review step
examines not only the product fonnulation, but also considers potential contaminants
from the ingredients, processing aids, and any other factors impacting contaminants in
the finished drinking water. Contaminants in the finished drinking water aIe'not
pennitted to exceed one-tenth of the EPA's regulated MCL (Maximum Contaminant
Level) when the product is added to drinking watez at its Maximum Use Level, unless it
can be documented that a limited number of sources of the contaminant occur in
drinking water.
NSF bas reviewed its files and has compiled a summary of om findings (Table 1) in
lieu of complete test reports. Individual test reports, as well as formulation infonnation
are protected by nondisclosure agreements with certification clients. '
NSF searched its files to determine the level of contaminants found in these
fluoridation products, when the product is dosed to water at the Maximum Use Level
(MUL). The exact number of laboratory tests perfonned is not readily available
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Page 6 of 10
This section provides responses to the 8 questions in your letter.
. .
Question 1. Please provide the identification and affiliation of each member of the
committee or committees contributine to the policies established for each of the
fluorine-bearin2 additives destined for the public water supplies. both current
committee members and those responsible for establishin2 product standards for
fluoride.
.
In response to an identified need for health-based standards dealing with drinking water
contact prodUCts, a consortium led by the National Sanitation Foundation (nowNSF)
worked to. develop voluntary third-party consensus standards for all direct and indirect
drinking water additives. Other consortium members were the American Water Works
Association (A WWA), the American Water Works Association Research Foundation
(AWWARF), the Association of State Drinking Water Administrators (ASDWA) and the
Conference of State Health and Environmental Managers (COSHEM, now inactive).
ANSIINSF 60 Drinking water treatment chemicals - Health effects was initially adopted
in December 1987, and was last revised in May 2000. It establishes minimum human
health effects requirements for the chemicals that are added directly to drinking water for
its treatment or other purposes. The standard was developed using a consensus standards
development process with representation of the major stakeholder interests, including
product manufacturers, product users such as consultants and water utilities, and
representatives from the regulatory/public health sectors. As an American National
Standard, each revision to ANSIINSF 60 also undergoes a public comment review. This
public comment process allows for any interested party to obtain a copy of the proposed
revision and to submit comments or objections to NSF. All comments received are .
handled in accordance with the due-process requirements set forth in the ANSI procedures
and NSF policies.
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Each edition of ANSIINSF60 contains a list of the committee members who oversee the
development and review of that edition of the standard. These committees consist of the
NSF Joint Committee for Drinking Water Additives, the balanced group of approximately
36 representatives from the user, regulatory and manufacturing sectors, and the NSF
Council of Public Health Consultants, which is a group of approximately 4S independent,
public health experts from government, academia and the environmental bealth
community. The current version of ANSl/NSF 60 (2000) is enclosed for your review
(Attachment 3), as well as a list of the membership of these committees when the
Standard was first adopted in 1987 (Attachments 7 and 8). Copies of the NSF Standanls
Development and Maintenance Policies (Attachment 5) and "Standards Update"
(Attachment 6) are also enclosed to provide further detail on the standards development
process.
Page S of 10
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,,8 true and complete copy of all tests that identify the full composition of each
niJorine-bearinl! additive. includin2 all attendant oreanic substances. radionuclides
Jlnd other chemicals.
Compositional analyses are not required by the NSF standard. The verification of
composition is perlonned during the annual unannounced plant inspection by NSF auditors
who verify sources and ratios of labeled ingredients. Separately, there are industry
standards from A WWA (American Water Works Association) (ANSIJAWWA B702-99 for
Sodium AuorosiIicate and ANSIJAWWA B703a-97 for FJuosilicic Acid) that provide for
compositional requirements.
!:opies of any and all tests or studies of each of the fluorine-bearine additives that
consider or indicate deeree of dissociation.
The standard requires testing for contaminants that are likely to be present in the product. A
study by N.T. Crosby, publisbedin.1969 in the Journal of Applied Chemistry (Volume 19),
establishes dissociation of fluorosilicates at 99% for Ippm fluoride concentrations in
drinking water.
Copies of anY and all studies that have been perfonned on laboratory animals us1nr
.r. "d ... n .d
JJydronuosl ICIC BCI, or SIICO uon es.
NSF does not perlonn animal testing, although these may be required under Standard 60 if
hazard/risk based action levels are exceeded. NSF toxicologists may review animal studies
during the toxicology evaluation step of the product certification process.
Copies of anY risk assessment documents in NSF JnternBtionalfiles that pertain to
fluorine-bearin, pesticides, such as cry91ite.' '
Fluorine-containing pesticides such as cryolite are not required analyses under the standard,
unless it is detennined to be part. of the fonnulation, or a potential contaminant. NSF would
test for this or any 'other contaminants if indicated during the fonnulation review step.
puestion 3. Have any studies on hydroOuosiUcic acid or silicofluorides been
;ub~itted to NSF under claimed Confidential Business Infonnation protection?
There have Dot been any studies OD hydrofluosilicic acid or silicofluoiides submitted to
NSF under claimed Confidential Business Information protection.
Pap 8 of 10
because we maintain records only on those tests where a contaminant was detected.
The results in Table 1 include initial product tests as well as annual product monitoring
tests. In total, these products have been tested more than 100 times in our laboratories.
Table 1 indicates that metals contamination of drinking water as a result of fluoride
chemical use is not an issue. There has not been a single fluoride product tested with a
metal concentration in excess of its corresponding MAL.
Silica and silicates, which make up a portion of the fluoridation chemicals mentioned
above, are addressed by the certification of sodium silicates to a level of 16 mgIL under
ANSI/NSF Standard 60. (See Attachment 15).
Beginning in early 1998, NSF went beyond Standard 60 requirements and voluntarily
began testing fluoridation chemicals for the presence of radionuclides (alpha and beta
emitters) utilizing EPA Test Method 900.0, as specified in Annex B of ANSUNSF
Standard 60. To date, w~ have not found any sample with a positive (detected) result, with
detection limits of 4 pCi/liter and 3 pCiIliter for gross alpha and gross beta, respectively.
Table 1
Number of Average Maximum ANSl/NSF US EPA
fluoride Contaminant Contaminant Standard 60 Maximum
Samples Concentration Concentration Maximum Contaminant
with in Samples in Samples Allowable Level
positive with Positive with positive Level (MQ..)
Test Test Results'" Test Results (MAL)
Results (uub) (uob) (nnb) (uub)
Antimonv 0 NA- NA 0.6 6
Arsenic 39 0.43 1.66 2.5** 50
Barium 1 o. 19 0.17 200 2000
Bervllium 5 0.21 0.3 0.4 4
Cadmium 3 0.06 0.1 0:5 5
Chromium 3 0.14 0.2 10 100
Couoer 8 0.49 0_55 130 1300
Lead 7 0.4 1.1 1.5 15
Mcn;w y 5 0.013 0.015 0.2 2
Nickel 0 NA NA NA NA
Selenium I 0.60 0.6 5 50
Thallium 6 0.03 0.05 0.2 2
Radionuclides 0 NA NA - -
"'Only those samples where a contaminant was detected contribute to the average. The average
contaminant concenrrationforall samples tested is significantly lower, and is affected by detection
limits and number of detections.
"'* ANSI/NSF Std 60 utilizes Canadian MACs and EPA MCLs in detennination of MALs.
Page 7 of 10
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. Question 7. Under what circumstances or authority is an additive certified when the
MAL of 10% of the establisbed MCL is exceeded?
. An MAL of greater than 10% of the MCL can be establisbed by the certification body in
. limited cases if it can be reasonably documented that there are no other significant sources
of the same contaminant, that together, would result in the finisbed drinking water
contaminant concentration exceeding the MCL. Fluoride bas an MAL of 1.2 mg /liter,
which is 30% of the MCL. This is justified on the basis of the limited number of other
potential sources of fluoride ion to drinking water. For example, water that naturally
contains sufficient fluoride is not additionally fluoridated, and fluoride is seldom present in
other additives. '
.
--
uestion 8. What tests and how often are the nonn t atio
:ietermine the exact consistency and concentratioJL41 of all contaminants ill
h,.dronuosilicic acid siliconuor"d 'd s .om Boride t e
~r NSF Inte..,..atipD8J mls to shlpmenlli by 1P8I)IIfacturen of lb. a~!litives? Are NSF
International test results compared with ~ertificates of A nalvses as a ouaUty
pssnrance mea..Qlft?
As indicated in question 2, the testing required by the standani is for regulated metals.
NSF additionally perfonns radionuclides analysis. Contaminant testing is performed
initially upon application, and at least annually thereafter. Samples are collected during
unannounced inspections by NSF auditors.
As mentioned previously, NSF tests products at least once per year. A contract signed by
the NSF Certified manufacturer precludes production or process changes without written
consent from NSF.
NSF test results are not routinely compared to Certificate of Analyses results. Certificates
of Analyses often report on parameters not requ~ under ANSVNSF Standard 60. For
example, the AWWA standards mentioned previously require testing for fluoride content,
moisture, impurities, etc. The A WWAstandards also incorporate the option of additional
purchaser specifications.
plf'.JlSe provide the committee with CQpies of any NSF International pubHcatio-,
~tudies: and reoorts relatlD2 to Ouoride.
As mentioned earlier, NSF relies on the U.S. EPA MCL and its supporting documentation,
as specified in the standard. See attachments listed in the cover letter.
Page 10 of 10
Question 4. What are the Maximum Contaminant Levels. or any other reeulatol1'
standards eswbJished for the fo))owin contaminants eithr sin arl in
combinati~n "itb another substance. or in the elements' variousfonns) or any other
contaminants re orted as resent in the nuorine-bearin sub tanc::es h drofluosilicic
acid and other siliconuorides used in fluoridation prouams?
Maximum Contaminant Levels (MCLs) can be found in Annex E of the enclosed copy of
ANSI/NSF 60. Annex E 'of Standard 60 lists the federally regulated MCLs. Of the
contaminants listed in your letter, MCLs exist fQr arsenic, barium, beryllium,. cadmium,
chromium, fluoride, lead, mercury, selenium, and dioxin (as 2,3,7,8-TCDD). Federal
regulatory standards have not been established for the remaining contaminants listed in
your letter.
. .
.
Question s. What tests are performed to identify the full and exact consiste~ of
tbe nuorine-bearin rod ct and determi tbe concen tio of
~ntaminants oreo~bination of contaminants in a sample? Upon what occasion or
fre uene are these tests. erfonned? Are Certificates of Anal s vided wi h ea
~hi;ment or sucb products from the manufacturer?
NSF tests certified products at least annually for prospective contaminants (See response to
Question 2). An NSF Certified company may produce many shipments during the course
of the year, but the company is contractually bound to not cbange the fonnulation ratios,
ingredients or add unauthorized sources of supply. Certificates of Analyses are typically
provided by the. vendor to the utility on a per sbipment basis. There are industry standards
from AWWA(American WaterWorks Association) (ANSllAWWA B702-99for Sodium
Fluorosilicate and ANSll A WWA B703a-97 for Fluosilicic Acid) that provide for affidavits
and Certificates of Analyses.
. Question 6. What is tbe purpose of establishine a maximum allowabl, level (MAL)
for additives ~trietin the con 'bution to drinki wat r an one u
}O% of the Maximum Contaminant Level (MCLl?
The purpose of establishing a maximum allowable level (MAL) for individual drinking
water additives products at 10% of the MCL is to recognize that contaminants may enter
drinking water from other points througbout the system,.inc1uding the source water, during
the treatment and distribution process, and either through direct addition or surface contact.
Limiting individual products to a contribution of 10% of the MCL for a given contaminant
provides an extra margin of safety so that it is unlikely that the summation of the
contributions from all potential sources will exceed the MCL at the tap.
"
Page 9 of 10
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~ DEPARTMENT OF HEALTH & HUMAN SERVICES
l
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tit
Public Health Service
Centers for Disease Control
and Prevention (COC)
Atlanta GA 30333
. ..
AUG 8 2000
The Honorable Kenneth Calvert
Cbainnan, Subcommittee on
Energy and Environment
Committee on Science
House of Representatives
Washington, D.C. 20515-6301
Dear Mr. Calvert:
Thank you for your letter requesting that the Centers for Disease Control and Prevention (CDC)
respond to comments and questions regarding the use of fluoride and enamel fluorosis.
I
CDC has recognized community water fluoridation as one of the great public health
achievements of the 20th century in its Morbidity and Mortality Weekly Report (MMWR) (copy
enclosed). Fluoridation of community drinking water is a major factor responsible for the
decline in dental caries (tooth decay) during the second half of the 20th century. Although other
fluoride-containing products are available, water fluoridation remains the most equitable and
cost-effective method of delivering fluoride to all members of most communities, regardless of
age, educational attainment, or income level. The per capita cost of water fluoridation over an
entire lifetime can be less than the cost of one dental filling; however, approximately 100 million
American children and adults (38 percent of Americans served by public water systems) do not
have access to water containing enough fluoride to protect their teeth.
Enclosed are COC's responses and copies of related publications, studies, and reports. We
appreciate the opportUnity to discuss the benefits of water fluoridation and hope this information
is helpful.
Sincerely,
p~
Jeffrey P. Kaplan, MD., M.P.H.
Director
Enclosures
1
ENCLOSURES
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Questions and Answers
MMWR Article - Ten Great Public Health Achievements-United States, 1900-1999
MMWR Article - Water Fluoridation and Costs of Medicaid Treannent for Dental Decay-
Louisiana, 1995-1996
Reference List
At-A-Glance - Improving Oral Health: Preventing Unnecessary Disease Among All Americans
Community Water Fluoridation Pamphlet
Water Fluoridation - nature's way to prevent tooth decay pamphlet
MMWR Article - Public Health Focus: Fluoridation of Community'Water Systems
MMWR Article - Engineering and Administrative Reconunendations for Water F"luoridation,
1995
MMWR Article - Knowledge of the Purpose of Community Water Fluoridation - United States,
1990
MMWR: Article - Fluoridation of Drinking Water to Prevent Dental Caries
National Fluoride Plan to Promote Oral Health, June 1996
Fluoride: The Benefits Can Last a Lifetime
Papers Published by Thomas G. Reeves, M.S., P.E. (CDC Fluoridation Engineer)
Water Fluoridation - A Manualfor Water Plant Operators
Water Fluoridation - A Manual for engineers and Technicians
Fluoridation Census 1992
Policy Statement on Community Water Fluoridation-July 22, 1992
Surgeon General Statement on Community Water Fluoridation-December 14, 1995
Correspondence Regarding Fluoride
Periodic Memoranda Over the Past 20 Years
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The Centers for Disease Control and Prevention's Responses to
Questions from the Honorable Kenneth Calvert, Chairman, Subcommittee on
Energy and Environment, Committee on Science, House of Representatives
Regarding the Use of Fluoride and Fluorosis '
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Question 1
Given that nonnal, healthy teeth do not display fluorosis, does CDC consider the appearance of
dental fluorosis in an individual as a sign of too much exposure to fluoride? If not, why not? If
so, at what incidence level in the population would CDC consider that the population as a whole
is receiving too much fluoride. If CDC does not consider dental fluorosis to be a sign of over
exposure, would eDC be comfortable with a 100% incidence of dental fluorosis in America's
children?
Given that nonnal, healthy teeth do.not display fluorosis, does CDC consider the appearance of
dental fluorosis in an individual as a sign of too much exposure to fluoride'? If not, why not'?
Response 1
Yes, CDC considers the appearance of the moderate to severe fonns of enamel fluorosis in an
individual as a sign of too much exposure to fluoride during the time the enamel of these teeth
had formed. Enamel fluorosis is the broad term applied to the range of certain visually detectable
changes in opacity (white spots) determined to be areas of fluoride-related hypominera1ization;
many developmental opacities in enamel are not fluoride-related. This cosmetic condition can
occur only during a relatively narrow period of childhood when young children ingest fluoride
during. susceptible periods of tooth enamel development.
Although the vast majority of enamel fluorosis today is of the mildest form that affects neither
cosmetic function nor tooth function, its increased prevalence in both non-fluoridated and
fluoridated areas suggests that during the first 6 to 8 years of life (the only time during which
fluorosis can develop), the total intake of fluoride has increased since the United States began to
use fluoride to prevent tooth decay. Since studies have demonstrated that fluoride intake from
water and the diet by children in fluoridated areas has not increased since water fluoridation
began in 1945, the increased intake by young children almost certainly derives from the
ingestion of fluoride from fluoride dental products. including the inadvertent swallowing of
toothpaste and inappropriate prescriptions of fluoride supplements.
Steps have been taken over the past 20 years to limit this condition while preserving the
substantial caries preventive benefits for children and ,adults. In 1979. infant formula
manufacrorers reduced the amount of fluoride in infant fonnula. Since 1986. the Environmental
Protection Agency regulations require that public water systems witb.natural fluoride
concentrations over two parts per million (ppm) annually notify their customers about use of
alternative water sources for children under age 8. In 1992, labels for toothpaste included
directions to use a pea-s~ amount of toothpaste for children under age 6. In 1994, the
3
American Dental Associati~n, the American Academy of Pediatrics, and the American Academy
of Pediatric Dentistry developed a revised schedule for fluoride supplements, which reduced the
.. fecomrnended amounts for children under age 6. In 1996, the Food and Drug Administration
posted further guidance on toothpaste labels to guide parents on proper supervision of young
children.
Question lA
If so, at what incidence level in the population would CDC consider that the population as a
whole is receiving too much fluoride.
RespODSe lA
The prevalence of moderate to severe enamel fluorosis is not necessarily an indication of the
fluoride intake of the population as a whole. Factors that can affect fluoride intake in this young
age group (less than age 6), such as inadvenent swallowing of toothpaste, can change with age
and do not affect the teeth once they are fonned. Early studies of fluoride by H. T. Dean
establishecl a "minimal threshold" (1.0 ppm) of fluoride in the water where there was maximal
caries (tooth decaY) prevention and enamel fluorosis that was "of no public health signifiCance."
At 1.0 ppm there was approximately 10-15 percent prevalence of very mild and mild enamel
fluorosis (barely noticeable) as well as a dramatic decrease in dental caries prevalence (greater
than 50 percent) and. as a result, a dramatic increase in the number of normal, healthy teeth.
CDC analyzed data from the 1986-1987 National Institute of Dental Research (NIDR) National
Survey of Oral Health, a survey designed to measure both the number of decayed, missing, and
filled pennanent teeth as well as the more exact number of tooth surl'aces affected. The overall ,
prevalence of very mild, mild, and moderate and severe fo.nns of enamel fluorosis in U.S. school
children was 23.5 percent, of which 18 percent was categorized as very mild, mild 4 percent, and
moderate. and severe 1.5 percent. This level, 23.5 percent, is considered below the level that
would be of public health significance, using the Community Fluorosis Index developed by Dean
(Dean 1942). In 2003, CDC expects to update data on enamel fluorosis prevalence and severity
after the first phase of the National Health and Examination Survey IV (NHA-S IV).
Question IB
If CDC does not consider dental fluorosis to be a sign of over exposure, would CDC be
comfortable with a 100% incidence of dental fluorosis. in America's children?
RespoDSe IB
CDC does not find 100 percent prevalence of any fOnD of enamel fluorosis as acceptable. Since
the time of the pioneering studies of fluoride in water in the 1 920-1 9308 by Dean, McKay, and
others, the existence of a low level of very mild and mild enamel fluorosis was, and still is,
.
It
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'regarded as far outweighed by the substantial reductions in tooth decay and its sequelae due to
optimal concentrations of fluoride.
. Question 2 '
What is. the cost nationwide of repairing fluorosed teeth? If you do not have data, what is COC's
estimate of the cost, and when will you have the data?
Response 2
COC is unaware of local, State or national data on the cost of repairing fluorosed teeth. It is not
currently possible to accurately estimate the cost of fluorosis-related treatment. Cunent insurance
coding for dental procedures does not include the reason for restoration or procedure, and there
are other causes of enamel opacities (white spots) that might prompt cosmetic treatment that are
not fluoride-related. Also, infonnation regarding the proportion of children with moderate or
severe enamel fluorosis who seek elective treatment is not available.
Question 3'
What is the basis for using the second most damaged tooth as the index for determining whether
dental fluorosis is present and its severity? In other words, why must at least two teeth present
with fluorosis before the diagnosis is made?
.
Response 3
Because enamel fluorosis typically occurs bilaterally and rarely occurs on only one tooth, one
should expect to find similar changes on both sides of the mouth (e.g., both central incisors).
Therefore, at least two teeth with opacities are considered when making a differential diagnosis.
The scores from Dean's Index are based on the most severe fonn recorded for at least two teeth
(Dean 1942).
Question 4
What is COC's view regarding the value of the Precautionary Principle as a basis for public
health protection?
Response 4
CDC encourages public health decisions that minimize disease and maximize good health. In
doing so, COC considers the accuracy and representativeness of scientific evidence regarding
both established and hypothetical risks and benefits.
Tbe precautionary principle focuses on risks for which scientific evidence is lacking. It is most
useful for public health protection when confronting newly-identified risks and where the
avoidance of risk poses no threat to health. The principle is less applicable when adequate
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5
scientific information on risks has been u'sed for making policy decisions. Also, it does not offer '-.
guid~ce in situations where interventions to reduce a risk to health would increase another
. 'health risk at the same time. In such situations, the weight of scientific evidence regarding risks
and benefits should be compared before a cbangeis made in. public health policy.
Question S
Please provide specific citations for the studies that CDC regards as most persuasive in proving
that ingested fluoride reduces incidence of dental caries? If the 1986- 1987 National Survey is
not included, why not? If it is included, please provide the rationale for that study using decayed
or filled surfaces, rather than decayed, missing or filled teeth, as the reported metric? If it is
included, how does CDC account for scatter among fluoridated, partially fluoridated and
non-fluoridated communities with respect to ranking for lowest caries incidence?
Please provide specific citations for thestu,dies that CDC regards as most persuasive in proving
that ingested fluoride reduces incidence of dental caries?
Response -
Dean HT, Arnold FA, Jay P, Knutson JW. Studies on mass control of dental caries through
fluoridation of the public water supply. Public Health Rep 1950;65:1403-1414.
Arnold FA Jr., Likins RC, Russell AL, Scott DB. Fifteenth year of the Grand Rapids fluoridation
study. J A Dent Assoc 1962;65:780-5.-
Ast DB, Fitzgerald B. Effectiveness of water fluoridation. J Am Dent Assoc 1962;65:581-7.
Blayney JR, Hill IN. Fluorine and dental caries.JAm DentAssoc 1967;74(SpecIssue):233-302.
Hutton WL, Linscott BW, Williams DB. Final report of local studies on water fluoridation in
Brantford. Can J Public Health 1956;47:89-92
Dean lIT, Jay P, Arnold FA Jr., Elvove E. Domestic water and dental caries U. A study of2,832
white children ages 12- 14 years of eight suburban Chicago communities, including L.
acidopbilus studies of 1,761 children. Public Health Rep 1941;56:761-92.
Dean lIT, Arnold FA Jr., Elvove E. Domestic water and dental caries. Additional studies of the
relation of fluoride in domestic waters to dental caries experience in 4,425 white children, ages
12 to 14 years, of 13 cities in 4 States. Public Health Rep 1942;57:1155-79.
u.S. Public Health Service, McClure FI, Ed. Auoride drinking waters: a s~lection ofPubli~
Health Service papers on dental fluorosis and dental caries; physiological effects, analysis, and
chemistry of fluoride. Public Health Service Publication No. 825. 1962.
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6 "
Backer-Dirks a, Houwink, Kwant GW. The results of 61/2 years of artificial drinking water in
_the Netherlands: The TIel-Culemborg experiment. Arch 0JaI Bioi 1961;5:284-300.
Backer-Dirks a. The relation between the fluoridation of water and dental caries experience.Int
DentJ 1967; 17:582-605.
a'Mullane DM, Whelton H, Costelloe P, et al. The results of water fluoridation in Ireland. J Pub
Health Dent 1996;36(Special Issue):259-64.
Murray JJ, Rugg-Gunn AJ. Water fluoridation and child dental health. water fluoridation and
adult dental health, community fluoridation scbemesthrougbout the world. In: Fluorides in
caries prevention. Dental practitioners' handbook No. 20. 2nd ed. Boston, MA:Wrigbt PSG,
1982:31 -73.
Newbron E. Effectiveness of water fluoridation. J Public Health Dent 1989;49(Spec Issue):979-
89.
Brunelle JA, Carlos JP. Recent trends in dental caries in U.S. children and the effect of water
'fluoridation. I Dent Res 1990;69(Spec Issue):723-7.
Question 5A
The NIDR's 1986-1987 National Survey is included in the list provided in Response 5 (Bronelle
1990). The survey was designed to measure both the number of decayed, missing, and filled
permanent teeth (DMFI') and the more exact number of tooth surfaces affected (DMFT versus
DMPS). This additional level of precision allows for more accurate assessment of effect and
analysis by surface type. Because the surface-specific analysis was used, we learned that almost
90 percent of the remaining decay is found in the pits and fissures (chewing surfaces) of
children's teeth; those surfaces that are not as affected by the protective benefit of fluoride.
Question 5B
If it is included, how does CDC account for scatter among fluoridated, partially fluoridated and
non-fluoridated communities with respect to ranking for lo~est caries incidence?
Response SB
CDC continues to analyze the data that indicate a significant "diffusion effect" for DOD-
fluoridated communities. Non-fluoridated communities in regions with a significant number of
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7
fluoridated communities have lower decay rates than non-fluoridated communities in regions
with 'only a few fluoridated cities. This indicates that non-fluoridated communities are also
, .deriving decay-preventive benefits from community water fluoridation by eating foods and
drinking beverages prepared and bottled in fluoridated communities. This may account in part
for the declining decay rates even in partially fluoridated and non-fluoridated communities.
Question 6
Does CDC subscribe to the recommendations of the American Dental Association (ADA) and
the American Medical Association (AMA) that children under six months of age should receive
no fluoride? If not, wbynot? If so, what measures does CDC recommend for families living in
communities with fluoridated water to prevent infant exposure to fluoride?
Response 6
The American Dental Association (ADA) and the American Medical Association (AMA) hav~
not made recommendations stating that children under 6 months should receive "no fluoride."
The ADA, the American Academy of Pediatrics (AAP), and the American Academy of Pediatric
Dentistry (AAPD) recommend that children living in non-fluoridated areas receive fluoride
supplements beginning at six months of age, but do not restrict intake of fluoride from other
sources such as foods, beverages, and water.
Question 6A
If so, what measures does CDC recommend for families living in communities with fluoridated
water to prevent infant exposure to fluoride?
,Response 6A
CDC recommends that clinicians follow the ADA, AAP, and AAPD supplement guidelines for
, children in non-fluoridated areas. In communities with fluoridated water below the 2 ppm level,
CDC does not recommend any measures to restrict intake from water.
Question 7
How many individuals in the Nation (CDC estimates) fall into the category called ""unusually
susceptible" in the Toxicological Profile for fluorides, Hydrogen Fluoride, and fluoride,
published by the Agency for Toxic Substances and Disease Registry (ATSDR)? What measures
does CDC recommend forunusually susceptible individuals who live in fluoridated
communities?
Response 7 A
The Toxicological Profile for fluorides, Hydrogen fluoride, and Fluorine states that "some
subsets of the population may be unusually susceptible to the toxic effects of fluoride and its
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npounds. These populations include the elderly; people with deficiencies of calcium,
~esium, and/or vitamin C; and people with cardiovascular and kidney problems:' These
~lations are hypothesized to be more susceptible because tbey may bave decreased kidney
nction that affects the clearance of fluoride from the body. Because there are no data available
IDcerning humans, tbese hypotheses are based on studies conducted on animals. This possible
lsceptibility is attributed to fluoride at levels greater than that used to fluoridate water (0.7 to
.2 ppm), or greater than the maximal natural levels allowed by the Environmental Protection
.gency (4ppm) for drinking water. CDC cannot estimate the number of people who maybe
nusually susceptible because we do not know the number of people in tbeUnited States who
,ave naturally occurring fluoride in their water at a level greater than 4ppm.
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CONGRESSMAN CALVERT INQUIRY
OF MAY 8, 2000
RESPONSE TO QUESTIONS
Question 1
On November 18, 1998, two EPA scientists, Drs. James Murphy and William Hirzy, wrote a
memorandum to Dr. Oscar Hernandez, Director of the Risk Assessment Division, Office of
Pollution Prevention and Toxics (OPPT) on the subject of the pending Children's Health Test
Rule. Drs. Murphy and Rirzy cited six recent studies that indicated that fluoride might pose a
risk of neurotoxicity for children. They also pointed out that a Reference Dose (calculated using
standard EP A methodology) and the cited studies would have a range of 0.000007 mg/kg/day to
0.003 mg/kg/day. They noted that no chronic studies of any kind appear to have been conducted
on hydrofluosilicic acid or its sodium salt - which are used in around 90% of water fluoridation
systems in the U.S. - and that the potential for those substances to form complexes with heavy
metals (such as lead) has not been studied.
Given the extremely wide spread exposure of millions of American children to fluoride, and in
particular, to hydrofluosiIicic acid and its sodium salt, along with the Administrator's concern for
the health of children, and these two scientists' positions at EP A, surely EP A has responded to
their'November 18, 1998, memorandum. Please provide a copy ofEPA's response, and what
action E,PA has taken to deal with the concerns raised in the November 18, 1998, memorandum.
Response
The response to Question 1 is divided into two segments. The first is the response from OPPT
regarding the memorandum to Dr. Hernandez from Drs. Murphy and Hirzy. The second part
provides infonnation on recent publications that discuss the potential for fluorosilicates to form
complexes with heavy metals.
I OPPT Response
On November 18, 1998, Drs. James Murphy and William Rirzy wrote a memorandum to
Dr. Oscar Hernandez which cited six studies that indicated that fluoride might pose a concern for
neurotoxicity in children. In addition, they suggested in their memorandum that fluoride would
be a good candidate chemical for a regulation which was under development at the time. That
regulation was intended to develop health effects data for chemicals to which children are
exposed. The proposed regulation or test rule was targeted to be completed December 30, 1998.
A formal response to the memorandum was not drafted because shortly thereafter EP A decided
to put the test rule on hold in order to develop, on a cooperative basis with interested
stakeholders, a Voluntary Children's Chemical Evaluation Program which was intended to serve
1
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'l-1:tt PAQ1i-CI
UNITED STATES ENVIRONMENTAL PROTECTION AGENCY
WASHINGTON. D.C. 20460
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SEP 5 2000
OFFICE OF
WATER
The Honorable Ken Calvert
Chairman
Subcommittee on Energy and The Environment
Committee on.Science
House of Representatives
Washington, D.C. 20515-6310
Dear Mr. Chairman:
This is in reply to the questions posed in your May 8, 2000, letter to Carol M. Browner,
Administrator of the United States Environmental Protection Agency (EPA). Your questions
primarily deal with fluoride and EP A's management of fluoride through our current regulatory
programs. I apologize for the delay in this response. The detailed nature of many of the
questions required both significant fact finding and inter-office coordination.
The Office of Water, Office of Air, Office of Solid Waste, Office of Pollution Prevention
and Toxics, Office of Pesticide Programs, and the Office of Research and Developmerit.
contributed information on the activities of their programs related to fluoride. The answers to the
technical questions were provided by the Office of Water and the Office of Pesticide Programs
an.d reviewed by the Office of Research and Development. We have included recent references
on the health effects of fluoride and other materials (memoranda, communications) as requested.
The scientific publications provided are either those cited in the enclosures or those published
over the past five years and collected by EP A as part of its routine surveillance of the fluoride
literature.
.
We hope the information provided addresses your concerns. Ifycu have any additional
questions, please feel free to contact me or have your staff call Dr. Joyce Donohue, at
(202)260-1318;
Sincerely~' ,
1. Charles Fox
Assistant Administrator
"
Enclosures
RecycledIRecyclable . Printed with Vegetable on Based Inks on 100% Reqdec:l Paper (40% Poslconsumer)
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Response
When EP A regulated fluoride levels in drinking water in 1986 by setting a Maximum
Contaminant Level (MCL), it was regulated on the basis of the opinion ofa group of experts
that mild dental fluorosis was not an adverse health effect. Thus, in the judgment of the experts,
mildly fluorotic teeth are still healthy. When dental fluorosis causes cracks and fissures, tooth
function is considered to be impaired. Therefore, following the logic of the fluoride drinking
water regulation, levels of fluoride ingestion sufficient to cause severe dental fluorosis in
individuals would be too much fluoride.
EP A Secondary Maximum Contaminant Level (SMCL) was established to warn the public
regarding the potential for development of dental fluorosis as a result of drinking water with
fluoride concentrations greater than 2 mg/L. Based on the data available in the mid-1980s, the
incidence of severe fluorosis was negligible at fluoride concentrations less than 2 mg/L (NAS,
1993). However, based on evidence froni recent studies that relate the concentrations of fluoride
in drinking water, to the incidence of severe dental fluorosis, the number of cases has increased in
the years since fluoride was regulated by EP A (Bothwell and Limeback, 1999; Ishii and
Suckling, 1991; NAS, 1993). At least apart of the increase appears to be due to the increased
fluoride exposure from dental products, processed foods, etc. (Bothwell and Limeback, 1999;
NAS,1993).
Because of considerable variability in the results of studies of dental fluorosis in the population
and the fact that those studies generally measure only the fluoride in the drinking water rather
than total fluoride exposure, it is not possible to provide an exposure value for the total fluoride
intake that causes severe dental fluorosis. In the recent review of the fluoride data by the
National Academy of Sciences (1997), the following upperlimitson fluoride intakes for infants
and children vulnerable to dental fluorosis were proposed:
.
o through 6 months
O.Tmg/day
.
7 through 12 months
0.9 mg/day
.
1 through three years
1.3 mg/day
.
4 through 8 years
2.2 mg/day
The NAS values are intended to protect against all dental fluorosis, not just severe dental
fluorosis. Accordingly, intakes that would protect against severe dental fluorosis would be
greater than the values above.
3
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the same purpose as the rule. This decision was publicized widely and it effectively preempted
consideration of any testing issues related to the test rule.
.
A voluntary program to obtain exposure and hazard information pertinent to the analysis of
children's risks evolved from series of stakeholder meetings over the past year. Participants in
this process were selected through an open process to ensure balanced participation from a
spectrum of stakeholders. The interested public was also encouraged to participate in these
stakeholder meetings. After considering the feedback from these meetings, OPPT has
coritemplated using a set of improved criteria, different from those used in the test rule, to select
chemicals for the program. These new criteria emphasize biomonitoring data which demonstrate
that a chemical is present in human blood/tissues/exhaled breath, and that this chemical is found
in indoor air, food or drinking water. Dr. Rirzy requested and was granted an opportunity to
address the attendees at a recent stakeholder meeting regarding his views on fluoride toxicity and
to reiterate his early suggestion that this chemical be considered for inclusion in the program.
EP A is evaluating all comments received through this activity and will determine whether the
chemical which is of interest to Dr. Rirzy is appropriate for inclusion in tpe voluntary program.
The launch of the voluntary program is expected later this year.
Drs. Murphy and Rirzy also stated in their memorandum that the Agency's Integrated Risk
Information System (IRIS) had developed a Reference Dose (RID) for fluoride, and that the
value for the RID may be reduced ifthe new studies that they cited were considered. As
discussed in the response to Question 9, EPA is required by the Safe Drinking Water Act to
review the MCLG/MCL for fluoride. That review will take place over the next two years. These
studies will be considered in that review and, as appropriate, changes to the RID and/or the
MCLG/MCL will proceed based on this and all other available information.
.
II Fluorosilicate Complexes with Heavy Metals
Two recent papers have reviewed the issues of fluorosilicate chemistry as applied to drinking
water fluoridation. These publications conclude that fluorosilicate hydrolysis'and dissociation
are greater than 99.9% complete and that complexes of metals with fluorosilicates are negligible,
with concentrations below 1 part per trillion (Urbansky and Schock,2000a,b)
Question 2
Given that normal healthy teeth do not display fluorosis, does EP A corisider the appearance of
dental fluorosis as a sign of too much exposure,to fluoride? Ifnot, why not? Ifso, at what
incidence level would EP A consider that the population is receiving too much fluoride?
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National Emission Standards for Hazardous Air Pollutants for Source Categories
40 CFR 63: Promul gated Stan~ards
Subpart AA - National Emission Standards for Hazardous Air Pollutants from Phosphoric
Acid Manufacturing Plants
Subpart BB - National Emission Standards for Hazardous Air Pollutants from Phosphate
Fertilizers Production Plants
Subpart LL - National Emission Standards for Hazardous Air Pollutants for Primary
Aluminum Reduction Plants
Subpart YY - National Emission Standards for Hazardous.Air Pollutants for Source
Categories Generic Maximum Achievable Control Technology Standards:
Hydrogen Fluoride Production
National Emission Standards for Hazardous Air Pollutants for Source Cateeories
Source Cateeorv
· Alumina Processing
· Clay Products Manufacturing
- Clay Minerals Processing (b)
- Brick, Structural Clay Products and
Ceramics Manufacturing (b)
- Lightweight Aggregate Production (b)
· Uranium Hexafluoride Production (b)
· Refractory Products Manufacturing
- Clay Refractory Manufacturing
Status
(b)
(b)
(a) proposed, (b) under development, or (c) under consideration
Office of Solid Waste
The Office of Solid Waste is in the process of proposing revisions to the fluoride and cyanide
treatment standards applicable to spent potliners from primary aluminum reduction (EP A
hazardous waste K088) under its Land Disposal Restrictions (LDR) program. The standards are
based on a relatively, new. type ofK088 vitrification technology that also recovers fluoride. If the
proposal is promulgated, it will result in the extraction, recovery and reuse of fluoride, the
destruction of toxic cyanide in the waste, and a reduction in the volume of treated K088 residuals
that are land disposed. The proposal is under review by OMB and will shortly enter final review
for signature by the Administrator.
5
What regulations does EP A have ~ either promulgated, under development, or under
consideration - to control fluoride emissions to the air, water, soil? Regarding emissions of
hydrofluosilicic acid,.which EPA has characterized as a water and air pollutant, how does EPA
explain its willingness to allow this substance to be bled into drinking water systems (especially
in the absence of any chronic toxicity studies on it) as long as the fluoride level does not exceed 4
mg/L? Is it EPA's policy that the "solution to pollution is dilution" as long as the pollutant is
applied directly into drinking water systems and not into fresh surface water?
.
Question 3
Response
The response to this question is divided into several sections. The first section deals with
regulations (promulgated, under development, or under consideration). That section.is
subdivided by the responsible office within EP A. The second section deals with fluoridation
chemicals..? i.e., hydrofluosilicic acid.
I. Re2ulations (Promul~ated. Under Development or Under Consideration)
Office of Air
The following is a list of EP A regulations that control fluoride emissions to the air:
New Source Perfonnance Standards 40 CFR 60: Promulgated Standards ~
Subpart S - Standards ofPerfonnance for Primary Aluminum Reduction Plants
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Subpart T - Standards ofPerfonnance for the Phosphate Fertilizer
Industry: Wet-Process Phosphoric Acid Plants
Subpart U - Standards ofPerfonnance forthe Phosphate Fertilizer
Industry: Superphosphoric Acid Plants
Subpart V - Standards ofPerfonnance for the Phosphate Fertilizer
Industry: Oiammonium Phosphate Plants
SubpartW- Standards ofPerfonnance for the Phosphate Fertilizer
Industry: Triple Superphosphate Plants
Subpart X - Standards of Performance for the Phosphate Fertilizer
Industry: Granular Triple Superphosphate Storage Facilities
National Emission Standards for Hazardous Air-Pollutants 40 CFR 61
None
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Part 436 - Mineral Mining and Processing Point Source Category
Subpart D
Industrial Sand Subcategory
Part 469 - Electrical and Electronic Components Point Source Category
Subpart A
Subpart B
. Subpart C
SubpartD
Semiconductor Subcategory
Electronic Crystals Subcategory
Cathode Ray Tube Subcategory
Luminescent Materials Subcategory
Part 471 - Nonferrous Metals Forming and Metal Powders Point Source Category
Subpart B
Subpart C
Subpart E
Subpart F
Subpart G
Subpart I
Magnesium Forming Subcategory
Nickel-Cobalt Forming Subcategory
Refractory Metals Forming Subcategory
Titanium Forming Subcategory
Uranium Forming Subcategory
Zirconium-Hafnium Forming Subcategory
II. Fluoridation Chemicals
EP Ais not involved with the decision of any drinking water system to fluoridate its water supply.
Those decisions are made by States and local communities. Individual systems make the
decisions regarding which fluoridation chemical to use, if fluoridation is practiced. Most States
require that systems select fluoridation chemicals certified against ANSI/NSF Standard 60:
Drinking Water Treatment Chemicals - Health Effects. The acronym ANSI/NSF indicated that
the Standard was developed by NSF International (formerly the National Sanitation Foundation)
and approved by American National Standards Institute. '
EPA supported the development of the Standards for Drinking Water Additives (ANSI/NSF
Standard 60 and 61) to insure that the chemicals used for fluoridation (sodium fluoride, sodium
silicofluoride, and hydrofluosilicic acid) did not contain impurities that might be deleterious to
health and were evaluated .against the Standard. Standard 60 requires that all fluoridation
chemicals be analyzed for the presence of regulated heavy metals (ANSI/NSF, 1998).
Question 4
What has EP A done to investigate the charges of science fraud made in the amicus curia brief
submitted by your headquarters professionals union in 1986 in the NRDC v. EP A law suit over
drinking water standards that was filed in that year (and subsequently reiterated byDrs. Robert
Carton and William Hirzy of the union in a 199.8 National Association of Environmental
Professionals publication)?
7
Office of Water
.
.
Under the Clean Water Act, EPA has promulgated effluent limitation's guidelines and standards
for fluoride in eight point source categories. The following list summarizes the location of these
fluoride regulations by part and subpart from the Code of Federal Regulations. In addition to the
regulations already promulgated and summarized below, EPA is considering effluent limitations
for fluoride for two additional point source categories: (I) Iron and Steel Manufacturing and (2)
Metal Products and Machinery. Both of these regulations are under development and have not
yet been proposed. EP A is not yet certain whether the regulations for these two point source
categories will include fluoride effluent limitations.
SummarY of Effluent Limitations and Standards for Fluoride
Part.415 - Inorganic Chemicals Manufacturing Point Source Category
SubpartH
Subpart W
Subpart BC
Hydrofluoric Apid Production Subcategory
Aluminum Fluoride Production Subcategory
Sodium Fluoride Production Subcategory
Part 418 - Fertilizer Manufacturing Point Source Category
Subpart A Phosphate Subcategory
Part 421 - Nonferrous Metals Manufacturing Point Source Category
Subpart B
Subpart C
Subpart I
Subpart K
Subpart 0
Subpart P
Subpart S
Subpart AA
Subpart AD
Primary Aluminum Smelting Subcategory
Secondary Aluminum Smelting Subcategory
Metallurgical Acid Plants Subcategory
Primary Columbium-Tantalum Subcategory
Primary Beryllium Subcategory
Primary and Secondary Germanium and Gallium
Primary Molybdenum and Rhenium Subcategory
Secondary Tin Subcategory
Secondary Uranium Subcategory
.
Part 422 - Phosphate Manufacturing Point Source Category
Subpart D
Subpart E
Subpart F
Defluorinated Phosphate Rock Subcategory
Defluorinated Phosphoric Acid Subcategory
Sodium Phosphates Subcategory
Part 426 - Glass Manufacturing Point Source Category
Subpart K
Subpart L
Subpart M
Television Picture Tube Envelope Manufacturing Subcategory
Incandescent Lamp Envelope Manufacturing Subcategory
Hand Pressed and Blown Glass Manufacturing Subcategory
.
6
.
. II.
..
. .
cited in your letter, including promotions, awards and transfers, such actions would be effected in
the routine course of Agency business and in compliance with appropriate Office of Personnel
Management regulations and EP A policy and practice.
Question 7
Fluoride is well recognized as a general enzyme poison (arising from its powerful hydrogen
bonding propensity that disrupts protein [and DNAlRNA structures] and it displays high acute
toxicity (ca. 5 mg/kg a threshold lethal dose), ranking as acute toxicant lying between lead and
arsenic. A host of chronic toxic effects of lead and arsenic are acknowledged by EP A (e.g.
hematopoietic effects, cardiovascular effects, neurologic effects, carcinogenicity, etc.). The EPA
view of fluoride toxicity appears to be that ingested fluoride strengthens teeth, or itwill kill, or
will inflict skeletal fluorosis, but has no other chronic toxic effects as its neighbors arsenic and
lead do. How does EP A explain this unique toxicological behavior of fluoride, especially in light
of its known effect on enzymes?
Response
The response to the question first considers,the statements regarding fluoride's hydrogen bonding
potential. and its potential effects 'on enzymes, and then respond to the portion of the question
relative to acute and chronic fluoride toxicity.
Fluoride and Hydrogen Bonding
There are several scientific problems with the statements made about the hydrogen bonding
potential of fluoride and its effects on enzymes. Hydrogen bonds are electrostatic interactions
between partially positive hydrogen atoms in molecules and partially negative atoms in the same
or neighboring molecules (Lehninger et al., 1993). Partial positive and negative charges within a
molecule are the product of differences in the affinity of covalently bonded atoms for electrons
resulting in bond polarity. Hydrogen fluoride, the simplest hydrogen-containing inorganic
fluorine compound, has a pKa of3.5. This means that the molecule can only participate in
hydrogen bond fonnation to any significant extent at pH values ofless than about 4.5. The pH
maintained in most mammalian cells is about 7 to 7.3, a pH range where only about one in 1,000
to one in 10,000 of the fluorines is present as hydrogen fluoride. The remainder of the fluorines
are present as monovalent, negative fluoride ions. The acid secreting cells of the stomach are an
exception to this generalization. The low pH of the gastric secretions would favor the presence
of the undissociated hydrogen fluoride, and hydrogen fluoride is capable of hydrogen bonding.
The primary interactions that would be displayed by the fluoride ion would be ion-ion
interactions or ion-dipole interactions rather than hydrogen bond interactions.
The distinction made above regarding the types of interactions expected between fluoride and
cellular constituents is more than simply semantic. For example, interactions of fluoride ions
with the hydrogen bonds in DNA are very unlikely since the negative charges on the DNAd
phosphate-sugar backbone and the pi-bonds of the DNA bases would tend to repel fluoride anion
9
. .
Response
In our attempt to answer this question, we consulted with our Office of General Counsel. Based
on the limited amount of information provided in the citation to the case, and the time that has
passed and associated turnover of key staff, we have not been able to locate the brief containing
the allegations of science fraud. If you have more detailed information regarding the case, we
would be pleased to further research the question.
.
Question 5
What has EPA done to investigate charges made by Office of Ground Water and Drinking Water
Senior Science Advisor, Dr. William Marcus, that data were tampered with and conclusions
improperly downgraded in the National Toxicology Program (NTP) cancer study on sodium
fluoride? Regarding the NTP study, mandated by Congress in 1977 to specifically exclude the
Public Health Service and National Institute of Health from involvement with it (because they
would not be unbiased), how is it that EPA did not challenge the down grading of the study
conclusions?
Response
The allegations were heard and discussed by Agency staff. The allegations were not
substantiated. There was no evidence that the NTP conducted its review by other than its
standard, rigorous review process, or that there was any downgrading of findings. Enclosed is a ~
copy of the peer review panel discussion on the study taken from the NTP report. Thi~ panel was .....
a subcommittee of the NTP Board of Scientific Counselors. Also enclosed is a copy of the NTP
process for quality control of its studies. In addition to quality control of study conduct, the steps
include reading of the pathology slides by independent, expert pathologists followed by
independent scientific peer review of report findings by a subcommittee of the Board. The Board
and its subcommittees are composed of experts whose integrity has not been challenged, and was
not challenged in the case of the fluoride study.
Question 6
What disciplinary action has been taken against the EPA employees involved in firing Dr.
Marcus (and thereby incurring unwarranted expenses to the tax payer)? What personnel actions
have been taken against those involved including promotions, awards, transfers, demotions,
fl. ?
mng, etc.. ,
Response
Based on the Agency's review of the Department of Labor (DOL) decision issued in
Dr. Marcus' case, no disciplinary action was required or taken with regard to relevant Agency
employees. With regard to any other personnel actions involving relevant EP A employees as
"
8
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.
.
. .
In 1991, the Department of Health and Human Services (DHHS) completed a review of
the benefits and risks of fluoride. Among other points, the DHHS review concludes that
optimal fluoridation of drinking water to about 1 mgIL does not pose a detectable cancer
risk in humans and recommended that the U. S. Public Health Service continue to support
optimal fluoridation.
In 1993, the Agency for Toxic Substances and Disease Registry, a division within the
Centers for Disease Control (CDC), published the Toxicological Profile for Fluorides,
Hydrogen Fluoride and Fluorine. A Minimum Risk Level (MRL) of 0.05 mg/kg/day
(3.5 mg/day for a 70-kg adult) was calculated for chronic oral exposure to fluoride. The
study used as the basis of the MRL was a study of women with osteoporosis who received
a 75-mg/day sodium fluoride supplement, a dose of about 0.48 mglkg/day, compared to a
group who received a placebo. Background fluoride exposure (diet, drinking water,
dental products) was not measured or considered in estimating the dose and there was no
comparison of the experimental group and the placebo group for their total fluoride
exposure. Accordingly, the MRL applies to exposures to fluoride in excess of the
background levels, rather than total fluoride exposure.
In 1998, the Institute of Medicine at NAS completed a review of fluoride as a nutrient.
They concluded that the adequate intake for fluoride ranges from 0.01 mg/day for infants
to 1 mg/day for children under age eight, the period when dental fluorosis can occur. For
adults and children more than eight, the recon1mendation ranges from 2 to 4 mg/day.
NAS also established an Upper Limit for a safe exposure in children older than age 8 and
for adults of 10 mg/day.
There is general agreement among these publications regarding critical effects and the
quantitative estimates of risk for effects on both bone and teeth. None of the publications listed
above have ignored data on other acute or chronic effects of fluoride including its relatively low
acutely toxic dose.
EP A understands that CDC is presently completing an assessment of fluoride and fluQridation.
CDC is the principal Federal agency involved in research on fluoridation in this country.
Question 8
. . ".
How many individuals in the nation does EP A estimate fall into the category depicted as
"unusually susceptible" in the Toxicological Profile for Fluorides, Hydrogen Fluoride, and
Fluorine, published by the Agency for Toxic Substances and Disease Registry? What measures
does EP A recommend for these unusually susceptible individuals who live in fluoridated
communities or communities whose water contains fluoride at the MCL?
11
preventing its disruption of the DNA hydrogen bonds. Interactionofthe fluoride ion with the
positively charged DNA-associated polyamines or histone proteins would be more likely.
However, to the knowledge of EPA, there has been no experimental investigation of fluoride ion
interactions with DNA-polyamines or histone proteins.
.
The results from studies of fluoride's mutagenicity and genotoxicity are consistent with the
hypothesis that the effects of fluoride on chromosomes and DNA are indirect rather than direct.
Most ofthe mutagenicity studies, particularly those using the Ames Assay, are negative (NAS,
1993). Although in vitro mouse lymphoma mutagenicity assays have some positive results, this
assay detects chromosomal damage as well as gene mutations. The results from many of the in
vitro studies of chromosomal effects are positive but the in vivo assays have approximately equal
numbers of positive and negative results (NAS, 1993). Thus, the effects of fluoride on DNA
appear to occur at the level of the chromosomes rather than the DNA bases.
Lack of hydrogen bonding potential of fluoride at physiological pH's would also determine the
nature of its interaction with proteins. Fluoride ions could influence protein structure and, thus,
enzyme activity by disrupting the electrostatic interactions between the acidic and basic amino
acids, or by interrupting hydrogen bond interactions of polar amino acid side chains. Fluoride's
ability to exert such an influence would be shared by other negative ions (i.e., chloride anions)
and would be concentration and enzyme-specific. Fluoride would also have to compete with
chloride and other intracellular negative ions for protein interaction sites. The small ionic radius
of fluoride would be a factor favoring interaction with positively charged amino acid side chains
that might not be accessible to larger ions.
.
It has been hypothesized (Spittle, 1994) that formation of relatively insoluble calcium or
magnesium complexes might disrupt the activities of enzymes using these divalent cations as
cofactors. This is a possible mechanism that might account for inhibition of some enzymes but
divalent cation complex formation would be an enzyme-specific rather than a general effect.
To the knowledge ofEPA, there has been no systematic evaluation of the ability of fluoride to
inhibit enzyme activities, or of the mechanism for such inhibition. Data on the specific enzymes
inhibited and the dose-response for the effects would be required for the data to be used for
quantitative risk assessment. An NAS (1993) report on the health effects of ingested fluoride
endorsed conducting research on the mechanism by which fluoride interacted with cells and
biomolecules, including enzymes, and research on specific mechanisms of enzyme inhibition
would be beneficial. .
II Fluoride Toxicitv
There have been independent evaluations of the toxicity of fluoride by the Public Health Service
(1991), EPA (1985), NAS (1993; 1998), and ATSDR (1993). In each of these reviews, the
critical adverse effects of fluoride ingestion were identified as the effects on bone and teeth rather
than other adverse effects. Brief descriptions of these evaluations are provided below.
10
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.,
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children and pregnant women. It will later be expanded to cover other at-risk populations. In
addition, EP A has made it a requirement for public water systems to provide their clients with
health effects information on contaminants in their water supply, including fluoride [Consumer
Confidence Rule FR 63(160): 4451'2-44536].
Revised public notification language for fluoride has recently been proposed [FR 65(87): 25982-
26049]. The new language suggests dental consultation in situations where there is a risk for
dental fluorosis because the water provided by their drinking water system has exceeded the
Secondary MCL for fluoride. The implementation manual for public notification is close to
completion.
In addition, please refer to the answer to Question II and EP A advice regarding fluoride
exposure and infants.
Question 9
Do you interpret Section 101 (b)(4) of the Safe Drinking Water Act of 1996 as requiring EPA to
set its MCL(G)s at a level that protects all persons, including sensitive populations, such as
infants, children, people who drink 4 or more liters of water per day, people with allergies or
hypersensitivity to fluoride and people with renal disease?
Response
. The Safe Drinking Water Act of 1996 does not have a Section 101(b)(4). Section 1412(b)(4)(a)
states that "Each maximum contaminant level goal established under this subsection shall be set
at the level at which no known or anticipated adverse effects on the health of persons occur and
which allows an adequate margin of safety."
.
As required by the SDWA [Section 1458(a)(I)], EPA is collecting information to identify groups
within the general population with increased sensitivity to contaminants such as infants, children,
the elderly, persons with allergies or hypersensitivity to chemicals. Some of the data that we
have collected in this process are cited in the response to Question 8 above. If the MCL/MCLG
for fluoride is selected for an in-depth evaluation as part of the six-year review of drinking water
regulations, additional data on sensitive populations and their dose-response to fluoride will be
collected andEP A will publish and seek public comment on its findings as required by the
SDWA Section 1412(b)(3)(C)(i)(V). .
Question 10
Is EP A satisfied that fluoride doses delivered to the public via drinking water under an MCL(G)
of 4 mgIL when added to the fluoride intake from dental products, pesticide residues, food and
beverages will not cause adverse health effects?
13
Response
Table 1 below summarizes those populations that the ATSDR Toxicological Profile (1993;
Section 2.7) identifies as sensitive and includes data on the prevalence in the United States of the
underlying physiological, nutritional, or age-related condition. It is important to note that the
population values in Table I are numbers of individuals that fall in each category. There are no
data to suggest that these individuals as a group are, or would be, sensitive to fluoride at the
levels found in the environment.
The demographic information for cardiovascular disease and renal disorders in Table 1 was
collected by the Office of Water as a component of an effort to identify sensitive populations in
the United States that might be sensitive to specific chemicals by virtue of their chronic disease
state (O'Dey et aI., 1998). Demographic data for the elderly come from a recently completed
study of water intakes by the Office of Water (Jacobs et al., 2000). Prevalence values have been
rounded to the nearest million and were extrapolated from the survey population to the U.S.
population. Data on nutrient deficiencies are from the U.S. Department of Agriculture 1994-
1996 Continuing Survey of Food Intake by Individuals (USDA, 1998). The values given are the
percent of the population consuming less than 75% of the Recommended Dietary Allowance for
the nutrient in question.
Table 1
Sensitive Populations
."
Sensitive Population Group (ATSDR, 1991) Estimated Population
Elderly 52,000,000 (>55 years)
Cardiovascular disease 22,000,000
Renal disorders 2,000,000
Vitamin C deficiency 27%
Magnesium deficiency 37%
Calcium deficiency 44%
Individuals that fall in each of the categories listed iil Table 1 have a number of specific risk
factors that impact their health status such as body weight, diet, and life style (e.g. smoking,
alcohol consumption). Advice on beneficial life style changes for each condition is best provided
by the medical community.
EP A is in the process of developing medical fact sheets to provide medical practitioners (doctors,
nurses, dietitians, etc.) with health data relative to drinking water contaminants that can be then
used in counseling patients. This work has just begun, and will init\ally focus on the elderly,
12
.
"
It
Response
.,
The 1993 NAS report on the health effects of ingested fluoride addressed the concern for fluoride
retention in persons with impaired renal function, a group which includes individuals with
diabetes. The NAS concluded that additional research was needed to adequately assess the risk.
EP A is not aware of recent data on the health effects of ingested fluoride in persons with
impaired renal clearance that expand our knowledge on this issue.
The Agency regulations for potable water do not apply to water used in dialysis. The American
Association for Medical Instruments (AAMI) establishes the standards that apply to dialysis
waters. The address for a contact at AAMI is as follows:
Dr. Ronald H. Abrahams
American Association of Medical Instruments
Renal Disease and Detoxification Committee
Suite 3330 Washington Boulevard
Arlington, VA 22201-4598
703 (525-4890)
.
Neither the NAS( 1993) report, nor the A TSDR (1993) Toxicological Profile on fluoride provides
data that identify any individuals with a fluoride-specific hypersensitivity or allergy. No
judgement can be made regarding the effects of fluoride in drinking water on such a population
without data from studies of such populations or knowledge of the mechanisms underlying the
adverse response.
Question 13
Does the incidence of dental fluorosis among at least an estimated 22% of American children
indicate that, at least among these children, an overdosing is occurring?
Response
TheNational Survey of Dental Caries in US School Children (1986-1987) reported a prevalence
of dental fluorosis of22.3%. Nearly all of the cases were mild to very mild. These data reflect
exposures that occurred before the EP A MCUMCLG was implemented.
A number of studies have been conducted since the National Survey of Dental Caries in US
School Children as indicated in the response to Question 10. Some of these studies indicate that
the prevalence of dental fluorosis appears to be increasing.
In 1993 NAS recommended that the most "effective approach to stabilizing the prevalence and
severity of dental fluorosis without jeopardizing the benefits to human health, is likely to come
. from the more judicious control of fluoride in foods, processed beverages, and dental products,
IS
, .
EPA continues to support the MCLG as protective of public health. The Agency realizes that the
use of fluoride in dental products has increased since fluoride was regulated in 1986. In 1998 the
EP A commissioned an evaluation of the exposure data for fluoride, including data on amounts in
foods and dental products.EP A found that the data published in the peer reviewed literature
were limited, and did not differ substantially from the data available when fluoride was regulated.
A copy of that draft report was included for your records when EP A responded to this question
last year.
.
Response
Over the past year we have collected recent publications covering the increased incidence of
dental fluorosis and the factors other than drinking water fluoride that appear to be contributing
to the increase (Barsden and Bjorvatn, 1999; Brothwell and Limeback, 1999; Den Besten, 1999;
Fitzsimons et aI., 1998; Horowitz, 1989; Ishii and Suckling, 1991; Villa et a1.1998). The
findings from those papers were used in making the proposed revision to the fluoride public,
notification language. If fluoride is selected for reevaluation of its MCLlMCLG, the Agency will
look carefully at relative sources of exposure during the revision process.
Question 11
What is the margin of safety for infants who consume drinking water containing 4 mgIL
fluoride?
Response
~
The Agency does not recommend that infants consume water containing 4 mgIL fluoride. The
Agency requires that all families who receive water from a system with greater than 2 mgIL
fluoride receive a public notification recommending that alternate sources of water be used for
infants and children in that family [40CFR 143.5]. Copies of the present public notification
statement and the proposed revision to that statement are enclosed for your records.
The Agency believes that the 2 mgIL SMCL protects children against dental fluorosis as well as
adverse health effects in situations where there are no other significant sources of exposure. The
Agency acknowledges that the MCL does not protect infants and children against dental .
fluorosis, a cosmetic effect rather than an adverse health effect.
Question 12
What is the margin of safety for persons receiving kidney dialysis treatment, diabetics, or those
who have a hypersensitivity or allergy to fluoride who consume drinking water containing 4
mgIL fluoride?
14
,
..
.
.
~
fluoride and cryolite. Hydrofluosilicic acid and its salts are not active ingredients in any
currently or formerly registered pesticide products. Accordingly, we have not conducted any risk
assessments on this chemical.
In 1993, EP A published a Reregistration Eligibility Document (RED) on sulfuryl fluoride. A fact
sheet outlining the basis for EPA's reregistration decision is enclosed. This pesticide has no food
uses and no other terrestrial uses. Accordingly, there is no dietary exposure through food or
drinking water. The pesticide is used primarily to fumigate structures. The Agency has
identified inhalation exposure as a possible hazard to persons who reenter treated structures. The
Agency required submission of exposure data to support the retention of the current reentry level
of 5 parts per million (ppm). (A reentry level is the concentration of sulfuryl fluoride in indoor
air that the Agency judges to be safe for persons reentering treated structures.) The Agency
announced in the RED that if these data were not submitted by August 1994, the Agency would
change the reentry level to 1 ppm.
The Agency is currently reviewing exposure data and a 90-day inltalation toxicity study in rats
required in the RED to characterize the neurotoxic effects of sulfuryl fluoride. EP A will .
reevaluate the reentry level for sulfuryl fluoride when it completes the review of these studies.
If the Agency finds that the use of sulfuryl fluoride results in significant exposures to infants and
children, the Agency may require submission of developmental neurotoxicity and other
neurotoxicity data on this compound. These studies were not routinely required before the
passage of the Food Quality Protection Act (FQPA) of 1996. However, in an April 1999 draft
report, an Agency task force recommended that such studies (among others) be routinely required
for all pesticides used on food or in ways that significantly expose infants and children. In
August 1999, EPA began to require developmental neurotoxicity and certain other neurotoxicity
data on pesticides known or suspected to have neurotoxic effects. Initially, EP A required
registrants of organophosphorus pesticide~ to submit such data, but the Agency plans to require
developmental neurotoxicity and other neurotoxicity data for all food use pesticides that are
known or suspected to have neurotoxic effects. Within a year, EP A will propose to amend its
data requirements in Part 158 of Title 40 of the Code of Federal Regulations to require the
developmental neurotoxicity and other neurotoxicity studies for all food use pesticides.
Sodium fluoride is used as a wood treatment to prevent rot. It is not used on food. The
pesticide uses of sodium fluoride do not appear likely to result in dietary exposure through
drinking water and it is not known whether the wood treatment use results in significant
exposures to infants and children. The Agency plans to issue a RED on sodium fluoride in 2004.
The Agency has not yet determined whether developmental neurotoxicity or other neurotoxicity
studies should be required for this pesticide.
Question 16
Have any studies on hydrofluosilicic acid or silicofluorides been submitted to EP A under claimed
Confidential Business Information Protection?
17
rather than a reduction in the recommendation for fluoride in drinking water." Control of
fluoride from these other sources (foods, beverages, and dental products) would require action by .-
the Food and Drug Administration.
Question 14
What steps has the Agency taken to address the hazards identified with fluoride exposure in the
following publications that appeared since EP A reaffirmed its drinking water standards for
fluoride? [Six publications are cited.]
Response
The Office of Water has reviewed each of the six references listed and participated in
discussions with the EPA Office of Research and Development (ORD) regarding the strengths
and weaknesses of each study. (See the enclosed memorandum from William Marcus dated
5/22/98 and the 6/3/98 response from Dr. Hugh Tilson ofORD.) The data presented in these
publications will be utilized in the review ofthe MCL values for presently regulated compounds
as discussed in the response to Question 9 above.
In 1999, EP A convened a group of experts to carefully consider the results of the Varner et a1.
(1998) study. A copy of the report of that conference is included. As a result of that conference,
EPA has requested that the National Toxicology Program consider the possibility of conducting
additional studies of the neurotoxicity of aluminum that include verification of the results
observed in the Varner et a1. study. ,;
-
Question 15
Please provide copies of any risk assessment documents in EP A files that pertain to fluorine-
bearing pesticides such as cryolite. '
Response
A copy of the cryolite risk assessment by the Office of Pesticide Programs is enclosed with the.
references to this response.
Our understanding is that you are concerned about those fluorine-bearing pesticides that produce
or act as free fluoride ion. You appear to be particularly concerned about the toxicity of
hydrofluosilicic acid and its salts. We further understand that you are concerned about the use of
fluorine-bearing pesticides that result in dietary exposures (Le., through food or drinking water).
Our review of our pesticide chemical database indicates that there are three active ingredients in
currently registered products that produce or act as free fluoride ion: sodium fluoride, sulfuryl
.
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16
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--
. .
. exposures or toxicity or to reflect pre- or post-natal toxicity of the pesticide. This determination
was based on current understanding of the information and procedures used to establish the need
for a lOX factor.
About a year later, EP A convened an intra-agency task force to examine the kinds of studies and
information needed to assess potential pre- and post-natal toxicity and exposure to infants and
children from pesticides. In 1999, the lOX Task Force prepared two draft papers, "Toxicology
Data Requirements for Assessing Risks of Pesticide Exposure to Children's Health" and
"Exposure Data Requirements for Assessing Risks of Pesticide Exposure to Children." These
papers supported the Office of Pesticide Programs' (OPP) draft policy guidance document on
implementation of the additional lOX FQPA safety factor entitled, "The Office of Pesticide
Programs' Policy on Determination of the Appropriate FQPA Safety Factor(s) for Use in the
Tolerance-Setting Process." It was accompanied by the "Standard Operating Procedures (SOP)
for Determining the Appropriate FQPA Safety Factor(s) for Use in Tolerance Assessment." All
of these papers were presented in May 1999 to the Agency's Scientific Advisory Panel (chartered
by the Federal Insecticide Fungicide and Rodenticide Act) and in July 1999, for public review
and comment (Federal Register of July 9, 1999; 64 FR 37001).
EP A has not revisited the December 1997 decision on cryolite because no one has petitioned the
Agency for a new tolerance for cryolite residues since then. The December 1997 action
established a time-limited tolerance for cryolite residues on potatoes and the processed animal
feed commodity potato waste which expires in November 2001. If the petitioner for the time-
limited tolerance petitions the Agency for a permanent tolerance, EPA would follow its new SOP
in making its lOX factor decision.
Question 19
Have the final rule and resulting risk assessment found in FR, Vol. 62, No. 234, Friday,
December 5, 1997, "Fluoride has been identified as the residue of toxicological concern in
cryolite and synthetic fluoride and the available data show that these compounds which are
approximately 52.8 % fluoride, act as a free fluoride." been applied to any other substances?'
Response
No. As explained above, there are only two pesticides, in addition to cryolite, that produce or act
as free fluoride: sodium fluoride and sulfuryl fluoride. EPA's 1993 reregistration eligibility
review of sulfuryl fluoride preceded the 1997,tolerance assessment of cryolite, so the conclusions
regarding cryolite were not available when EPA reviewed sulfuryl fluoride. EPA's reregistration
eligibility review of sodium fluoride is scheduled for 2004. The Agency will consider the
applicability of the findings on cryolite to sodium fluoride when it conducts the reregistration
eligibility review of this compound.
19
. .
The Office of Pollution Prevention and Toxics has checked their Confidential Business
Information files and cannot identify any studies ofhydrofluosilicic acid or silicofluorides that
were submitted to EP A under claimed Confidential Business Information Protection.
.
Response
Through Mr. George Glasser from Florida, the Office of Water became aware ofa
nonconfidential submission in November 1992, by Rhone-Poulenc under TSCA Section 8(e).
The submission includes data on hydrofluosilicic acid from three studies (skin irritation, eye
irritation and acute oral LD-50). A copy of that submission has been included with this response.
Question 17
Does the EPA support the recommendations made in the draft report of the Joint Science
Advisory Board Scientific Advisory Panel Subcommittee on Data from Testing of Human
subjects that states, "... in no case should developing humans be exposed to neurotoxic
chemicals"?
Response
The passage you have quoted appears in a draft report that has not been officially submitted to
the Agency. We are not certain about the context of this passage or even whether it will appear
in its current form when the report is presented to us. Accordingly, it would be premature to ..a4a
comment on it. ...
Question 18
Has the so called "lOx factor" been considered or applied in any way for fluorine-bearing
pesticides under the FQPA? '
Response
Our understanding is that you are concerned about those fluorine-bearing pesticides that produce
or act as free fluoride ion, so we have interpreted this question as applying only to those
pesticides that produce or act as free fluoride. There are three fluoride pesticides: cryolite,
sulfuryl fluoride and sodium fluoride. Of these, only cryolite is used iil or on food and, thus, is
the only pesticide in the group that is subject to the requirements of section 408 of the Federal
Food Drug and Cosmetic Act (FFDCA). The requirement to assess the need for a "lOX factor"
appears in section 408 of the FFDCA.
In a Federal Reeister notice of December 5, 1997 (62 FR 64294), EPA detenninedthat a lOX
factor was not required to account for completeness of data regarding infants and children's
18
~
"
~
. National Academy of Sciences (NAS). 1993. Health Effects oflngested Fluoride. National
." Academy Press. Washington, D.C.
National Academy of Sciences (NAS). 1997. Dietary Reference Intakes for calcium,
phosphorous, magnesium, vitamin D and fluoride. National Academy Press. Washington, D.C.
.
.
. .
O'Day. R.O., Rench, 1., Oen, R., and A. Castro. 1998. Demographic distribution of sensitive
population groups. SRA Technologies, Falls Church, VA for the United States. Environmental
Protection Agency, Office of Water Contract Number 68-C6-0036.
Public Health Service. 1991. Review of fluorine benefits and risks. Report of the Ad Hoc
Subcommittee on Fluoride of the Committee to Coordinate Environmental Health and Related
Programs. Department of Health and Human Services, Public Health Service
Riggs, B.L., Hodgson, S.F., O'Fallen, M., Chao, E.Y., Wahner, H.W.,Muhs, J.M., Cedel, S., and
L.J. Melton. 1990. Effect of fluoride on the fracture rate in postmenopausal women with
osteoporosis. N. Engl. J. Med. 322:802-809.
Spittle, B. 1994. Phycopharmacology of fluoride: a review. Internt. Clin. Psycopharmacol. 9:79-
82.
United States Department of Agriculture (USDA). 1998. Food and nutrient intakes by individuals
in the United States by sex and age, 1994-96. Nationwide Food Surveys Report No. 96-2.
Agriculture Research Service.
United States Environmental Protection Agency (USEPA). 1985. Drinking Water Criteria
Document on Fluoride. Office of Water.
Urbansky, E.T. and M.R. Schock. 2000a. Can fluoridation affect lead(II) in potable water?
Hexafluorosilicate and fluoride equilibria in aqueous solution. International Journal of
Environmental Studies. in press.
Urbansky, E.T. and M.R. Schock. 2000b. Can Fluoridation Affect Water Lead(II) Levels and
Lead(II) Neurotoxicity? Proceedings of the Anierican Water Works Association Annual
Conference, June 11-15, 2000, Denver, CO (on CD-ROM).
Villa, A.E., Guerrero, S., Icaza, G., Villalobos, J., and M. Anabalon. 1998. Dental fluorosis in
Chilean children: evaluation of risk factors. .
21
What is the Water Quality Criterion under the Clean Water Act for protection of aquatic life (and
for protection of human health) for fluoride?
.
Question 20
Response
There are no water quality criteria for fluoride either for the protection of aquatic life or for the
protection of human health. Pollutants for which water quality criteria are developed are selected
based on their toxicity, persistence, and exposure to target organisms. EPA has not developed an
aquatic life criterion for fluoride because the risk associated with other pollutants is greater. The
equations used to calculate human health criteria require that EPAhave established an RiD or
cancer risk value. Although there is an RID for fluoride based on dental fluorosis, it is a
cosmetic effect rather than an adverse health effect. Thus, the RID is not an appropriate value to
use for a human health water quality criterion.
References
Agency for Toxic Substances and Disease Registry (ATSDR). 1993. Toxicological profile of
fluorides, hydrogen fluoride and fluorine. U.S. Department of Health and Human Services.
Public Health Service. Atlanta GA.
Bardsen, A, and K. Bjorvatn. 1998. Risk periods in the development of dental fluorosis. Clin.
Oral Invest. 2:155-160.;
-
Bothwell, DJ., and H. Limeback. 1999. Fluorosis risk in grade 2 students residing in a rural area
with widely varying natural fluoride. Community Dent. Oral Epidemeol. 27: 130-136.
Den Besten, P.K. 1999. Mechanism and timing of fluoride effects on developing enamel. J.
Public Health Dent. 59(4):247-251.
Fitzsimons, D., Dwyer, J.T., Palmer, C. and L.D.Boyd. 1998. Nutrition and oral health
guidelines for pregnant women, infants and children. J. Am. Diet. Assoc. 98:182-189.
Horowitz, H.S. 1989. Fluoride and enamel defects. 1989. Adv. Dent. Res. 3(2):143-146.
Ishii, T., and G. Suckling. 1991. The severity of dental fluorosis in children exposed to water
with a high fluoride content for various periods of time. J. Dent. Res. 70(6):952-956.
Jacobs, H.L., Du, 1., and H.D. Kahn. 2000. Estimated per capita water ingestion in the United
States. United States Environmental Protection Agency. Office of Water. EPA-822-00-008.
Lehninger, A.L., Nelson, D.L., and M.M. Cox. 1993. Principles of Biochemistry. Worth
publishers. New york, NY.
~
20
~ . DEPARTMENT OF HEALTH &. HUMAN SERVICES
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Public Health Service
Food and Drug Administration
Rockville MD 20857
DEe 2 1 2Cm
The Honorable Ken Calvert
Chairman
Subcommittee on Energy and Environment
Committee on Science
House of Representatives
Washington, D.C. 20515-6301
Dear Mr. Chairman:
Thank you for the letter of May 8, 2000, to Dr. Jane E.
Henney, Commissioner of Food and Drugs, regarding the
use of fluoride in drinking water and drug products.
We apologize for the delay in responding to you.
We have restated each of your questions, followed by our
response.
1.
If health claims are made for fluoride-containing
products (e.g. that they reduce dental caries incidence
or reduce pathology from osteoporosis), do such claims
mandate that the fluoride-containing product be
considered a drug, and thus subject the product to
applicable regulatory controls?
Fluoride, when used in the diagnosis, cure, mitigation,
treatment, or prevention of disease in man or animal, is a
drug that is subject to Food and Drug Administration (FDA)
regulation. FDA published a final rule on October 6, 1995,
for artticaries drug products for over-the-counter (OTe) human
use (copy enclosed). This rule establishes the conditions
under which OTC anticaries drug products are generally
recognized as safe and effective and not misbranded. The rule
has provisions for active ingredients, packaging conditions,
labeling, and testing procedures that are required by
manufacturers in order to market anticaries products. A new
drug application (NDA) may be filed for a product containing
fluoride that does not meet the provisions stated in the final
rule. As you know, the Environmental Protection Agency
regulates fluoride in the water supply.
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.' ,I. Page 2 - The Honorable Ken Calvert
2.
Are there any New Drug Applications (NDA) on file, that
have been approved, or that have been rejected, that
involve a fluoride-containing product (including
fluoride-containing vitamin products) intended for
ingestion with the stated aim of reducing dental caries?
If any such NDA's have been rejected, on what grounds
were they rejected? If any such NDA have been approved,
please provide the data on safety and efficacy that FDA
found persuasive.
No NDAs have been approved or rejected for fluoride drugs
meant for ingestion. Several NDAs have been approved for
fluoride topical products such as dentifrices and gels.
Fluoride products in the form of liquid and tablets meant for
ingestion were in use prior to enactment of the Kefauver-
Harris Amendments (Drug Amendments of 1962) to the Food, Drug,
and Cosmetic Act in which efficacy became a requirement, in
addition to safety, for drugs marketed in the United States
(U.S.). Drugs in use prior to 1962 are being reviewed under a
process known as the drug efficacy study implementation
(DESI). The DESI review of fluoride-containing products has
not been completed.
3. Does FDA consider dental fluorosis a sign of over
exposure to fluoride?
Dental fluorosis is indicative of greater than optimal
ingestion of fluoride. In 1988, the U.S. Surgeon General
reported that dental fluorosis, while not a desirable
condition, should be considered a cosmetic effect rather than
an adverse health effect. Surgeon General M. Joycelyn Elders
reaffirmed this position in 1994.
4. Does FDA have any action-level or other regulatory
restriction or policy statement on fluoride exposure
aimed at minimizing chronic toxicity in adults or
children?
The monograph for OTC anticaries drug products sets acceptable
concentrations for fluoride dentifrices, gels and rinses (all
for topical use only). This monograph also describes the
acceptable dosing regimens and labeling including warnings and
directions for use. FDA's principal safety concern regarding
fluoride in OTC drugs is the incidence of fluorosis in
..
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Page 3 - The Honorable Ken Calvert
children. Children under two years of age do not have control
of their swallowing reflex and do not have the skills to
expectorate toothpaste properly. Young children are most
susceptible to mild fluorosis as a result of improper use and
swallowing of a fluoride toothpaste. These concerns are
addressed in the monograph by mandating maximum
concentrations, labeling that specifies directions for use and
age restrictions; and package size limits.
Thanks again for contacting us concerning this matter. If you
have further questions, please let us know.
&~
Melinda K. Pla1sier
Associate Commissioner
"for Legislation
Enclosure
"Final Rule/Federal Register - October 6, 1995
Over-the-Counter Anticaries Drug Products"
.
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UN~DSTATESENvmONMEHTALPROTEcnoNAGENCY
NATIONAL RISK MANAGEtoIENT RESEARCH LABORATORY
CINCINNATI. OH 45211
November 16, 2000
oFn:E OF
~SUfCH ItIII:J DElELOPMENT
Roger D. M8JlCrs
Researcl1Professor of Government
Dartmouth Collc&e
l.lepaJ'UI1CDt of Government
6108 Silsby Hall
Hanover, New Hampshire 03755-3547
Dear Professor Masters:
We have received your letter dated September 27,2000, requesting empirical scientir~
data we may have on the health effects of fluosilicic acid or sodium silicofluOride. and manganese
neurotoxicity .
To answer your first question on whether we have in our possession empirical scientific
data on the effects of fluosilicic acid or sodiwn silicofluoride on health and behavior. our answer
. is no. Health effects research is primarily conducted by our National Health and Environmental
Effects Research Laboratory (NHEERL). We have contacted our colleagues at NHEERL and
they report that with the exception of some acute toxicity data., they were unable to find any
information on the effects of silicofluorides on health and behavior.
In answer to your question on empirical information we may have on manganese
neurotoxicity. NHEERL scientists forwarded to us severalltWluscripts with reference s.ectioDS
that contain information on the neurotoxicity of manganese. These are enclosed for your
information.
I apologize for the delay in responding to your request and hope you find the enclosed
information useful.
Sincerely.
Qkzf L. ~
Robert C. Thurnau, Chief
Treatment Technology Evaluation Branch
Water Supply and Wa~ Resources Division
-- Enclosures
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UNITED STATES ENVIRONMENTAL PROTECTION AGENCY
NATIONAL RISK MANAGEMENT RESEARCH LABORATORY
CINCINNATI, OH 45268
March 15, 2001
Roger D. Masters, Ph.D.
Research Professor of Government
Dartmouth College, 6108 Silsby Hall
Hanover, New Hampshire 03755-3547
OFFICE OF
RESEARCH AND DEVELOPMENT
Dear Dr. Masters:
Thank you for your letter dated December 19, 2000. I apologize for the delay in my
response. To formulate a reply to you, it was necessary to coordinate with our program office in
Washington.
A recent communication to you (November 29,2000) from Jeanette Wiltse, Director,
Health and Ecological Division indicated that the U.S. Environmental Protection Agency (EPA)
endorsed the use of fluosilicate compounds for fluoridation of public drinking water supplies.
Supporting the endorsement is the ANSIINSF Standard 60, Drinking Water Chemicals - Health
Effects. This is the official agency position on this matter.
In January, representatives from the Office of Research and Development (ORD) and
the Offices of Science and Technology and Ground Water and Drinking Water met to discuss a
number of water related issues including Fluoridation. Several fluoride chemistry related
research needs were identified including; (1) accurate and precise values for the stability
constants of mixed f1uorohydroxo complexes with aluminum (III), iron (III) and other metal
cations likely to be found under drinking water conditions and (2) a kinetic model for the
dissociation and hydroloysis of fluosilicates and stepwise equilibrium constants for the partial
hydrolysis products.
As a result of these discussions, ORD is exploring options to initiate research in the
identified research areas.
If we have additional information on this issue, we will forward it to you:
Sincerely,
a~,t. l {2,,~ ~
Sally C. Gutierrez
Director
Water Supply and Water Resources
Division
RecycledlRecyclable. Printed with Vegetable Oil Based Inks on 100% Recycled Paper (40% Postconsumer)
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REQUEST FOR ASSISTANCE
Measur.ement of Fluorosilicates in Drinking Water
1.0. INTRODUCfION
The improvemcnt of the quality of the nation's drinking water is an important goal and research to
extend the boundaries of knowledge in this area is a function that govcrnment serves well. The Watcr
Supply and Water Resources Division (WSWRD) of the National Risk Management Research
Laboratory (NRMRL) is involved in a wide range of efforts, one of which is thc revicw and
advancement of the science on regulated contaminants. Much of the nation's drinking water is
fluoridated, and fluoride is regulated by thc EP A at a maximum contaminant level of 4.0 mg L-'. The
division has completed a review of the scientific literature and has identified certain arcas for which
additional infonnation is desired. The division seeks to promote the public welfare by researching
basic liquid aqueous phase solution chemistry ofrcgulated contaminants and ~liciting competent
researchers capable of completing research projects that fill identified gaps in the scientific literdture.
To that end, the division seeks to fund a proposal on the measurement of fluorosilieate species in
drinking water.
2.0. RESEARCH OBJECTIVES
2.1. Background
Hexafluorosilieie acid (H2SiF/>) and sodium hexafluorosilicate (Na2SiF/>) arc the most commonly
used fluoridating agents by potable water systems in the U.S. These species dissociate and hydrolyze
to produce fluoride anion (F""). The rclease of fluoride proceeds through a complex, multi-step
equilibrium process that is not well-understood. A variety of models have been proposed, and the
speciation remains a matter of debate as docs the existence of some fluorosilieates. A review of the
relevant chemical literature detailing the complexities, disagreement, and scientific facts has been
prepared by the EP A. This revicw is available to prospective applicants, and they arc encouraged to
request a copy prior to preparing a proposal.
In addition to the silieon(lV) present from the fluoridating agent, many natural water supplies contain
soluble oxo- and hydroxosilicates, which further complicates the speciation. The EPA seeks
information on the utility of techniques and methods for monitoring the species fonned during the
dissociation and hydrolysis ofhexafluorosilieate as wcll as those species present once equilibrium
is achieved. These data arc expectcd to aid in the development of phannacokinetie and toxieokinetie
studies and to further the understanding of the fate of fluoride, including its interactions with other
species in drinking water. As such, the results of this study will be of use to state agencies, water
utilities, and other governmental or scientific bodies who seek to ensure the quality of the nation's
drinking water supplies.
2.2. Objective
The primary objective of this RF A is to investigate the rcactions that take place when fluorosilieates
arc added to drinking watcr supplies and what concentrations of which fluorosilicate species may
monitored in finished drinking water supplies and what techniqucs may bc used for such monitoring.
A secondary objective of this RF A is to explore what spectroscopic or other techniques arc most
amenable to determination of equilibrium constants for fluorosilicatc systcms, which engage in
multiple, simultaneous, and complex equilibria. A tcrtiary objective is to consider what techniques
might be. applied to kinctic and mechanistic studies of the dissociation and hydrolysis of
hexafluorosilicatc. Conditions in finishcd drinking water include total fluoride conccntrations on the
orderof20 ~M and total silicon(lV) coneentrdtions onthe orderof300 ~M. Collaboration by skilled
experimentalists with expertise in inorganic chemistry and the analytical techniques is encouraged.
REQUEST FOR ASSISTANCE (RF A)
MEASUREMENT OFFLUOROSILICA TES IN DRINKING WATER
Announccmcnt datc: April 25, 2002
An offcror must submit thc application (original plus four copics) so as to be reecived by
Thc applieation should be addressed
as follows:
Edward T. Urbansky
U.S. Environmental Protection Agency
National Risk Managcment Rcsearch Laboratory
Water Supply and Water Resources Division
26 West Martin Luther King Drive, MS 681
Cincinnati, Ohio 45268
An application received after the above time and datc will not bc considered unless there is elear
evidence that the application was mishandlcd by EP A aftcr its timely receipt.
Questions regarding this RF A should bc directed by electronic mail to
urbansky.edward@epa.gov
Applicants will bc notified by letter as to the disposition of thcir prcapplication (accepted/not
accepted) and informcd of the identity of thc successful proposal.
Proprictary Information: In aceordancc with 40 CFR 40.150, applications consideredrelcvant to EP A
research objectivcs will bc vicwed for technical merit by at least one rcviewer within the EP A and
at lcast two revicwers outsidc of thc EP A. Thercfore, proposals submitted in response to this
compctitive solicitation will not be considered ifthe applicant asserts a claim of confidentiality for
technical infonnation contained therein.
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tl=~=~:!:.~":..;cals Contribute to Arsenk Levels
and.. Cia.., M. Huntley
Arsenic is an issue that water utilities no longer can
avoid. The US Environmental Protection Agency is expected
to propose a reduction in the federal drinking water
standard on arsenic from 50 pglL to 5 Jlg/L later this year,
although USEPA is also considering setting the maximum
contaminant level at 3 pg/L, 10 pglL, and 20 pg/L. The final
arsenic rule is due by Jan. 1, 2001.
Utilities should test their sources of water for arsenic and
compare them with the proposed levels of 3, 5, and 10 pg/L. .
However, testing source water alone may not be suffident to
determine the arsenic load in finished water. Some
treatment chemicals may also contain trace amounts of
arsenic. Utilities should review and estimate the maximum
~ible arsenic concentrations contributed by the
cIl.elnicals they use in drinking water treatment. Even trace
~()UIlts add up and may contribute a substantial portion-
~bly up to 10 percent-of a 3 or
5..PiIL maximum contaminant level.
Connecticut Experience
The South Central Connecticut Regional Water Authority
has three surface water treatment plants (SWfPs) and five
wellfields. Recently, SCCRWA calculated the arsenic burden
derived from chemicals routinely used to treat surface and
etr' .. dwater at these facilities. Those chemicals are listed in
e1.
To estimate the trace arsenic levels in the bulk treatment
chemicals, data from the suppliers' analysis reports or
product specifications were used. The resulting trace arsenic
concentrations in the finished water that were contributed
J:,y ,the treatment chemicals were computed by one of the
fOllOWing two methods:
,.....1. For those chemicals with dosages expressed as mg/L
of product chemicals (such as polymer, sulfuric add,
bimetallic zinc metaphosphate, and potassium
~anganate), the resulting trace arsenic concentration
In the finished water was computed by multiplying the
c::bemical dosage by the trace arsenic level in the bulk
treatment chemical.
2. For other chemicals (such as alum, ferric chloride,
caustic soda, and fluorosilidc add), a dilution factor was
determined by dividing the chemical concentration by the
chemical dosage. The resulting trace arsenic concentration
In the finished water was computed by dividing the trace
arsenic level in the bulk treatment chemical by the dUution
factoL
Information produced by several calculations is tabulated
asfoliows:
.~le 2 shows the maximum possible arsenic cOncentratims
.. '~ntributed by treatment chemIcals for Olle surface water
'::J~~ent plant that uses alum (0.279Jlg/L ~c. .
"'.;tontributed). ... ,
.~ble 3 shows the maximum possible arsenic . .
.~pcentrations contributed by tr.eatmentchemicals for.
the wellfield, which uses sodium hypochlorite for
disinfection (0.249 pglL arsenic cOntributed).
FenIc chIorlde
Synthetic polymer A
Synthetic polymer B
ChlorIne
Sodium hypochlorite
BImetallic zinc metaphosphate
FIuorosIIicIc acid
Not used
NotuMd
Not uMd
Notuaed
4
1
5
5
Not used
3
3
Table 1. Chemicals routinely used by the South Central
Connecticut Regional Water Authority" and the number
of facilities where they are used.
. Table 4 shows the range of maximum arsenic
contribution by treatment chemicals for the SCCRWA
(range of all compounds, 0.0002-0.245 pg/L).
. Table 5 compares in finished water the calculated amount
of arsenic that is contributed by treatment chemicals with
the analytical result (overall calculated range,
0.248-0.306 pg/Li analytical result <1 pg/L in all cases).
These data show that in finished water the theoretical
arsenic concentrations attributable to normal dosages of
water treatment chemicals are extremely low (Tables 2, 3,
and 4). This conclusion is supported by the analytical data
(Table 5), which show arsenic concentrations to be below
1.0 J1g/L in all of the SCCRWA's surface ~d groundwater
treatment facility finished waters.
Conclusion
If the standard were set at 3 Jlg/L, about 10 percent of the
MCL would come from the treatment chemicals, hardly a
minimal amount. It is also interesting to note that about
90 percent of the arsenic that would be contributed by
treatment chemicals is attributable to fluoride addition.
If your processes include the addition of chemicals, ask
your manufacturer for the amount of arsenic in each. If
necessary, obtain conversion charts for diluted products, as
well. Then calculate how much arsenic those chemicals will
add to your finished water. If the total is close to the MCLs
proposed by USEPA, you have reason for concern.
To find out more about the proposed arsenic rule, go to
the agency's Web site, <www.epa.gov/safewater/
arsenic.html>, or call the Safe Drinking Water Hotline at
(800) 426-2791.
., Cheng-nan "Mike" Wens, PhD, DEE, is seniOr water qutllity
engineer, Darrell B. Smith is vice president of water qutllity
and research, and Gary M. Huntley.is water treatment
manager for South Central Connecticut Regional Water
Authority, 90 Sargent Drive, New Haven, CT 06511;
(203) 624-6671.
Opflow
: Treat"!ent Am~unt of Arsenic Dosage -Calculation of Contribution Ars.enlc
Chemical In Product Contribution
Bimetallic zinc < 2 mgIL
meta os hate
Potassium
permanganate
(KMn04)
Chlorine All manulaclurer reports indicate that arsenic is not present in gaseous chlorine.
Total arsenic contributed by treatment chemicals
50% alum 0.25 mgIL 10 m!1l'
Polymer A < 0.5 mgIL 2.0 m!1l
50% Sodium 1.5m!1l 12.5 mgIL.
hydroxide (maximum) (maximum)
(NaOH)
Auoroslcic Maximum = 60 mg/l. 1.0 mgIL'
acid (H2SiF6) Normal = 28 m!1l asF
1.7m!1l
4.8 m!1l
0.35 m!1l
* Based on dry equivalents.
Chemical concentration 0150% alum = 650 mg/mL
DiulIon factor = 650 x 1,000 .;. 10 = 65,000
Arsenic contribution = 0;25 .;. 65,000 mg/L
Arsenic contribution = 0.5 m!1l x 2 mg/L
Chemical concentretion 0150% NaOH = no mg/mL
DIution factor = (770 x 1,000) .;. 12.5 = 61,600
Arsenic contribulIon = 1.5 .;. 61,600 m!1l.
H2SiF6 solution contains 20% F or 244.8 mg/ml. at F
F dosage = 1.0 m!1l as F
Dilution factor = 244.8 x 1,000.;. 1.0 = 244,800
Maximum arsenic contrIbulion =
60 /244,800 mgIL = 0.2451Jg/1..
Normal arsenic conbibulion = 28 .;. 244,800 "9'l = 0.11419L
Arsenic contribution = 2 mg/L x 1.7 m!1l
Table 2. Arsenic
contributed by
chemicals used to
treat surface water
at Lake Call1ard
Water Treatment
Plant
.
0.00385
I/g/\..
0.0011Jg/1..
0.0241Jg/1..
0.1141Jg/1..
(1lOIm8I)
0.245 !Ig/L
(maximum)
Arsenic contribution = 4.8 m!1l x 0.35 mg/\..
0.003411WL
0.00168
!Ig/L
o
lI.279l'S11l
(maximum)
Treatment Amount of Arsenic .. . Arsenic
Chemical in Product Dosage Calculallon of ContributIOn ContributIon
Table 3. Anenlc
contributed by
chemicals used
to treat
groundwater at
North Cheshire
Wellfleld
Sodium 0.8 m!1l 1.2mg/\.. 1 Ib of chlorine reads with 1.128 Ib of caustic soc:fa to 0.00096
hypochlorite (maximum) produce 1.05 Ib of NaOCl. An excess of caustic soc:fa is IJg/I..
(NaOCI) used as a stabilizer. Based on the arsenic concentration
in the 50% caustic soda, tha maximum arsenic
concentration In the NaOCI is estimated to be 0.8 mg/\...
Arsenic contribution = 0.8 mg/\.. x 1.2 mg/l. .
. Fluorosilicic 6Omg/\.. 1.0 mg/\.. Dilution factor = 244.8 x 1,000 + 1.0 = 244,800 0.245 I/g/\..
acid (HzSiFe) (maximum) asF Maximum arsenic contribution = 60 .;. 244,800 mg/\.. .
Bimetallic zlnc < 2 mg/l. 1.7mg/\.. Arsenic contribution = 2 mg/\.. x 1.7 mg/\.. 0.00341Jg/1..
metaphosphate
Total arsenic conlrIbuled by treatment chemicals 0.249 I'WL
(maximum)
. Range of Range of Maximum
Treatment Chemical Chemical Dosage Arsenic Contribution
. (mg/L) (119/L in finished water)
Table 5. Malmum finished wateranenlc
. concentrations based on chemical dosages .
applied In the treatll1ent"facllltles .
Sodium hydroxide
Sulfuric acid
Alum
Potassium permanganate
Ferric chloride
Synthetic polymer A
Synthetic polymer B
Chlorine
SOdium hypochlorite
Bimetallic zinc metaphosphate
Ruorosillcicacid
8.0-12.5
20
10-80
0.30-0.35
7
2.0
4.0
1.2-2.8
1.2
1.5-1.7
1.0
October 2000
Table 4. Maximum finished water
anenlc concentrations based on
chemical dosages applied In the
treatment facilities
0.015&-0.024
0.0002
0.00385-0.0308
0.0014-0.00168
0.037
0.001
0.004
0.000
0.00096
0.0030-0.0034
0.245
Trace Arsenic
Concentration (119/L)
Calculated Analytical
Treatment Facility Maximum Result
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Lake Gaillard WTP'
Lake SaJtonstaJl WTP . <1
West River WTP . <1
North Cheshire Wellfleld <1
All olherwellflelds (N=4) <1
* Water treatment plant
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Table 7-1
Comparative Toxicity of Inorganic Fluorides6
Extremely Tox;c
Hydrogen fluoride (anhydrous)
Silicon tetrafluoride
Hydrofluoric acid (aqueous)
Hydrofluorosilicic acid
Very Tox;c
Easily soluble fluorides a~ fluorosilicates
Sodium fluoride
Potassium fluoride
Ammonium fluoride
Sodium fluorosilicate
Potassium fluorosilicate
Ammonium fluorosilicate
Moderately Tox;c
Poorly soluble (almost insoluble) fluorides
Cryolite
Calcium fluoride
Table 7-2
Lethal Dose of Fluorides in Adult Guinea Pigs'
CHAPTER 7
HF
SiF4
HF
H2 SiF 6
NaF
KF
NH.F
Na:zSiF 6
K2 SiF 6
(NH4 )2SiF 6
Na3 AIF 6
CaF2
Compound
NaF
CaF2
AIF3
HF (aqueous)
H2 SiF 6
Na2 SiF 6
AI2 (SiF 6)3
Oral (mglkg)
250
>5,000
600
80
200
250
5,000
Subcutaneous (mg/kg)
400
>5,000.
3,000
100
250
500
4,000
Table 7-2 shows the acute toxicity. of the. most important fluo-
ride salts to guinea pigs, expressed in mi))jgrams per kilogram of
body weight. It also demonstrates the difference in the lethal dose
foJIowing oral and subcutaneous administration.
7. Simonin, P., and Pierron A.: Toxiciti brute des derives nuores. C .R.SE. .
ances Soc. Bioi. Fil.. 12.4:133.134. 1937.
In: Waldbott GL, M.D., A W Burgstahler, Ph.D., HL McKinney, Ph.D. Fluoridation: The Great
Dilemma Lawrence Kansas: Coronado Press, Inc., 1978:
'. " :: - 0 ~~ ... 0 " . . 0_ 0" , '. - :
.. . ~ ' - . ~
.
COMPTES RENDUS HEBDOMADAIRES
DES SEANCES ET MEMOJRES
DB LA
SOCIETE DE BIOLOGIE
~
ET DE SES FILJALES ET ASSOCIEES:
LES SOCIETES DE BlOLOGlE D'ALGER, DE BORDEAUX, l.lLLE,
LYON, MARSEILLE, NANCY. STRASBOURG, ATHtNES. BARCELONE.
BELGilADE, MONTEVlDEO, MONTREAL;
LES SOCIETE:; DE BlOLOGlE ARGENTINE
(BUENOS-AIRES, CORDOBA,! ROSARIO),
BELGE, DRESJLJENNE (RlO DE JANEIRO, SAO PAULO)
CHJLIENNE (CONGEPClON, SANTIAGO), DANOlS'E, MEXICAINE,.
POLONAISE (LWOW,VAHSOVIE, POZNAN), POR1'UGAISE
~LI~BONNE, ponTO, COI~IBRE). HOUMAINE (DUCAnE~T, CLUJ,
JASSY), 1'CHECOSLOV AQUE, DE SUEDE E1' DE LETTONIE;
LA socm'i'E FHANr.O-JAPONAISE DE BIOLOGlE.
(80. annee)
.
ANNEE 1937 - TOME
(CENT VINGT-QUATRIE.ME TOME DE LA COLLECTION)'
PARIS
l\lASSON ET Cie, EDITEURS
LlDRAIHES DE L ACADf:MJE DE MtDECINE.
1:10, JlOllLEVAl\D SAUlT-Gill MAl" (6.)
1937
.
JeuroToxicology@ 21(6): 1091-1100,2000
:opyright @ 2000 by Intox Press, Ine.
.
.~
Association of Silicofluoride Treated Water
with Elevated Blood Lead
RD. MAsTERst, M.J. COPLAN2, B.T. HaNEl AND J.E. DYKEsl
IFoundation for Neuroscience and Society, Dartmouth College, Hanover, NH, USA; 21ntellequity, Natick,
MA, USA
Abstract: Previous epidemiological studies have associated silicofluoride-treated community
water with enhanced child blood lead parameters. Chronic, low-level dosage of silicofluo-
. ride (SiF) has never been adequately tested for health effects in humans. We report here on
a statistical study of 151,225 venous blood lead (VBL) tests taken from children ages 0-6
inclusive, living in 105 communities of populations from 15,000 to 75,000. The tests are part
of a sample collected by the New York State Department of Children's Health, mostly from
1994-1998. Community fluoridation status was determined from the CDC 1992 Fluoridation
Census. Covariates were assigned to each community using the 1990 U.S. Census. Blood
lead measures were divided into groups based on race and age. Logistic regressions were
carried out for each race/age group, as well as above and below the median of 7 covariates
to test the relationship between known risk fadors for lead uptake, exposure to SiF-treated
water, and VBL > 10pg/dL. RESULTS: For every age/race group, there was a consistently
significant association of SiF treated community water and elevated blood lead. Logistic
regressions above and below the median value of seven covariates show an effect of silico-
fluoride on blood lead independent of those covariates. The highest likelihood of children
having VBL> 10pgldL occurs when they are both exposed to SiF treated water and likely to
be subject to another risk fador known to be associated with high blood lead (e.g., old
housing). Results are consistent with prior analyses of surveys of children's blood lead in
Massachusetts andNHANES III. These data contradict the null hypothesis that there is no
difference between the toxic effects of SiF and sodium fluoride, pointing to the need for
chemical studies and comprehensive animal testing of water treated with commercial grade
silicofluorides. t> 2000 Intox Press, Inc.
.~
(ey Words: Lead Neurotoxicity, Silicofluorides, Water Fluoridation, Venous Blood Tests, Public Health
INTRODUCTION
Over 91 % of US fluoridated water is treated with
~ither sodium silicofluoride (Na2SiF) or fluosilicic acid
H SiF ) - henceforth, the silicofluorides or SiFs. Less
h~n 10% is treated with simple sodium fluoride (NaF).
Vhereas NaF was the model compound used in the
940s for demonstrating safety and efficacy, and has
leen submitted to exhaustive animal testing for
lecades (e.g., McClure, 1962; Largent, 1961; Dunipace
tal., 1995, 1996, 1998a, 1998b; Jackson et aI., 1997), the
amecannot be said of the SiFs. The Assistant
~dministrator of the EPA recently acknowledged (Fox,
999) that his agency knew of no study of human health
ffects of chronic low-level exposure to either of the
,iFs. Here we report data suggesting that SiF may
enhance the uptake of lead from other environmental
sources.
As is well known, many environmental and
behavioral risk factors have previously been associated
with increased lead levels among children. Among these
are age, race, sex, income (or poverty), size of community
(esp. between urban areas of greater and less than 1
million as well as between urban, suburban, and rural
communities), location of community (including presence
of soils with high lead levels), age of housing (presence of
lead paint), lead in excess of 15 ppb in public water
supplies, individual calcium or iron deficiency, maternal
smoking, parental education and alcohol consumption
(e.g., Needleman, 1992; Hense et aI., 1992; Cezard et aI.,
1992; Weitzman et aI., 1993). Using community rates, a
recent study of over 238,000 Massachusetts children found
. ase send requests for reprints to Dr. Roger D. Masters, Dep~rtment of Govemment, Dartmouth College, 6108 Silsby Hall, Hinman Box 6108,
lanover, NH 03755-3547, USA, Phone: (603) 646-2153, Fax: (603) 646-0508, E-mail: roger.d.masters@dartmouth.edu
ubmitted: Decmber 15, 1999 Accepted: July 14.2000
or permission to photocopy Neurotoxicology (0161-813X) contact the Copyright Clearance Center. 978-750-8400, Fax: 978.750-4470
~
. rz~~
.~
.1
DEPARTMENT Of HEALTH &. HUMAN SERVICES
Public HeaJlh ServicI
National Instllutes of Heallh
National Institute of Diabetes and
Digestive and KJdney DIseases
Sethesda. Maryland 20892
January 4, 1991
Wini SUko
1507 N. Fife St.
Tacoma, WA 98406
Dear H3. S11k.o:
.tour letter tQ Surgeon Gener;alDr. Antonia Novello hu been fowarded to
the Nation",l In.tHute of Diabetes And Digestive and lUdney Diseases of
the National In.tHutes of Health (NUl), the local point within the
Federal Government for biomedical relearch. .
I am enclo~ing lame booklets on Insulin~ependent and noninsulin~ependent
diabetes th.llt explain when to suspect diabetes and how various testa are
uled to diagnole it. Tau are absolutely correct in .tating that many
people have diabetes but clon"t know it. tn the United States,
approximAtelY hall of the estimated 12 million people who have the diseaae
don"t renUze it. nle .ymptolllll of dlabetu include rapid weight loss,
exceulve thint, frequent ur1naHon. (Other l'Iymptom. are listed in the
enclosed information.) nle. rapLdlty of detection and control usually
depends on hQw long an individual waiU before aeeinga doctor.
Treatment depends on whether the diseaee 18 ineulln~ependent or
nonlnsul!n dependent, as well ;as other facton euch ae the patient",
weight, lifelltyle and diet. Diabetic care also depends on whet,her the
individual suffers froll complicatione as.ociated with diabetes, euch as
kidney. failure, corona~ artery dile..e, etc.
Re8earch, "lao part of NIH,
1 hope thh information ie helpful.
s;;;t ~a~ l..iclkt
~thy ~nZfelder
HI0D~ Informatioa Office
.~
.~
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MUNICIPAL UTILITY DISTRICT ACT
Div.6
apportionment of expenses among public agencies served, or any . combination
of the foregoing. .
(Stats.l951, c. 764, p. 2232, ~ 12813. Amended by Stats.1963, c. 1345, p. 2870, ~ 3, eff.
July 11, 1963; Stats.1965, c. 210, p. 1173, ~ 3; Stats.1977, c. 128, p. 563., ~ 3.)
~ 12813
Historical and Statutory Notes
Intent of 5tats.1965. c. i 10, see Historical
and Statutory Notes under Public Utilities Code
!j 11503.
Derivation: 5tats.1915. c. 531, p. 878. !j 23.
5tats.1921, .c. 218, p. 257, !j 18, amended
5tats.1929, c. 31, p. 67, !j 8; 5tats.1931, c. 75,
p. 95. !j 9; 5tats.1941, c. 321, p. 1503. !j 32.
Amended as !j 862. 5tats.1947, c. 97, p. 598,
!j 1.
Municipal Corporations e=o911.
WE5TLAW Topic No. 268.
C,J.5. Municipal Corporations!j!j 1907, 1908.
Library References
Background and general effect of 1965
amendment. Rev. of 1965 Code Leg. (Cont.
Educ. of Bar, 1965) page 236.
Notes of Decisions
Dry Dock Co. v. East Bay Mun. Util. Dist.
(1932) 14 P.2d 828, 126 C.A.349.
2. Levy of taxes
Levy of tax by municipal utility district to take
care of bonded debt on property purchased was
valid and not "impairment of oHigation of con.
tract nor infringement of vested rights of tax-
payers. General Engineering & Dry Dock Co.
v. East Bav Mun. Uti!. Dist. (1932) 14 P.2d 828,
126 C.A. 349. .,
Credit lending 1
Levy of taxes 2
1. Credit lending
Purchase by municipal utility district of water
company's assets subject to mortgage indebted-
ness was not giving or lending of credit of such
utility district to another within prohibitory pro-
visions of Constitution. General Engineering &
~ 12814. Addition of fluorine or fluorine compounds to public water sup-
plies: approval of voters
A district may add fluorine or fluorine compounds to the water supply of the
district only if the voters of the district have approved the addition of the
fluorine and fluorine compounds to the .water supply. If a majority of the
voters of a district voting upon the proposition at an election called and held as
prescribed in Section 12815 have voted in favor of the addition of fluorine and
fluorine compounds to the water supply of the district, the district shall, subject
to the provisions of Article 1 (commencing at Section 4010), Chapter 7, Part 1,
Division 5 of the Health and Safety Code, add to water intended for consump-
tion or use by the public, including domestic, industrial, and other uses,
fluorine and fluorine compounds.
(Added by Stats.1959, c. 1152, p. 3244, ~ 1.)
Section 4 of Stats.1959,
provided:
'The Legislature hereby declares that it is not
the intent of the Legislature in enacting Sec-
Historical and Statutory Notes
c. 1152, p. 3245, tions 12814 and 12815 of the Public Utilities
Code to indicate legislative approval or disap.
proval of the principle of fluoridation of water."
300
POWEF
Ch. 6
Liberty,
Strong (F
Waters
WESTL
C.J.5. \
District a
Limltatio:
1. Distii
TheEa
under the
fluoride (
to the p\
~ 128
The
submitt
voters ;
water s
on whi
manneJ
TIle elf
with a
ed. Al
propos
12815.
(Added
~ 1.)
Legist:
Historic;
Utilities
Munic
WE51
Consolie
. '
el
Ordinance enacted by the voters of the City of Watsonville11/5/02:
e~
e~
In order to ensure that the public water of Watsonville is safe to drink, it
shall be unlawful and a public nuisance for any person, agent, or any public
or private water system, to add any product, substance, or chemical to the
public water supply for the purpose of treating or affecting the physical or
mental functions of the body of any person, rather than to make water safe
or potable, unless the substance meets the following criteria:
1) The substance must have been specifically approved by the U. S. Food
and Drug Administration for safety and effectiveness with a margin of
safety that is protective for all adverse health and cosmetic effects at all
ranges of unrestricted consumption.
2) The substance, at Maximum Use Levels, must contain no contaminants
at concentrations that exceed U.S. Maximum Contaminant Level Goals or
California Public Health Goals, whichever is more protective.
If any provision of this act or the application thereof to any person or
circumstance is held invalid, that invalidity may not affect other provisions
or applications of this act that can be given effect without the invalid
provision or application, and to this end the provisions of this act are
severable.
1 of the Complaint and are irreJevant to the issue of plaintiffs' erroneous allegation that the state
2 law requiring fluoridation is unconstitutional facially or "as applied." The plaintiffs' extrinsic
3 evidence does not cure the FAC's defect that the fluoridation issue concerns a permit - not a plan.
4 There is no "approval" under the law other than issuance of a permit or amended permit There
5 has not been a complete pennit application submitted by the City or issuance of a permit by the
6 Department, and none has been alleged by plaintiffs in the F AC. Likewise, the Department does
7 not approve a fluoridation substance. But rather, when a facility is built and the permit is
8 completed with the precise trademark and manufacturer of the substance, the Department will, if
9 appropriate, issue a permit The plaintiffs' allegation on page 3, line 16 of the FACmakes an
10 inaccurate and baseless statement that the state will demand the City fluoridate with the
11 particular substance complained of by plaintiffs. Plaintiffs have failed to make any allegation
12 supported by law thatthe Department could act in such a manner. The Departmentcannot be
13 enjoined from doing what it is not doing and in fact cannot do. The Department is limited to
14 issu~g a permit, and requiring fluoridation by a substance approved by the American National
. ~ 15 Standards Institute (ANSI) and National Sanitary Foundation (NSF). (See Health and Safety
16 Code section 116525, et seq., 116550 and Title 22, California Code of Regulations, section
.~
17 64700). Accordingly, the declaration attaching discovery submitted to the plaintiffs by the City
18 are not properly before this Court, irrelevant and should be disregarded.
19 11/
20 III
21 1/1
22 III
23 1/1
24 11/
25 III
26 III
27 III
.- 28
4.
DEFENDANT'S REPLY TO nm OPPOSrnON OF PLAINTIFFS TOnm DBMURRBR TO
THE FOURTH AMENDED COMPLAINT AND OBJECI'ION TO EXTRINSIC EVIDENCE
1 Bll.L LOCKYER, Attorney General
of the State ofCalifomia
2 JoHN" H. SANDERS,.
Lead Supervising Deputy Attorney General
3 KAREN L. FRIED, Deputy Attorney General
State Bar No. 74420
4 300 South Spring Street, Suite 9 North
Los Angeles, California 90013
5 Telephone: (213) 897-2438/Fax: (213) 897-2805
6 Attorneys for Defendant
Califomja Department of Health Services
.
7
8
9
10
11 SHIRLEY MACY, an individual; PAULCOSHOW,
an individual; ROBIN WINTON,.an individual;
12 SABRINA GESE, an individual; OWEN
MORRISON, an individual; JOY ALSOBROOK, an
13 individual; AL MCGOWEN, an individual; JIM
PETERSEN, an individual; ROES 1 through 1,000,
14 in~lusive, on behalf of themselves, on behalf of the
general public, and. on behalf of all persons similarly
IS . situated,
IN THE SUPERIOR COURT OF THE STATE OF CALIFORNIA
SAN DIEGO COUNTY, NORTH COUNTY DISTRICf
16
17
18
19
20
21
22.
23 COMES NOW Respondent, California Department of Health Services (Department), and
Plaintiffs,
Case No.: GIN 015280
DEFENDANT'S REPLY TO THE
OPPOSITION OF PLAINTIFFS TO
THE DEMURRER TO THE
FOURm AMENDED
COMPLAINT AND OBJECfION
TO EXTRINSIC EVIDENCE
PROFFERED BY PLAINTIFFS IN
THEIR OPPOSITION
Date: March 27, 2003
Time: 3 :00 p.m. .
Judge: Hon. Dana M, Sabraw
Dept.: 27
v,
CITY OF ESCONDIDO, STATE OF CALIFORNIA.
and DOES 1 through 100, inclusive,
Defendants.
24 in response to Plaintiffs' Memorandum of Points and Authorities in Opposition to the Dem1Jl1'eI'
.25 to the Fourth Amended Com.plaint submits the following ReplyinSupport of its Demurrer and
26 Objection to Extrinsic Evidence Proffered by Plaintiffs.
27 1/1
28
l.
DEFENDANT'S REPLY TO THE OPPOSITION OF pLAINTIFFS 10 1lIE DEMURRER TO
THE FOURTH AMENDED COMPLAINT AND OBJECTION TO EXl"RINSIC BVlDENCB
.
!
j
Page 1 of:
Superior Court
San Diego County. State of California
Business
Return to Reauest Rulina I Trouble orintina?
The following is a TELEPHONIC, ruling for 3/27/2003,
Department 27, the Honorable DANA M. SABRAW presiding.
Case Number GIN015280
The Court declines to consider the Nordrehaug declaration or the exhibits attached thereto. These matters
constitute extrinsic evidence which cannot be considered in ruling on a demurrer. (See Ion Equipment
Corp. v Nelson (1980) 110 CaI.App.3d 868).
Defendant's general demurrer to Plaintiffs Fourth Amended Complaint based on the argument the
complaint is not ripe for judicial review is overruled. Defendant argues in the moving papers it has "yet to
approve or even see a complete permit application. . . " (moving papers page 7 lines 22-24 and page 8
lines 8-9). .
~is argument is improper as it is based. on matters outside the four comers of the complaint. Thus, based
~. the holding in Ion Equipment Corp, supra it cannot be considered in ruling on this motion. However,
even ifthe argument is construed as requiring Plaintiff to allege these matters, Plaintiff has sufficiently pled
approval in paragraph 69 of the Fourth Amended Complaint which infers submission of a completed
application.
In the reply, Defendant argues Plaintiffs allegations in para. 69 are insufficient as Plaintiff has not alleged
Defendant issued a permit. As this argument differs from the one made by Defendant in its moving papers
quoted above, and because plaintiff has been raised for the first time in the reply, to which Plaintiff cannot
respond, it cannot be considered in ruling on this demurrer.
In addition, Defendant cites to no section of Title 22 or the Health and Safety Code which specifies what
action the Dept. takes after receipt of a completed application, Le., whether it issues a permit or approves a
permit application.
Defendant's special demurrer to the fourth amended complaint based on the failure to name an
indispensable party is overruled. This defect does not appear on the face of the pleading and therefore, the
demurrer based on misjoinder will not lie. In addition, Defendant has not demonstrated the entities listed
are in fact indispensable as defined by CCP 389(b).
Defendant's special demurrer to the fourth amended complaint based on the failure to specifically allege the
laws purportedly violated is overruled. Plaintiff has cured this defect by alleging in para. 14 the State's
approval of the City's Plan "is illegal under State law (Penal Code Section 374.8) and in violation of the
United States constitution, Amendment IX and XIV, and California Constitution Art. I, Section 7(a).
.intiffs further allege in para. 72 and elsewhere, Defendant's conduct "violates the fundamental rights of
1Ie:IIC:\ WINDOWS\TEMP\triNNNHD.htm 3/27/0:
Page 2 of:
Rlaintiff and other similarly situated residents of Escondido to preserve their health from such govemment-
imposed practices as may prejudice or annoy it. . ." Thus, Plaintiffs have done more than merely recite the
laws allegedly violated. .
.Defendant's special demurrer for uncertainty based on the argument the complaint fails to "evidence"
Defendant permitted or sanctioned the actions of which Plaintiff complains and Plaintiffs claimed injuries
are speculative is overruled. As stated above, Plaintiff alleges in para. 69 Defendant approved the City's
Plan of fluoridation. Thus, Plaintiffs have adequately alleged Defendan "sanctioned" that plan. Defendant
does not support its argument Plaintiffs injuries are speculative.
Defendant's special demurrer for uncertainty based on the argument Plaintiffs have not alleged the
existence of an actual controversy is overruled. The court overruled Defendant's identical demurrer to the
Third Amended Complaint. Where a prior demurrer was sustained as to some causes of action but
overruled as to others, and plaintiff then amends the complaint, defendants may not demurrer against on
the same grounds to those portions of the amended pleading to which an earlier demurrer was overruled.
(Bennett v Suncloud (1997) 56 Cal.App.4th 91).
As the court pointed out in its Jan. 9, 2003 ruling, "Plaintiffs' complaint, when read as a whole establishes
the existence of an actual controversy between the parties".
Defendant's special demurrer for uncertainty based on Plaintiffs' complaint simply referring to some generic
"industrial grade Hydrofluorosilic acid" which might be used by the City without specifically identifying the
compound is overruled. Defendant has not adequately explained how the failure to allege the exact
compound at issue prevents it from answering the complaint.
Defendant's special demurrer for uncertainty based on Plaintiffs attaching numerous allegedly irrelevant
exhibits and background allegations and request to strike the allegations on pages 12-24 and the
.orresponding exhibits is overru. led. The inclusion of these allegedly irrelevant allegations and exhibits does
ot render the complaint so uncertain, vague, or ambiguous Defendant cannot determine how to answer
the allegations against it.
If the parties wish to orally argue this motion, they are required to contact the court at (760) 806-6346 and
opposing parties within two court days following this tentative telephonic ruling date. Parties will be required
to file a declaration proving notice given. If oral argument is requested it will be heard Friday, April 04, 2003,
at 1 :30 p.m. in Department 27 formerly Department 24.
This ruling file posted to web server: Thu, Mar 27, 2003, 12:23 AM
ThIs ruling file retrieved by browser: Thu, Mar 27, 2003, 12:25 AM
A PIe8II8 eend queBllons or~ IJbout IhIs page III /he s.-rior CtJutl WsbmasIer San DIego SUperior Coutt,
. SyaI8ms Gmltp. 330 Wesl8ID8dW8y, S8n DIego. CA 92101
.
lle://C:\ WINDOWS\TEMP\triNNNHD.htm
3/27/0:
.
';an Diego Superior Court, Ruling for Case GIN015280
Page 1 of:
Superior Court
San Diego County, State of California
Business
Return '\0 B"QII'"'' RIlling I Irr" ,hi.. printing?
The following is a TELEPHONIC, ruling for 1/9/2003,
Department 27, the Honorable DANA M. SABRAW presiding.
Case Number GIN015280
Defendant State of California's Special Demurrer based on a defect in the parties is sustained with ten days
leave to amend to name the proper State Agency and/or officers against whom Plaintiffs are seeking relief.
(See State v Superior Court (1974) 12 Cal.3d 237).
Defendant State of California's General Demurrer to Plaintiffs' Third Amended Complaint based on the
argument fluoridation is legal is overruled. Plaintiffs maintain they are not facially attacking the legislation
mandating fluoridation of the City of Escondidots drinking water. However, a review of the allegations made
in the third amended complaint suggests such an attack has been alleged. (See e.g., para 14 lines 17-18,
~ra. 70 lines 11-12, para. 73 lines 9-14). .
~vertheless, Plaintiffs are also alleging the fluoridation legislation as applied by the plan of the City of
Escondido is illegal and Unconstitutional. (See e.g., Para. 14 lines 18-19). Thus, Plaintiffs appear to have
combined facial and "as applied" attacks on the subject legislation.
A general demurrer does not lie to only part of a cause of action. If there are sufficient allegations to entitle
Plaintiff to relief, other allegations cannot be challenged by general demurrer. (Financial Corp. of America v
Wilburn (1987) 189 Cal.App.3d 764). As the moving papers do not address the legal sufficiency of the
allegations that the legislation as applied in this case is illegal and Unconstitutional, the general demurrer
must be overruled.
Defendant State of California's General Demurrer to the Third Amended Complaint based on the running of
the Statute of Limitations is overruled as this defect is not revealed on the face of the pleading. It is unclear
to what legislation Defendants are referring in making this argument, Le., the California Safe Drinking Water
Act, the implementing regulations, or the City's plan of fluoridation.
In addition, the question of waiver involves issues of fact which cannot be determined in a demurrer. (See
e.g., Estate of Crane (1946) 73 Cal.App.2d 93)
Defendant State of California's Special Demurrer to the Third Amended Complaint for uncertainty based on
Plaintiffs failure to make reference to any pertinent sections of either the U.S. or Calif. Constitutions which
were allegedly violated is sustained with ten days leave to amend to allege the specific Constitutional
violations at issue against the State. Plaintiffs maintain they have alleged specific Constitutional violations
in para. 14 of the Third Amended Complaint. However, the allegations are addressed only to "the City's
.ision and plan to inject contaminated Hydrofluorosilic acid into the public drinking water. . . II and there
no specific violations alleged against the State of California.
Ittp:/lwww.sandiego.courts.ca.gov/scripts/seekrulingfile.cgi
1/9/0::
",an Diego Superior Court, Ruling for Case GIN015280
Page 2 of:
If.fendant State of California's Special Demurrer to the Third Amended Complaint for uncertainty based on
failure to allege a contractual relationship between the parties or facts showing the existence of an
actual controversy is overruled. Nothing in CCP Section 1060 limits the availability of Declaratory Relief to
only parties in a contractual relationship. In addition, Plaintiffs complaint, when read as a whole establishes
the existence of an actual controversy between the parties.
Defendant State of California's Special Demurrer to the Third Amended Complaint for uncertainty based on
the failure to clearly allege the "legal rights and duties of the respective parties" at issue in this lawsuit is
sustained.
As the above ruling on Defendant's general demurrer points out, Plaintiffs appear in the Third Amended
Complaint to be making both a facial and "as applied" attack to fluoridation legislation. However, in the
opposition to the instant motion, Plaintiffs .maintain their attack is lias applied" only. Therefore, Plaintiffs are
granted leave to amend to clarify the nature of this action as against the State of California and to specify
the particular legislation involved.
If the parties wish to orally argue this motion, they are required to contact the court at (760)806-6346 and
opposing parties within two court days following this tentative telephonic ruling date. Parties will be required
to file a declaration proving notice given. If oral argument is requested it will be heard Friday, January 17,
2003, at 1 :30 p.m. in Department 27 formerly Department 24. .
This ruling file posted to web server. Thu. Jen 9, 2003, 12:52 AM
This ruling file retrieved by browser: Thu, Jan 9, 2003, 3:08 PM
.
A. ... PleBse send qUBsllons or commenls Bboullhis psgB 10 Ihe "'''p''nft' ,,~.., WA"~D.'A' Ssn ~ Supsrlor COlIIt,
.. Systems Group. 330 Wesl Srosdwsy. SBn Diego. CA 92101
.
Ittp://www.sandiego.courts.ca.gov/scriptslseekrulingfile.cgi
1I9/0~
.
.
.
Superior Court San Diego Connty, State of California
The following is a TELEPHONIC, ruling for 8122102,
Department 24, the Honorable DANA M. SABRA W presiding.
Case Nmnber GIN015280
MACY vs CITY OF ESCONDIDO
(D-DEMURRER) EPP
DEFENDANT'S REQUEST FOR JUDICIAL NOTICE IS GRANTED.
DEFENDANT'S GENERAL DEMURRER TO THE FIRST CAUSE OF ACTION
FOR DECLARATORY RELIEF BASED ON FAILURE TO STATE A CAUSE OF
ACTION IS OVERRULED. PLAINTIFFS HAVE ALLEGED FACTS
ESTABLISIDNG THE EXISTENCE OF AN ACTUAL CONTROVERSY
SUFFICIENT TOWITHSTAND A GENERAL DEMURRER. BY THIS ACTION,
PLAINTIFFS SEEK TO CHALLENGE THE CONSTITUTIONALITY OF THE
CITY'S ALLEGED DECISION TO UTILIZE HYDROFLUOROSICILIC ACID AT
EXCESSIVE QUANTITIES IN THEIR PLAN OF WATER FLUORIDATION.
DEFENDANT'S GENERAL DEMURRER TO THE SECOND CAUSE OF ACTION
FOR INJUNCTIVE RELIEF BASED ON A FAILURE TO STATE A CAUSE OF
ACTION IS OVERRULED. PLAINTIFFS HAVE PLED SUFFICIENT FACTS TO
ALLEGE DEFENDANT IS THREATENING AN ILLEGAL EXPENDITURE OF
PUBLIC FUNDS, BYITS PLAN TO UTILIZE HYDROFLUOROSILIC ACID IN
THE CITY'S WATER SUPPLY. DEFENDANT CITES TO NO AUTHORITY
WHICH REQUIRES THAT THE FUNDS ACTUALLY HAVE BEEN EXPENDED
BEFORE PLAINTIFFS CAN SEEK INJUNCTIVE RELIEF PURSUANT TO CCP
SECTION 526a. DEFENDANTS ARGUMENT THAT ANY EXPENDITURE MADE
liTO PREVENT TOOTH DECAY AND TO COMPLY WITH STATE MANDATES
ARE NOT ILLEGAL EXPENDITURES" IGNORES PLAINTIFFS' ALLEGATIONS
THAT THE SPECIFIC PLAN OF FLUORIDATION TO BE IMPLE:MENTED BY
THE CITY IS UNCONSTITUTIONAL.
DEFENDANT'S SPECIAL DEMURRER TO THE SECOND AMENDED
COMPLAINT BASED ON UNCERTAINTY IS SUSTAINED WITH TEN DAYS
LEAVE TO AMEND TO ALLEGE THE OPERATIVE FACTS AGAINST THE
STATE OF CALIFORNIA SEPARATE FROM THE OPERATIVE FACTS AGAINST
THE CITY OF ESCONDIDO. PLAINTIFFS ARGUE IN THEIR OPPOSITION
BRIEF THAT THE SECOND AMENDED COMPLAINT NO LONGER ALLEGES
THE CITY IS LIABLE AS A RESULT OF ITS IMPLEMENTATION OF STATE-
MANDATED FLUORIDATION OF ITS WATER SUPPLY. INSTEAD,
PLAINTIFFS CLAIM THEIR ACTION AGAINST THE CITY IS BASED ON THE
SPECIFIC MANNER IN WlllCH THE CITY HAS DECIDED TO IMPLEMENT
FLUORIDATION. THE ALLEGATIONS OF THE SECOND AMENDED
COMPLAINT, HOWEVER, APPEAR TO ALLEGE BOTH THEORIES OF
LIABILITY AGAINST THE CITY. (SEE E.G., PARA 55(a) AND (c)).
THEREFORE, TO CLARIFY WIDCH OF THE THEORIES OF LIABILITY APPLY
TO THE CITY, PLAINTIFFS ARE ORDERED TO SEPARATE THE
ALLEGATIONS wmCH PERTAIN TO THE STATE FROM THOSE PERTAINING
TO THE CITY EITHER BY SEPARATING THE ALLEGATIONS IN SECTION III
OF THE SECOND AMENDED COMPLAINT, ENTITLED "F ACTUAL
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ALLEGATIONS," OR BY ALLEGING SEPARATE CAUSES OF ACTION
AGAINST EACH NAMED DEFENDANT. IN ITS CURRENT FORM, THE
SECOND AMENDED COMPLAINT CANNOT BE ADEQUATELY RESPONDED
TO BY THE CITY.
IF THE PARTIES WISH TO ORALLY ARGUE THIS MOTION, THEY ARE
REQUIRED TO CONTACT THE COURT AT (760) 806-6346 AND OPPOSING
PARTIES WITHIN TWO COURT DAYS FOLLOWING TIllS TENTATIVE
RULING DATE. PARTIES WILL BE REQUIRED TO FILE A DECLARATION
PROVING NOTICE GIVEN. IF ORAL ARGUMENT ISREQUESTEDIT WILL BE
HEARD FRIDAY, AUGUST 30, 2002 AT 1:30 P.M. IN DEPARTMENT 24.
Review of the California Oral Health
el NeedsAssessment 1993-94
City of Escondido
Jan. 2000
Page 1
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Summary
The intent of this paper is to provide the City of Escondido with an independent review of the
California Oral Health Needs Assessment 1993-94. In the review context, I have concentrated on
. the issues that are .expected to be most important: the relationship between prevalence of dental
caries (cavities in teeth) and such factors as use of fluoridated water, use of fluoride supplements,
use of dental sealants, prevalence of specific infant feeding practices, and occurrence of Baby
Bottle Tooth Decay. It must be emphasized, however, that this review is not exhaustive and is
concerned primarilY with the scientific merits of one particular study; I have not addressed more
. general issues such as .the pros and cons of water fluoridation or the use of fluorideslilpplements.
I would like to commend the originators of the study for their obvious care and thoroughness in
designing the study and collecting the data. The data collected during the California Oral Health
Needs AssessmeQ.t 1993-94 constitute a valuable resource for addressing a number of import.ant
questions.
However, the data analysis as reported by Pollick et al. (1994) stands inneed of imProvement in
two key areas:
1. All sources of uncertainty should be considered, including sample representativeness.
errors or ambiguity in data collection or recording, and absence or incompleteness of
relevant data. In particular, uncertainties in individual fluoride exposures should be
addressed. Regional fluoridation status should not ~ used as a surrogate for total
fluoride exposure due to -the potential for misclassification of individuals.
2. Analysis of endpoints such as caries experience should include both incidence (caries
or no caries) and severity (number of caries) and should account, on an individual.
basis, for all factors that might affect the endpoint, including total fluoride exposure,
presence of dental sealants, history of dental visits, history of Baby Bottle Tooth.
Decay, and economic factors; . .
The results of the study as reported by Pollick et at (1994) do not support its primary conclusion,
namely that increased fluoridation of public water supplies and increased supplementation of
fluoride in nonfluoridated areas are warranted. The differences in caries incidence (percentage of
children with and without caries) with fluoridation status as reported by Pollick et aI. (1994) are
probably due to other factors, primarily economic status and presence or absence of dental
sealants.
f2 SENES o..lIldpllOC.
~ c.n...............,....
.c::::::::::::J SENES Oak Ri~ge inc.
l .ENE~ Center for Risk Analysis
. . F. Owen Hoffman, Ph.D., President
SpecialisI8 in ~ ,.ut:I8er
end EtM<>Irt-*' sa.-.
CuIrIilm AppIc:afions in Human HeeIrh
and rcoIOgIc:aI ~..-Jt
.
January 31, 2000
Mr. John E. Hoagland .
Deputy Director of Public Works
City of Escondida
201 North Broadway
E~ondido, CA 92025
Re: Consulting Agre~ment-Independent Review of California Oral Health Needs
Assessment (A-2336)
Dear Mr. Hoagland:
I am enclosing an original and five photocopies .of my review of the California Oral Health
Needs Assessment.l apologize . for my delay in completing this review; we have had more work .
. ~helast few months than I had anticipated. If you or others at the City of Escondido have any
questions about the review, or. if I or SENES Oak Ridge. Inc., can. be of further assistance tQ. the
City of Escondido, please do not hesitate to call me at (865) 483-6111. (The 865 area. code is
rClatively new, arid some people have reported difficulty with it; if that should happen, try the old .
area code, 423). .
Sincerely,
.~/tf~
Kathleen M. Thiessen, Ph.D.
Senior Scientist
.
102 Donner Drive. Oak RidQe. Tennessee 37830 .. Tel: (865) 483-6111 . Fax (865) 481-()()60 E-Mail: senesor@senes.com
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STATEMENT OF
Dr. J. WILLIAM HIRZY
NATIONAL TREASURY EMPLOYEES UNION CHAPTER 280
BEFORE THE
SUBCOMMITTEE ON WILDLIFE, FISHERIES AND DRINKING WATER
UNITED STATES SENATE
JUNE 29, 2000
Good morning Mr. Chairman and Members of the Subcommittee. I appreciate the
opportunity to appear before this Subcommittee to present the views of the union, of which I am
a Vice-President, on the subject of fluoridation of public water supplies.
Our union is comprised of and represents the professional employees at the headquarters
location of the U.S. Environmental Protection Agency in Washington D.C. Our members include
toxicologists, biologists, chemists, engineers, lawyers and others defined by law as
"professionals." The work we do includes evaluation of toxicity, exposure and economic
information for management's use in formulating public health and environmental protection
policy. I am not here as a representative ofEPA, but rather as a representative ofEPA
headquarters professional employees, .through their duly elected labor union. The union first got
involved in this issue in 1985 as a matter of professional ethics. In 1997 we most recently voted
to oppose fluoridation. Our opposition has strengthened since then.
Summa" of Recommendations
1) We ask that you order an independent review of a cancer bioassay previously mandated by
Congressional committee and subsequently performed by Battelle Memorial Institute with
appropriate blinding and instructions that all reviewer's independent determinations be reported
to this Committee.
2) We ask that you order that the two waste products of the fertilizer industry that are now used
in.90% of fluoridation programs, for which EP A states they are not able to identify any chronic
studies, be used in any future toxicity studies, rather than a substitute chemical. Further, since
federal agencies are actively advocating that each man woman and child drink, eat and bathe in
these chemicals, silicofluorides should be placed at the head of the list for establishing a MCL
that complies with the Safe Drinking Water Act. This means that the MCL be protective of the
most sensitive of our population, including infants, with an appropriate margin of safety for
ingestion over an entire lifetime.
3) We ask that you order an epidemiology study comparing childTenWitbdentalfluor6sistbu
those not displaying overdose during growth and development years for behavioral and other
disorders.
4) We ask that you convene a joint Congressional Committee to give the only substance that is
being mandated for ingestion throughout this country the full hearing that it deserves.
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National Review of Fluoridation The Subcommittee's hearing today can only begin to get at
the issues surrounding the policy of water fluoridation in the United State~ a massive
experiment that has been TUn on the American public, without informed consent, for over fifty
years. The last Congressional hearings on this subject were held in 1977. Much knowledge has
been gained in the intervening years. It is high time for a national review of this policy by a Joint
Select Committee of Congress. New hearings should explore,.at minimum, these points:
1) excessive and un-controlled fluoride exposures;
2) altered findings of a cancer bioassay;
3) the results and implications of recent brain effects research;
4) the ''protected pollutant" status of fluoride within EP A:,
5) the altered recommendations to EPA ofa 1983 Surgeon General's Panel on fluoride;
6) the results of a fifty-year experiment on fluoridation in two New Yode communities;
7) the findings of fact in three landmark lawsuits sillce 1978;
8) the findings and implications of recent research linking the predominant fluoridation chemical
with elevated blood-lead levels in children and anti-social behavior; and
9) changing views among dental researchers on the efficacy of water fluoridation
Fluoride Exposures Are Excessive and Un-controlled According to a study by the National
Institute of Dental Research, 66 percent of America's children ill fluoridated communities show
the visible sign of over-exposure and fluoride toxicity, dental fluorosis (1). That result is from a
survey done in the mid-1980's and the figure today is undoubtedly much higher.
Centers for Disease Control and EP A claim that dental fluorosis is only a "cosmetic"
effect. God did not create humans with fluOTOSed teeth. That effect occurs when children ingest
more fluoride than their bodies can handle with the metabolic processes we were born with, and
their teeth are damaged as a result. And not only their teeth. Children's bones and other tissues,
as well as their developing teeth are accumulating too much fluoride, We can see the effect on
teeth. Few researchers, if any, are looking for the effects of excessive fluoride exposure on bone
and other tissues in American children. What has been reported so far in this connection is
disturbing. One example is epidemiological evidence (28, 2b) showing elevated bone cancer in
young men related to consumption of fluoridated drinking water.
Without trying to ascribe a cause and effect relationship beforehand, we do know that
American children in large numbers are afflicted with hyperactivity-attention deficit disorder,
that autism seems to be on the rise, that bone fractures in young athletes and military personnel
are on the rise, that earlier onset of puberty in young women is occurring. There are biologically
plausible mechanisms described in peer-reviewed research on fluoride that can link some of
these effects to fluoride exposures (e.g. 3,4,5,6). Considering the economic and human costs of
these conditions, we believe that Congress should order epidemiology studies that use dental
fluorosis as an index of exposure to determine if there are . links between such effects and fluoride
over-exposure.
In the interim, while this epidemiology is conducted, we believe that a national
moratorium on water fluoridation should be instituted. There will be a hue and cry from some
quarters, predicting increased dental caries, but Europe has about the same rate of dental caries
as the U.S. (7) and most European countries do not fluoridate (8). I am submitting letters from
European and Asi~ authorities on this point. There are studies in the U. S. of localities that have
interrupted fluoridation with no discernable increase in dental caries rates (e.g., 9). And people
who want the freedom of choice to continue to ingest fluoride caD do so by other ....ea,D5.
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Cancer Bioassav Findine:s In 1990, the results of the National Toxicology Program cancer
bioassay on sodium fluoride were published (10), the initial findings of which would have ended
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fluoridation. But a special commission was hastily convened to review the findings, resulting in
the salvation of fluoridation through systematic down-grading of the evidence of carcinogenicity.
The final, published version of the NTP report says that there is, "equivocal evidence of
carcinogenicity in male rats," changed from "clear evidence of carcinogenicity in male rats."
The change prompted Dr. William Marcus, who was then Senior Science Adviser and
Toxicologist in the Office of Drinking Water, to blow the whistle about the issue (22), which led
to his firing by EP A Dr. Marcus sued EP A, won his case and was reinstated with back pay,
benefits and compensatory damages. I am submitting material from Dr. Marcus to the
Subcommittee dealing with the cancer and neurotoxicity.risks posed by fluoridation.
We believe the Subcommittee should call for an independent review of the tumor slides
from the bioassay, as was called for by Dr. Marcus (22), with the results to be presented in a
hearing before a Select Committee of the Congress. The scientists who conducted the original
study, the original reviewers of the study, and the '1"eview commission" members should be
called, and an explanation given for the changed findings.
Brain Effects Research Since 1994 there have been six publications that link fluoride exposure
to direct adverse effects on the brain. Two epidemiology studies from China indicate depression
ofl.Q. in children (11,12). Another paper (3) shows a link between prenatal exposure of animals
to fluoride and subsequent birth of off-spring which are hyperactive throughout life. A 1998
paper shows brain and kidney damage in animals given the "optimal" dosage of fluoride, viz.
one part per million (13). And another (14) shows decreased levels ofa key substance in the
brain that may explain the results in the other paper from that journal. Another publication (5)
links fluoride dosing to adverse effects on the brain's pineal gland and pre-mature onset of
sexual maturity in animals. Earlier onset of menstruation of girls in fluoridated Newburg, New
York has also been reported (6).
Given the national concern over incidence of attention deficit-hyperactivity disorder and
autism in our children, we believe that the authors of these studies should be called before a
Select Committee, along with those who have critiqued their studies, so the American public and
the Congress can understand the implications of this work.
Fluoride as a Protected Pollutant The classic example ofEPA's protective treatment of this
substance, recognized the world over and in the U.S. before the linguistic de-toxification
campaign of the 1940's and 1950's as a major environmental pollutant, is the 1983 statement by
EPA's then Deputy Assistant Administrator for Water, Rebecca Hanmer (15), that EPA views
the use ofhydrofluosilicic acid recovered from the waste stream of phosphate fertilizer
manufacture as,
"...an ideal solution to a long standing problem. By recovering by-product fluosilicic acid
(sic) from fertilizer manufacturing, water and air pollution are minimized, and water
authorities have a low-cost source of fluoride..."
In other words, the solution to pollution is dilution, as long as the pollutant is dumped
straight into drinking water systems and not into rivers or the atmosphere. I am submitting a
copy of her letter.
Other Federal entities are also protective of fluoride. Congressman Calvert of the House
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Science Committee has sent letters of inquiry to EP A and other Federal entities on the matter of
fluoride, answers to which have not yet been received.
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We believe that EP A and other Federal officials should be called to testify on the manner
in which fluoride has ~een protected. The union will be happy to assist the Congress in
identifying targets for an inquiry. For instance, hydrofluosilicic acid does not appear on the
Toxic Release Inventory list of chemicals, and there is a remarkable discrepancy among the
Maximum Contaminant Levels for fluoride, arsenic and lead, given the relative toxicities of
these substances.
Sur2eon General's Panel on Fluoride We believe that EP A staff and managers should be
called to testify, along with members of the 1983 Surgeon General's panel and officials of the
Department of Human Services, to explain how the original recommendations of the Surgeon
General's panel (16) were altered to allow EPA to set otherwise unjustifiable drinking water
standards for fluoride.
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Kin2ston and Newbul"2. New York Results In 1998, the resuhs ofa fifty-year fluoridation
experiment involving Kingston, New York: (un-fluoridated) and Newburg, New York
(fluoridated) were published (17). In summary, there is no overall significant difference in rates
of dental decay in children in the two cities, but children in the fluoridated city show
significantly higher rates of dental fluorosis than children in the un-fluoridated city.
We believe that the authors of this study and representatives of the Centers For Disease
Control and EP A should be called before a Select Committee to explain the increase in dental
fluorosis among American children and the implications of that increase for skeletal and other
effects as the children mature, including bone cancer, stress fractures and arthritis.
Findin2s of Fact bv Jud2es In three landmark cases adjudicated since 1978 in Pennsylvania,
Illinois and Texas (18), judges with no interest except finding fact and administering justice
heard prolonged testimony from proponents and opponents of fluoridation and made
dispassionate fil)dings of fact. I cite one such instance here.
In November, 1978, Judge John Flaherty, now Chief Justice of the Supreme Court of
Pennsylvania, issued findings in the case, Aitkenhead v. Borough of West View, tried before him
in the Allegheny Court of Common Pleas. Testimony in the case filled 2800 transcript pages and
fully elucidated the benefits and risks of water fluoridation as understood in 1978. Judge Flaherty
issued an injunction against fluoridation in the case, but the injunction was overturned on
jurisdictional grounds. His findings of fact were not disturbed by appellate action. Judge
Flaherty, in a July, 1979 letter to the Mayor of Aukland New Zealand wrote the following about
the case:
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''In my view, the evidence is quite convincing that the addition of sodium fluoride to the
public water supply at one part per million is extremely deleterious to the human body,
and, a review of the evidence will disclose that there was no convincing evidence to the
contrary...
''Prior to hearing this case, I gave the matter of fluoridation little, if any, thought, but I
received quite an education, and noted that the proponents of fluoridation do nothing
more than try to impune (sic) the objectivity of those who oppose fluoridation."
In the Dlinois decision, Judge Ronald Niemann concludes: "This record is barren of any
credible and reputable scientific epidemiological studies and or analysis of statistical data which
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would support the Dlinois Legislature's determination that fluoridation of the water supplies is
both a safe and effective means of promoting public heahh."
Judge Anthony Farris in Texas found: ""[That] the artificial fluoridation of public water
supplies, such as contemplated by {Houston} City ordinance No. 80-2530 may cause or
contribute to the cause of cancer, genetic damage, intolerant reactions, and chronic toxicity,
including dental mottling, in man; that the said artificial fluoridation may aggravate malnutrition
and existing illness in man; and that the value of said artificial fluoridation is in some doubt as to
reduction of tooth decay in man."
The significance of Judge Flaherty's statement and his and the other two judges' findings
of fact is this:. proponents of fluoridation are fond of reciting endorsement statements by
authorities, such as those by CDC and the American Dental Association, both of which have
long-standing commitments that are hard if not impossible to recant, on the safety and efficacy of
fluoridation. Now come three truly independent servants of justice, the judges in these three
cases, and they find that fluoridation of water supplies is not justified.
Proponents of fluoridation are absolutely right about one thing: there is no real
controversy about fluoridation when tbe facts are heard by an open mind.
I am submitting a copy of the excerpted letter from Judge Flaherty and another letter
referenced in it that was sent to Judge Flaherty by Dr. Pett"J" Sammartino, then Chancellor of
Fairleigh Dickenson University. I am also submitting a reprint copy of an article in the Spring
1999 issue"ofthe Florida State University Journal of Land Use and Environmental Law by Jack
Graham and Dr. Pierre Morin, titled "'Highlights in North American Litigation During the
Twentieth Century on Artificial Fluoridation of Public Water. Mr. Graham was chieflitigator in
the case before Judge Flaherty and in the other two cases (in Dlinois and Texas).
We believe that Mr. Graham should be called before a Select Committee along wit~ if
appropriate, the judges in these three cases who could relate their experience as trial judges in
these cases.
Bvdrofluosllicic Acid There are no chronic toxicity data on the predominant chemical,
hydrofluosilicic acid and its sodium salt, used to fluoridate American communities. Newly
published studies (19) indicate a link between use of these chemicals and elevated level of lead
in children's blood and anti-social behavior. Material from the authors of these studies has been
submitted by them independently.
We believe the authors of these papers and their critics should be called before a Select
Committee to explain to you and the American people what these papers mean for continuation
of the policy of fluoridation.
Chao2in2 Views on Efficacv and Risk In recent years, two prominent dental researchers who
were leaders of the pro-fluoridation movement announced reversals of their former positions
because they concluded that water fluoridation is not an effective means of reducing dental caries
and that it poses serious risks to human health. The late Dr. John Colquhoun was Principal
Dental Officer of Aukland, New Zealand, and he published his reasons for changing sides in
1997 (20). In 1999, Dr. Hardy Limeback, Head of Preventive Dentistry, University of Toronto,
announced his change of views, then published a statement (21) dated April 2000. I am
submitting a copy of Dr. Limeback's publications.
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We believe that Dr. Lirneback, along with fluoridation proponents who have not changed
their minds, such as Drs. Ernest Newbrun and Herschel Horowitz, should be called before a
Select Committee to testify on the reasons for their respective positions.
Thank you for you consideration, and I will be happy to take questions.
CITATIONS
l.Dental caries and dental fluorosis at varying water fluoride concentrations.
Heller, K.E, Eklund, S.A. and Burt, B.A. J. Pub. Health Dent. .5Z 136.43 (1997).
2a. A brief report on the association of drinking water fluoridation and the
incidence of osteosarcoma among young males. Cohn, P.O. New Jersey
Department of Health (1992).
2b. Time trends for bone and joint cancers and osteosarcomas in the
Surveillance, Epidemiology and End Results (SEER) Program. National Cancer
I nstitute. I n: Review of fluoride: benefits and risks. Department of Health and Human
Services.1991: F1.F7.
3.Neurotoxicity of sodium fluoride in rats. Mullenix, P.J., Denbesten, P.K.,
Schunior, A. and Kernan, W.J.Neurotoxicol. Teratol.lI 169.177 (1995)
. ~ 4a. Fluoride and bone - quantity versus quality [editorial] N. Engl 1. Med. 322845.;6(1990)
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4b. Summary of workshop on drinking water fluoride influence on hip fracture and bone health.
Gordon, S.L. and Corbin, S.B. Natl Ins!. Health. April 10, 1991.
5. Effect of fluoride on the physiology of the pineal gland. Luke, J.A. Caries
Research 28 204 (1994).
6. Newburgh-Kingston caries.fluorine study XIII. Pediatric findings after ten
years. Schlesinger, E.R., Overton, D.E., Chase, H.C., and Cantwell, K.T. JADA 52
296.306 (1956).
7. WHO oral heahh country/area profile programme. Department of Non -Communicable
Diseases Surveillance/Oral Health. WHO Collaborating Centre, Malmo University, Sweden.
URL:
www.whocollab.odont.lu.selcountriesa1phab.html
8. Letters from government authorities in response to inquiries on fluoridation status by E.
Albright. Eugene Albright: contact through 1. W. Hirzy, P.O. Box 76082, Washington, D.C.
20013.
9. The effects of a break in water fluoridation on the development of dental caries and fluorosis.
Burt B.A, Keels ., Heller KE. 1. Dent. Res. 2000 Feb;79(2):761-9.
10. Toxicology and carcinogenesis studies of sodium fluoride in F344/N rats and
B6C3F1 mice. NTP Report No. 393 (1991).
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11. Effect of high fluoride water supply on children's intelligence. Zhao, L.B.,
Liang, G.H., Zhang, D.N., and Wu, X.R Fluoride 22 190.192 (1996)
12. Effect of fluoride exposure on intelligence in children. Li, X.S., Ztii, J.L., and
Gao, RD. Fluoride 28 (1995).
13. Chronic administration of aluminum. fluoride or sodium.fluoride to rats in
drinking water: alterations in neuronal and cerebrovascular integrity. Varner, J.A.,
Jensen, K.F., Horvath, W. And Isaacson, RL. Brain Research 784 284.298 (1998).
14. Influence of chronic fluorosis on membrane lipids in rat brain. Z.Z. Guan, Y.N.
Wang, K.Q. Xiao, D.Y. Dai, Y.H. Chen, J.L. Liu, P. Sindelar and G. Dallner,
Neurotoxico/ogy and Teratology 20537.542 (1998).
15. Letter from Rebecca Hanmer, Deputy Assistant Administrator for Water, to
Leslie Russell re: EPA view on use of by.product fluosilicic (sic) acid as low cost
source of fluoride to water authorities. March 30, 1983.
16.Transcript of proceedings. Surgeon General's (Koop) ad hoc committee on
non-dental effects of fluoride. April 18.19, 1983. National Institutes of. Health.
Bethesda, MD.
17. Recommendations for fluoride use in children. Kumar, J.V. and Green, E.L.
New York State Dent. J. (1998) 40.47.
18. Highlights in North American litigation during the twentieth century on
artificial fluoridation of public water supplies. Graham, J.R and Morin, P. Journal
of Land Use and Environmental Law 14 195-248 (Spring 1999) Florida State University
College of Law.
19. Water treatment with silicofluorides and lead toxicity. Masters, R.D. and
Coplan, M.J. Intern. J. Environ. Studies ~ 435.49 (1999).
20. Why I changed my mind about water fluoridation. Colquhoun, J. Perspectives
in Bioi. And Medicine 41 1-16 (1997).
21. Letter. limeback, H. April 2000. Faculty of Dentistry, U'niversity of Toronto.
22.. Memorandum: Subject Fluoride Conference to Review the NTP Draft Fluoride
Report; From: Wm. L. Marcus, Senior Science Advisor ODW; To: Alan B. Hais,
Acting Director Criteria & Standards Division Office of Drinking Water. May 1,
1990.
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Esteemed Voices Against Fluoride
Page 1 of 3
Esteemed Voices have, for 50 years, warned
the American public that water fluoridation
has dangerous long-term consequences to health:
"I am appalled at the prospect of using water as a vehicle for drugs. Fluoride is a corrosive
poison that will produce serious effects on a long range basis. Any attempt to use water this
way is deplorable."
Dr. Charles Gordon Heyd, Past President of the American Medical Association.
"fluoridation ... it is the greatest fraud that has ever been perpetrated and it has been
perpetrated on more people than any other fraud has. "
Professor Albert Schatz, Ph.D. (Microbiology), Discoverer of streptomycin & Nobel Prize
Winner.
Join voices with the medical professionals who see fluoride as a health hazard.
William Marcus, Ph.D., D.A.B.T. (Toxicology), former U.S.
EPA, Senior Science Advisor, Office of Drinking Water. *
Albert W. Burgstahler, PILD. (Organic Chern, Environ. Fluoride)
Robert J. Carton, Ph.D. (Environ. Sciences and Risk Assessment).
Paul Connett, Ph.D. (Environmental Chemistry and Toxicology).
Richard Foulkes, M.D., fmr. Consult. to Health Minstr., BC,
Canada
J. William Hirzy, Ph.D. (Chern and Risk Assess) Sr.VP,
NFFE,EPA
RobertL. Isaacson, Ph.D. (Neurobehavioral Science). Dist.
Prof. David C. Kennedy, D.D.S., Inter. Acad. Oral Med. and
Toxicology.
Harold D. Kletschka, M.D., F.A.C.S.(finr. Chair. ofBio-
Medicus,Inc)
Lennart Krook, D. V.M., Ph.D. (pathology) Cornell Univ.and
NYSC.
Richard A Kunin, MD., Pres., Soc. for orthomotecuia
HIth.Medicine
Gene W. Nfler, Ph.D. (Biochemistry and Toxicology).
Phyllis Mullemy, Ph.D. Owmacology and Neumtoxicology)
John Colquhoun, BDS, MPhlL Ph.D., DipEd., Prin. Dent. Ofc.
NZ.
John AYiamouyiannis, Ph.D. (Biochemistry)
A K. Susheela, Ph.D., F.ASc., F.AM.S. (Ifistocryochemistry)
Benedict J. Gallo, Ph.D.(Botany). Research Mcrobiologist.
Norman R. Mancuso,Ph.D. (Chemistry) Apollo Project Scientist.
Andrew Berna-Ificks, Hazardous Substance Engineer, Cal EPA
Jason Kupperschmidt, B.C. (Chem. Engr)
Rudolph Ziegelbecker, Ph.D. (phys.) Inst. of Environ
Hlth.Austria
MA Krikker M.D., Hemochromatosis Found, Albany, N. Y.
Dean Burk, Ph.D. (Biochemistry) former Senior Chemist and
http://www.garynull.com/lssueslFluoridelFluorideVoices.htm
John R. Lee, M.D. (physician)
J. C. Smart, Ph-D. (Chemistry) UCB
Gerard F. Judd, Ph.D. (Chemistry)
Gerson Jacobs, MD.
Michael F. Ziff, D.D.S..
Harvey Petraborg, MD.
Robert I H. Mick,D.D.S. E. R- Cooper, M.D.
C. T. Betts, D.D.S.
I E. Waters, D.D.S.
Allen London, D.D.S.
Edward A McLaughlin, M.D.
Philip E. Zafagna, M.D.
George W. Heard, D.D.S.
Charles Dillon, D.D.S., 1.D.
S. Leslie A Russell, D.M.D. (dentist)
Casimir R. Sheft, D.D.S.
Jonathan Forman, M.D.
Ross Pringle, D.D.S.
A B. MacWhimiie, D.D.S.
AC. Baumann, D.D.S.
Kirk Youngman, D.M.D.
1. A Alesen, M.D.
Paul W. Sheeran, D.M.D.
Thomas F. Evans, D.D.S.
Robert Davis, D.D.S.
William I Filante, MD.
Joyal W. Taylor, D.D.S.
Michael Ohnstad, D.D.S.
Sheridan B. Mianasen, D.D.S
Scott McAdoo, D.D.S.
Tony Lees, B.D.S. DentI Surgn
8/1 0/2003
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Esteemed Voices Against Fluoride
Director Cytochemistry Section, National Cancer Institute.
Harold Warner, Prof Of Research; Chief, Biomedical Engineer
Div.
Sheila L. M. Gibson, M.D., B. Sc., M.F. Horn. (Research
Physician)
James B. Patrick, Ph.D. (Chemistry) , Antibiotics Research.
I. R. B. Mann, Senior Lecturer in Environ. Studies, U. of
Auckland.
Bruce J. Spittle, Ph.D., Psycho. Med., U. of Otago Med. Sch., NZ
George 1. Waldbott, MD., fladr. Inter Soc for Fl. Res. and j.
Fluoride
Alfred Taylor, Ph.D, Research Scientist, Clayton Fnd. Biochem.
Insl.
Ludwik Gross, M.D, fmr Chief of Cancer Res. Vetrans Admin,
N.Y.
Dr. Daniel Zaskin, Chf. Diagnostician, Columbia Sch of Dental
Surg.
Geoffrey E. Smith, L.D.S., RC.S. Dental Surgeon.
Philip R- N. Sutton, D.D.Sc., 1.D.S., F.R.AC.D.S.
Brian A. Dementi~ Ph.D. (Biochemistry and Toxicology)
John P. Flaherty, Chief Justice, Supreme Court of Pennsylvania
Simon Beisler, M.D., Chief of Urology, Roosevelt Hosp. N.Y.
Fred Squier, M.D., Head of Oral Surgery, Lenox Hill Hosp. N.Y.
John Garlock, M.D., Consulting Surgeon, ML Sinai Hosp. N.Y.
Edgar A Lawrence, M.D., Dir. of Medicine, Lenox Hill
Girard F. Oberrender, M.D., Dir. of Otolaryugology, Lenox Hill
Frederick B. Exner, M.D. Fellow of the Am. CoIl. Of Radiology.
Charles C. Bass, M.D., Dean Emeritus, Tulane Univ. Med. Sch.
Alton Ochsner, M.D., head, Dept of Surgery, Tulane Univ. Med.
Sch.
Alfred I Murray, M.S.T. (Chemistry).
Mark Diesendorf, Ph-D. (INUthematics).
John J. Miller, Ph.D. (Biochemistry)
Paul I-L Phillips, Ph.D. (Biochemistry)
Kaj Roholm, M.D., Ph.D. (Biochemistry)
Hubert A Arnold, Ph.D. (Math) UCDavis
James W. Benfield, AB., D.D.S., F.A.C.D.
Eugene Peterson, Ph.D. (Chem.Engr.) UCB.
Cornelius Steelink, Prof Erner. Chern.
John Thomson, Ph.D. (Biochemistry)
D. Skinner, B. Sc., MD. C.AF.C.I.
Richard Manus, Ph.D. (physics) UCBerkely
Laura Nader, Ph.D. (Anthropology)UCB
D. W. Hanson, Ph.D. (Chem. Engr.)UCB
C. J. King, Ph.D. (Chern. Engr.)UCB
J. B. Neilands, Ph.D. (Biochemistry)UCB
Giovanni Ames, Ph.D. (Biochem.) UCB
Page 2 of 3
Frederick W. Howe, D.D.S.
Ellsworth D. Foreman, D.M.D.
Robert D. Stephan, D.D.S.
Carl Mestman, D.D.S.
Hans Moolenburgh, M.D.
Peter Mansfield, M.D.
William F. Corell, M.D.
F. Logan Stanfield, M.D.
Julian Whitaker, MD.
Robert C. Atkins, M.D.
James A Paar, M.D.
Kemieth H. Rudolph, M.D.
Jonathan Wright M.D.
John McDougall, MD.
Steven M. Rachlin, M.D.
John R Lilliendahl, Jr. D.D.S.
Hal A. Huggins, D.D.S.
Herbert-H. Robinson, D.D.S.
James P. Hammond, MD.
Philip Sukel, D.D.S.
Deloss E. Winkler, Ph.D. (Chem.)
Andrew Weil, UD, Health Advocate
Thomas M. DeStefimo, A.B., D.D.S.
Harlee S.Strauss, Ph.D. (Molecular Biology)
Geoffrey Dobbs, Ph.D. (Botony) ARC.S.
Frederick I. Scott, B.E., M.S., Chern. Engr.
Thomas D. Hinesly, Prof. of Soil Ecology
Roy E. Hanford, MD. (phys. and Surgeon)
Stanley Monteith, MD., rel. Ortho. Surgeon.
G. A Samotjoi, Ph.D. (Chemistry) UCB
Henry Cheung, Ph.D. (Chern. Engr.)Alexis T
Bell, Ph.D. (Chem. Engr.)UCB
Note: The information on this website is not a substitute for diagnosis and treatment by a qualified, licensed
professional.
http://www.garynull.com/Issues/Fluoride/FluorideVoices.htm
8/10/2003
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Fluoride
Robert & Kerry Broe
Sodium j1uoride is the most violent protoplasmic poison known to science. The National Library of Medicine's
computerized data service on toxic substances rates fluorides 4-5 (very toxic-extremely toxic) on a scale of five.
Scheele discoveredj1uorine in 1771, but Moissan did not produce it in gaseous elemental purity until 1886. Fluoride is
added to the water supply of most American cities for the purpose of dental hygiene. The reader will be amazed to find
out that such a result is not only unlikely but the reverse of the actual outcome. The u.S. has been fluoridating drinking
water for so many decades that people hardly think about it. Very few articles appear about fluoridation in newspapers
and magazines any more. At least chlorine will evaporate from a glass of water if you let it sit for an hour or so. Not so
with fluoride. Even cooking, food processing, filtration, or digestion will not remove fluoride. Fluoride goes right up
the food chain. It accumulates in fat cells when ingested or absorbed through the skin or mucous membranes. Fluoride
drops, tablets; and vitamins are more likely to damage children's teeth than to prevent cavities, according to mainstream
dental groups such as the Canadian Dental Association and the Western Australia Health Department's Dental Service.
Both organizations have stopped recommending regular fluoride supplementation.
The American Dental Association (ADA), the American Medical Association (AMA) and the World Health
Organization (WHO) all endorse fluoridation, and many established scientific bodies have declared that its advantages
are not debatable. Before fluoridation's implementation in 1945 and popular acceptance in 1950, sodiumj1uoride, a by-
product of aluminum manufacture, was known as an intractable industrial pollutant. Waterworks engineers warned that
water containing I part-per-million (ppm) fluoride is contaminated. The devilish plot to put fluoride in drinking water
has been backed in Washington since an ex-employee of the Aluminum Company of America was made Secretary of
the Public Health Administration. Fluoride is a very toxic substance, which is why it is the active ingredient in a
number of pesticides. Two grams of fluoride is enough to kill an adult, and 500 mg is enough to kill a child. A tube of
toothpaste can have as much as 1,500 mgs., and fluoride gel contains up to 6,000 mgs. In the U.S., people have died,
and many have become sick, when faltering fluoridation equipment has pumped excess fluoride into the water.
Poor nutrition exacerbates the toxic effects of fluoride exposure, which is one reason why it's wrong to target poor
communities with fluoridation (poor nutrition is more prevalent in low income communities). Subsets of the population
may be unusually susceptible to the toxic effects of fluoride and its compounds. These populations include the elderly,
people with deficiencies of calcium, magnesium and/or vitamin C, and people with cardiovascular and kidney
problems.
Ninety-eight percent of Western Europe has rejected water fluoridation. This includes Austria, Belgium, Denmark,
Finland, France, Germany, Italy, Luxembourg, Netherlands, Norway, and Sweden. The predominant reason for
Europe's rejection is the belief that public drinking water is not the appropriate vehicle with which to deliver
medication to a population. Fluoride is not an essential nutrient, which means that no human disease (including dental
decay) has ever been linked to a fluoride deficiency. Fluoridation adds between 0.1 and 1.6 parts per billion (ppb)
arsenic to drinking water, and therefore violates the EPA's Maximum Contaminant Level Goal for arsenic-which is 0
ppb. When water fluoridation began 50 years ago, it was believed that fluoride needed to be ingested in order to be
effective.
This is no longer the view of the dental establishment, which now generally concedes that fluoride's benefits are
derived primarily from topical application. No fluoride products designed for ingestion have ever been approved as safe
or effective by the U.S. Food and Drug Administration (FDA). Fluoridated water can appropriately be classified as an
unapproved prescription drug. Fluoride is ineffective at preventing the most common type of dental decay pits and
fissures. Pit & fissure decay-which is the decay found in the crevices of the chewing surfaces-accounts for upwards of
85% of dental decay now experienced ~ the U.S. Despite the fact that nearly all large U.S. cities have been fluoridated
for decades, dental decay is currently rampant in virtually all poor urban areas. Routinely prescribed to U.S. children
who don't drink fluoridated water (starting with toothless six month oIds), fluoride supplements were never tested for
safety and efficacy by the U.S. F.D.A. These supplements comprise one category of many different medications the
FDA officially "grandfathered" in, (they were sold before drug testing was required by law). Current research shows
that many of the old fluoride studies were flawed. Fluoride's benefits are merely topical, not systemic, as was once
thought.
Moreover, ingested fluoride can result in unwanted side effects, including dental fluorosis (spotted, stained, or pitted
teeth). Brian A. Burt of the University of Michigan School of Public Health states that "fluoride supplements should no
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longer be used for young children in North America ...the risks of using supplements in infants and young children
outweigh the benefits." Euan Swan, author of the Canadian Dental Association's (CDA) new fluoride supplement
guidelines, said, "The evidence supporting the effectiveness of dietary.fluoride supplements is relatively weak. There's
better evidence indicating that they contribute to dental fluorosis." "The notion that systemic fluorides are needed in
nonfluoridated areas is an outdated one that should be abandoned altogether," says Canada's leading fluoride authority,
Hardy Limeback, head of the Department of Preventive Dentistry at the University of Toronto and past president of the
Canadian Association for Dental research. He says, "We are now spending more money treating dental fluorosis than
we would spend treating new decay if water fluoridation was halted. "
Forms of Fluoride
There are five forms of fluoride that are often discussed and sometimes get confused. First, there is elemental jluorine, which
is a gas and the most reactive element in the periodic table. It reacts with every other element except three of the noble gases.
It even reacts with asbestos. Free fluorine is not produced in nature. Fluorine is not put in our drinking water! Fluorine is
found in the form of hydrogen jluoride, another gas. It etches glass. It dissolves in water to form a weak acid. It is a pollutant
emitted by metal smelters, the oil industry, ceramic and brick industries, coal fired power stations, incinerators, and a number
of other industries. It's been responsible for many deaths in air pollution incidents. Then there is thejluoride ion. The fluoride
ion cannot be placed in a bottle by itself. It is a negative ion; it must be accompanied by positive ions. Negative ions are
formed when metals react with non-metals (fluorine is a nonmetal). When this happens, the metal transfers one or more of its
electrons (negative particles) to the non-metal. The result is a positively charged metal ion and a negatively charged ion. In
the solid form, these positive ions and negative ions appear in a tidy three-dimensional arrangement. This internal
arrangement gives rise to the crystalline shape of these substances. For example, table salt (sodium cWoride) has crystals in
the shape of a cube. When these substances (salts) are disSQlyed in water the positive ions and negative ions separate.
Sodium cWoride is very soluble in water; calcium fluoride is far less soluble. Ten percent of the water fluoridated in the U.S.
is fluoridated with sodium fluoride. Complex ions are positive metal ions that are surrounded by negative ions or neutral
molecules that have a stronger bonding than simply electrostatic attraction. Thus they have different properties from the
parent ions. Thus, AIF4 has different properties from the parent Al 3+ ion and the F- ions. It is this ability of the fluoride ion
to form complexes with so many ions - including a lot of toxic ones, and others that are needed by the body-which might help
to explain why this unreactive species (in the chemical sense) can be so biologically active and dangerous. Another form of
fluoride that we meet is hexafluoro silicic acid (H2SiF6) and its sodium salt sodium jluorosilicate (Na2SiF6). These
substances are used to fluoridate 90% of the fluoridated water in the U.S. They are waste products from the superphosphate
industry. Pro-fluoridation people claim that when these substances are diluted and dissolved in water, they completely
dissolve into Si02 and fluoride ion. This is disputed, as there are still some silicon fluoride complexes left when the water
reaches our taps. These complexes facilitate the uptake of lead into the blood. Over 50% of the communities in the United
States use, fluorosilicic acid or sodium jluorosilicate to fluoridate drinking water. Neither the EPA nor the Centers for
Disease Control and Prevention can provide one safety study proving the product is safe for long-term, low-level consump-
tion. Not one clinical study with animal models has ever been done with the products. Interestingly, all the people who say
this product is 'safe' have no concept of how it is produced. The last form of fluoride that we meet is the organojluoride
group. These are compounds which have fluorine covalently bonded to carbon atoms. One of the organofluorines, which you
have probably handled, is the plastic PTFE. This is poly tetra fluoro ethylene, used in non-stick frying pans. It consists of
long chains of carbon attached to itself with two fluorines attached to each carbon. It is very stable and resistant to chemical
attack.
Fluorine is frequently added to pharmaceuticals. These drugs, when they are metabolized, break down in the body and
produce fluoride ion. The net result is that these drugs carry fluoride into very sensitive places, like the brain, where it can
cause problems. Little investigation has been done on this aspect of organofluorines. There are other organofluorines that are
very toxic in their own right- the toxicity has nothing to do with the fluoride ion itself; or the formation of the fluoride ion.
Substances like jluorocitrate are very toxic because they bind to an enzyme involved in sugar metabolism, and they don't let
go-they block it-they prevent it from handling the citrate, and it usually changes into something else. This rather unreactive
chemical species calledjluoride ions can interfere with biological systems in three profound ways: a) by forming hydrogen
bonds with key groups in proteins and nucleic acids, b) can complex with metal ions like aluminum, beryllium, lead and
carbon) can interfere with enzymes that use magnesium ions as a co-factor. For many enzymes, magnesium helps to align the
enzyme with the substrate it is working on, and fluoride can interfere with this alignment.
We're swallowing more fluoride each day with every glass of water. Since 1945, when fluoride was first put into the
municipal water system in Newburgh, New York, 75% of the United States water supply has been fluoridated. Other countries
are taking a suspicious look at fluoride. Sweden abandoned fluoridation on the recommendation of a special fluoride
commission. Denmark, Holland, Finland, France, Gennany and Japan have also rejected it, citing public health concerns.
Plans to make fluoridation mandatory in Britain were suspended in 1998 after the British Home Secretary intervened and
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urged the Health Secretary to review the negative evidence. Disreputable and power-hWlgI)' persons in high places have been
know to experiment with fluoride to see if it "could not be used to subjugate the people of a whole community more quickly
than fighting them into submission," according to William Guy Carr, a retired commander from the Royal Canadian Navy.
Fluoride In Toothpaste
Contrary to its public image as a benign substance used solely to reduce tooth decay, fluoride is extremely corrosive, more
toxic than lead and just slightly less toxic than arsenic. Sodium fluoride, the active ingredient in most brands of toothpaste,
was originally sold as a rat poison. If a three-year-old ate half a tube of the toothpaste, it could kill him. "Fluoridated
toothpaste contains 1,000-2,000 mgs of fluoride. Fluoridated drinking water contains one to four parts per million. Fluoride is
absorbed through mucous membranes in the mouth. A child may not consunie the whole tube, but smaller amoWlts daily are
certainly a hazard to anyone.
It is estimated that children swallow or absorb approximately I mg. of fluoride at each brushing with such toothpaste. In
1987 the Journal of Pediatrics issued a warning that children should use no more than "one-third of one pea-sized dollop
of toothpaste" when brushing their teeth. Allowing for the 4-ppm standard to which the EP A has raised fluoride, and based
upon accurate water consumption figures, approximately 50% of children under five are receiving a daily dose of fluoride
known to cause skeletal fluorosis. Is the possible saving of 0.8% of one tooth surface over a seventeen-year period worth
the risk of skeletal fluorisis, cancer, AIDS? Implementation of sOWld nutritional principles, removal of pollutants that
reduce natural immunity and appropriate health education proves more effective in resolving the problems of tooth decay
along with many other modern degenerative diseases.
Just as you lock your doors against unwanted intrusion, you must take the necessary steps to protect yourselves from this
daily poisoning. It will have to be done by you. No one else will do it for you. Terry Leader, a dental hygienist from Long
Island, witnessed, 1969, a child given topical fluoride, who then went into convulsions and died in the dentist's chair. She
pleads: "I just wish parents would read before they subject their children to something so dangerous. It's not going to save
them money. Good oral hygiene prevents tooth decay; fluoride doesn't. The mystique behind many 'miracle' drugs is the
belief that, like heat-seeking missiles they will zoom right to the enemy symptom and zap it neatly out of existence. So
with fluoride, our bodies should deliver all the fluoride directly to our teeth where it will supposedly harden the enamel
and form an indestructible barrier to tooth decay. Such magical thinking bears little relationship to biochemical reality.
Fluoride In Water
Corporations have a lot invested in fluoridation, which allows them to dispose of industrial pollution via dilution. Today,
the most common product used for fluoridation is hydrofluosilicic acid, which is not a natural substance but a waste
product coming straight from the scrubbers of the phosphate fertilizer industry. When phosphate is mined, they have to get
rid of the attached fluorine or it would kill the plants. So they put the phosphate through a sulfuric acid wash to separate
the fluorine out into what is called hazardous waste liquor. The fluorine is captured by a scrubber system since they can't
let it go out into the air because it would kill all the plants And animals aroWld. If they had to dispose of this liquor as
hazardous industrial waste, it would cost them $1.40 a gallon or more to neutralize it--depending on how much cadmium,
lead, uranium, and arsenic are also present. They don't want to pay that, so instead they call it a product and we pay them
approximately 3 cents a gallon to dump in our water. Data collected in the largest survey to date-of over 39,000 American
schoolchildren ages 5 to 17 in 84 communities, showed that children living in fluoridated areas had tooth decay rates
nearly identical with those living in fluoridated areas.
The cells that produce the collagen matrix that forms enamel are poisoned to the point that they can no longer produce
opalescent pearl like enamel. Fluorotic enamel is irregular in texture, porous, chalky white to brown in color and brittle. In
severe cases, the enamel forms incompletely and corners easily break off the teeth. Even proponents of fluoridation
acknowledge that fluorosis increases with the level of fluoride in the water. Currently, an estimated 22% of American
children exhibit the symptoms of fluorosis. This is not just a cosmetic fla~ it's proof of the fact that the body has been
overdosed with fluoride and has not been able to handle it. Bottle-fed babies (whose formula is made with fluoridated
water) are most likely to develop dental fluorosis. Mother's milk has virtually no fluoride present. Those children who are
deficient in protein, calcium, magnesium, phosphorous, and vitamin C are especially vulnerable to fluoride poisoning. The
accumulation of fluoride is greatly increased if the person has impaired kidney function. In short, the weakest members of
our society, the undernourished and the underfed, are the very children that fluoridation was to allegedly benefit. In some
poorer communities, as much as 80% of the children have fluorosis." But don't assume that if your child is healthy and
well nourished, he or she runs no risk. Look at the toothpaste, and read the directions-"Children 2 to 6 years: To minimize
swallowing, use a pea-sized amount, and supervise brushing and rinsing until good habits are established." Tempted by
bubble-gum flavors and artificial sweeteners, a child can easily ingest more than the recommended amount. Studies show
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that children under four inadvertently swallow 50% to 100% of the toothpaste they put in their mouths, simply because
they lack a fully developed gag reflex. The American Dental Association will not give toothpaste its seal of approval
unless it includes fluoride.
Dental jluorosis is just the fIrst, visible evidence of much more serious changes in the body. When fluoride accumulates at
high concentrations in the bones, they become weak and brittle. Victims of this debilitating condition, called skeletal
jluorosis can only hobble forward, stiff and hunched. The osteoarthritis that afflicts many people in this country may
actually be a misdiagnosed stage of skeletal t7uorosis. Recent studies have linked fluoride to an increased incidence of hip
fractures, damage to the central nervous system, and cancer. In. China, researchers correlated dental fluorosis with a 10
point reduction in IQ. Low levels of fluoride in the drinking water oftest animals produced pathological changes in the
brain similar to those in humans with Alzheimer's disease. Another study demonstrated how fluoride interferes with the
brain's pineal gland and inhibits its production of melatonin. What will happen when the fIrst generation of fluoride-fed
children turns 70, after accumulating this poison over a lifetime in their bones? Cavities are not life-threatening, but
fluoridation comes with real risks and negligible benefIts. Even if you believe in the value of fluoride, no one should be
allowed to use our drinking water as a delivery system. A lot of people consider Vitamin C benefIcial, but so far it doesn't
flow out of the tap. Water is our most precious resource, and we have no business adding anything to it, other than what's
necessary to make it safe to drink. It is our responsibility to maintain this gift, as pure and pristine as possible, for each
and every person to enjoy. In. 1990, Dr. William Marcus, chief toxicologist for the EPA's Office of Drinking Water, was
disturbed to fInd data from a study reporting specifIc fluoride-related cancers altered or omitted in the fInal National
Toxicology Program report.
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When he demanded an independent review of the raw data, he was fIred. Later, an investigation by the Senate
Environment and Public Works Committee corroborated his charges and produced evidence that government scientists had
been pressured to portray fluoride more positively. Because fluorine is the most negatively charged and interactive
element of all, it bonds with practically everything and does not exist separately in nature, despite its rank as the 13th most
abundant element in the earth's crust. But most of it stays buried there, unless it is mined and brought to the surface or
created as a by-product of various manufacturing processes. It's kind of a bully; it aggressively seeks out other electrons
and is prized for its ability to disrupt and reconfigure other molecular bonds.
One reason people have been reluctant to expose the problems of fluoride is that it cuts across so many industries. In. its
various forms, fluoride is used to etch glass, ceramics and computer chips; refIne petroleum products; separate out heavy
metal and power rockets. Our air is contaminated by fluoride emissions from the production of iron, steel, copper,
aluminum and plastics. Fluoride is one of the world's most widely used pesticides. If you walk past a house tented for
termites, they're probably spraying sulfuryl jluoride (Vikaue) to kill the bugs.
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Fluorinated Drugs
Many psychoactive drugs are fluorinated. The fluorine atom is attached to the active ingredients in many drugs in order to
allow them to penetrate into the brain or other targeted organs more easily. Because the fluoride enhances the penetrating
power of the active ingredient, less of the active ingredient needs to be made, and the manufacturer can save money. But
the side effects of all the fluoride containing medications is scarcely ever discussed as a general health issue. The primary
ingredients of most psychoactive drugs suppress enzyme production, and the fluorine ion is also an enzyme inhibitor. The
one particular side effect common to almost all fluorinated drugs, which is mentioned in the Physician's Desk Reference,
is memory loss. These drugs, including Prozac (fluoxetene)and Paxil-antidepression drugs, contain three Fluorine atoms in
each molecule that quickly kill the brain-issued enzymes that normally maintain mood stability.
Prozac and Paxil contain the fluoride containing Fluorophenyl compounds and are also known to cause liver disease.
Organic fluoride compounds undergo extensive transformation in the liver, and in many instances the resulting metabolites
may have higher activity and/or greater toxicity than the original compound. Prozac has caused hepatitis and has also been
shown to promote tumors in the liver. Rophypnol (flunitrazepam, or "RoofIes,")-the date rape drug-is fluorinated Valium,
which is about 20-30 times more potent than Valium alone. Phen-Fen (Fenjluramine) a weight-loss drug, fluorinated
corticosteroids and fluorinated psychoactive drugs all contain fluoride. In. 2000, a U.S. district judge approved a $3.75
billion national settlement of health claims stemming from Fen-Phen. More than 9,000 lawsuits have been flIed against
American Home Products, maker of Fenjluramine. People taking such drugs might exceed 5 mg in just one prescribed
application.
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We are essentially putting psychoactive drugs into the water supply. If you go in for surgery, you'll usually be given a
fluoride-based anesthetic because fluoride is virulent enough to throw you into an immediate coma. Sevoflurane, one of
many fluorinated agents used in anesthesia, such as florinated Halothane, is thought to be responsible for renal failure.
Hydrogen fluoride is the only toxic element in the nerve gas Sarin (1500 times more poisonous than cyanide) used in the
Japanese subway attack. On August 8th, 2001, Baycola cholesterol-lowering drug taken by 700,000 Americans-was pulled
off the market. It had been linked to 31 U.S. deaths. Bayer AG the maker of the drug would not disclose the total number
of deaths worldwide. Scientists have found that all fluoride compounds interfere with thyroid hormones. Numerous
congenital abnormalities have been reported due to first trimester exposure to Fluconsazole, a systemic anti-fungal agent.
There have been numerous fluorinated drugs removed from the market recently. Most have been shown to cause serious
adverse cardiac effects, probably due to fluoride's adverse effects on thyroid hormone activity.
Fluoride in the Food Chain
So now we have fluoride in our water, which means we're mass-medicating the population, although we can't control the
dose because everyone drinks varying amounts. Back when safety levels in the water were set at 1 ppm, there was
basically no other source. Since then, fluoride has been added to toothpaste, mouth rinses and dental floss. Dentists treat
the teeth topically with fluoride, and doctors prescribe fluoride supplements. And, of course, if fluoride is in the water, it's
in the food chain. Food is irrigated, washed, and processed with fluoridated water; we're consuming much more fluoride
than we think. Independent lab reports show high levels in common products: .98 to 1.2 ppm in Coca-Cola, 1 ppm in
Minute Maid orange juice, 2.1 ppm in Fruit Loops, 10 ppm in Wheaties, 6.8 ppm in Gerber's white grape juice which is
often used as a sweetener in baby foods. Grapes are commonly sprayed with an insecticide that contains fluoride.A 1996
study published in the Journal of the American Dental Association warned parents to limit their children's intake of juices
due to excessive fluoride content. In fact, according to a 1993 government survey, children in non-fluoridated
communities are already receiving at least 3 times the amount of fluoride recommended for total consumption, while
children in fluoridated communities are receiving 4.6 to 7 times the recommended amount. The National Research Council
of Canada has done extensive research on the many environmental sources of fluorides and the multiple avenues by which
they enter the human food chain. Most packaged foods are processed with fluoridated water, and many fruits and
vegetables contain fluorides in pesticide and fertilizer residues. When fluoridation first began, exposure to fluoride from
sources other than fluoridated water was minimal. Today that is not the case.
People now receive fluoride from a whole host of sources, including pesticide residues, fluoridated dental products,
mechanically de-boned meat, fluoride air pollution, and processed foods & beverages prepared with fluoridated water
(soda, juice, beer, cereal, etc). It has now reached the point where most people receive the "optimal" I mg.lday of
fluoride without ever drinking a glass of fluoridated water. Foods such as sardines, tea, lettuce, spinach, and others
have particularly high fluoride contents. If fluoride is ingested, even though a person is eating a nutritious diet and
taking the best supplements in the world, all the good nutrition is rendered almost completely ineffective, and
development or advancement of d,egenerative disease will ensue. The harmful effects of fluoride have been known for
over one hundred years. How much more evidence is needed before we, the victims, stop this behavior modification
program, being literally forced down out throats? Some beer-drinking men consume over six liters of fluoridated water
a day from beer alone.
Fluoride in Nature
In any case, fluoride is unavoidable in the diet, since it is the thirteenth most abundant element and is extremely
reactive, forming many compounds available to the human body. Fluorine occurs in nature as calcium fluoride. Sodium
fluoride is an industrial waste product from the aluminum and phosphate fertilizer industries. Since the 1920s and
1930s, it has been sold as a potent roach and rat killer. Sodium fluoride (NaF) is over five hundred times more soluble
than calcium fluoride (CaF2). It requires eighty times more CaF2 to kill a rat than NaF Fluoridation critics never
accepted the transformation of sodium fluoride from dangerous chemical to benign cavity fighter.
Fluoride in Industry
The first fluoride compound purposely put in the public water was sodium fluoride, a toxic by-product of the aluminum
industry. During World War II, as Alcoa accelerated production to meet the need for more warplanes, they produced
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more of this pollutant and faced mounting damage claims. Eager to put a positive spin on fluoride, the U.S. Public
Health Service-then under the command of Treasury Secretary Andrew Mellon, a founder and major stockholder of
Alcoa-sent a dentist in its employ out West to investigate certain towns where fluoride occurs naturally in the water.
This dentist observed that the inhabitants had fewer cavities than average although they also had stained and eroded
teeth.
In 1939, a scientist funded by Alcoa solved the disposal problem when he proposed adding fluoride to drinking water to
reduce tooth decay. Then in the 1940s the unimpeded production of fluoride became a matter of national security-
fluoride was the key substance used to separate the uranium isotope to build the atomic bomb. Millions of tons of
fluoride were required. In 1944, according to declassified documents, an accident at a DuPont plant in New Jersey
producing fluoride for the Manhattan Project released large quantities into the atmosphere. Crops. were poisoned,
animals were crippled, and people were sickened. The fluoride even etched windows in the local school. Scientists
scrambled to gloss over the adverse effects in the interests of the war effort. Defense contractors and the govenunent
needed to create public support for fluoride and protect themselves from liability as well.
Fluoride's Effects on Physiology
The average consumer of fluoridated water is usually not aware that sodium fluoride, or hydrofluosilicic acid, is rated as
more toxic than lead in chemistry indexes and only slightly less toxic than arsenic. Fluoride is not an essential nutrient
and, according to the National Academy of Sciences, has never been shown to be necessary for human life. Drs. Roger
Berry and Wilfred Trillwood at Oxford United Hospitals concluded that Sodium fluoride kills human cells at 1/20 the
strength of fluoridated drinking water. Biochemical research has established that chemical poisons like fluoride form
hydrogen bonds with protein amide groups together. Thus: since DNA strands are connected by hydrogen bonds,
fluoride will damage chromosomes. General Chemistry, McQuarrie and Rock, U. Cal., 1984, discusses fluorine,
"Because its electro-negativity is higher than that of any other element, fluorine occurs with a positive oxidation state
in any compound." Thus, fluorine is the most reactive element known to chemists, and its greatest affinity is for
calcium.
Nature, The International Journal of Science, Jan. 15, 1987, let the cat out of the bag, further exposing the Fluoridation
Fiasco. It published university studies showing that water boiled in an aluminum utensil for 10 minutes acquired 0.2-
ppm of aluminum, which is a cause of Alzheimer's disease. If water is fluoridated at lppm, in ten minutes, 200 ppm of
Aluminum are released 1,000 times more aluminum! Fluorine may cause irreversible loss of potassium from the human
red cell. Fluorine increases excretion of iron-thus leading to anemia. Even at 10 mg. per liter, fluorine causes anemia,
lymphocytosis and leukopenia. Blood levels of vitamin B 12 are lowered. Damaging effects of fluorine may be found in
the stomach, duodenum, small intestines, liver, spleen, lungs, brain, pancreas, adrenals and thyroid.
Liver and muscle glycogen depletion and lactic acid accumulation, with increased blood sugar. Especially serious
damage occurs in the spinal cord, with neurological symptoms following. The pituitary gland takes up several times as
much fluorine as any other soft tissue, which is especially dangerous because the pituitary is the master gland of the
endocrine system. Fluorine may cause anoxia in newborns and shorten their survival. Fluoride inhibits neuromuscular
activity. Human Biochemistry, Orten and Neuhause, 9th Ed., tells us, "Calcium is needed by all cells. It is required for
physiologic balance. "
A particular and important effect of the calcium ion is on nervous tissue. If the ionic calcium of the blood falls, the
nervous system becomes hyperirritable. "Calcium is the main structural mineral in the body. Osteoporosis is a result of
calcium loss in the skeleton. During the last trimester of pregnancy, between 200 and 300 mg. of calcium are deposited
every day in the skeleton ofthe fetus. Pregnant women are given synthetic prenatal vitamins with added fluoride. Anyone
with a calcium deficiency can experience muscle spasms and convulsions. Also, the tissue levels of two poisonous metals,
lead and cadmium, increase, and blood clotting is adversely affected causing thrombosis and embolism. Oxygen
deprivation in heart muscle is increased, with calcium deficiency causing arhythmias.
Fluoride is a mutagen. Rats dosed with fluoride had a statistically significant increase in bone tumors. Fluoride-dosed rats
had tumors of the thyroid, oral cavity and rare tumors of the liver. Female infertility is associated with elevated levels of
fluoride (>3 ppm). One ppm fluoride in water facilitates the uptake of aluminum into the brain ofrats, producing the type
of brain tangles (amyloid deposits) that are associated with Alzheimers disease and other types of dementia. Fluoridated
water was associated with elevated levels of lead in children's blood.
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Lead is associated with a variety of neurological problems, including reduced intelligence, aggression and hyperactivity.
Recently released reports by the New York State Department of Public Health and an expert panel appointed by the U.S.
Surgeon General dispute the American Dental Association's blanket claim that there are no adverse health effects from
fluoridation. Fluoridation's effectiveness may be less than earlier studies had indicated, according to a new study by the
National Institute for Dental Research. The largest study in the 50 years since fluoridation of U.S. water supplies began
covers almost 40,000 children, aged 5 to 17, in 84 areas across the country. The Journal of the American Dental
Association, Vol. 23, 1936, pp. 569-570, states. "There is an increasing amount of evidence of the injurious effects of
fluorine, especially the chronic intoxication resulting from the ingestion of minute amounts of fluorine over long periods
of time. It adds, "Toxicity data suggests that fluorine, lead and arsenic belong to the same group, as far as the ability to
cause some symptoms of toxicity in minute dosage is concerned." Small daily doses of lead or arsenic are believed to be
harmful. Fluoride is in the same category.
The U.S. Department of Agriculture in 1939 surveyed and reported on the effects of fluoride. Fluorine was shown to be the
cause of a disfiguring dental disease known as mottled enamel or fluorosis. Fluorine interferes with the normal process of
calcification of teeth during the process of their formation, so that affected teeth, in addition to being unusually discolored
and ugly in appearance, are structurally weak and deteriorate early in life. For this reason, it is especially important that
fluorine be avoided during the period of tooth formation, from birth to the age of 12 years. Pediatricians report that over
30% of U.S. children have some degree of noticeable dental fluorosis, or mottling of the teeth from exposure to
excessively high levels of fluoride. There is an almost infinite array of fluoride-based toothpastes, mouthwashes,
dentifrices, tablets and vitamins on pharmacy shelves, many of which warn (in very tiny print) that they should not be used
if the fluoride concentration in drinking water exceeds 0.7-ppm. The sources of fluorine intoxication are...(among others)
... drinking water containing 1 ppm or more of fluorine." It is estimated that approximately 40 million Americans suffer
from arthritis, the most common type being osteoarthritis. Fluoride stimulates abnormal bone development. High dose
fluoride treatment increases bone mass, but the newly formed bone is structurally unsound. Thus, instead of reducing hip
fracture, high doses of fluoride increase hip fracture. Kyphosis (skeletal fluorosis spinal curvature) was very prevalent
among a community whose drinking water contained 7.4 ppm fluoride. It's alarming to learn of these adverse effects of
fluoride at 1.1 parts per million when the U.S. EP A raised the safe level for fluoride up to 4.0 parts per million. Who is
being protected, the people or the firms that sell fluoride and the manufacturers who produce fluoride as a by-product they
can't get rid of? Yes, the fluoride producers cannot dispose of this waste product unless all of us drink a little bit each day.
Thyroid Dysfunction
Up until the 1950s, European doctors used fluoride to reduce the activity of the thyroid gland for people suffering from
overactive thyroid (hyperthyroidism). The daily dose of fluoride which people are now receiving in fluoridated
communities (1.6 to 6.6 mg/day) actually exceeds the dose of fluoride found to depress the thyroid gland (2.3 to 4.5
mg/day). Hypothyroidism is currently one of the most common medical problems in the U.S. Synthroid, the drug doctors
prescribe to treat hypothyroidism, was the fourth most prescribed drug in the U.S. in 2000. Symptoms of hypothyroidism
include depression, fatigue, weight gain, muscle and joint pains, increased cholesterol levels and heart disease. From a
recent University of York report, considered the "final word on fluoridation," it was shown that symptoms described in the
literature on fluoride's adverse health effects are identical to those observed in thyroid dysfunction, and the condition
known as dental fluorosis is a direct result offluoride-induced iodine deficiency during the time of enamel formation. It
showed an increase in thyroid cancers in the fluoridated areas when compared to non-fluoridated areas. In China, where
entire villages are being relocated due to fluoride contamination, fluoride is being openly acknowledged as the cause of
thyroid cancer, Kaschin-Beck disease and iodine deficiency. It has been established since the 1930s that the thyroid
hormones control tooth eruption. Fluoridation delays the eruption of teeth because of its hypothyroid effect. Dental
fluorosis is a sign of thyroid dysfunction. Any anti-thyroid substance administered during the time of enamel formation
will produce the effects seen in dental fluorosis. Fluorides actually cause cavities. There are countless papers-some of
them found in the York Report-clearly state that the dental defects seen in fluorosis predispose to caries. Hyperthyroidism,
caused after iodine was added to public water supplies in the early 1920s, led to the use of fluorides as anti-thyroid
medication. Fluorides are the worst endocrine disruptor imaginable.
What was once known as fluoride-iodine antagonism can now be explained in detail by thousands of papers showing the
fluoride power on G-protein activation. The biochemical activity of fluoride mimics TSH (thyroid-stimulating-hormone)
on G-protein activation-molecular on/off switches by which all thyroid hormone activity is regulated. Three-quarters of the
world's population is suffering from iodine deficiency in areas, which are identical to endemic fluorosis areas. Tooth decay
is an epidemic in certain U.S. populations, whether or not they live in fluoridated cities. Eighty percent of decay occurs in
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25% of the population, most of them poor and minorities. Well-meaning, but misguided dentists and hygienists are still
pushing to get more of the U.s. fluoridated by the year 2010, primarily because they believe it will help poor children who
suffer from needless dental pain every year that interferes with their eating, learning, and sleeping. One problem is that
dentists want more money to actually treat poor children. Well-nourished children who practice good dental hygiene
usually have the least decay.
Politics and Suppression of Truth
When the fluoridation campaign began, it was determined that the optimal dose was I milligram per day, which translates
to 1 part per million (ppm) in the water supply (assuming an individual drinks I liter of water a day). Officials concurred
that concentrations of 2 ppm would not be acceptable because that would produce too many cases of dental fluorosis. But
over the decades the maximum allowable contaminant level (fluoride is classified as a contaminant by the EPA), inched up
to 2.4 ppm. Then in 1985 when the EPA increased the allowance to 4 ppm, something unprecedented occurred. The union
representing employees at EPA headquarters in Washington D.C.-some 1500 scientists, engineers and other professionals-
revolted against their own management and filed an Amicus curiae brief in court to support a lawsuit brought by the
National Resources Defense Council against the EPA. As the brief stated, in their professional opinion, allowable fluoride
levels should have been reduced rather than raised. They alleged that evidence of adverse effects was manipulated or
ignored in order to arrive at a preordained political conclusion. Why was this allowed when the Federal Register of
November 14, 1985, stated that the Office of Drinking Water received II out of 12 studies confirming the carcinogenicity
(cancer-causing potential) of fluoride during a comment period on the safe allowable levels of fluoride in drinking water?
An article titled "Chronic Fluorine Intoxication" in a 1943 issue of the Journal of the American Medical Association
(JAMA) declared, "Fluorides are general protoplasmic poisons, probably because of their capacity to modify the
metabolism of cells by changing the permeability of the cell membrane and by inhibiting certain enzyme systems...
Slander and smear campaigns have been commonplace in the frenzy of the fluoridation wars. The late Dr. John A.
Yiamouyiannis, a biochemist and former biochemical editor of the prestigious Journal of the Chemical Abstracts Service,
the world's largest chemical information center, was removed from his post in 1969 when he began to publish articles
critical of fluoridation. Since thousands of articles routinely passed through his hands, many of which showed the negative
effects of even miniscule amounts of fluoride on enzyme function and the immune system, he began to question its use for
human consumption. He says he was told by his editorin-chief at the time, Dr. Russell Rowlett, that the Chemical
Abstracts Service's federal funding ($1.1 million) was in jeopardy and that if Yiamouyiannis did not "cease and desist" in
his attack of fluoridation, he would be fired. When Yiamouyiannis did not comply, he was put on probation and ultimately
forced to resign. He continued to be an outspoken critic of fluoridation until the time of his death. He has written a paper
saying the NIDR data show no difference in decay rates between areas with fluoridated and unfluoridated water supplies.
Research scientists have produced a report saying the same data, showing 18% less decay in the fluoridated areas, a
difference they call significant, but which is far below the 40 to 60% reduction claimed by the ADA.
In the summer of 1988, an article in the 100,000-member American Chemical Society's trade journal Chemical and
Engineering News s. examined the evidence on safety and effectiveness of fluoride and found many unresolved questions:
"If the lifeblood of science is open debate of evidence, scientific journals are the veins and arteries of the body scientific.
Yet journal editors often have refused, for political reasons, to publish information that raises questions about
fluoridation." Submissions critical of fluoridation are returned as "inappropriate for publication." The bulk of the social
science literature on fluoridation is scientifically proven and indeed scientifically unquestionable. The many studies that
fall into this category make no examination of the scientific evidence, but rely entirely on the endorsements of dental and
medical authorities. Those promoting fluoridation have had almost exclusive access to the resources of authority, even
while claiming that scientific truth was their strongest plank and that opponents to fluoridation are spurred by personal or
political motivation. Therefore, opposition to fluoridation has always been treated as an anomaly, to be explained away as
the activity offringe groups and "quacks. n
The problem began in 1950 when key public health and professional bodies such as the United States Public Health
Service and the ADA came out supporting fluoridation. Almost overnight, the scientific issues were treated as closed.
Fluoridation was considered scientifically proved and, furthermore, criticisms of fluoridation were treated as political
rather than scientific. Opponents were classified as cranks rather than as rational critics. The climate is the same today.
The combination of direct attacks on public opponents of fluoridation, fears about loss of grants, and the general labeling
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of them as ignorant and misguided, combine to discourage scientists from doing research or speaking out on the issues.
The relative lack of open opposition, in turn, encourages a perception of the fringe nature of critics. The pro-
fluoridationists, through their control over dental and medical associations, their control mehealth authorities, and their
influence over editorial policy of journals and publishers, have exerted power to stop expression of antifluoridation views
by professionals. Nevertheless, not all critics of fluoridation have been effectively silenced.
Brian Dementi, toxicologist at the Virginia State Department of Health, discussed in his 1981 report, Fluoride in
Drinking Water, the many scientific papers showing fluoride to be both mutagenic and carcinogenic. Dementi contends
that there has not been nearly enough research done to warrant the claim that fluoridation is absolutely safe. He
concludes, "The weight of the evidence from studies on mutagenic effects of fluoride indicates that the substance is
mutagenic (causes mutations) at low concentrations." He adds that "there appears to be virtually no margin of safety for
fluoride of the nature generally sought after or required for exposures to toxic substances." Dementi's report includes a
1969 study that shows an average 48% reduction in the activity of the enzyme succinic dehydrogenase in the kidneys of
golden hamsters that drank water containing l-ppm sodium fluoride. He discusses a study done in 1975 in which
monkeys exposed to fluoride at the l-ppm level for 18 months exhibited cytochemical changes in their kidneys.
A 1979 report stated, "The available evidence suggests that some patients with long-term renal failure are being
affected by drinking water with as little as 2-ppm fluoride." In his report, which was deleted from Virginia Health
Department files because it was "too old," Dementi chronicles the research on fluoride mutagenesis. He writes that in
1977 researchers observed leucocytes in cows suffering from fluorosis (a systemic poisoning caused by excessive
fluoride which can lead to severe crippling). The chromosomal aberration rate was over twice that of controls. The
authors concluded, "These data suggest that inorganic fluor compounds represent a potential genetic hazard to
mammals." Similarly, another 1977 study by a team who added sodium fluoride to drinking water at various
concentrations and noticed the effects on mouse cells (bone marrow and spermatocytes), showed "statistically sig-
nificant increases in chromosomal aberrations in both types of cells even at drinking water levels as low as l-ppm
sodium fluoride." Dementi states, "Any perturbation of this complex system must be viewed, a priori, as cause for
concern." The largest epidemiological study ever done on fluoridated water and carcinogenicity was conducted in 1977
by Yiamouyiannis and Dr. Dean Burk, retired head of cytochemistry at the National Cancer Institute, in which they
monitored cancer rates over a twenty-year period in ten fluoridated American cities and ten non-fluoridated ones. After
controlling for population differences in age, race and sex, the researchers found an increased cancer mortality rate in
persons over age forty-five in fluoridated cities. The study was validated in three courts of law in the u.s. Further
studies on DNA and DNA-repair systems have shown that fluoride inhibits or interferes with the ability of DNA to
repair itself, thus providing a clue as to how fluoride might exert a carcinogenic impact on human cells. The New
Jersey Department of Health had conducted a study and found the incidence of osteosarcoma to be significantly higher
in fluoridated communities versus non-fluoridated ones.
The New Jersey findings supported similar ones by larger national studies and by the National Toxicology Program. In
a 1989 Medical Tribune, a weekly publication for health professionals revealed that a panel appointed to study the issue
in 1983 by C. Everett Koop, then surgeon general, also raised questions about health effects. All mention of those
issues was edited out of the panel's [mal report. The omission of health concerns from the panel's final report is
"shocking," charged Robert Carton, an EPA scientist and president of the union that represents the agency's scientific
staff. The immune system, the body's National Guard, so to speak, using white blood cells, is disrupted and rendered
much less effective from the effects of fluoride. These white blood cells are calcium dependent. One consequence is
hypersensitivity or "allergy" which will bring increased, more severe or longer-lasting colds, flus and other ills. Since
studies have revealed that fluoride, taken over a long period of time, breaks down the immune system, some researchers
feel that it is therefore conducive to AIDS. The Cape Cod News, August 20, 1986, observed that the three longest
fluoridated areas in the U.S.-New York, D.C. & San Francisco-are the most prolific with AIDS. L.A. and San Antonio,
on the other hand, have never been fluoridated, and this plague has been miniscule in these cities." Though these two
cities have large homosexual communities, AIDS isn't as prevalent. Dean Burk, Chief Chemist Emeritus at U.S. Cancer
Institute, states, "In point of fact, fluoride causes more cancer death, and causes it faster than any other chemical."
(Fluoride and Cancer," Congressional Record H7l76-6, July 21, 1975, by Dean Burk and J.A. Yiamouyiannis).
Several studies, including one carried on over a period of years at the University of Wisconsin and published in 1963,
show that fluoridated areas have an exceptional number of stillbirths. Scientists know that fluoride passes through the
placenta. Dr. lonel Rapaport, University of Wisconsin, "carried out two studies showing that mongolism, a birth defect
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characterized by mental and physical retardation, occurs more often in areas where there is a relatively high fluoride
content in the water." According to the Grand Rapids Press, July 28, 1955, following widely publicized fluoridation
experiments in Grand Rapids, Michigan: "Deaths rose sharply after four years of fluoridation which began in 1945.
Deaths from cancer, heart disease, intracranial (brain) disease, diabetes and hardening of the arteries increased 25 to 50
percent over those in Michigan as a whole." The I.AM-A. for Feb. 10, 1961 states, "Fluorine also tends to accumulate in
the bones, leading to hyper-calcification and brittleness. Ligaments and tendons also become calcified. Serious
symptoms may ensue, such as loss of mobility of joints, easy fracture and pressure on the spinal cord. Other defects
include baldness in young men, anemia and decreased blood clotting power. In women, painful menstruation, lowered
. birth rate, high incidence of fracture, thyroid alterations and liver damage."
When one drinks sodium fluoride (NaF) in water, they excrete calcium fluoride (CaF2) in their urine. This calcium was
stolen from the body. In 1936 50 percent of Americans were calcium deficient. The AMA journal of the same year
reported that out of 4,000 persons checked in at a New York hospital, only two were not suffering from calcium
deficiency. The situation is worse today. Fluoride in drinking or cooking water can disrupt the enzymatic activity of
proteins. Dr. John Yiamouyiannis (Fluoride The Aging Factor, Health Action Press, 1983) observed, "If the shape (or
conformation) of the protein is greatly distorted by fluoride, the body's immune system will no longer be able to
recognize the protein and will attempt to destroy it. "
The summer 1959 issue of Clinical Physiology reported on page 96, a study done by experimental embryologist James D.
Eberrt and published in Scientific American March 1959. It relates: ".. .he found that sodium fluoride in low concentrations
blocked, almost completely, the regions destined to form heart muscle but left the developing brain and spinal cord intact."
He correlated this with the high incidence ofvent,icullll' septal defect, which was relatively uncommon before the 1950s,
and fluoridation. Most of the advanced Western European countries have banned fluoridation or given it up. The United
States is the most fluoridated country, and it has the highest tooth decay rate in the world! So is fluoridation the "biggest
hoax ever inflicted on humanity" or a modern miracle opposed by a small, ignorant minority?
Noncfluoridated toothpaste is available at your local health food store or co-op. Children and parents who are truly
concerned about their children can refuse fluoride "swish" programs in public schools. The Union of Scientists and
professionals at EP A headquarters has voted to oppose fluoridation and has called upon Congress to issue a "national
moratorium" on the sixty year old policy. The toxicity of fluoride is so great and the purported benefits associated with it
are so small-if there is any at all-that requiring every man, woman and child in America to ingest is criminal behavior on
the part of the government.
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The Tribune, Mesa, AZ
Sunday, December 5, 1999
"Why'd you do it, Doc? Why'd you toss the fluoride folks overboard?" I had just tracked down Dr. Hardy
Limeback, B.Sc., Ph.D in Biochemistry, D.D.S., head of the Department of Preventive Dentistry for the
University of Toronto, and president of the Canadian Association for Dental Research. (Whew.) Dr.
Limeback is Canada's leading fluoride authority and, until recently, the country's primary promoter of the
controversial additive.
In a surprising newsmaker interview this past April, Dr. Limeback announced a dramatic change of heart.
"Children under three should never use fluoridated toothpaste," he counseled. "Or drink fluoridated water.
And baby formula must never be made up using Toronto tap water. Never."
Why, I wondered? What could have caused such a powerful paradigm shift? "It's been building up for a
couple of years," Limeback told me during a recent telephone interview.
"But certainly the crowning blow was the realization that we have been dumping contaminated fluoride
into water reservoirs for half a century. The vast majority of all fluoride additives come from Tampa Bay,
Florida smokestack scrubbers. The additives are a toxic byproduct of the super-phosphate fertilizer
industry. "
"Tragically," he continued, "that means we're not just dumping toxic fluoride into our drinking water. We're
also exposing innocent, unsuspecting people to deadly elements: lead, arsenic and radium, all of them
carcinogenic. Because of the cumulative properties of toxins, the detrimental effects on human health are
catastrophic. "
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A recent study at the University of Toronto confrrmed Dr. Limeback's worst fears. "Residents of cities that
fluoridate have double the fluoride in their hip bones vis-a-vis the balance of the population. Worse, we
discovered that fluoride is actually altering the basic architecture of human bones." Skeletal fluorosis is a
debilitating condition that occurs when fluoride accumulates in bones, making them extremely weak and
brittle. The earliest symptoms? "Mottled and brittle teeth," Dr. Limeback told me. "In Canada we are now
spending more money treating dental fluorosis than we do treating cavities. That includes my own
practice. "
One of the most obvious living experiments today, Dr. Limeback believes, is a proof-positive comparison
between any two Canadian cities. "Here in Toronto we've been fluoridating for 36 years. Yet Vancouver,
which has never fluoridated, has a cavity rate lower than Toronto's." And, he pointed out, cavity rates are
low all across the industrialized world, including Europe, which is 98% fluoride free. Low because of
improved standards ofliving, less refined sugar, regular dental checkups, flossing and frequent brushing.
Now less than 2 cavities per child Canada-wide, he said.
"I don't get it, Doc. Last month, the Centers for Disease Control (CDq ran a puff piece all across America
saying the stuff was better than sliced bread. What's the story?" "Unfortunately," he replied, "the CDC is
basing its position on data that is 50 years old, and questionable at best. Absolutely no one has done
research on fluorosilicates, which is the junk they're dumping into the drinking water." "On the other hand,"
he added, "the evidence against systemic fluoride in-take continues to pour in."
"But Doc, the dentists." "I have absolutely no training in toxicity," he stated fmnly. "Your well-intentioned
dentist is simply following 50 years of misinformation from public health and the dental association. Me,
too. Unfortunately, we were wrong."
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Last week, Dr. Hardy Limeback addressed his faculty and students at the University of Toronto,
Department of Dentistry. In a poignant, memorable meeting, he apologized to those gathered before him.
"Speaking as the head of preventive dentistry, I told them that I had unintentionally mislead my colleagues
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and my students. For the past 15 years, I had refused to study the toxicology information that is readily
available to anyone. Poisoning our children was the furthest thing from my mind."
"The truth," he confessed to me, "was a bitter pill to swallow. But swallow it I did."
South of the border, the paradigm shift has yet to dawn. After half a century of delusion, the CDC,
American Dental Association and Public Health stubbornly and skillfully continue to manipulate public
opinion in favor of fluoridation.
Meantime, study after study is delivering the death knell of the deadly toxin. Sure, fluoridation will be
around for a long time yet, but ultimately its supporters need to ready the life rafts. The poisonous waters of
doubt and confusion are bound to get choppier.
"Are lawsuits inevitable?" I asked the good doctor. "Remember tobacco," was his short, succinct reply.
Welcome, Dr. Hardy Limeback, to the far side of the fluoride equation. It's lonely over here, but in our
society loneliness and truth frequently travel hand in hand. Thank you for the undeniable courage of your
convictions.
Want more scientific information about fluoride/tluoridation? Find it on the net.
International Society for Fluoride Research http://www.fluoride-ioumal.com
Dental Fluorosis http://www.inter-view.net/-sherrell
IAOMT Risk Assessment for ingested fluoride http://www.SaveTeeth.org
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.
INTRODUCTION
There are four reports included in this document:
I. The first report is from the Centers for Disease Control and Prevention
(CDC) in Atlanta, GA. It is entitled "Recommendations for Using Fluoride
to Prevent and Control Dental Caries in the United States."
II. The second report, published by the National Academy Press and
prepared by The Committee on Toxicology for the National Research
Council, is titled "Health Effects of Ingested Fluoride," and was published
in 1993.
III. The third report is the new project, "Toxicologic Risk of Fluoride in
Drinking Water." This new study, commissioned by the EPA and CDC, will
be prepared by the National Research Council. Its primary purpose is to
report on additional and current toxicologic findings in areas that were
identified in "The Health Effects of Ingested Fluoride Study" completed in
1993.
Following these reports is an article published by the CDC and featured in
the MMWR Weekly newsletter published online titled, "Populations
Receiving Optimally Fluoridated Public Drinking Water---United States,
2000," as well as the "Surgeon General Statement on Community Water
Fluoridation," published by the Department of Health & Human Services in
2001.
IV. The fourth report is Pinellas County Utilities' estimate of the costs of the
construction of facilities and operation of fluoride addition equipment to
the Utilities System drinking water supply.
The Summary of I. "Recommendations for Using Fluoride to Prevent and Control
Dental Caries in the United States" and the Conclusion of II. "Health Effects of
Ingested Fluoride" are reprinted here for quick reference. The Summary of our
Cost Estimation Proposal is also provided.
.
.
.
SUMMARY: REPORT NO. I
"Recommendations for Using Fluoride to Prevent and Control Dental
Caries in the United States"
Widespread use of fluoride has been a major factor in the decline in the
prevalence and severity of dental caries (Le., tooth decay) in the United States
and other economically developed countries. When used appropriately, fluoride
is both safe and effective in preventing and controlling dental caries. All U.S.
residents are likely exposed to some degree to fluoride, which is available from
multiple sources. Both healthcare professionals and the public have sought
guidance on selecting the best way to provide and receive fluoride. During the
late 1990s, CDC convened a workgroup to develop recommendations for using
fluoride to prevent and control dental caries in the United States. This report
includes these recommendations, as well as a) critical analysis of the scientific
evidence regarding the efficacy and effectiveness of fluoride modalities in
preventing and controlling dental caries, b) ordinal grading of the quality of the
evidence, and c) assessment of the strength of each recommendation.
Because frequent. exposure to small amounts of fluoride each day will best
reduce the risk for dental caries in all age groups, the workgroup recommends
that all personal drink water with an optimal fluoride concentration and brush
their teeth twice daily with fluoride toothpaste. For persons at high risk for
dental caries, additional fluoride measures might be needed. Measured use of
fluoride modalities is particularly appropriate during the time of anterior tooth
enamel development (Le., age <6 years).
The recommendations in this report guide dental and other healthcare providers,
public health officials, policy makers, and the public in the use of fluoride to
achieve maximum protection against dental caries while using resources
efficiently and reducing the likelihood of enamel fluorosis. The recommendations
address public health and professional practice, self-care, consumer product
industries and health agencies, and further research. Adoption of these
recommendations could further reduce dental caries in the United States and
save public and private resources.
.
.
.
CONCLUSIONS: REPORT NO. II
"Health Effects of Ingested Fluoride"
Based on its review of available data on the toxicity of fluoride, the
subcommittee (Subcommittee on Health Effects of Ingested Fluoride) concludes
that the U.S. Environmental Protection Agency (EPA)'s current MCL (maximum
contaminant level) of 4 mg/L for fluoride in drinking water is appropriate as an
interim standard. At that level, a small percentage of the U.S. population will
exhibit moderate or even severe dental fluorosis. However, the question of
whether to consider dental fluorosis a cosmetic effect or an adverse health effect
and the balancing of the health risks and health benefits of fluoride are matters
to be determined by regulatory agencies and are beyond the charge or expertise
of this subcommittee.
The subcommittee found inconsistencies in the fluoride toxicity database and
gaps in knowledge. Accordingly, it recommends further research in the areas of
fluoride intake, dental fluorosis, bone strength and fractures, and carcinogenicity.
The subcommittee. further recommends that EPA's interim standard of 4 mg/L
should be reviewed when results of new research become available and, if
necessary, revised accordingly.
.
COST ESTIMATE SUMMARY
· The facilities for which cost estimates are provided herein are
temporary.
· The estimated cost of construction is $295,000.00.
· New fluoridation facilities would be constructed in the Plant Detention
Blending Facility now under design.
· Very little, if any, of this equipment would be usable in the new plant.
· Annual operating cost is estimated to be $115,000. Operating cost in
the new plant would be approximately the same.
,.
· These costs will have a minimal impact on annual expenses and will
not require an increase in water rates.
.
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.
Health Effects of Ingested Fluoride (1993)
hllp:llwww.nap.edulopenbooki030904975Xh1tmUR1.html. copyright 1993, 2000 The National Academy of Sciences, all rights reserved
Health Effects of
Ingested Fluoride
\.
Subcommittee on Health Effects of Ingested Fluoride
Committee on Toxicology
Board on Environmental Studies and Toxicology
Commission on Life Sciences
National Research Council
NA TIONAL ACADEMY PRESS
Washington, D.C. 1993
.
Health Effects of Ingested Fluoride (1993)
hltP1/www.n~.edu/openbookl030904975X1htmI/1.html. copyright 1993, 2000 The National Academy of Sciences, an rights reserved
.
HEALTH EFFECTS OF
INGESTED FLUORIDE
EXECUTIVE SUMMARY
INTRODUCTION
Fluoridation of drinking water has been a subject of controversy for
decades. Over the past 50 years, the incidence of dental caries (cavities)
has declined considerably in the United States, an important health ad-
vance that most scientists attribute principally to increased access to
fluoridated water and dental products. According to the U.S. Centers for
Disease Control and Prevention, approximately 132 million Americans
now receive drinking water that contains fluoride, either naturally oc-
curring or added, at concentrations of 0.7 milligrams per liter (mg/L) or
higher. Since the 1960s, the U .S, Public Health Service (PHS) has
recommended an "optimal" fluoride concentration of 0.7-1.2 rng/L to
prevent dental caries and minimize dental fluorosis. However, there has
been an increase in the prevalence of dental tluorosis a mottling oftooth
enamel that ranges from barely discernible enamel flecks in it<; mildest
forms to staining and pitting in its severest forms; the severest forms are
rare in the United States. EPAconsiders dental fluorosis to be a cosmet-
ic effect and not an adverse health effect.
Recent findings have renewed longstanding concerns of those who op-
pose water fluoridation, claiming that ingestion of fluoride can lead to a
variety of unwanted effects. One animal study reported an equivocal
increase in osteosarcomas (malignant bone tumors) in male rats, but not
in female rats, at very high concentrations (100-175 mglL). However,
.
.
.
Health Effects of Ingested Fluoride (1993)
hltp:/lwww.nap..,a,/openbooklD30904975XihlmIl4.hlml.copyrighll993, 2DOO The Nalional Academy 01 Sciences, all rights reserved
4 Health Effects of Ingested Fluoride
from the alimentary tract. Because of its chemical affinity for calcium
compounds, about half of that fluoride becomes associated with teeth and
hones within 24 hours of ingestion. In growing children, even more of
the ingested fluoride is retained because of the large surface area provid-
ed by numerous and loosely organized bone crystallites. The remaining
fluoride is eliminated almost exclusively by the kidneys, and the rate of
renal clearance is directly related to urinary pH. Asa result, diet, drugs,
metabolism, and other factors can affect the extent to which fluoride;is
retained in the body. .
Recommendations for further research are (1) to determine and
compare intake of fluoride from all sources (this recommendation
has implications for research design in several of the areas that
follow); and (2) to determine the metabolic characteristics of flUe>;"
ride in infants, young children, and the elderly, as well as in pa-
tients with progressive renal disease.
~.
'-
DENTAL FLUOROSIS
Fluoride prevents tooth decay by enhancing the remineralization of
enamel that is under attack, as well as inhibiting the production of acid
by decay-causing bacteria in dental plaque. Fluoride is also a normal
constituent of the enamel itself, incorporated into the crystalline structure
of the developing tooth and enhancing its resistance to acid dissolution.
One side effect of too much fluoride ingested in early childhood while
teeth are forming, however, is dental fluorosis; the enamel cover.ing of
the teeth fails to crystallize properly ,leading to defects that range from
barely discernible to severe brown stain, surface pitting, and brittleness.
Fluoride intake by children 2-5 years old is particularly important be-
cause the anterior (front) permanent teeth are at the early-maturation
stage, during which they are particularly susceptible to fluoride-induced
changes, De~tal fluorosis also is a dose-respoIL~e condition: the greater
the fluoride intake during tooth development, the more severe the dental
fluorosis. Depending upon the amount and time (relative to tooth devel-
opment) of fluoride absorbed, severity of dental fluorosis can range from
barely discernible to severe manifestations of stained and pitted tooth
enamel. PHS's recommended fluoride concentration in drinking water,
.
-.
Health Effects of Ingested Fluoride(19~.~)i . ,
http://www.nv.edu/openbook/030904975Xihtml/5.html.COpyright 1993, 2000 The National Academy of SCiences. all nghlS reserved
.
E;cecut;ve Summary 5
0.7-1.2 rng/L, was designed to maximize prevention of dental caries
while limiting the prevalence of dental fluorosis to about 10% of the
population, virtually all of it mild to very mild.
A 1991 report from PHS of the U.S. Department of Health and
Human Services compiled the results of independent investigations
conducted duringt:he 1980s on dental fluorosis in 24 cities and compared
them with a series of PHS surveys conducted during the late 1930s and
early 1940s in 21 cities. That comparison showed that the prevalence of
dental fluorosis, most of it very mild to mild, had increased. The 1980s
data showed th~t the .mean prevalence of dental fluorosis in four cities
with optimally fluoridated water supplies was around 22% (17% very
mild, 4% mild, 0.8% moderate, and 0.1 % severe). In another city with
a water fluoride concentration in the range of 1.8-2.2 mg/L, dental
fluorosis prevalencewas 53% (23% very mild, 17% mild, 8% moderate,
and 5% severe). tn two other cities with water fluoride concentrations
greater than 3.7 mg/L, prevalence was around 84% (25% very mild,
27% mild, 19% moderate, and 14% severe). The data in the PHS report
also showed that the greatest relative increase in fluorosis prevalence
since the early studies was in communities with very low water fluoride
concentrations, demonstrating the influence of sources of fluoride other
than water. Those sources make it difficult to estimate fluoride exposure;
they represent a source of po~sible error in estimating fluoride intake in
studies of the relation between fluoride exposure and dental fluorosis,
Moreover, there is disagreement on whether dental fluorosis (even
moderate~to-severe dental fluorosis, in which substantial tooth enamel is
affected and dental ~reatment might be required) is a cosmetic problem
or an adverse health effect. .
In general, the evidence supports the conclusion that tluoridation at the
recommended concentrations, in the absence of fluoride from other
sources, results in a prevalence of mild-to-very-mild (cosmetic) dental
fluorosis in about 10% of the population and almost no cases of moderate
or severe dental fluorosis. At 5 or more time..1i the recommended con-
centration, . the proportion of moderate-to-severe dental fluorosis is
substantially higher. The most effective approach to controlling the
prevalence and severity of dental fluorosis, without jeopardizing the
benefits of fluoride to oral health, is likely to come from more judicious
control of fluoride in foods, processed beverages, and dental products,
especially those items used by young children.
~
.
.
.
Health Effects of Ingested Fluoride (1993)
http://www.n.p.edulopenbookJ030904975Xlhlml/B.hlml.copyrightl993.2OooTheNZ::.:;.naIAcodemy of Sciences, all rights reserved
6 Heallh Effects of Ingested Fluoride
Recommendations for further research are to identify sources of
fluoride during the critical stages of tooth development in childhood
and evaluate the contribution of each source to dental fluorosis.
Further research should be aimed at the goal of minimizing ex-
posure to fluoride concomitant with maintaining effectiveness in
preventing caries.
FLUQRIDE AND BoNE FRACTURES
~..
"
The effect of fluoride on bone strength, hip fractures, and skeletal
fluorosis in humans has been addressed in two types of studies. The first
type involves clinical trials of the effectiveness of high concentrations of
fluoride supplements in strengthening bones and preventing further
fractures in patients with osteoporosis; this treatment has been used
primarily in Europe for almost 30 years. When conducted using proper
control groups, these studies showed little or no benefit even at dosages
of 20-32 mg per day, well over 10 times the exposure from fluoridated
drinking water. If anything, the treated groups experienced a greater
number of new fractures, including painful stress fractures ,in bones other
than the vertebrae.
The second type of human study involves epidemiological investiga-
tions. These studies compared the rate of bone fracture in populations
of the elderly that differed in their exposure to natural or added fluoride
in drinking water. Geographic and time-trend analyses were made; time-
trend analysis is considered the stronger methodology because there is
less opportunity for confounding by other risk factors. Of the six epide-
miological studies that used geographic comparisons (where no actual
intake data were available), four found a weak association between
fluoride in drinking water and the risk of hip fracture. Two additional
studies examined time trends in bone fracture before and after water
fluoridation: one found no association and the other a negative associa-
tion. Only two additional studies collected information on individual ex-
posure: one (essentially a geographic comparison) found an increased
risk of hip fracture at water fluoride concentrations of 4 mglL, and the
other observed no difference in risk.
Studies with several species of experimental animals have yielded var-
ious outcomes. Most of the studies indicated little or no effect on bone
strength, even with very high fluoride intake and very high concentrations
.
Health Effects of Ingested Fluoride (1993)
http://www.ne.;l.edu/openbooJ<...03C904975X1htmll7.html. copyright 1993, 2000 The NationBl Academy of Sciances, all rights reserved
.
Executive Summary 7
of fluoride in bone, The subcommittee identified many potential prob-
lems in the experimental design of the animal studies, including the lack
of suitable control groups with reasonably low fluoride exposures.
However, the subcommittee concluded that the weight of evidence indi-
cates that bone strength is not adversely affected in animals that are fed
a nutritionally adequate diet unless there is long-term ingestion of fluoride
at concentrations of at least 50 mglL of drinking water or 50 mg/kg in
diet.
In view of the conflicting results and limitations of the current data
base on fluoride and the risk of hip or other fractures, the subcommittee
concludes that there is no basis at this time to recommend that EP A
lower the current standard for fluoride in drinking water for this end
point. However, the subcommittee recommends additional research to
improve the current data base.
A recommendation for further researCh is to conduct additional
studies of hip and other fractures in geographical areas with high
and low fluoride concentrations in drinking water and to make use
of individual information about water consumption. These studies
should also collect individual information on bone fluoride concen-
trations and intake of fluoride from all sources, as well as repro-
ductive history, past and current hormonal status, intake of dietary
and supplemental calcium and other cations, bone density, and other
factors that might influence risk of hip fracture.
.'
EFFECTS OF FLUORIDE ON
THE RENAL SYSTEM
Renal excretion is the major route of elimination for inorganic fluoride
from the body. As a result, kidney cells are exposed to relatively high
fluoride concentrations, making the kidney a potential site for acute
fluoride toxicity. Animal studies have shown that very high water
fluoride concentrations of 100-380 mg/L can lead to necrosis of proximal
and renal tubules, interstitial nephritis, and dilation of renal tubules.
However, human epidemiological studies have found no increase in renal
disease in populations with long-term exposureto fluoride at concentra-
tions of up to 8 mglL of drinking water.
The subcommittee concludes that available evidence shows that the
.
.
Health Effects of Ingested Fluoride (1993)
hllp:Jlwww.nap.edu/openbookl030904975XlhlmIl8.hlml, copyright 1993, 2000 The Nztional Academy of Sciences, all rights reserved
8 Health Effects of Ingested Fluoride
threshold dose of fluoride in drinking water for renal toxicity in animals
is approximately 50 mg/L. The subcommittee therefore believes that
ingestion of fluoride at currently recommended concentrations is not
likely to produce kidney toxicity in humans.
EFFECTS OF FLUORIDE ON
THE GASTROINTESTINAL SYSTEM
.
In the acid environment of the stomach, fluoride and hydrogen ions
can combine to form hydrogen fluoride, which, at sufficiently high con-
centrations, can be irritating to the mucous membranes of the stomach
lining. Experimental studies with several animal species have shown
dose-dependent adverse effects, such as chronic gastritis and other lesions
of the stomach, at fluoride concentrations of 190 mglL and higher.
Reports of gastrointestinal effects in humans often involve workers ex-
posed to unknown concentrations oifluoride in the workplace, so that the
contribution of fluoride exposure to the risk of adverse health effects is
unknown. The subcommittee noted that these workers could also be
exposed to other toxic substances present in the work environment.
There have been few studies of the gastrointestinal effects" of fluoride at
low concentrations, .
The subcommittee concludes that the available data show that the
concentrations of fluoride found in drinking water in the United States
are not likely to produce adverse effects in the gastrointestinal system.
EFFECTS OF FLUQRJDE ON
HTPERSENSITMTY AND THE IMMUNE SYSTEM
Few animal and human data on sodium fluoride-related hypersen-
sitivity reactions are found in the literature. In animal studies, exces~
sivelyhigh doses, inappropriate routes of administration of fluoride, or
both were used. Thus, the predictive value of those data, in relation to
human exposures at accepted exposure levels, is questionable. Reports
of hypersensitivity reactions in humans resulting from exposure to sodium
fluoride are mostly anecdotal.
.
Health Effects of Ingested Fluoride (1993) . .
hnp:llwww.nap.edJ!openbOOkl030904975X/html/9.html. copyri9ht 1993, 2000 The NsJionaJ Academy of Sciences, all nghts reserved
.
&ecutive Summary 9
The literature pertaining to immunological effects of fluoride is limit-
ed. Although direct exposure to high concentrations of sodium fluoride
in vitro affects a variety of enzymatic activities, the relevance of the
effects in vivo is unclear. Standardized immunotoxicity tests of sodium
fluoride at relevant concentrations and routes of administration have not
been conducted. The weight of evidence shows that fluoride is unlikely
to produce hypersensitivity and other immunological effects.
EFFECTS OF FLUORIDE ON REPRODUCTION
There have been reports of adverse effects on reproductive outcomes
associated with high levels of fluoride intake in many animal species. In
most of the studies, however, the fluoride concentrations associated with
adverse effects were far higher than those encountered in drinking water.
The apparent threshold concentration for inducing reproductive effects
was 100 mg/L in mice, rats, foxes, and cattle; 100-200 mg/L in minks,
owls, and kestrels; and over 500 mg/L in hens.
Based on these findings; the subcommittee concludes that the fluoride
concentrations associated with adverse reproductive effects in ani~als are
far higher than those to which human populations are exposed.
Consequently, ingestion of fluoride at current concentrations should have
no adverse effects on human reproduction.
.~
GENOTOXICITY
Fluoride has been tested extensively for its genotoxicity. It does not
damage DNA or induce mutations in microbial systems, but it has pro-
duced mutations and chromosomal damage in several in vitro tests with
mammalian cells. Sodium fluoride, in particular, inhibits protein and
DNA synthesis and has been reported to cause chromosomal aberrations
in human cells. The lowest effective dose in these cell-culture studies
was a fluoride concentration of approximately 10 ILg/mL, whereas the
normal concentration in human plasma is 0.02-0.06 ILg/mL, even in areas
where drinking water is fluoridated, which means that there is a large
margin of safety.
Sodium fluoride and other fluoride salts also have been tested for
.
.
Health Effects of Ingested Fluoride (1993)
htlP:llwww.nap.e6J...openbooklO3090497SXhltmV10.html. copyright 1993, 2000 Tr.e Ne!ionaJ Academy of Sciences. all rights reserved
10 Health Effects of Ingested FIU()ride
genotoxicity in the fruit fly Drosophila, as well as in mice and rats. The
subcommittee's review of the results of these in vivo studies was incon-
clusive, however, because of differences in protocols and insufficient de-
tail to support a thorough analysis. There are no published studies on the
genetic or cytogenetic effects of fluoride in humans.
The subcommittee concludes that the genotox.icity of fluoride should
not be of concern at the concentrations found in the plasma of most
people in the United States,
CARCINOGENICITY
~.
More than 50 epidemiological studies have examined the relation be-
tween fluoride concentrations in drinking water and human cancer. Most
studies compared geographic or temporal patterns of cancer occurrences
with distributions of fluoride in drinking water. These studies provide
no credible evidence for an association between fluoride in drinking
water and the risk of cancer. The existence of such an extensive epide-
miological data base oil fluoride with no consistent evidence of carcino-
genic effects suggests that, if there is any increase in cancer risk due to
exposure to fluoride, it is likely to be small. However, most of these
studies used geographic and temporal comparisons of cancer rates and
hence are of limited sensitivity. Further analytical studies with accurate
information on individual fluoride exposures and disease diagnoses are
therefore desirable.
The subcommittee also reviewed the literature on the potential car-
cinogenic effects of fluoride in 'animals. Although the results of earlier
animal studies were largely negative, the studies were not conducted
using current bioassay techniques and are thus of limited value. The
subcommittee placed greater weight on two recent studies. The first,
conducted by the National Toxicology Program (NTP), administered fluo-
ride at concentrations of up to 175 mglL of drinking water. Although the
results were negative for male and female mice and female rats, there
was some evidence of a dose-related increase in the incidence of osteosar-
comas in male rats. However. these results were not confirmed by a
second study conducted by Procter & Gamble, in which fluoride was
administered in the diet at doses higher than those in the NTP study.
The Procter & Gamble study did produce a significant dose-related in-
.
Health Effects of Ingested Fluoride (1993)
http://www.nap.edu/openbookl030!l04975Xlhtml/11.html. eopyright 1993, 2000 The National Academy of Sciences, all rights reserved
.
Executive Summary 11
crease in the incidence of osteomas (benign bone tumors) in male and
female mice. However, these lesions were not considered to be neoplas-
tic and, in any event, have no known counterpart in human pathology.
The subcommittee concludes that the available laboratory data are
insufficient to demonstrate a carcinogenic effect of fluoride in animals.
The subcommittee also concludes that the weight of the evidence from the
epidemiological studies completed to date does not support the hypothesis
of an association between fluoride exposure and increased cancer risk in
humans.
Nonetheless, the subcommittee recommends conducting one or
more carefully designed analytical epidemiological (case-control or
cohort) studies to more fully evaluate the relation between fluoride
exposure and cancer, especially osteosarcomas, at various sites,
including bones and joInts. In conducting such studies, it is im-
portant that individual exposure to fluoride from all sources be
determined as accurately as possible.
CONCLUSIONS
.
Based on its review of available data on the toxicity of fluoride, the
subcommittee concludes that EP A's current MCL of 4 mg/L for fluoride
in drinking water is appropriate as an interim standard, At that level, a
small percentage of the U.S. population will exhibit moderate or even
severe dental fluorosis. However, the question of whether to consider
dental fluorosis a cosmetic effect or an adverse health effect and the
balancing of the health risks and health benefits of fluoride are matters
to be determined by regulatory agencies and are beyond the charge or
expertise of this subcommittee. .
The subcommittee found inconsistencies in the fluoride toxicity data
base and gaps in knowledge. Accordingly, it recommends further re-
search in the areas of fluoride intake, dental fluorosis, bone strength and
fractures, and carcinogenicity. The subcommittee further recommends
that EPA's interim standard of 4 mglL should be reviewed when results
of new research become available and, if necessary, revised accordingly.
.
.
"'.
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t-
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Toxicologic Risk of Fluoride in Drinking Water
Page 1 of 4
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<,.,..')) ':1 -" . ...:,.;",,' " >\'","<":~.;-:"''::-'"'' '~-':Tl: ,'-c~. '- ";~ > "~- -., l_ ,., ~--1"' -; ~ ,;..-' ~: :-<^~ 't::~ ",,-;: ~;:~" -~
The Current Projects System
Project Title: Toxicologic Risk of Fluoride in Drinking
Water
Date Posted: 07/08/2003
Project Identification Number: BEST-K-02-05-A
Major Unit:
Division on Earth and Life Studies
Sub Unit:
Board on Environmental Studies and Toxicology
Committee Membership:
JOHN DOULL (Chair) is professor emeritus of
pharmacology and toxicology at the University of Kansas
Medical School. His distinguished career in toxicology
includes service in a variety of leadership positions and on
numerous scientific advisory committees. Most notably he
is past-president of the Society of Toxicology and the
American Board of Toxicology. Dr. Doull is the recipient of
many awards, including the International Achievement
Award from the International Society for Regulatory
Toxicology and Pharmacology, the Commanders Award
for Public Service from the Department of the Army, and
the Stockinger Award from ACGIH, and he was the first
recipient of the John Doull Award, which was established
by the Central States Chapter of the Society of Toxicology
to recognize his contributions to the discipline of
toxicology. He is former chair of the NRC Committee on
Toxicology and currently serves as vice chair of the Board
on Environmental Studies and Toxicology. He is a National
Associate of the National Academies. Dr. Doull received
his M.D. and Ph.D. in pharmacology from the University of
Chicago.
KIM BOEKELHEIDE is professor and acting chair of the
Department of Pathology and Laboratory Medicine at
Brown University. His research interests are in male
. reproductive toxicology, particularly in the area of
examining the potential roles of stem cell proliferation
kinetics and local paracrine growth factors in regulation of
spermatogenesis following toxicant-induced injury. He is a
member of the Board of Scientific Counselors of the
National Toxicology Program and was chair of the NIH
Center for Scientific Review Special Emphasis Panel, Fetal
Basis of Adult Disease: Role of the Environment. Dr.
Boekelheide received his M.D. and Ph.D. in pathology
from Duke University.
Toxicologic Risk of Fluoride in Drinking Water
Page2of4
tsAKtsAKA rAKI::iHIAN IS a pracllclng oemlst In
Washington, DC, and is a former faculty member at
Georgetown University Dental School. She is a fellow of
the Academy of General Dentistry, past-president of the
Capitol Academy of Dentistry, and a member of the Board
of Directors of the District of Columbia Dental Society, an
affiliate of the American Dental Association. Prior to
attending dental school, Dr. Farishian was a toxicologist at
the U.S. Environmental Protection Agency and was on the
biomedical research staff of the Wistar Institute of the
University of Pennsylvania. She received her D.D.S. from
the Georgetown University Dental School.
.
ROBERT L. ISAACSON is a distinguished professor of
psychology at Binghamton University. His research
interests are in behavioral neuroscience, particularly the
study of recovery from brain damage, functions of the
limbic system, mechanisms responsible for neuronal cell
death, and the neurotoxic effects of certain fluoride
complexes. He is a past president of the International
Behavioral Neuroscience Society and is recipient of the
Society's Lifetime Achievement Award. He serves on a
number of editorial boards, including that of Brain
Research. He has received fellow status in several
scientific societies. He has served as chairperson and
member of several committees of the Society for
Neuroscience. In the past he has served as a member of
grant review panels for NIH, NIMH, and NSF. He received
his Ph. D. from the University of Michigan.
JUDITH B. KLOTZ is an adjunct associate professor at the
University of Medicine and Dentistry of New Jersey. Before
joining the university, she was program manager of the
cancer surveillance and environmental epidemiology
programs at the New Jersey Department of Health and
Senior Services. Her research interests are in
epidemiological studies of cancer incidence and
reproductive outcomes, gene-environment interactions,
evaluation of biological exposures to environmental
contaminants, and the application of health risk
assessment and epidemiology to public policy. She
received her M.S. in genetics from the University of
Michigan and her Dr P.H, in environmental health sciences
from Columbia University School of Public Health.
.
JAYANTH V. KUMAR is director of the Oral Health
Surveillance & Research unit, Bureau of Dental Health at
the New York State Department of Health. He also holds
an appointment as an associate professor in the
Department of Health Policy, Management, and Behavior
at the School of Public Health of the University at Albany,
State University of New York. His research interests are in
exposure to fluoride, its effects on oral health, and health
promotion and disease prevention strategies. Dr. Kumar
received his dental degree from Bangalore University,
M.P.H. from Johns Hopkins University, and post-doctoral
certificate in dental public health from the New York State
Department of Health.
CHARLES POOLE is an associate professor in the
Department of Epidemiology at the University of North
Carolina School of Public Health. Previously,-he was with
.. - . . ... - ... .. .., - - .-
.
httn:/ /www4.nationalacademies.org.../22ed6a 7bcd08a4698525 6dOfD060 116f?OpenDocumen 7/29/2003
Toxicologic Risk of Fluoride in Drinking Water
Page 3 of 4
.
me t;;oston university ::icnoOI or ....UbIlC Healtn. Ur. ....60Ie.(s
work currently focuses on the development and utilization
of epidemiologic methods and principles, including
problem definition, study design, data collection, statistical
analysis, and the interpretation and application of research
results, including systematic review and meta-analysis. His
research experience includes studies in environmental and
occupational epidemiology and other substantive areas.
Dr. Poole was an epidemiologist in the Office of Pesticides
and Toxic Substances of the U.S. Environmental
Protection Agency for five years and worked for a decade
as an epidemiologic consultant, both with a firm and
independently. He received his M.P.H in health
administration from the University of North Carolina School
of Public Health and his Sc.D. in epidemiology from the
Harvard School of Public Health. Dr. Poole was a member
of the 10M Committee on Gulf War and Health: Review of
the Literature on Pesticides and Solvents and the NRC
Committee on Estimating the Health-Risk-Reduction
Benefits of Proposed Air Pollution Regulations.
!~.
J. EDWARD PUZAS is the Donald and Mary Clark
Professor of Orthopaedics at the University of Rochester
School of Medicine and Dentistry. He also holds faculty
appointments in biochemistry, biomedical engineering,
oncology, and pathology and laboratory medicine. He is
director of university?s Osteoporosis Center and Center
for Musculoskeletal Research. His research interests are
in all aspects of bone, cartilage, orthopaedic, and dental
biology, with a particular interest in diseases of the
skeleton, such as osteoporosis and some skeletal
cancers. He 'also directs the osteotoxicology research core
at the university?s NIEHS center program at the University
of Rochester Medical Center, where he conducts research
on adverse impacts of environmental agents on skeletal
tissue. He has won several awards for his research,
including the Kappa Delta Prize for Outstanding
Orthopaedic Research and the Kroc Foundation Award for
Excellence in Cartilage and Bone Research. Dr. Puzas is
president of the Orthopaedic Research Society. He
received his M,S. and Ph.D. in radiation biology and
biophysics from the University of Rochester.
.
NU-MAY RUBY REED is a staff toxicologist with the
California Environmental Protection Agency?s Department
of Pesticide Regulation, where she is the lead person on
risk assessment issues in the Health Assessment Section.
Her research interests are in evaluating health risks and
developing dietary assessment guidelines for pesticides.
She has been on several Cal/EPA working groups that
initiate, research, and revise risk assessment guidelines
and policies, and represented her department in task
forces on community concerns and emergency response,
risk management guidance, and public education. Dr.
Reed is also a lecturer on health risk assessment at the
University of California at Davis. She received her Ph.D.
from the University of California at Davis, and is a
diplomate of the American Board of Toxicology.
KATHLEEN M. THIESSEN is a senior scientist at SENES
Oak Ridge, Inc., Center for Risk Analysis. She has
extensive experience evaluating exposures, doses, and
Toxicologic Risk of Fluoride in Drinlcing Water
Page 4 of 4
risks to human health from environmental contaminants
and in the use of uncertainty analysis for environmental
and health risk assessment. More recently, Dr. Thiessen
has led a working group on dose reconstruction for the
International Atomic Energy Agency?s Biosphere Modeling
and Assessment Methods program, She received her
Ph.D. in genetics from the University of Tennessee-Oak
_ Ridge Graduate School of Biomedical Sciences.
.
BERNARD M. WAGNER is emeritus research professor of
"pathology at New York University Medical Center. His
research interests include toxicology, diseases of the
connective tissue, and comparative pathology. Dr. Wagner
is an honorary memberof the-;A.merrcan College of
Veterinary Pathologists and a fellow of the Royal College
of Pathologists. He received his M.D, from Hahnemann
Medical College. He has served on several NRC
. - committees; including service in the early 1990s as chair
of the Subcommittee on Health Eff\3cts of Ingested
Fluoride. . . .
THOMAS WEBSTER is assistant professor in the
Department of Environmental Health at the Boston
'University School of Public Health. His research interests
include methods in environmental epidemiology,
mathematical modeling, and the sources, fate and hazards
of persistent organic pollutants"particularly dioxins. He
received his D.Sc. in environmental health from Boston
University School of Public Health,
There has been a change in committee membership with
the appointment of Dr. Robert Isaacson.
.
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Populatiol1S Rece;'ving Optimally FJ...king Water --- United Statewysiwyg://23/http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5107a2.htm
, '
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~.
1 _ C' ~
Populations Receiving Optimally Fluoridated
.'Public Drinking Water --- United States, 2000
Dental caries (i.e., tooth decay) is a transmissible, multi-factor disease that affects 50% of children
aged 5--9 years, 67% of adolescents aged 12--17 years (1), and 94% of adults aged :::18 years (2) in
,the United States. During the second half of the 20th century (J), a major decline in the prevalence
and severity of dental caries resulted from the identification of fluoride as an effective method of
preventing caries. Fluoridation of the public. water supply is the most equitable, cost-effective, and
cost-saving method of delivering fluoride to the community (::L5). In the United States during 2000,
approximately 162 million persons (65.8% of the population served by public water systems) received
optimally fluoridated water compared with 144 million (62.1%) in 1992 (6). This report presents
state-specific data on the status of water fluoridation in the United States and describes a new
surveillance system designed to routinely produce state and national data to monitor fluoridation in .
the public water supply. The results of this report indicate slow progress toward increasing access to
optimally fluoridated water for persons using public water systems. Data from the new surveillance
system can heighten public awareness ofthis effective caries prevention measure and can be used to
identify areas where additional health promotion efforts are needed.
The 2000 and 2010 national health goals include objectives (13.9 and 21.9, respectively) (7,8) to
- increase the 1989 and 1992 national baseline fluoridation levels (61 % and 62%, respectively) (6,9) to
75% of the U.S. population served by community water systems that receive water with optimal levels
of fluoride (0.7--1.2 ppm depending on the average maximum daily air temperature of the area). The
U.S. Environmental Protection Agency (EPA) does not regulate the addition of fluoride to water, and
EP A's Safe Drinking Water Information System (SDWlS) actively tracks fluoride concentrations only
in water systems with naturally occurring fluoride levels above the established regulatory limits (:::2.0
ppm).
During 1998--2000, CDC developed the Water Fluoridation Reporting System (WFRS), a
surveillance database that included CDC's 1992 water fluoridation census (6) and EPA'sSDWIS. To
ensure that initial data were accurate and complete, in 2000, CDC sent state-specific reports generated
from WFRS to the oral health contact at each state health agency for review; updated information was
returned, and nonrespondents were contacted through telephone calls and electronic messages. In July
2001, each state received its preliminary public water system data and was asked to submit
corrections. Alabama, California, Kansas, Louisiana, Montana, Rhode Island, Texas, and Wyoming
had not updated their data by September 1, 2001; therefore, existing WFRS data were used in this
report.
.
Fluoridation percentages were determined by dividing the number of persons using public water
systems with fluoride levels considered optimal (naturally occurring and adjusted) for the state by the
total population of the state served by public water systems. When the population served by public
water systems exceeded the 2000 population census for that state, the state census was used as the
population using the public water supplies. This might occur as a result of the methods used by water
systems to estimate the population served, These states were Alabama, Hawaii, Louisiana,
Massachusetts, Missouri, Utah, and \Vyoming. .
., ,.,,,-, ,..,n(\""l 0.'1'(\ ^.
.
.
.
Populations Receiving Optimally F1...king Water -- United Statewysiwyg://23/http://www.cdc.gov/mmwr/preview/mmwrhtmVmm5l07a2.htm
In the United States during 2000, approximately 162 million persons (65.8% of the population served
. by public water systems) received optimally fluoridated water compared with 144 million .(62.1 %) in
1992 (6); state-specific percentages (Table 1) ranged from 2% (Utah) to 100% (District of Columbia)
(median: 76.7%). In 27 states during 1992--2000, the proportion increased (range: 0.8%--63.8%
. [Georgia and Nevada, respectively]; median: 4.9%), and in 23 states, the proportion decreased (range:
from --0.1 % to --6.0% [Iowa and Alaska, respectively]; median: 2.9%); the District of Columbia
remained 100% fluoridated. Delaware, Maine, Missouri, Nebraska, and Virginia reached 75% in 2000
and Oklahoma reached 74.6%. The national objective has been met by 26 states, and the small
increase from 1992 to 2000 of 3.7 percentage points has left a gap of 9.2 percentage points from the
overall target.
. Reported by: D Apanian, MS, D lvfalvitz, DrPH. S Presson, DDS, Div of Oral Health, National
Center for Chronic Disease Prevention and Health Promotion, CDC.
Editorial Note:
.
WFRS data indicate that during the 1990s, the estimated proportion of the U.S. population using
public water supplies that maintained optimally fluoridated water increased from 62.1 % to 65.8%.
This modest progress occurred as the result of substantial increases in coverage in a few states and, in
some instances, because several large metropolitan areas commenced fluoridation (e.g., Clark County
[Las Vegas], Nevada; Los Angeles and Sacramento, California; and :tv1anchester, New Hampshire).
The findings in this report are subject to at least three limitations. First, nonresponses might have
affected the accuracy of some states' final water fluoridation percentages by not accounting for
changes in status. Second, use of the 2000 U.S. census data as the denominator for calculating water -
fluoridation percentages in seven states might have resulted in the percentages being underestimated
because, in most states, the number of persons using public water systems was probably less than the
2000 U.S. census population. Finally, three states (Kentucky, Rhode Island, and South Dakota)
reported their 1992 fluoridation rates as 100%; in these states, the apP81ent decrease from 1992 to
2000 in the percentage of persons using public water supplies receiving optimally fluorioated water
represents an error correction in reporting methods rather than a true decrease.
WFRS will become an increasingly valuable tool for monitoring state and annually updating national
water fluoridation data as more users register and routinely participate in entering data and receiving
reports. WFRS updates and reports \vill assist states in monitoring the extent and consistency of water
fluoridation. During 2002, CDC will provide online information on \-vater fluoridation for states that
update their data electronically.
Although the new WFRS online site might facilitate public knowledge about optimally fluoridated
water, efforts to convince jurisdictions to provide such water must address 1) the perception by some
scientists, policymakers, and members of the public that dental caries is no longer a public health
problem or that fluoridation is no longer necessary or effective; 2) the often complex political process
involved in adopting water fluoridation; and 3) unsubstantiated claims by opponents of water
fluoridation about its alleged adverse health effects (10). To reach the goal of 75% of the public water
drinking population supplied \\-ith optimally fluoridated water, policymakers and public health
officials at the federal, state, and local levels will need to devise new promotion and funding
approaches to gain support for this prevention measure.
Acknowledgements
.
This report is based on data contributed by state health, natural resources, and environmental
departments. S Randlett, Alaska Dept of Environmental Conservation. K Hayward, Arizona Dept of
Health Svcs. L Mouden, DDS, Arkansas Dept of Health. D Brunson, MP H. Colorado Dept of Public
Health and Environment. H Link, Connecticut Dept of Public Health. H Davis, DDS, Florida Dept of
Health. E Alderman, DDS, Georgia Dept of Human Resources. M Greer, DMD, Hawaii Dept of
Health. L Penny, Idaho Dept of Health and Welfare. L Lampiris, DDS, Illinois Dept of Public Health.
D Cain, Indiana State Dept of Health. M Magnant, Iowa Dept of Public Health. R Murphy, Kentucky
..... .,...-1....,..,....... ,.., ...." "....
pulations Receiving Optimally Fl...king Water m United Statev,')"siwyg://23/http://www,cdc.gov/mmwr/preview/mmwrhtmUmm51 07a2.htri:::.
Dept for Public Hea}th. S Russ, Maine Dept of Human Svcs. N Rei/man, Maryland Dept of the
Environment. F Barker, Massachusetts Dept of Public Health. J Shekter, Michigan Dept of
Environmental Quality. D Rindall, Minnesota Dept of Health. J Young, DMD, Mississippi State Dept
of Health. M Logston, Missouri Dept of Natural Resources. K McFarland, DDS, Nebraska Health
.and Human Svcs System. C Lawson, Nevada State Health Div. A Pelletier, MD, New Hampshire Dept
of Health and Human Svcs. F Dickert, New Jersey Dept of Environmental Protection. R Romero,
DDS, New Mexico Dept of Health. E Green, DDS, New York State Dept of Health. R King, DDS,
North Carolina Dept of Health and Human Svcs.. G Stewart, MP A, North Dakota Dept of Health. J
Pierson, Ohio Dept of Health. MMorgan, DDS, Oklahoma State Dept of Health. K Salis, Oregon
Health Div. N Gardner, DDS, Pennsylvania Dept of Health. R Lala, DDS, South Carolina Dept of
Health and Environmental Control. M Baker, South Dakota Dept of Health. W Wells, Tennessee Dept
.. of Environment and Conservation. K Zinner, MPH, Utah Dept of Health. A Lund, Vermont Dept of
Health. K Day, DDS, Virginia Dept of Health. T Wi/son, Washington Dept of Health. G Black, DDS,
West Virginia Bur of Public Health. W LeMay, DDS, Wisconsin Div of Public Health.
References
.
1. Kaste LM, Selwitz RH, Oldakowski RJ, Brunelle JA, Winn DM, Brown LJ. Coronal caries in the
primary and permanent dentition. of children and adolescents 1--17 years of age: United States,
1988--1991. J Dent Res 1996;75:631--41.
2. Winn DM, Brunelle JA, Selwitz RH, et al. Coronal and root caries in the dentition of adults in
the United States, 1988--1991. J Dent Res 1996;75:642--51.
3. CDC. Achievements in public health. 1900--1999: fluoridation of drinking water to prevent
dental caries. MMWR 1999:48:933--40.
4. CDC. Recommendations for using fluoride to prevent and control dental caries in the United
States. MMWR 200l;50(No. RR-14):26.
5. Griffm SO, Jones K, Tomar SL. An economic evaluation of community water fluoridation. J
Public Health Dent 2001 ;61 :78--86.
6. CDC. National Center for Prevention Services. Fluoridation census 1992 summary. Atlanta, .
Georgia: US Department of Health and Human Services, Public Health Service, CDC, 1993.
7. US Department of Health and Human Services. Healthy people 2000: national health promotion
and disease prevention objectives---full report, with commentary. Washington, DC: US
Department of Health and Human Services, Public Health Service, 1990:357--8.
8. US Department of Health and Human Ser;ices. Healthy people 2010---understanding and
improving health. 2nd ed. Wasnington, DC: US Government Printing Office, November
2000:21-28.
9. CDC. National Center for Prevention Services. Fluoridation census 1989 summary. Atlanta,
Georgia: US Department of Health and Human Services, Public Health Service, CDC, 1991.
10. Hodge HC. Evaluation of some objections to water fluoridation. In: Newbrun E, ed. Fluorides
and Dental Caries: Contemporary Concepts for Practitioners and Students. 3rd ed. Springfield,
Illinois: Charles C Thomas, 1986:221--55.
Table 1
.
_r c
2/27/2002 8:30 A~'
Toxicologic Risk of Fluoride in Drinking Water
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The Current Projects System
Project Title: Toxicologic Risk of Fluoride in Drinking
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Date Posted: <Posted: 03/20/2003>
Project Identification Number: BEST-K-02-05-A
Major Unit:
Division on Earth and Life Studies
Sub Unit:
Board on Environmental Studies and Toxicoloqy
Project Scope:
Asubcommittee of the National Research Council?s
(NRC) Committee on Toxicology (COT) will review
toxicologic, epidemiologic, and clinical data published
since 1993, and exposure data on orally ingested fluoride
from drinking water and otheF sources (e.g., food,
toothpaste, dental rinses). Based on those reviews the
subcommittee will evaluate independently the scientific
and technical basis of the U.S. Environmental Agency?s
(EPA) maximum contaminant level (MCL) of 4 milligram
per liter (mg/L) and secondary maximum contaminant level
(SMCL) of 2 mg/L in drinking water. The subcommittee will
advise EPA on the adequacy of its fluoride MCL and
SMCL to protect children and others from adverse effects.
The subcommittee will determine the relative contribution
of various fluoride sources (e.g., food, dental-hygiene
products) to total exposure. The subcommittee wm also
identify data gaps and make recommendations for future
research relevant to setting the MCL and SMCL for
fluoride.
Sponsor: U.S. Environmental Protection Agency
The approximate start date for the project is November 15,
2002,
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approximately 24 months
Project Duration: 24 months
Links to Project Information:
Committee Membershi~
Meeting 1 - 08/12/2003
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Toxicologic Risk of Fluoride in Drinking Water
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T"'> _ ___nO ___ -r /"H'I'''nn'J
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P0pulations.Receiving Optimally FLking Water --- United StatewYsiwyg://23lhttp://www.cdc.gov/mmwr/preview/mmwrhtmUmmSl07a2.htm
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TABLE t. Number of persons and percentage of the population receiving optimally fluoridated wator ltIrough public water
systems (PWS), by state - Unillld Statos, 1992 and 2000
2000 2lIOO 2000 1992
lluorldalacS Iolal PWS pel'Cllll'ltage percentage
Slale population popUlatlon fluoridated fluoridated (9)
Alabama' 3.967,05l1 4.447,100 811.2% 82.6'r.
Alasl<.a 270.099 .olBll.371 55.2% 612%
Arizona. 2.700.354 4.BM.065 55.~ 49.1I'r.
AJ1<.ar=s' 1,455,767 2,431,477 59.ll% Sll.7'%
Caiiiomla 9,551,961 33,238.057 28.7% IS.7'f.
Colerado' 2.852.386 3.700,061 76.~. 81.~
Connecticut 2,3118,227 2.701,178 8S..B% 85.1l%
Delaware 505.747 624.923 eo~. 67.4%
District 01 Colurnl:ia 595,000 595.000 100,0% 100.0%
Aor1da 9,407.494 15,033.S74 62.6% Sll.3%.
Gllotgla. 6,161.139 6.lS34.&:35 92.9% 92.1%
Havtair 109,147 1,211,537 9.0% 13.0%
Idaho 383.720 845,780 45,4% 48.3%
IBI~ 10.453.837 11,192286 93,4% 9S.2%
1nt2ana 4,232.1107 4,441.502 9S.3'f. 118.6%
Iowa 2.181,&49 2.390.661 91.3'f. 91.4'7.
Kansas 1 ;S13.:lOG 2,421,2.74 62.5% 58..4".
Kantucl<y 3,235.053 3.367.812 lloS.1~ loo.~.
Loulslana' 2.37S.702 4.4GB.976 53.r.. 5S.7'f.
Maine 466,208 618,033 75.4% S5.B'l'.
Malyland' 4.124.953 4,547.908 9O.~ 85.8':'.
Massacrosel1S" 3.546.099 6.349.097 SS,IF.. 57 .~.
Michigan 6,568,151 7,242.531 9O,7':\, 88.5%
Mlnnasota 3,714.465 3.7SO.942 118.r.v 93.4~~
MlsslssIppI 1 ,2Z7 ~8 2,66S.075 46.0% 48,4%
Mlssourl" 4,502.722 5,595.211 80.5% 71.4'7.
Montana 143.092 645.452 22.2% 25.9%
NGbrasl<a' llGO,262 1,243.713 77.7"!. 62.1%
Nevada' 1,078.479 1,&:37.105 55.1F,. 2.1%
New Hampshire 347.007 807.438 43.0% 24.0%
NewJe<sey 1.120,410 7.208,514 15.50/. 16.2.%
New Mexico 1.187.404 1,54a.084 76.~ 66~.
tlaliYor'\(t 12.000.000 17.e90,198 67.B'l'. 69.7%
Notlh Catolina 4.aS2.220 5.837.936 83.3"'. 78.57.
NC<th Oakola 531,738 557,595 95.4~. lloS.4%
Ohio 8.355,002 9,535.188 87.6% 87.9'%
Oklahcma' 2.164.330 2,900.000 74.G'l'. Sll.~.
oregon' .612.485 2.700,000 22.7% 24.8%
PennsyIVanl.1 5.825.328 10,750,095 54.2% 50.9%
RMde Island 842.797 llB9.786 85. 1% 1oo.0'l~
SOUll'o CaroII....... 3.086.974 3,383.434 1l1.2% 90.0%
South Dal<ota' 553.503 626.221 B8.4~ 1oo.~.
_ Temessse 4,749,493 5.025.998 S4.5% 92.0'>.".
Te><as 11,888,046 18.072,6S0 65,7~~ 64.~.
Utah'- 43.816 2.233.169 2.0'>.". 3.1~
VBrmoot 240.579 443.ll<l1 54.2'l~ 57.4%
Vilglnla 5.677,551 6.085.436 93.3"'. 72.1 'f.
W:lShington' 2.644.893 4.925.540 57.8% 53.27.
West VIrgInia' 1.207,000 1,387,000 87.0% 82.1%
Wisconsin 3.108.738 3,481.285 89.3% 93.~~
"'Iyoming' 1411.774 493.782 30.3% 35,7'%
Tolal 162.067.341 246,120 616 65.1l"Jl, 62.1.,..
; Reported PWS popLAallon axce_lOW state j:lopulallon: PWS populaUon..'aS ~ to the 2000 U.S. census 01 slale popuIaliOns.
Complete data were not available 1m'll Water RuoricJ.alion Re.por11ng System; addillonal inlOl'mallon was obIalned "om Slat.$.
Return to toP.
Change In
pet'C8l\tage
11192-2000
6.6
~.O
5.6
1.2
13.0
-1.8
2.9
13.5
0.0
4.3
0.8
-4.0
-2.9
-1.8
--3.3
-0.1
4.1
--3.9
-2.5
19.6
4.9
-1.2
2.2
4.8
-2.4
g,1
-3.7
15.6
63.8
19.0
-OJ
10.5
-1.9
4..8
-1.0
-<l.3
16.6
.-2.1
3.3
-14.9
1.2
-11.6
2.5
1.7
-1.1
-32
21.2
4.6
4.9
-3,7
-5.4
3.7
.~....... .A.......... .... _.... . ...
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CDC DOH
770-488-5575
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DEPARTMENT OF HEALTH &.. HUMAN SERVlCES
Public Health Service
Office of the Surgeon Gen ~rilt
Roclr;ville MD 20857
DEe 3 i 00 I
SURGEON GENERAL STATEMENT ON coMMUNITY WATER FLUORIDATION
For more than half a century, community water fluoridation has been the cornerstone of caries
prevention in the United States. As noted in my May 2000 report, Or~l Health in Af'(lerica: A
Report of the Surgeon Gener~l. community water fluoridation contiIiues to be the most cost-
efIcct1ve, practical and safe means for reducing and controlling the occurrence of tooth decay in
a community, In thousands of communities in the United States where naturally-occurring '.
fluoride levels are deficient, small amounts of fluoride have been added to drinking water
supplies with dramatic results. More than 50 years of scientific research has found that people
living in communities with fluoridated water have healthier teeth and fewer cavities than those
l~ving where the water is not fluoridated.
-
Almost two-thirds of the United States population served by public water supplies consume
water with optimal fluoride levels. Of the 50 largest cities in thc country, 43 are fluoridated. A
significant advantage of water fluoridation is that anyone; regardless of socioeconomic level, can
enjoy thcse health benefits during their daily lives-at home, work, or at school or play-simply
by drinking fluoridated water or beverages prepared with fluoridated watec Water fluoridation
is a powerful strategy in our efforts to eliminate health disparities among populations.
Unfortunately, over one-third of the U.S. population (100 million people) is without this critical
public health measure. .
The U.S. Ccnters for Disease Control and Prevention has recognized the fluoridation of drinking
water as one often great public health achievements of the twentieth century. Water fluoridation
has helped improve the quality of life in the U.S. through reduced. pain and suffering related to
tooth decay 7 reduced time lost from school and work, and less money spent to restore, remove, or
replace decayed teeth. Fluoridation is the single most effective public health measure to prevent
tooth decay and improve oral health over a lifetime, for both children and adults,
Water fluoridation continues to be a highly cost-effective strategy; even in areas where the
overall caries level has declined and the cost of implementing water fluoridation has increased.
Compared to the cost of restorative treatment, water fluoridation actually provides cost savings, a
rare characteristic for community-based disease prevention strategies.
While we can be pleased with what has already been accomplished, it is clear that there is much
yet to be done. I join previous Surgeons General in acknowledging the continuing public health
role for community water fluoridation in enhancing the oral health of all Americans. .
Sincerely yours,
David Satcher, M.D., Ph.D.
Surgeon General
.
Fluoridation Costs Proposal
Prepared by
Dennis Janovsky
&.
Larry Trepany
~.
References:
Water Quality and Treatment Handbook (AWWA)
Robert Powell (PCU)
William Lovins III, PE, PhD (Boyle)
Kurt Peters (City of Safety Harbor)
David Brown (Town of Belleair)
Wayne Koch (PCU)
Mike Hamant (Allied Universal)
.
.
SUMMARY
. The facilities for which cost estimates are provided herein are
temporary.
. The estimated cost of construction is $295,000.00.
. New fluoridation facilities would be constructed in the Plant Detention
Blending Facility now under design.
. Very little, if any, of this equipment would be usable in the new plant.
.
. Annual operating cost is estimated to be $115,000. Operating cost in
the new plant would be approximately the same.
. These costs will have a minimal impact on annual expenses and will
not require an increase in water rates.
.
.
I
,.
.
Fluoride Application Costs
At Keller Connector
. Construction of Fluoride Feed Facility
. Bulk Fluoride delivery for star-up (5000 gallons)
. Tap 60" above ground North and South pipe for injection point
. 316 stainless steel injection probes
. Startup and Training
Construction Costs
5,000 Gallons HSS
2 60-inch x 2" taps
2 Injection Probes
Startup & Training
$138,000.00
$1,525.00
$6,000.00
$1,500.00
$3,000.00
$150,025.00
Total Cost
Note: Above costs do not include on-line analyzers, $8,000 additional if utilized.
.
~.
.
Fluoride Application CostS
At Keller Water Treatment Facility
. Construction of Fluoride Feed Facility
. Bulk Fluoride delivery for startup (5000 gallons)
. Tap for injection point
. Startup and Training
Construction Costs
5,000 Gallons HSS
Injection Point
Startup & Training
$138,000.00
$1,525.00
$3,000.00
$3,000.00
$145,525.00
Total Cost
Note: Above costs do not include on-line analyzers, $8,000 additional if utilized.
.
Annual Operation & Maintenance Costs
. Fluoride (Hydrofluosilic Acid) HSS
. Plant Operator (Operations Specialist)
. Maintenance (Electrical Mechanical Technician)
. Power Costs
Chemical Costs
Plant Operator
Maintenance
Power Costs
$32,836.00
$48,180.00
$32,032.00
$2.000.00
$115,048.00
.
Total Annual Costs
.
Jle \ Lib
.
Paul Connett, PhD
Professor of Chemistry, St. Lawrence University, Canton NY
· Cover letter
· Communities which have rejected Fluoridation since 1990
· Statements from European Health, Water & Environmental Authorities on
Water Fluoridation
· The Phosphate Fertilizer Industry: An Environmental Overview
· A Bibliography of Scientific Literature on Fluoride
.
Paul Connett, PhD has accumulated the most information on fluoride of anyone individual
that we know of He is working on the National Research Council study and presented it
to NRC on Aug 12, 2003.
Dr. Connett is willing to have an open debate with your advisors. He has found that most
advisors, when challenged, have refused to debate this issue in public with experts who
have studied the issue for years.
How can a person in good conscience force a substance on the public which cannot be
defended in open public debate? It is a matter of integrity to not rush through this vote but
instead invite the pro-fluoride advisers to debate Dr. Connett, who has agreed to come to
Pinellas County at no charge.
He can present the arguments that he gave to the NRC in August in Washington, which
reviews the safe drinking water standard for fluoride for the US EP A. Should the pro-
fluoride advisers still refuse to debate or speak with Dr. Connett, he is prepared to present
his review of the latest scientific evidence to you, the Commission, directly.
.
Pinellas County Citizens for Safe Drinking Water
Angela Schrader 727 772.9236
.
.
.
August 20,2003
Re: No fluoridation of our drinking water
Hello Fellow Citizens and Commissioners,
We are a group of citizens who are against putting fluoride into our water supply.
Dr Paul Connett is working on the National Research Council study. He is willing to have an open debate with
your advisors, who when challenged, have refused to debate this issue in public with experts who have studied
the issue for years. How can you in good conscience force a practice on the public which cannot be defended in
open public debate?
It is a matter of integrity to not rush through this vote but instead invite your advisers to debate Dr. Paul Connett,
who has agreed to come to Pinellas County without fee. He will present the arguments he has recently presented
to the National Research Council (August 12, 2003 in Washington, DC) which is reviewing the safe drinking
water standard for fluoride for the US EPA. Should your advisers still refuse to debate or engage Dr. Connett, he
is prepared to present his review of the latest scientific evidence to you directly.
The body of information that is presented by both sides can be hard to understand because it involves dosage as
well as formulation. There is much conflicting data, how does ene know what to believe?
We strongly support the City Commission in taking the very responsible position to have all pertinent fluoride
research at hand before implementing any fluoridation into our water system. It is obvious that there are
definite gaps in the knowledge, thus the existence of severe contradictions in the presentations.
Water fluoridation is a peculiarly American phenomenon. It started at a time when asbestos lined our pipes, lead
was added to gasoline and paint, PCBs filled our transformers and DDT was deemed so "safe and effective" that
officials felt no qualms spraying kids in school classrooms and seated at picnic tables. One by one all these
chemicals have been banned, but fluoridation remains untouched.
For over 50 years US government officials have confidently and enthusiastically claimed that fluoridation is
"safe and effective." However, they are seldom prepared to defend the practice in open public debate. Actually,
there are so many arguments against fluoridation that it can get overwhelming.
To simplify things it helps to separate the ethical from the scientific arguments.
For those for whom ethical concerns are paramount, the issue of fluoridation isvery simple to resolve. It is
simply not ethical; we simply shouldn't be forcing medication on people without their "informed consent."
The bad news is that ethical arguments are not very influential in Washington DC unless politicians are very
conscious of millions of people watching them.
The good news is that the ethical arguments are buttressed by solid common sense arguments and scientific
studies which convincingly show that fluoridation is neither "safe and effective" nor necessary. I have
summarized the arguments in several categories:
Fluoridation is UNETInCAL because:
1) It violates the individual's right to informed consent to medication.
2) The municipality cannot control the dose of the patient.
3) The municipality cannot track each individual's response.
4) It ignores the fact that some people are more vulnerable to fluoride's toxic effects than others. Some
people will suffer while others may benefiL
Pinellas County Citizens for Safe Drinking Water
Angela Schrader 727 772.9236
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August 20, 2003
Page 2
5) It violates the Nuremberg code for human experimentation.
As stated by the recent recipient of the Nobel Prize for Medicine (2000), Dr. Arvid Carlsson:
"I am quite convinced that water fluoridation, in a not-too-distant future, will be consigned to
medical history.. . Water fluoridation goes against leading principles of pharmacotherapy, which
is progressing from a stereotyped medication - of the type 1 tablet 3 times a day - to a much
more individualized therapy as regards both dosage and selection of drugs. The addition of
drugs to the drinking water means exactly the opposite of an individualized therapy."
As stated by Dr. Peter Mansfield, a physician from the UK and advisory board member of the recent government
review of fluoridation (McDonagh et al 2000):
"No physician in his right senses would prescribe for a person he has never met, whose
medical history he does not know, a substance which is intended to create bodily change, with
the advice: 'Take as much as you like, but you will take it for the rest of your life because some
children suffer from tooth decay. ' It is a preposterous notion."
Fluoridation is UNNECESSARY because:
1) Children can have perfectly good teeth without being exposed to fluoride.
2) The promoters (CDC, 1999, 2001) admit that the benefits are topical not systemic, so fluoridated
toothpaste, which is universally available, is a more rational approach to delivering fluoride to the target
organ (teeth) while minimizing exposure to the rest of the body.
3) The vast Iilajority of west em Europe has rejected water fluoridation, but has been equally successful as
the US, if not more so, in tackling tooth decay.
4) If fluoride was necessaty for strong teeth one would expect to find it in breast milk, but the level there is
0.01 ppm, which is 100 times LESS than in fluoridated tap water (10M, 1997).
5) Children in non-fluoridated communities are already getting the so-called "optimal" doses from other
sources (Heller et aI, 1997). In fact, many are already being over-exposed to fluoride.
Fluoridation is INEFFECTIVE because:
1) Major dental researchers concede that fluoride's benefits are topical not systemic (Fejerskov 1981;
Carlos 1983; CDC 1999,2001; Limeback 1999; Locker 1999; Featherstone 2000).
2) Major dental researchers also concede that fluoride is ineffective at preventing pit and fissure tooth
decay, which is 85% of the tooth decay experienced by children (JADA 1984; Gray 1987; White 1993;
Pinkham 1999).
3) Several studies indicate that dental decay is coming down just as fast, if not faster, in non-fluoridated
industrialized countries as fluoridated ones (Diesendorf, 1986; Colquhoun, 1994; World Health
Organization, Online).
4) The largest survey conducted in the US showed only a minute difference in tooth decay between
children who had lived all their lives in fluoridated compared to non-fluoridated communities. The
difference was not clinically significant nor shown to be statistically significant (Brunelle & Carlos,
1990).
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August 20, 2003
Page 3
5) The worst tooth decay in the United States occurs in the poor neighborhoods of our largest cities, the
vast majority of which have been fluoridated for decades.
6) When fluoridation has been halted in communities in Finland, fonner East Gennany, Cuba and Canada,
tooth decay did not go up but continued to go down (Maupome et aI, 2001; Kunzel and Fischer, 1997,
2000; Kunzel et aI, 2000 and Seppa et aI, 2000).
Fluoridation is UNSAFE because:
1) It accumulates in our bones and makes them more brittle and prone to fracture. The weight of evidence
from animal studies, clinical studies and epidemiological studies on this is overwhelming. Lifetime
exposure to fluoride will contribute to higher rates of hip fracture in the elderly.
2) It accumulates in our pineal gland, possibly lowering the production of melatonin a very important
regulatory honnone (Luke, 1997,2001).
3) It damages the enamel (dental fluorosis) of a high percentage of children. Between 30 and 50% of
children have dental fluorosis on at least two teeth in optimally fluoridated communities (Heller et aI,
1997 andMcDonagh etal, 2000).
4) There are serious, but yet unproven, concerns about a connection between fluoridation and
osteosarcoma in young men (Cohn, 1992), as well as fluoridation and the current epidemics of both
arthritis and hypothyroidism.
5) In animal studies fluoride at 1 ppm in drinking water increases the uptake of aluminum into the brain
(Varner et aI, 1998).
6) Counties with 3 ppm or more of fluoride in their water have lower fertility rates (Freni, 1994).
7) In human studies the fluoridating agents most commonly used in the US not only increase the uptake of
lead into children's blood (Masters and Coplan, 1999, 2000) but are also associated with an increase in
violent behavior.
8) The margin of safety between the so-called therapeutic benefit of reducing dental decay and many of
these end points is either nonexistent or precariously low.
Fluoridation is INEQUITABLE, because:
1) It will go to all households, and the poor cannot afford to avoid it, if they want to, because they will not
be able to purchase bottled water or expensive removal equipment.
2) The poor are more likely to suffer poor nutrition which is known to make children more vulnerable to
fluoride's toxic effects (MassIer & Schour 1952; Marier & Rose 1977; A TSDR 1993; Teotia et aI,
1998).
3) Very rarely, if ever, do governments offer to pay the costs of those who are unfortunate enough to get
dental fluorosis severe enough to require expensive treatment.
Fluoridation is INEFFICIENT and NOT COST -EFFECTIVE because:
1) Only a small fraction of the water fluoridated actually reaches the target. Most of it ends up being used
to wash the dishes, to flush the toilet or to water our lawns and gardens.
2) It would be totally cost-prohibitive to use pharmaceutical grade sodium fluoride (the substance which
has been tested) as a fluoridating agent for the public water supply. Water fluoridation is artificially
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August 20, 2003
Page 4
cheap because, unknown to most people, the fluoridating agent is an unpurified hazardous waste
product from the phosphate fertilizer industry.
3) If it was deemed appropriate to swallow fluoride (even though its major benefits are topical not
systemic) a safer and more cost-effective approach would be to provide fluoridated bottle water in
supermarkets free of charge. This approach would allow both the quality and the dose to be controlled.
Moreover, it would not force it on people who don't want it.
Fluoridation is UNSCIENTIFICALLY PROMOTED. For example:
1) In 1950, the US Public Health Service enthusiastically endorsed fluoridation before one single trial had
been completed.
2) Even though we are getting many more sources of fluoride today than we were in 1945, the so-called
"optimal concentration" of 1 ppm has remained unchanged.
3) The US Public health Service has never felt obliged to monitor the fluoride levels in our bones even
though they have known for years that 50% of the fluoride we swallow each day accumulates there.
4) Officials that promote fluoridation never check to see what the levels of dental fluorosis are in the
communities before they fluoridate, even though they know that this level indicates whether children
are being overdosed or not.
5) No US agency has yet to respond to Luke's finding that fluoride accumulates in the human pineal gland,
even though her finding was published in 1994 (abstract), 1997 (ph. D. thesis), 1998 (paper presented at
conference of the International Society for Fluoride Research), and 2001 (published in Caries
Research).
6) The CDC's 1999,2001 reports advocating fluoridation were both six years out of date in the research
they cited on health concerns.
Fluoridation is UNDEFENDABLE IN OPEN PUBLIC DEBATE.
The proponents of water fluoridation refuse to defend this practice in open debate because they know that they
would lose that debate. A vast majority of the health officials around the US and in other countries who promote
water fluoridation do so based upon someone else's advice and not based upon a first hand familiarity with the
scientific literature. This second hand information produces second rate confidence when they are challenged to
defend their position. Their position has more to do with faith than it does with reason.
Those who pull the strings of these public health 'puppets' do know the issues, and are cynically playing for time
and hoping that they can continue to fool people with the recitation of a long list of "authorities" which support
fluoridation instead of engaging the key issues. As Brian Martin made clear in his book Scientific Knowledge in
Controversy: The Social Dynamics of the Fluoridation Debate (1991), the promotion of fluoridation is based
upon the exercise of political power not on rational analysis. The question to answer, therefore, is: "Why is the
US Public Health Service choosing to exercise its power in this way?"
Motivations - especially those which have operated over several generations of decision makers - are. always
difficult to ascertain. However, whether intended or not, fluoridation has served to distract us from several key
issues. It has distracted us from:
a) The failure of one of the richest countries in the world to provide decent dental care for poor people.
b) The failure of 80% of American dentists to treat children on Medicaid.
c) The failure of the public health community to fight the huge Qver consumption of sugary foods by our
nation's children, even to the point of turning a blind eye to the wholesale introduction of soft drink
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August 20, 2003
Page 5
machines into our schools. Their attitude seems to be iffluoride can stop dental decay why bother
controlling sugar intake.
d) The failure to adequately address the health and ecological effects of fluoride pollution from large
industry. Despite the damage which fluoride pollution has caused, and is still causing, few environmentalists
have ever conceived of fluoride as a 'pollutant.'
e) The failure of the US EP A to develop a Maximum Contaminant Level (MCL) for fluoride in water
which can be scientifically defended.
f) The fact that more and more organofluorine compounds are being introduced into commerce in the
form of plastics, pharmaceuticals and pesticides. Despite the fact that some of these compounds pose just as
much a threat to our health and environment as their chlorinated and brominated counterparts (i.e. they are
highly persistent and fat soluble and many accumulate in the food chains and our body fat), those
organizations and agencies which have acted to limit the wide-scale dissemination of these other
halogenated products, seem to have a blind spot for the dangers posed by organofluorine compounds.
So while fluoridation is neither effective nor safe, it continues to provide a convenient cover for many of the
interests which stand to profit from the public being misinformed about fluoride.
Unfortunately, because government officials have put so much of their credibility on the line defending
fluoridation, it will be very difficult for them to speak honestly and openly about the issue. As with the case of
mercury amalgams, it is difficult for institutions such as the American Dental Association to concede health risks
because of the liabilities waiting in the wings if they were to do so. .
However, difficult as it may be, it is nonetheless essential - in order to protect millions of people from
wmecessary hann - that the US Government begin to move away from its anachronistic, and increasingly absurd,
status quo on this issue. There are precedents. They were able to do this with hormone replacement therapy.
But getting any honest action out of the US Government on this is going to be difficult. Effecting change is like
driving a nail through wood - science can sharpen the nail but we need the weight of public opinion to drive it
home. Thus, it is going to require a sustained effort to educate the American people and then recruiting their help
to put sustained pressure on our political representatives. At the very least we need a moratorium on fluoridation
(which simply means turning off the tap for a few months) until there has been a full Congressional hearing on
the key issues with testimony offered by scientists on both sides. With the issue of education we are in better
shape than ever before. Most of the key studies are available on the internet and there are videotaped interviews
with many of the scientists and protagonists whose work has been so important to a modern re-evaluation of this
Issue.
With this new infonnation, more and more communities are rejecting new fluoridation proposals at the local
level. On the national level, there have been some hopeful developments as well, such as the EP A Headquarters
Union coming out against fluoridation and the Sierra Club seeking to have the issue re-examined. However,
there is still a huge need for other national groups to get involved in order to make this the national issue it
desperately needs to be.
I hope that if there are RFW readers who disagree with me on this, they will rebut these arguments. If they can't
then I hope they will get off the fence and help end one of the silliest policies ever inflicted on the citizens of the
US. It is time to end this folly of water fluoridation without further delay. It is not going to be easy.
Fluoridation represents a very powerful ''belief system" backed up by special interests and by entrenched
governmental power and influence.
Paul Connett
For Pinellas County Citizens for Safe Drinking Water
Communities which have Rejected Fluoridation Since 1990
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FLUOR I DE
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Page 1 of3
Communities which have Rejected
Fluoridation Since 1990
Compiled by Maureen Jones & Fluoride Action Network
"In about 60% of 2000 referenda held in the U.S. since 1950, fluoridation
has been voted down." - Zev Ramba, Washington Bureau Editor of AGD Impact
(the publication of the Academy of General Dentistry). Quoted in the Chemical &
Engineering News (8/1/88).
"Avoid a referendum. The statistics are that 3 out of 4 fluoridation
referenda fail.". Susan Allen, RDH, BS Fluoridation Coordinator, Public Health
Dental Program, State Health Office, Florida. May 7, 1990. (See letter)
''The fact that nearly 3 out of every 5 communities which vote on the issue
have rejected fluoridation, year after year, does in alllikeliliood represent
a collective judgment on the part of the public that, when all things are
considered, fluoridation is not an acceptable public health measure." -
Edward Groth III, PhD Dissertation, Stanford University, May 1973
Burns Lake, British Columbi~ Canada
Dutton-Dunwich. Ontario. Canada
West Ele:in. Ontario. Canada
Sequim. Washine:t:on State
York. Nebraska
Canton. New York
Shaler, Pennsylvania
Billings, Montana
Kalispell. Montana
WashoeCoun~.Nevada
Methuen, Massachusetts
Redding. California
Watsonville. California
Texarkana. Arkansas
Ashdown. Arkansas
Oneida, New York
Franklin, North Carolina
Plainville. Massachusetts
Monroe, Louisiana
Colorado Springs. Colorado
Kennewick. Washington
Benninton. Vermont
Lanai. Hawaii
Cobalt. Ontario. Canada
Erie. Colorado
Modesto, C..alifornia
Worcester. Massachusetts
Flagstaff. Arizona
Sutherlin. Oregon
Kamloops. British Columbia Canada
White Salmon. Washington
Goldendale. Washington
http://www.tluoridealeft.org/communities.htm
June 25, 2003
June 2003
June 2003
May 7, 2003
May 6, 2003
February 18, 2003
February 11, 2003
November 5, 2002
November 5, 2002
November 5, 2002
November 5, 2002
November 5, 2002
November 5, 2002
November 5, 2002
November 5, 2002
August 6, 2002
May 2002
April 1, 2002
February 26, 2002
January16,2002
January 15, 2002
January 8, 2002
January 2002
December 11, 2001
November 2001
November 7, 2001
November 7, 2001
November 7, 2001
November 7, 2001
October 13, 2001
September 2001
September 2001
8/21/2003
Communities which have Rejected Fluoridation Since 1990
Page 2 of3
.
BishoDville. South Carolina June 2001
Harper. Kansas May 31, 2001
Brewster, Massachusetts May 15, 2001
McPherson, Kansas April 3, 2001
Norridgewock, Maine May 5, 2001
Blue River, WISCOnsin February 2001
Willamina Oregon January 2001
Itha~.NewYork Novemberh2000
Spokane. Washington November 7, 2000
Brattleboro. Vermont November 7, 2000
Wenatchee, Washington November 7, 2000
Shawano. Wisconsin November 7, 2000
Nibly City, Utah November 7, 2000
Hyrwn City, Utah November 7, 2000
Providence City, Utah November 7, 2000
Smithfield City, Utah November 7, 2000
Logan City, Utah November 7, 2000
River Heights, Utah November 7, 2000
Pequannock. New Jersev November 7, 2000
Ozark, Missouri November 7, 2000
Wooster. Ohio November 7, 2000
Squamish, British Columbia, Canada October 16, 2000
Woodside. California September 2000
Ste. Genevieve. Missouri August 8, 2000
Wmfield, Kansas March 6, 2000
WUmington, Massachusetts February 15, 2000
Santa Barbara, California November 23, 1999
Johnstown, New York November 19,1999
Tooele, Utah November 2, 1999
Wichita, Kansas October 26, 1999
Bo~ Raton, Florida October 25, 1999
EI Carjon, California April 27, 1999
Escondido. California April 7, 1999
Helix Water District, California April 7, 1999
Lakeside Water District, California April 6, 1999
Hutchinson, Kansas March 30, 1999
Riverview Water Disbict, California March 24, 1999
La Mesa. California March 9, 1999
Santa Cruz, California March 4, 1999 ...banned
Bremerton, California February 2, 1999
Olympia, Washington December 15,1999
Seward, Nebraska November 3, 1998
Whitehorse, Yukon Territory, Canada July 28, 1998... quit after 30 years
Grand Island, Nebraska May 13, 1998... quit
Norfolk, Nebraksa May 13, 1998
North Platte, Nebraska May 13, 1998
Washington, Missouri April 7, 1998
Kitmat, British Columbia, Canada, Canada March 1998... quit
Hot Springs, Arkansas February 1998
Ridgefield, Oregon December 22, 1997
Largo, Florida July 15,1997
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http://www.f1uoridealert.org!communities.htm
8/21/2003
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Communities which have Rejected Fluoridation Since 1990
Page 3 of3
Clearwater, Florida July 15,1997
North Redington Beach, Florida July 15, 1997
Amsterdam, New York May 21,1997
Suisun City, California May 1, 1997
Yardly, Pennsylvannia April 16, 1997
Village of Orfordville, WISCOnsin December 9, 1996
Western Nassau County, New York November 21,1996... quit after 23 years
Kelowna, British Columbia, Canada November 16, 1996... quit after 42 years
Gothenberg, Nebraska December 1996
Bloomer, WISconsin November 6, 1996
Kodiak, Alaska July 12, 1996
Carle Place, New York February 1,1996,.. quit
Wmter Springs, Florida January 10, 1996
Pasco, Florida December 14, 1995
York, Pennsylvannia July 29,1995
Thurmont, Maryland February 3, 1994
Albany, New York December 8, 1994
Middletown, Maryland November 1993... quit
Sarnia, Ontario, Canada January 30, 1993
Barnstable, (Cape Cod) Massachusetts November 4, 1993
Wagoner, Oklahoma June 17,1993
Redwood Valley, California February 6, 1993
Los Altos Hills (Purissima) California 1993
Campbell River, British Columbia, Canada April 1993... quit after 33 years
Port Hardy, British Columbia, Canada November 1993... quit after 19 years
Squamish, British Columbia, Canada November 1993.., quit after 20 years
Fort Smith, Arkansas November 3, 1992
Milltown, WISCOnsin October 17,1992
Bellingham, Washington May 19, 1992
Comox/Courtenay, British Columbia, February 1992
Canada
Palm Beach County, Florida
Ketchikan, Alaska
Suffolk County, New York
Davis, California
Morgan Hill, California
October 22, 1991
October 2, 1991
August 15, 1991
December 14, 1990... 5th rejection
March 7, 1990... quit
Fluoride Action Network I 802-859-3363 I infola>fluoridealert.o~
http://www.f1uoridealert.org/communities.htm
8/21/2003
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Statements from European Health, Water & Environment Authorities on Water Fluoridati.,. Page 1 of 4
FLUORIDE
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Statements from European Health, Water, &
Environment Authorities on Water Fluoridation
UPDATE: On April 9, 2003, the City Parliament of Basel. Switzerland voted 73 to
23 to stop Basel's 41 year water fluoridation program. Basel was the only city in
Switzerland tofluoridate its water, and the only city in continental western Europe,
outside of afew areas in Spain. To learn more about Basel's decision, click here.
:-:~-:~~o:".:o:~~"o;o:<i:'lv.~-:-:-:o:o;~v.~~-:-:-:-:~o:~'to:-:-:o:o;o;-:-:-:";"';-:-:o;o;-:-:"i:o;o;o;"lo;-:-;-;,\-:0;-;-;-:-:-:-:-:0;0;-:-:-:-:0;-:-:-:-:-:-:-:-:-:-:-:-:0;0;0;-:-:-:-:-:-:-:-:-:-:0;-:-:-:-:-:-:-:-:-:-:-:-:-:-;-:-:0;0;";-:-:-:-:-:-:-:-:0;';-:-:-:-:-:-:0;-:-:-:-:-:-:-:'
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Germany:
"Generally, in Germany fluoridation of drinking water is forbidden. The relevant
German law allows exceptions to the fluoridation ban on application. The
argumentation of the Federal Ministry of Health against a general permission of
fluoridation of drinking water is the problematic nature of compuls[ory]
medication." (Gerda Hankel-Khan, Embassy of Federal Republic ofGermany,
September 16,1999). www.fluoridealert.org/germany.iDeg
II
France:
"Fluoride chemicals are not included in the list [of 'chemicals for drinking water
treatment']. This is due to ethical as well as medical considerations." (Louis Sanchez,
Directeur de la Protection de l'Environment, August 25, 2000).
www.fluoridealert.org/france.ipeg
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Belgium:
''This water treatment has never been of use in Belgium and will never be (we hope so)
into the future. The main reason for that is the fundamental position of the drinking
water sector that it is not its task to deliver medicinal treatment to people. This is the
sole responsibility of health services." (Chr. Legros, Directeur, Belgaqua, Brussels,
Belgium, February 28,2000). www.fluoridation.com/c-belgium.htm
Luxembourg:
"Fluoride has never been added to the public water supplies in Luxembourg. In our
views, the drinking water isn't the suitable way for medicinal treatment and that people
needing an addition of fluoride can decide by their own to use the most appropriate
way, like the intake of fluoride tablets, to cover their [daily] needs." (Jean-Marie RIES,
Head, Water Department, Administration De L'Environment, May 3,2000).
www.fluoridealert.org/luxembourg.ipeg
http://www.fluoridealert.org/govt-statements.htm
8/21/2003
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Statements from European Health, Water & Environment Authorities on Water Fluoridati... Page 2 of 4
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Finland:
"We do not favor or recommend fluoridation of drinking water. There are better ways
of providing the fluoride our teeth need." (Paavo Poteri, Acting Managing Director,
Helsinki Water, Finland, February 7, 2000). www.fluoridation.com/c-finland.htm
"Artificial fluoridation of drinking water supplies has been practiced in Finland only in
one town, Kuopio, situated in eastern Finland and with a population of about 80,000
people (1.6% of the Finnish population). Fluoridation started in 1959 and finished in
1992 as a result of the resistance of local population. The most usual grounds for the
resistance presented in this context were an individual's right to drinking water without
additional chemicals used for the medication of limited population groups. A concept of
"force-feeding" was also mentioned.
Drinking water fluoridation is not prohibited in Finland but no municipalities have
turned out to be willing to practice it. Water suppliers, naturally, have always been
against dosing of fluoride chemicals into water." (Leena H iisvirta, M.Sc., Chief
Engineer, Ministry of Social Affairs and Health, Finland, January 12,1996.)
www.fluoridealert.ora/finland.fpeg
...
...
Denmark:
"We are pleased to inform you that according to the Danish Ministry of Environment
and Energy, toxic fluorides have never been added to the public water supplies.
Consequently, no Danish city has ever been fluoridated." (Klaus Werner, Royal Danish
Embassy, Washington DC, December 22,1999). www.f1.uoridation.com/c-
denmark.htm
1:-:::.
II"
Norway:
"In Norway we had a rather intense discussion on this subject some 20 years ago, and
the conclusion was that drinking water should not be fluoridated." (Truls Krogh & Torii
Hofshagen, FolJcehelsa Statens instituttfor folkeheise (National Institute of Public
Health) Oslo, Norway, March 1, 2000). www.fluoridation.com/c-norway.htm
.....
1I11~...'.'" v:::l:
Sweden:
"Drinking water fluoridation is not allowed in Sweden...New scientific documentation
or changes in dental health situation that could alter the conclusions of the
Commission have not been shown." (Gunnar Guzikowski, Chief Government
Inspector, Livsmedels Verket -- National Food Administration Drinking Water
Division, Sweden, February 28,2000). www.fluoridation.com/c-sweden.htm
(See statement blJ Dr. Arvid Carlsson. the Nobel Laureate in Medicine, who helped
lead the campaign to preventjluoridation in Sweden in the late 19705.)
http://www.fluoridealert.org!govt-statements.htm
8/21/2003
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Statements from European Health, Water & Environment Authorities on Water Fluoridati... Page 3 of 4
Netherlands:
"From the end of the 1960s until the beginning of the 1970S drinking water in various
places in the Netherlands was fluoridated to prevent caries. However, in its judgement
of 22 June 1973 in case No. 10683 (Budding and co. versus the City of Amsterdam) the
Supreme Court (Hoge Road) ruled there was no legal basis for fluoridation. After that
judgement, amendment to the Water Supply Act was prepared to provide a legal basis
for fluoridation. During the process it became clear that there was not enough support
from Parlement [sic] for this amendment and the proposal was withdrawn." (Wilfred
Reinhold, LegalAdvisor, Directorate Drinking Water, Netherlands, January 15,
2000). www.fluoridation.com/c-netherlands.htm
'"
--r-
Northern Ireland:
"The water supply in Northern Ireland has never been artificially fluoridated except in
2 small localities where fluoride was added to the water for about 30 years up to last
year. Fluoridation ceased at these locations for operational reasons. At this time, there
are no plans to commence fluoridation of water supplies in Northern Ireland." (G.J.
Grimes, Departmentfor Regional Development, Belfast, November 6, 2000).
www,fluoridealert.org/Northern-lreland.ipeg
Austria:
"Toxic fluorides have never been added to the public water supplies in Austria." (M.
Eisenhut, Head of Water Department, Osterreichische Yereinigung fur das Gas-und
Wasserfach Schubertring 14, A-1015 Wien, Austria, February 17, 2000).
www.fluoridation.com/c-austria.htm
..
Czech Republic:
"Since 1993, drinking water has not been treated with fluoride in public water supplies
throughout the Czech Republic. Although fluoridation of drinking water has not
actually been proscribed it is not under consideration because this form of
supplementation is considered:
· uneconomical (only 0.5496 of water suitable for drinking is used as such; the
remainder is employed for hygiene etc. Furthermore, an increasing amount of
consumers (particularly children) are using bottled water for drinking
(underground water usually with fluor)
· unecological (environmental load by a foreign substance)
. unethical ("forced medication")
· toxicologically and phyiologically debateable (fluoridation represents an
untargeted form of supplementation which disregards actual individual intake
and requirements and may lead to excessive health~threatening intake in
certain population groups; [and] complexation of fluor in water into non
biological active forms of fluor." (Dr. B. Havlik, Ministerstuo Zdravotnictui
Geske Republiky, October 14,1999). www.fluoridealert.ora/czech.ioeg
http://www.fluoridealert.orglgovt-statements.htm
8/21/2003
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The Phosphate Fertilizer Industry: An Environmental Ovetview
Page 1 of 12
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The Phosphate Fertilizer Industry:
An Environmental Overview
by Michael Connett
Fluoride Action Network
May 2003
1) Introduction
2) Effects of Fluoride Pollution
3) Litigation from Fluoride Damage
4) Scrubbing aw~ the problem
5) A Missed Opportunity: Little Demand for Silicofluorides
6) Fluoridation: "An ideal solution to a long-standing problem"?
7) Recent Findine:s on Silicofluorides
8) Gvpsum Stacks & 'Slime Ponds'
9) Radiation Hazard
10) Will radioactive gypsum be added to roads?
11) Commercial Uranium Production
12) Cold War Secrets & Worker Health
13) Wastewater Issues
14) References
15) Photographs of the Phosphate Industry
16) Further Reading
1) Introduction (back to tOD)
They call them "wet scrubbers" - the pollution control devices used by the phosphate
industty to capture fluoride gases produced in the production of commercial fertilizer.
In the past, when the industty let these gases escape, vegetation became scorched,
crops destroyed, and cattle crippled.
Today, with the development of sophisticated air-pollution control technology, less of
the fluoride escapes into the atmosphere, and the type of pollution that threatened the
survival of some communities in the 1950S and 60S, is but a thing of the past (at least
in the US and other wealthy countries).
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.
However, the impacts of the industry's fluoride emissions are still being felt, although
more subtly, by millions of people - people who, for the most part, do not live anywhere
near a phosphate plant.
That's because, after being captured in the scrubbers, the fluoride acid
(hydrofluorosilicic acid), a classified hazardous waste, is barreled up and sold,
unrefined, to communities across the country. Communities add hydrofluorosilicic acid
to their water supplies as the primary fluoride chemical for water fluoridation.
Even if you don't live in a community where fluoride is added to water, you'll still be
getting a dose of it through cereal, soda, juice, beer and any other processed food and
drink manufactured with fluoridated water.
Meanwhile, if the phosphate industry has its way, it may soon be distributing another
of its by-products to communities across the country. That waste product is radium,
which may soon be added to a roadbed near you - if the EP A buckles and industry has
its way.
2) Effects of Fluoride Pollution (backtotopl
Central Florida knows it well. So too does Garrison Montana, Cubatao Brazil, and any
other community where phosphate industries have had inefficient, or non-existent,
pollution control: Fluoride.
The Canadian Broadcasting Corporation (GBe) called the phophate industry a
"pandora's box." That, while it brought wealth to rural communities, it also brought
ecological devastation. The GBG described the effects of one particular phosphate plant
in Dunville, Ontario:
.
"Farmers noticed it first... Something mysterious burned the peppers,
burned the fruit, dwarfed and shriveled the grains, damaged everything
that grew. Something in the air destroyed the crops. Anyone could see
it... They noticed it first in 1961. Again in '62. Worse each year. Plants
that didn't burn, were dwarfed, Grain yields cut in half...Finally, a
greater disaster revealed the source of the trouble. A plume from a silver
stack, once the symbol of Dunville's progress, spreading for miles
around poison - fluorine. It was identified by veterinarians. There was
no doubt. What happened to the cattle was unmistakable, and it broke
the farmer's hearts. Fluorosis - swollen joints, falling teeth, pain until
cattle lie down and die. Hundreds of them. The cause - fluorine
poisoning from the air."
Fluoride has been, and remains to this day, one of the largest environmental liabilities
of the phosphate industry. The source of the problem lies in the fact that raw
phosphate ore contains high concentrations of fluoride, usually between 20,000 to
40,000 parts per million (equivalent to 2 to 4% of the ore).
When this ore is processed into water-soluble phosphate (via the addition of sulfuric
acid), the fluoride content of the ore is vaporized into the air, forming highly toxic
gaseous compounds (hydrogen fluoride and silicon tetrafluoride).
In the past, when the industry had little, if any, pollution control, the fluoride gases
were frequently emitted in large volumes into surrounding communities, causing
serious environmental damage.
.
In Polk County. Florida, the creation of multiple phosphate plants in the 1940S caused
damage to nearly 25,000 acres of citrus groves and "mass fluoride poisoning" of cattle.
It is estimated that, as a result of fluoride contamination, "the cattle population of Polk
County dropped 30,000 head" between 1953 and 1960, and "an estimated 150,000
acres of cattle land were abandoned" (Linton 1970).
According to the former president of the Polk County Cattlemen's Association:
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The Phosphate Fertilizer Industry: An Environmental Overview
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"Around 1953 we noticed a change in our cattle... We watched our cattle
become gaunt and starved, their legs became deformed; they lost their
teeth. Reproduction fell off and when a cow did have a calf, it was also
affected by this malady or was a stillborn" (ibid).
In the 1960s, air pollution emitted by another phosphate plant in Garrison, Montana
was severe enough to be branded "the worst in the nation" by a 1967 National Air
Pollution Conference in Washington, D.C.
As in Polk County, and other communities downwind of fluoride emissions. the cattle
in Garrison were poisoned by fluoride. As described in a 1969 ~ from Good
Housekeeping:
"The blight had afflicted cattle too. Some lay in the pasture, barely able
to move. Others limped and staggered on swollen legs, or painfully sank
down and tried to graze on their knees... Ingested day after day, the
excessive fluoride had caused tooth and bone disease in the cattle, so
that they could not tolerate the anguish of standing or walking. Even
eating or drinking was an agony. Their ultimate fate was dehydration,
starvation - and death."
3) Litigation from Fluoride Damage (back to top)
Damage to vegetation and livestock, caused by fluoride emissions from large industry,
has resulted, as one might expect, in a great deal of expensive litigation. In 1983, Dr.
Leonard Weinstein of Cornell University, stated that" certainly, there has been more
litigation on alleged damage by fluoride than all other pollutants combined" (Weinstein
1983). While Weinstein was referring to fluoride pollution in general, his comments
give an indication of the problem facing the phosphate industry - one of the most
notorious emitters of fluoride - in its early days.
So too does an estimate from Dr. Edward Groth, currently a Senior Scientist at
Consumers Union. According to an article written by Groth, fluoride pollution between
the years 1957 to 1968, "was responsible for more damage claims against industry than
all twenty (nationally monitored air pollutants) combined."
The primary reason for the litigation against fluoride emitters was "the painful,
economically disastrous, debilitating disease" that fluoride causes to livestock (Hodge
& Smith 1977). As noted in a 1970 review by the US Deparbnent of Agriculture (USDA),
"Airborne fluorides have caused more worldwide damage to domestic
animals than any other air pollutant" (Lillie 1970).
Another review on air pollution reached the same conclusion. According to Ender
(1969):
"The most important problem concerning damage to animals by air
pollution is, no doubt, the poisoning of domestic animals caused by
fluorine in smoke, gas, or dust from various industries; industrial
fluorosis in livestock is today a disorder well known by veterinarians in
all industrialized countries. II
According to a review discussing "Fluorine toxicosis and industry", Shupe noted that:
"Air pollution damage to agricultural production in the United States in
1967 was estimated at $500,000,000. Fluoride damage to livestock and
vegetation was a substantial part of this amount" (Shupe 1970).
4) Scrubbing away the problem (back to top)
Due to the inevitable liabilities that fluoride pollution presented, and to an increasingly
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The Phosphate Fertilizer Industry: An Environmental Overview
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stringent set of environmental regulations, the phosphate industry began cleaning up
its act.
As noted by Ervin Bellack, a chemist for the US Public Health Service:
"In the manufacture of super-phosphate fertilizer, phosphate rock is
acidulated with sulfuric acid, and the fluoride content of the rock
evolves as volatile silicofluorides. In the past, much of this volatile
material was vented to the atmosphere, contributing heavily to
pollution of the air and land surrounding the manufacturing site. As
awareness of the pollution problem increased, scrubbers were added to
strip particulate and gaseous components from the waste
gas..." (Bellack 1970)
A 1979 review, published in the jounUu Phosphorous & Potassium, added:
"The fluorine compounds liberated during the acidulation of phosphate
rock are now rightly regarded as a menace and the industry is now
obliged to suppress emissions-containing vapors to within very low
limits in most parts of the world...
In the past, little attention was paid to the emission of gaseous fluorine
compounds in the fertilizer industry. But today fluorine recovery is
increasingly necessary because of stringent environmental restrictions
which demand drastic reductions in the quantities of volatile and toxic
fluorine compounds emitted into the waste gases. These compounds
now have to be recovered and converted into harmless by-products for
disposal or, more desirably, into marketable products" (Denzinger
1979).
5) A Missed Opportunity: Little Demand for Silicotluorides (back to top)
Considering the great demand among big industry for fluoride chemicals as a material
used in a wide variety of commercial products and industrial processes, the phosphate
industry could have made quite a handsome profit selling its fluoride wastes to
industry. This was indeed the hope among some industry analysts, including the
authors of the review noted above (Denzinger 1979).
However, the US phosphate industry has thus far been unable to take advantage of this
market. The principal reason for this failure stems from the fact that fluoride captured
in the scrubbers is combined with silica. The resulting silicofluoride complex has, in
turn, proved difficult for the industry to separate and purify in an economically-viable
process.
As it now stands, silicofluoride complexes (hydrofluorosilicic acid & sodium
silicofluoride) are of little use to industry.
Thus, while US industry continues to satisfy its growing demand for high-grade
fluoride chemicals by importing calcium fluoride from abroad (primarily from Mexico,
China, and South Africa), the phosphate industry continues dumping large volumes of
fluoride into the acidic wastewater ponds that lie at the top of the mountainous waste
piles which surround the industry.
In 1995, the Tampa Tribune summed up the situation as follows:
"The U.S. demand for fluorine, which was 400,000 tons, is expected to
jump 25 percent by next year... Even though 600,000 tons of fluorine
are contained in the 20 million tons of phosphate rock mined in Florida,
the fluorine market has been inaccessible because the fluorine is tied up
with silica, a hard, glassy material."
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Of course, not all of the phosphate industry's fluoride waste is disposed of in the ponds.
As noted earlier, the phosphate industry has found at least one regular consumer of its
silicofluorides: municipal water-treatment facilities.
According to recent estimates. the phosphate industry sells approximately 200,000
tons of silicofluorides (hydrofluorosilicic acid & sodium silicofluoride) to US
communities each year for use as a water fluoridation agent (Coplan & Masters 2001).
6) Fluoridation: "An ideal solution to a long-standing problem"? (back to tOD)
In 1983, Rebecca Hanmer, the Deputy Assistant Administrator for Water at the US
Environmental Protection Agency, described the policy of using the phosphate
industry's silicofluorides for fluoridation as follows:
"In regard to the use of fluosilicic acid as the source of fluoride for
fluoridation, this agency regards such use as an ideal solution to a long
standing problem. By recovering by-product fluosilicic acid from
fertilizer manufacturing, water and air pollution are minimized, and
water authorities have a low-cost source of fluoride available to
them." (See letter)
Another EP A official, Dr. J. WIlliam Hi14y, the current Senior Vice-President of EP A
Headquarters Union, recently expressed a different view on the matter. According to
Hirzy:
"'If this stuff gets out into the air, it's a pollutant; if it gets into the river,
it's a pollutant; if it gets into the lake it's a pollutant; but if it goes right
into your drinking water system, it's not a pollutant. That's amazing...
There's got to be a better way to manage this stuff' (Hirzy 2000).
7) Recent Findings on Silicotluorides (back to top)
Adding to Hirzy's, and the EP A Union's, concerns are three recent findings.
First and foremost are two recent studies reporting a relationship between water
treated with silicofluorides and elevated levels oflead in children's blood (Masters &
Coplan 1999, 2000). The authors of these studies speculate that the silicofluoride
complex may increase the uptake oflead (derived from other environmental sources,
such as lead paint) into the bloodstream.
The second finding is the recent, and quite remarkable concession from the EP A, that
despite 50 years of water fluoridation, the EP A has no chronic health studies on
silicofluorides. All safety studies on fluoride to date have been conducted using
pharmaceutical-grade sodium fluoride, not industrial-grade silicofluorides. A similar
concession has also been obtained from the respective authorities in England.
The defense made by agencies promoting water fluoridation, such as the US Centers
for Disease Control, to the lack of such studies, is that when the silicofluoride complex
is diluted into water, it dissociates into free fluoride ions or other fluoride compounds
(e.g. aluminum-fluoride), and thus the treated water, when consumed, will have no
remaining silicofluoride residues (Urbansky & Schock, 2000).
This argument, while supported by a good deal of theoretical calculation is backed by a
notable lack oflaboratory data. Moreover, a recently obtained and translated PhD
dissertation from a German chemist (Westendorf 1975) contradicts the claims.
According to the dissertation, not only do the silicofluorides not fully dissociate, the
remaining silicofluoride complexes are more potent inhibitors of cholinesterase, an
enzyme vital to the functioning of the central nervous system.
The third finding, although perhaps of less concern, is that the silicofluorides, as
obtained from the scrubbers of the phosphate industry, contain a wide variety of
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The Phosphate Fertilizer Industry: An Environmental Overview
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impurities present in the process water - including arsenic, lead, and possibly
radionuclides. While these impurities occur at low concentrations, especially after
dilution into the water, their purposeful addition to water supplies directly violates
EPA public health goals. For instance, the EPA's Maximum Contaminant Level Goal for
arsenic, a known human carcinogen, is 0 parts per billion. However, according to the
National Sanitation Foundation. the addition of silicofluorides to the water supply will
add, on average, about 0.1 to 0.43 ppb, and as much as 1.6 ppb, arsenic to the water.
As noted by the Salt Lake Tribune.
"Those who had visions of sterile white laboratories when they voted for
fluoride weren't thinking of fluorosilicic acid. Improbable as this
sounds, much of it is recovered from the scrubbing solution that scours
toxins from smokestacks at phosphate fertilizer plants."
8) Gypsum Stacks & 'Slime Ponds' Cbackto top)
To make 1 pound of commercial fertilizer, the phosphate industry creates 5 pounds of
contaminated. phosphogypsum slurry (calcium sulfate). This slurry is piped from the
processing facilities up into the acidic wastewater ponds that sit atop the mountainous
waste piles known as gypsum stacks. (See photos)
According to the EPA, ~2 million tons of new gypsum waste is created each year by the
phosphate industry in Central Florida alone. (Central Florida is the heart of the US
phosphate industry). The EPA estimates that the current stockpile of waste in Central
Florida's gypsum stacks has reached "nearly 1 billion metric tons." (The average
gypsum stack takes up about 135 acres of surface area - equal to about 100 football
fields - and can go as high as 200 feet,)
9) Radiation Hazard Cbacktotop)
It is sort of a misnomer, however, to call these stacks "gypsum" stacks. Indeed, if the
stacks were simply gypsum, they probably wouldn't exist, as gypsum can be readily
sold for various purposes (e.g. as a building material). What can't be readily sold,
however, is radioactive gypsum, which is about the only type of gypsum the phosphate
industry has to offer.
The source of the gypsum's radioactivity is the presence of uranium, and uranium's
various decay products (i.e. radium), in raw, phosphate ore. As noted. by the Sarasota
Herald Tribune
"there is a natural and unavoidable connection between phosphate
mining and radioactive material. It is because phosphate and uranium
were laid down at the same time and in the same place by the same
geological processes millions of years ago. They go together. Mine
phosphate, you get uranium."
While uranium, and its decay-products, naturally occur in phosphate ore, their
concentrations in the gypsum waste, after the extraction of soluble phosphate, are up
to 60 times greater.
The gypsum has therefore been classified. as a "Naturally Occurring Radioactive
Material". or NORM waste, although some, including the EPA, have questioned.
whether this classification understates the problem. According to the Tampa Tribune,
the gypsum "is among the most concentrated. radioactive waste that comes from
natural materials."
It is so concentrated, in fact, that "it can't be dumped. at the one landfill in the country
licensed to take only NORM waste."
Thus, according to US News & World Report, the EPA is currently "weighing whether
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to classify the gypsum stacks as hazardous waste under federal statutes, which would
force the industry to provide strict safeguards" (to nearly 1 billion tons of waste).
One of EPA's main concerns with gypsum stacks centers around the fact that radium-
226 breaks down into radon gas. When radon gas is fonned, it can become airborne,
leading to potentially elevated exposures downwind of the stacks. Such airborne
exposures are of particular concern to areas like Progress Village. Florida. where "a
new gypsum stack is rising a few hundred yards from a grade school."
According to US News & World Report, there is evidence to suggest that cancer rates
downwind of the stacks may be elevated. A 1995 ~ in the magazine stated:
"Some epidemiological studies suggest that lung cancer rates among
nonsmoking men in the phosphate region are up to twice as high as the
state average. Acute leukemia rates among adults are also double the
average. An industry-sponsored study of male phosphate workers,
however, found lung cancer rates no higher than the state average.
There is no proof that mine wastes cause cancer, but the evidence is
worrisome."
10) Will radioactive gypsum be added to roads? (back to tOD)
With the growing realization that gypsum stacks represent a serious environmental
threat to Central Florida, both now and for generations to come, the phosphate
industry has been looking into ways of reducing the size of the stacks (and the size of
their liability.)
In an interesting parallel to fluoride, the phosphate industry is looking to turn its
gypsum waste into a marketable product: as a potential cover for landfills, as a soil
conditioner, and as a base material for roads.
According to Robert Vanderslice, head of Phosphate Management for Florida's
Department of Environmental Protection, the gypsum is a "good material to replace
lime rock in roads, Lime rock will run out at some time, and we're still building a lot of
roads. Building roads with phosphogypsum would consume quite a bit of gypsum."
In 1995, a "Phosphogypsum Fact-Finding Forum" organized by the Florida Institute of
Phosphate Research, presented a "message aimed straight at Washington: Relax the
rules on using gypsum and the mountains will gradually disappear."
As of yet, however, the EPA does not appear willing to relax its rules and lift its ban on
commercial uses of gypsum. According to the Tampa Tribune, "EPA's limit for use is 10
picocuries of radium per gram, well below the levels usually found in the mounds."
A recent statement from the EPA reads:
"Only two uses (for the gypsum) are pennitted: limited agricultural use
and research. Other uses may be proposed, but otherwise the
phosphogypsum must be returned to mines or stored in stacks."
11) Commercial Uranium Production (back to tOD)
While the presence of uranium decay-products makes gypsum a tough sell for the
phosphate industry, the uranium has, at various times, presented the industry with a
business opportunity of its own.
One of the lesser-known-facts about the phosphate industry is that its processing
facilities have produced and sold sizeable quantities of uranium.
In 1997, just two phosphate plants in Louisiana produced Q!>O.ooo pounds of
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commercial uranium, which amounted to roughly 16% of the domestically produced
uranium in the US.
In 1998, the same two plants produced another 950,000 pounds, but due to declining
market prices for uranium, both plants have since ceased production.
If market prices improve, however, 4 US phosphate plants (2 in Louisiana & 2 in
Florida) would have the capacity to produce a combined 2.75 million pounds of
uranium per year, according to the Department of Energy (DOE). The DOE has termed
these 4 facilities "Nonconventional Uranium Plants."
12) Cold War Secrets & Worker Health (back to tOD)
The Department of Energy has not always been so open about the uranium-making
potential of the phosphate industry. During the Cold War, its predecessor institution,
the Atomic Energy Commission (AEC), kept this fact closely under wraps - even to the
workers who were, unknowingly, handling large quantities of the radioactive material.
In Joliet. Illinois, it has only recently come to light that the local phosphate plant had
secretly produced some 2 million pounds of uranium for the US government in the
years 1952 to 1962. According to local newspaper reports. the cancer rates of people
who worked at the plant, especially "Building 51\" where the uranium was processed,
are unusually high.
"We used to kind of joke that if you worked for Blockson, you got cancer," quipped
Vmce Driscoll, the son of a cancer-stricken worker.
Today, with the Cold War over, it is becoming clear that workers in the phosphate
industry need special protection. According to a report from the European
Commission:
" Processing and waste handling in the phosphate industry is associated
with radiation levels of concern for workers and the public. The level of
protection for these groups should be more similar to the level of
protection that is state of the art in other industries, particularly the
nuclear industry."
13) Wastewater Issues (backtotoD)
While the radioactivity of the gypsum stacks has probably been the key health concern
of the EP A, it is not the only one.
Resting atop the phosphate industry's gypsum piles are highly-acidic wastewater
ponds, littered with toxic contaminants, including fluoride, arsenic, cadmium,
chromium, lead, mercury, and the various decay-products of uranium. This
combination of acidity and toxins makes for a poisonous, high-volume, cocktail, which,
when leaked into the environment, wreaks havoc to waterways and fish populations. As
noted by the St. Petersb~ Times. "Spills from these stacks have periodically poisoned
the Tampa Bay environs. "
One spill, in 1997, from a now-defunct gypsum stack in Florida, "killed more than a
million fIsh."
"Strike the Alafia River off your list of fishing spots," wrote one iournalist after the spill.
"It's gone, dead as a sewer pipe, killed by the carelessness of yet another phosphate
company."
Today, the same gypsum stack which caused this particular spill, is considered by
Florida's Department of Environmental Protection to be "the most serious pollution
threat in the state." That's because tropical rains over the past couple of years have
brought the wastewater to the edge of the stack's walls.
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As noted by the Tampa Tribune. "The gypsum mound is near capacity, and a wet spring
or a tropical storm could cause a catastrophic spill."
To prevent such a spill, which was all but inevitable, the EP A recently agreed to let
Florida pursue "Option Z": To load 500-600 million gallons of the wastewater onto
barges and dump it directly into the Gulf of Mexico.
The dumping of the wastewater into the Gulf represents the latest in a series of high-
profile embarrasments for Florida's phosphate industry; one of the most dramatic of
which happened on June 15, 1994.
On that day, a massive, IS-story sinkhole appeared in the middle of an 80 million ton
gypsum stack. The hole was so big that, according to US News & W orId Report. it
"could be as big as 2 million cubic feet, enough to swallow 400 railroad
boxcars. Local wags call it Disney World's newest attraction -- 'Journey
to the Center of the Earth. ...
But, as US News noted,
"there's nothing amusing about it. The cave-in dumped 4 million to 6
million cubic feet of toxic and radioactive gypsum and waste water into
the Floridan aquifer, which provides 90 percent of the state's drinking
water. "
And so it goes.
As summarized by the Tampa Tribune:
"It's not like you can padlock the doors and walk away. The complexities
of keeping a phosphate processing plant operating are becoming clear
to government regulators now overseeing two of them. Ponds full of 1.5
billion gallons of acid and three mountains of radioactive waste mean
you just can't shut off the machinery and turn out the lights. The state
could be stuck with the plants for years. And taxpayers would be stuck
with the tab."
...................................................................................................................................................................................................................................................................................................................................................................................
14) REFERENCES (back to tOll)
Full citations of the studies listed above, can be accessed at:
htt;p: / /www.fluoridealert.org/phosphate/overview-refs.htm
Note: Full-text copies of all newspaper articles cited in this article can be accessed by
clicking on the links within the text.
.................................................................................................................................................................................................................................................................................................................................................v........""".............................................v.................
15) PHOTOGRAPHS OF THE PHOSPHATE INDUSTRY (back to top)
Photographs of the phosphate industry are available at:
htt;p: / /www.fluoridealert.org/phosphate/photographs.htm
..."..""""...,...""...""".......".............."".."...............".."............".."....~....................""..""..""...."............................".........."............................"...."............................"........."""....."....................".......".....................,...............,...........................
16) FURTHER READING (back to tOll)
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Page 10 of 12
.
(Many thanks to Anita Knightfor continually supplying FAN with newspaper articles
on the phosphate industry in Florida.)
Fluoride Pollution Issues
.
. Stu<!y to Address Cancer. Bone Problems. & Other Health Concerns Near
Coronet Tampa Tribune July 13, 2003
· Neighbors fear health effects of blowing gypsum The Edmonton Journal June
14, 2003
. Fears over level of toxic fluoride: Homegrown produce threatened by emissions
Otago Daily Times (New Zealand) June 9, 2003
· Concerns over high levels of fluoride - Otago Daily Times (New Zealand) June
4, 2003
· Oswal Phosphate Plant facing Closure due to Fluoride Contamination - India
Business Insight June 13 & 18,2002
. Investigation into Buffalo deaths near Phosphate plant - The Hindu December
9, 2002
. Superfund site might pose greater risk. legal fight shows Pensacola News
Journal (Florida) September 15, 2002
. Air of Death Canadian Broadcasting Company 1967
. The Town that Refused to Die Good Housekeeping January 1969.
. Death in the Air: Air Pollution from Phosphate Fertilizer Production
Synthesis/Regeneration Fall 2002
· Terracide: America's Destruction of Her Living Environment Ron M. Linton,
Little, Brown and Company, 1970
· Fluoride-tainted Pasture Grass May Harm Cattle The Tampa Tribune February
16,1984
· Air Pollution from Stauffer Chemical Phosphate Plant Ombudsman Report,
Agencyfor Toxic Substances and Disease Registry, December 29,2000
· Old plant may contaminate Anclote River. report says Tampa Tribune March
21,1994
. EP A Amends Phosphoric Acid and Fertilizer Rules Chemical Engineering
Progress August 1,2002
· A host of roasted daffodils - The Guardian (UK) December 15,1988
· Technology Developed to Capture HF Emissions from Phosphate Ponds Tampa
Tribune April 17, 1993
· Keysville air quali1;y to be monitored East Hillsborough Tribune January 20,
1986
· Assessment of the vegetation risk by fluoride emissions from fertiliser
industries at Cubatao. Brazil Science of the Total Environment 1996
· Chromosomal aberrations and micronuclei in lymphocytes of workers at a
phosphate fertilizer factory Mutation Research, Volume 393, 1997
· Sedimentary Fluorite in TamDa Bav. Florida Environmental Letters, Vol. 60,
1974
· Fluorine Recovery in the Phosphate Indust:Iy: a review Phosphorous &
Potassium #103 SEPI'/Ocr 1979, pages 33-39.
· Recovery of fluosilicic acid and fluoride bearing waters for the production of a
mixture of silica and precipitated calcium fluoride usable for the Droduction of
~ International Fertilizer Industry Association's 2000 Technical
Conference in New Orleans
Fluoridation Chemicals
.
· What's in the Water? - Salt Lake Tribune June 16,2002
· Dartmouth Researcher Warns of Chemicals Added to Drinking Water
Dartmouth News March 15, 2001
· EPA Admits to Having No Studies on the Health Effects of Silicofluorides Letter
from EPA s Robert Thurnau to Roger Masters, November 16,2000
· Fluoridation Chemicals Have Not Been Safety Tested - Here's the Proof
NationalPure Water Association (UK) August 2002
· A Resolution on the Silicofluoride Controversy Dr. Robert Carton & Myron
Coplan, 2001 (Resolution submitted to the American Public Health Association
for consideration at October 21-25, 2001 conference in Atlanta, Georgia)
· The Official Spinninl!: of Pollution into an Elixir George Glasser 2000
· Letter from Rebecca Hanmer. EPA's Depu1;y Assistant Administrator for Water.
http://www.fluoridealeft.org/phosphate/overview.htm
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The Phosphate Fertilizer Industry: An Environmental Overview
Page 11 of 12
~.
.
Phosphogypsum Stacks
· About Phosphogypsum US Environmental Protection Agency
· FreqJ,lently Asked Questions US Environmental Protection Agency
· Waste bvpassesfedecal regulation despite radioactivity Tampa Tribune July 21
1991
· Tally conference will debate use of phosphate byproduct Tampa Tribune
December 3,1995
· G)'psum finds ecological concerns stacked against it The Tampa Bay Business
Journal December 6, 1996
Wastewater Issues
.
· DEP says Piney Point bil!:e:est threat to environment - The Herald Tribune June
25,2003
· Waste Water Heading To Gulf With Federal OK - Tampa Tribune April 11, 200;:;
· !'loo-million gallons of acidic waste headine: to gulf - St. Petersburg Times April
5, 2003
· G)'psum Stacks Cleanup Costly - Tampa Tribune March 15,2003
· Dumping Acidic Water In Gulf Is Best Of Dismal Alternatives - Tampa Tribune
February 22, 2003
· DEP Aims To Up Dump In Bay - Tampa Tribune January 10,2003
· DEP let phosphate waste flow into preserve - St. Petersburg Times November
22, 2001
· Phosphate Disch~e to Resuine Tampa Tribune December 14, 2001
· Groups seek solution for wastewater woes - Bradenton Herald December 11,
2001
· Mulbeny bailout tops $lM - Herald Tribune Newscoast June 17, 2001
· Phosphate plants under close eye Tampa Tribune March 17,2001
· Sinkholes and Stacks; Neighbors claim Florida's Phosphate Mines are a Hazard
US News & World Report June 12,1995
· Coronet Working to Control Arsenic Tampa Tribune December 30, 2002
· Phosphate industry hits another low Tampa Tribune December 19,1997
Fluoride & Radon Air Emisionsfrom Waste Ponds
· Neighbors fear health effects of blowing gypsum The Edmonton Journal June
14, 2003
· Regional planners OK phosphate gypsum stack Tampa Tribune August 23,
1994
· Fluoride-tainted Pasture Grass May Harm Cattle The Tampa Tribune February
16,1984
· Gaseous Fluoride Emissions from GVDSum Settling and Cooling Ponds Florida
Scientist Vol. 50 NO.2 Spring 1987 No, 2
· Technology Developed to Capture HF Emissions from Phosphate Ponds Tampa
Tribune April 17, 1993
Radiation Hazards
.
· Cancer mvsterv deepens: Uranium secret long al!:o in Joliet area. prompts
Q!lestions - The Herald News October 1,2001
· Buildinl!: !\/): Was a killer in our midst? - The Herald News September 17, 2000
· Radiation victims urged to file claims - The Herald News July 19, 2001
· Workers share stories about health woes - The Herald News April 3, 2001
· Waste bvpasses federal regulation despite radioactivily Tampa Tribune July 21,
1991
· Tallv conference will debate use of phosphate byproduct Tampa Tribune
December 3,1995
· Sinkholes and Stacks; Neighbors claim Florida's Phosphate Mines are a Hazard
US News & World Report June 12, 1995
· Phosphate mining lega<tYfeared Sarasota Herald Tribune June 14, 1995
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Ine t'nospnate l'ertll1zer InduStry: An Environmental Overview
Page 12 of 12
. About Phosphogypsum US Environmental Protection Agency
. Frequently Asked Ouestions US Environmental Protection Agency
. Yellowcake Production at Stauffer Chemical from Agencyfor Toxic Substances
and Disease Registry, Ombudsman Report of Findings and Recommendations
Regarding the Stauffer Chemical Company Site Tarpon Springs, Florida,
December 29, 2000
. Handling of radium and uranium contaminated waste piles and other wastes
from phosphate ore processing Nuclear Science and Technology, Report EUR
15448 EN European Commission, Luxembourg 1995.
. Eastern Michaud Flats ContaIninationAgencyfor Toxic Substances and
Disease Registry, Superfund Site Assessment Branch, October 21,1998
· A Study of Radium-226 and Radon-222 Concentrations in Ground Water Near
a Phosphate Mining and Manufacturing Facility The Water Resources Research
Institute March 1984
Mining Issues
· A mining showdown at Horse Creek - St. Petersburg Times November 12, 2001
. Opposition builds to stop mine - St. Petersburg Times June 18, 2001
· Campahm to protect creek has few allies - St. Petersburg Times July 20,1999
· Mining Threat - St. Petersburg Times June 20, 2001
. Reclaimed mine is not as safe as once thought - Tallahassee Democrat
February 17,2002
· One Third of Fish Species in Peace River May be Histoiy Sun Herald February
9, 2002
· Sheep Herd Dies from Contamination at Phosphate Mine Articles from Idaho
State Journal July 2001
· A Study of Radium-226 and Radon-222 Concentrations in Ground Water Near
a Phosphate Mining and Manufacturing Facility The Water Resources Research
Institute March 1984
Politics/Greenwashing
· Florida Institute of Phosphate Research Accused of Whitewashing The Ledger
January 14, 2002
· Phosphate industry aims to be corporate neighbor Herald Sun (Florida)
December 2, 2002
· Mining Threat - St. Petersburg Times June 20, 2001
Other
· Phosphate Fertilizer Pollution in Israel (Haifa Chemical) Greenpeace June 8,
1998
· Greenpeace Action Alert on Phosphate IndustIy Pollution in Mediterranean
Greenpeace Mediterranean September 21, 2000
Back to top
Fluoride Action Network I 802-859-3363 I infolalfluoridealert.org
http://www.f1uoridealert.org/phosphate/overview.htm
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A Bibliography of Scientific Literature on Fluoride
Page 1 of 54
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A Bibliography of Scientific Literature on Fluoride
I Contents I
L FLUORIDE & BONE X. FLUORIDE & REPRODUCTIVE SYSTEM
. Clinical trials . Animal studies
. Animal studies . Hwnan studies
. FluoridationlHip fracture studies
. Fluoride concentrations in bone XL FLUORIDE & THE IMMUNE SYSTEM
. Factors which increase accumulation ofF
xu. ALLERGYIHYPERSENSITIVITY TO FLUORIDE
II. SKELETAL FLUOROSIS
xm DOWN'S SYNDROME
. Endemic fluorosis
. Industrial fluorosis XIV. FLUORIDE & CARIES (I'ooth Decay)
. Livestock fluorosis
. Decline of caries in western. industrialized societies
m. FLUORIDE & THE BRAIN . NIDR's national survey of dental health in US
. Fluoridation cessation studies
. LeaminglBehavior . CritiQue of early fluoridation trials
. Synergistic effects offluoride/alwninwn . Fluoride's topical vs. systemic effects
. Other . Fluoride and pit & fissure decay
. Fluoride & baby bottle tooth decay
IV. SILICOFLUORIDES & LEAD UPTAKE . Elevated fluoride exposure increases tooth decay
. Fluoride & delayed eruption of teeth
V. FLUORIDE & THE PINEAL GLAND
XV. DENTAL FLUOROSIS
VI. FLUORIDE & CANCER
. Mechanism of action
. US National Toxicology Program's bioassay . Current rates of dental fluorosis
· Recent epidemiological studies . Dental fluorosis prevalence among African-Americans
. Occupational fluoride/cancer . PerceptionsIPsvchololrical effects of dental fluorosis
. Fluoride & mutagenicity . Dental fluorosis & bone fracture
. Fluorosis & Caries
Vu. FLUORIDE & THE THYROID . Risk factors for fluorosis
· Fluoride treatment for hyperthyroidism XVL FLUORIDE: NOT an ESSENTIAL NUTRIENT
. Fluoride & goiter
. Fluoride/iodine interactions
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A Bibliography of Scientific Literature on Fluoride
Page 2 of 54
. Other xvn. SOURCES OF FLUORIDE EXPOSURE
vm. FLUORIDE & the KIDNEYS xvm NUTRITONAL DEFICIENCIES EXACERBATE
FLUORIDE'S TOXICITY
. Kidnev damage in skeletal fluorosis XIX. ACUTE TOXICITY of FLUORIDE
. Fluoride-induced Nephrotoxicity
. Kidnev aihnents heightening susceptibility xx. SYSTEMIC FLUORIDE NEVER APPROVED BY FDA
to fluoride toxicity
. Fluoride/Kidney Stones - Association XXL ALTERNATIVES TO FLUORIDE
. Fluoride/Kidnev Stones - No association
VIX. FLUORIDE & GASTOINTESTINAL XXn. REVIEWS of the SCIENTIFIC LITERATURE
DISORDERS
I. FLUORIDE & BONE (back to top)
** For a listing offluoride/bone research with notes and excerpts, click here
Fluoride & Bone: Clinical Trials (back to top)
Balena R, et aI. (1998). Effects of different regimens of sodium fluoride treatment for
osteoporosis on the structure, remodeling and mineralization of bone. Osteoporosis
International 8(5):428-35. (See abstract)
Bayley TA, et aI. (1990). Fluoride-induced fractures: relation to osteogenic effect. Journal
of Bone and Mineral Research 5(Suppl1):S217-22. (See abstract)
Brown JP, Josse RG. (2002). 2002 clinical practice guidelines for the diagnosis and
management of osteoporosis in Canada. Canadian Medical Association Journal 167(10
Suppl): S 1-S34. (See abstract)
Boivin G, et aI. (1993). Relationship between bone fluoride content and histological
evidence of calcification defects in osteoporotic women treated long term with sodium
fluoride. Osteoporosis International 3(4):204-8. (See abstract)
Dambacher MA, et aI. (1986). Long-term fluoride therapy of postmenopausal osteoporosis.
Bone 7: 199-205. (See abstract)
Fratzl P, et aI. (1994). Abnormal bone mineralization after fluoride treatment in
osteoporosis: a small-angle x-ray-scattering study. Journal of Bone and Mineral Research 9
(10):1541-9. (See abstract)
Gerster JC, et aI. (1983). Bilateral fractures of femoral neck in patients with moderate renal
failure receiving fluoride for spinal osteoporosis. British Medical Journal (Clin Res Ed) 287
(6394):723-5. (See abstract)
Gutteridge DR, et al. (2002). A randomized trial of sodium fluoride (60 mg) +/- estrogen in
postmenopausal osteoporotic vertebral fractures: increased vertebral fractures and
peripheral bone loss with sodium fluoride; concurrent estrogen prevents peripheral loss, but
not vertebral fractures. Osteoporosis International 13(2): 158-70. (See abstract)
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A Bibliography of Scientific Literature on Fluoride
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Gutteridge DR, et al. (1990). Spontaneous hip fractures in fluoride-treated patients:
potential causative factors. Journal of Bone and Mineral Research 5 Suppl 1: S205-15. (See
abstract)
Haguenauer D, et al. (2000). Fluoride for the treatment of postmenopausal osteoporotic
fractures: a meta-analysis. Osteoporosis International 11(9):727-38. (See abstract)
Hedlund LR, Gallagher JC. (1989). Increased incidence of hip fracture in osteoporotic
women treated with sodium fluoride. Journal of Bone andMineral Research 4:223-5. (See
ab stract)
Inkovaara JA. (1991). Is fluoride treatment justified today? Calcified Tissue International
49 Suppl:S68-9. (See abstract)
Inkovaara J, et al. (1975). Prophylactic fluoride treatment and aged bones. BritishMedical
Journal 3(5975):73-4. (See abstract)
Kleerekoper M, et al. (1991). A randomized trial of sodium fluoride as a treatment for
postmenopausal osteoporosis. Osteoporosis International 1(3): 155-61. (See abstract)
Kragstrup J, et al. (1989). Effects of sodium fluoride, vitamin D, and calcium on cortical
bone remodeling in osteoporotic patients. Calcified Tissue International 45: 337-41. (See
ab stract)
Lindsay R. (1990). Fluoride and Bone - Quantity Versus Quality. Editorial. New England
Journal of Medicine 322: 845-846. (See editorial)
Melton LJ. (1990). Fluoride in the prevention of osteoporosis and fractures. Journal of Bone
andMineral Research 5(Suppl. 1):163-167. (See abstract)
Meunier PJ, et al. (1998). Fluoride salts are no better at preventing new vertebral fractures
than calcium-vitamin D in postmenopausal osteoporosis: the FA VOStudy. Osteoporosis
International 8: 4-12. (See abstract)
O'Duffy JD, et al. (1986). Mechanism of acute lower extremity pain syndrome in fluoride-
treated osteoporotic patients. American Journal of Medicine 80: 561-6. (See abstract)
Grcel P, et al. (1990). Stress fractures of the lower limbs in osteoporotic patients treated
with fluoride. Journal of Bone andMineral Research 5(Suppll): SI91-4. (See abstract)
Orcel P, et al. (1987). [Spontaneous fissures and fractures of the legs in patients with
osteoporosis treated with sodium fluoride]. PresseMed. 16: 571-5. (See abstract)
Pak CY, et al. (1995). Treatment of postmenopausal osteoporosis with slow-release sodium
fluoride. Final report of a randomized controlled trial. Annals of Internal Medicine 123:
401-8. (See abstract)
Patel S, et al. (1996). Fluoride pharmacokinetics and changes in lumbar spine and hip bone
mineral density. Bone 19(6):651-5. (See abstract)
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A Bibliography of Scientific Literature on Fluoride
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Riggs BL, et al. (1990). Effect of Fluoride treatment on the Fracture Rates in
Postmenopausal Women with Osteoporosis. New England Journal of Medicine 322:802-
809. (See abstract)
Schnitzler CM, et al. (1990). Bone fragility of the peripheral skeleton during fluoride
therapy for osteoporosis. Clinical Orthopaedics (261):268-7S. (See abstract)
Schnitzler CM, Solomon L. (198S). Trabecular stress fractures during fluoride therapy for
osteoporosis. Skeletal Radioliology 14(4):276-9. (See abstract)
Sogaard CH, et al. (1994). Marked decrease in trabecular bone quality after five years of
sodium fluoride therapy--assessed by biomechanical testing of iliac crest bone biopsies in
osteoporotic patients. Bone lS(4): 393-99. (See abstract)
Vigorita VJ, SudaMK. (1983). The microscopic morphology offluoride...;induced bone.
Clinical Orthopaedics 177:274-82. (See abstract)
Fluoride & Bone: Animal Studies (back to top)
_ For a listing offluoride/bone research with notes and excerpts, click here
Bohatyrewicz A. (1999). Effects of fluoride on mechanical properties of femoral bone in
growing rats. Fluoride 32: 47-S4. (See abstract)
Burnell TW, et al. (1986). Effect of dietary fluorine on growth, blood and bone
characteristics of growing-finishing pigs. Journal of Animal Science 63: 20S3-67. (See
ab stract)
Carter DR, Beaupre GS. (1990). Effects of fluoride treatment on bone strength. Journal of
Bone and Mineral Research S Suppl1:S177-84. (See abstract)
Chachra D, et al. (1999). The effect of fluoride treatment on bone mineral in rabbits.
Calcified Tissue International 64: 34S-S1. (See abstract)
Gedalia I, et al. (1964). Effects of estrogen on bone composition in rats at low and high
fluoride intake. Endocrinology 7S: 201-20S. (See abstract)
Giavaresi G, et al. (1999). The mechanical properties of fluoride-treated bone in the
ovariectomized rat. Calcified Tissue International6S: 237-41. (See abstract)
Lafage MIl, et al. (199S). Comparison of alendronate and sodium fluoride effects on
cancellous and cortical bone in minipigs. A one-year study. Journal of Clinical
Investigation 9S: 2127-33. (See abstract)
Lundy MW, et al. (199S). Histomorphometric analysis of iliac crest bone biopsies in
placebo-treated versus fluoride-treated subjects. Osteoporosis InternationalS: 11S-29. (See
ab stract)
Jiang Y, et al. (1996). Effects oflow-dose long-tenn sodium fluoride preventive treatment
on rat bone mass and biomechanical properties. Calcified Tissue InternationalS8: 30-9.
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A Bibliography of Scientific Literature on Fluoride
Page 5 of 54
(See abstract)
Mosekilde L, et al. (1987). Compressive strength, ash weight, and volume of vertebral
trabecular bone in experimental fluorosis in pigs. Calcified Tissue International 40: 318-22.
(See abstract)
Riggins RS, et al. (1976). The effect of fluoride supplementation on the strength of
osteopenic bone. Clinical Orthopaedics (114):352-7. (See abstract)
Riggins RS, et al. (1974). The Effects of Sodium Fluoride on Bone Breaking Strength.
Calcified Tissue Research 14: 283-289. (See abstract)
Robin JC, et al. (1980). Studies on osteoporosis m. Effect of estrogens and fluoride.
Journal of Medicine 11: 1-14. (See abstract)
Rockert H. (1963). X-ray absorption and x-ray fluorescence micro-analysis of mineralized
tissue of rats which have ingested fluoridated water. Acta Pathologica et Microbiologica
Scandinavica 59: 32-38.
Silva MJ, Ulrich SR. (2000). In vitro sodium fluoride exposure decreases torsional and
bending strength and increases ductility of mouse femora. Journal of Biomechanics 33
(2):231-4. (See abstract)
Snow GR, Anderson C. (1986). Short-tenn chronic fluoride administration and trabecular
bone remodeling in beagles: a pilot study. Calcified Tissue International 38(4):217-21. (See
abstract)
Sogaard CR, et al. (1995). Effects offluoride on rat vertebral body biomechanical
competence and bone mass. Bone 16(1): 163-9. (See abstract)
Turner CR, et al. (1997). Fluoride treatment increased serum IGF-l, bone turnover, and
bone mass, but not bone strength, in rabbits. Calcified Tissue International 61(1):77-83.
(See abstract)
Turner CR, et al. (1996). High fluoride intakes cause osteomalacia and diminished bone
strength in rats with renal deficiency. Bone 19(6):595-601.(See abstract)
Turner CR, et al. (1996). Reductions in bone strength after fluoride treatment are not
reflected in tissue-level acoustic measurements. Bone 19(6):603-7. (See abstract)
Turner CR, et al. (1992). The effects of fluoridated water on bone strength. Journal of
Orthopaedic Research 10(4):581-7. (See abstract)
Turner RT, et al. (1989). The effects offluoride on bone and implant histomorphometry in
growing rats. Journal of Bone and Mineral Research 4(4):477-84. (See abstract)
Uslu B. (1983). Effect offluoride on collagen synthesis in the rat. Research and
ExperimentalMedicine 182(1):7-12. (See abstract) .
Wolinsky I, et al. (1972). Effects of fluoride on metabolism and mechanical properties of rat
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A Bibliography of Scientific Literature on Fluoride
Page 6 of 54
bone. American Journal of Physiology 223(1): 46-50. (See abstract)
Zhang X, Qiu MC, Liu WB. (1994). [Effects of pollution with fluoride on bone dynamics of
periosteum in iliac of domestic pigs]. Zhonghua Yu Fang Yi Xue Za Zhi 28(6):360-2. (See
abstract)
Fluoridation/Hip fracture Studies (back to top)
.. For a listing of fluoride/bone research with notes and excerpts, click here
a) Studies reporting association between fluoridated water (~ 1.2 ppm fluoride) & hip fracture.
(back to top)
a) Cooper C, et al. (1990). Water fluoride concentration and fracture of the proximal femur.
Journal of Epidemiology and Community Health 44: 17-19.
b) Cooper C, et al. (1991). Water fluoridation and hip fracture. Letter. Journal of the
American Medical Association 266: 513-514. (A reanalysis of data presented in 1990
paper). (See letter)
Danielson C, et al. (1992). Hip fractures and fluoridation in Utah's elderly population.
Journal of the American Medical Association 268(6): 746-748. (See abstract)
Hegmann KT, et al. (2000). The effects offluoridation on degenerative joint disease (DID)
and hip Fractures. Abstract # 71 of the 33rd annual meeting of the Society for
Epidemiological Research. American Journal of Epidemiology S 18. (See abstract).
Jacobsen SJ, et al. (1992). The association between water fluoridation and hip fracture
among white women and men aged 65 years and older; a national ecologic study. Annals of
Epidemiology 2: 617-626. (See abstract)
Jacobsen SJ, et al. (1990). Regional variation in the incidence of hip fracture: US white
women aged 65 years and olders. Journal of the American Medical Association 264(4):
500-2. (See excerpt)
a) Jacqmin-Gadda H, et al. (1995). Fluorine concentration in drinking water and fractures in
the elderly. Journal of the American Medical Association 273: 775-776 (letter). (See letter)
b) Jacqmin-Gadda H, et al. (1998). Risk factors for fractures in the elderly. Epidemiology 9
(4): 417-423. (An elaboration of the 1995 study referred to in the JAMA letter). (See
abstract)
Keller C. (1991) Fluorides in drinking water. Unpublished results. Discussed in: Gordon
SL, Corbin SB. (1992). SummaI)' of Workshop on Drinking Water Fluoride Influence on
Hip Fracture on Bone Health. Osteoporosis International 2: 109-117. (See excerpt)
Kurttio PN, et al. (1999). Exposure to natural fluoride in well water and hip fracture: A
cohort analysis in Finland. American Journal of Epidemiology 150(8): 817-824. (See
ab stract)
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.
May DS, Wilson MG. (1992). Hip fractures in relation to water fluoridation: an ecologic
analysis. Unpublished results. Discussed in: Gordon SL, Corbin SB. (1992). Summary of
Workshop on Drinking Water Fluoride Influence on Hip Fracture on Bone Health.
Osteoporosis International 2: 109-117. (See excerpt)
Suarez-Almazor M, et al. (1993). The fluoridation of drinking water and hip fracture
hospitalization rates in two Canadian communities. American Journal of Public Health 83:
689-693. (See abstract)
The authors of this study conclude there is no association between fluoridation
and hip fracture. However, their own data reveals a significant increase in hip
fracture for men living in the fluoridated area. According to the study,
"although a statistically significant increase in the risk of hip fracture was
observed among Edmonton men, this increase was relatively small (RR= 1.12). "
b) Studies reporting association between water-fluoride levels higher than fluoridated water (2 to
5 ppm) & hip fracture. (back to top)
Alarcon-Herrera MT, et al. (2001). Well Water Fluoride, Dental fluorosis, Bone Fractures
in the Guadiana Valley of Mexico. Fluoride 34(2): 139-149.(See study)
Li Y, et al. (2001). Effect oflong-tenn exposure to fluoride in drinking water on risks of
bone fractures. Journal of Bone and Mineral Research 16(5):932-9. (See abstract)
.
Sowers M, et al. (1991). A prospective study of bone mineral content and fracture in
communities with differential fluoride exposure. American Journal of Epidemiology 133:
649-660. (See abstract)
c) Studies reporting no association between fluoridated water & hip fracture: (back to top)
(Note that in 3 of these 9studies, an association was found between fluoride and some form of fracture _
i.e. distalforearm, even hip. See notes and quotes below,)
Amala I, et al. (1986). Hip fracture incidence not affected by fluoridation. Osteofluorosis
studied in Finland. Acta Orthopaedica Scandinavica 57: 344-348. (See abstract)
Cauley J. et al. (1995). Effects of fluoridated drinking water on bone mass and fractures: the
study of osteoporotic fractures. Journal of Bone andMineral Research 10(7): 1076-86. (See
abstract)
Feskanich D, et al. (1998). Use of toenail fluoride levels as an indicator for the risk of hip
and forearm fractures in women. Epidemiology 9(4): 412-6. (See abstract)
While this study didn't find an association between water fluoride and hip
fracture, it didfind an association - albeit non-significant 1.6 (0.8-3.1) _
between fluoride exposure and elevated rates of forearm fracture.
.
Hillier S, et al. (2000). Fluoride in drinking water and risk of hip fracture in the UK: a case
control study. The Lancet 335: 265-2690. (See abstract)
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Jacobsen SJ, et al. (1993). Hip fracture incidence before and after the fluoridation of the
public water supply, Rochester, Minnesota. American Journal of Public Health 83: 743-
745. (See abstract)
Karagas MR, et al. (1996). Patterns of fracture among the United States elderly: Geographic
and fluoride effects. Annals of Epidemiology 6 (3): 209-216. (See abstract I See critique of
study) .
As with Feskanich (1998) this study didn'tfind an association between
fluoridation & hip fracture, but it did find an association between fluoridation
and distal forearm fracture, as well as proximal humerus fracture.
"Independent of geographic effects, men in fluoridated areas had modestly
higher rates of fractures of the distal forearm and proximal humerus than did
men in norifluoridated areas. "
Lehmann R, et al. (1998). Drinking water fluoridation: Bone mineral density and hip
fracture incidence. Bone 22: 273-278. (See abstract)
Madans J, et al. (1983). The relationship between hip fracture and water fluoridation: an
analysis of national data. American Journal of Public Health 73: 296-298. (See abstract)
Phipps KR, et al. (2000). Community water fluoridation, bone mineral density and
fractures: prospective study of effects in older women. British Medical Journal 321 : 860-4.
(See abstract I See Study I See BMJ letter responding to study I See critique of study)
As with Feskanich (1998) andKaragas (1996), this study didn'tfind an
association between water fluoride & hip fracture, but it did find an
association between water fluoride and other types of fracture - in this case,
wrist fracture. "There was a non-significant trend toward an increased risk of
wrist fracture. "
See also:
Bernstein DS, et al. (1966). Prevalence of osteoporosis in high- and low-fluoride areas in
North Dakota. Journal of the American Medical Association 198: 499-504. (See abstract &
critique)
Lee JR. (1993), Fluoridation & hip fracture. Fluoride 26(4): 274-277. (See paper)
National Research Council. (1993). Fluoride exposure and risk of bone fracture. In: Health
Effects of Ingested Fluoride. Report of the Subcommittee on Health Effects of Ingested
Fluoride. National Academy Press, Washington, DC. (See chapter)
Fluoride Concentrations in Bone (back to top)
Alhava EM, et al. (1980). The Effect of Drinking Water Fluoridation on the Fluoride
Content, Strength and Mineral Density of Human Bone. Acta Orthopaedica Scandinavica
51: 413-420.
Bohatyrewicz A. (2001). Bone fluoride in proximal femur fractures. Fluoride 34: 227-235.
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Page 9 of 54
.
Amala I, et al. (1985). Effects of fluoride on bone in Finland. Histomorphometry of cadaver
bone from low and high fluoride areas. Acta Orthopaedica Scandinavica 56(2): 161-6.
Boivin G, et al. (1988). Fluoride content in human iliac bone: results in controls, patients
with fluorosis, and osteoporotic patients treated with fluoride. Journal of Bone and Mineral
Research 3(5):497-502.
Call RA, et at. (1965). Histological and chemical studies in man on effects offluoride.
Public Health Reports 80: 529-538.
Charen J, et at. (1979). Bone fluoride concentrations associated with fluoridated drinking
water. Calcified Tissue International 27(2):95-9.
Eble DM, et al. (1992). Fluoride concentrations in human and rat bone. Journal of Public
Health Dentistry 52: 288-291.
Glock GE, et at. (1941). The retention and elimination of fluoride in bones. Biochemical
Journal 35: 1235-1239.
Hefti A, Marthaler TM. (1981). Bone fluoride concentrations after 16 years of drinking
water fluoridation. Caries Research 15(1):85-9.
Jackson D, Weidman SM. (1958). Fluorine in human bone related to age and the water
supply of different regions. Journal of Pathological Bacteriology 76: 451-459.
. Kuo HC, Stamm JW. (1974). Fluoride levels in human rib bone: a preliminary study.
Canadian Journal of Public Health 65(5):359-61.
Parkins FM, et al. (1974). Relationships of human plasma fluoride and bone fluoride to age.
Calcified Tissue Research 16: 335-338.
Richards A, et al. (1994). Normal age-related changes in fluoride content of vertebral
trabecular bone - Relation to bone quality. Bone 15: 21-26.
Smith FA, et at. (1953). Age increase and fluoride content in human bone. (abstract).
Federation Proceedings 12: 368.
Stein ill, Granik G. (1980). Human vertebral bone: Relation of strength, porosity, and
mineralization to fluoride content. Calcified Tissue International 32: 189-194.
Sogaard CH, et al. (1994). Marked decrease in trabecular bone quality after five years of
sodium fluoride therapy--assessed by biomechanical testing of iliac crest bone biopsies in
osteoporotic patients. Bone 15(4): 393-99.
Wix P, Mohamedally SM. (1980). The significance of age-dependent fluoride accumulation
in bone in relation to daily intake offluoride. Fluoride 13: 100-104.
.
Zipkin L, et al. (1958). Fluoride deposition in human bones after prolonged ingestion of
fluoride in drinking water. US Public Health Reports 73:732-740.
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Factors which increase accumulation of fluoride in bone (back to top)
. a) Kidney problems
Adams PH, Jowsey J. (1965). Sodium Fluoride in the Treatment of Osteoporosis and Other
Bone Diseases. Annals of Internal Medicine 63(6): 1151-1155. (See excerpt)
Arnala I, et al. (1985). Effects offluoride on bone in Finland. Histomorphometry of cadaver
bone from low and high fluoride areas. Acta Orthopaedica Scandinavica 56(2): 161-6.
Call RA, et at. (1965). Histological and chemical studies in man on effects of fluoride.
Public Health Reports 80: 529-538.
Gerster JC, et at. (1983). Bilateral fractures offemoral neck in patients with moderate renal
failure receiving fluoride for spinal osteoporosis. British Medical Journal (Clin Res Ed) 287
(6394):723-5. (See abstract)
Hefti A, Marthaler TM. (1981). Bone fluoride concentrations after 16 years of drinking
water fluoridation. Caries Research 15(1):85-9.
Juncos LI, Donadio JV Jr. (1972). Renal failure and fluorosis. Journal of the American
Medical Association 222(7):783-5. (See abstract)
.
Kono K, et al. (1984). Urinary fluoride excretion in fluoride exposed workers with
diminished renal function. Industrial Health 22(1):33-40. (See abstract)
Linsman JF, McMurray CA. (1943). Fluoride osteosclerosis from drinking water. Radiology
40: 474- 484.
Noel C, et al. (1985). [Risk of bone disease as a result offluoride intake in chronic renal
insufficiency]. (Article in French). Nephrologie 1985;6(4):181-5. (See abstract)
Spak CJ, et at. (1985). Renal clearance of fluoride in children and adolescents. Pediatrics 75
(3):575-9. (See abstract)
Turner CH, et at. (1996). High fluoride intakes cause osteomalacia and diminished bone
strength in rats with renal deficiency. Bone 19(6):595-601.(See abstract)
Welsch M, et al. (1990). [Iatrogenic fluorosis. 2 cases]. Therapie 45(5):419-22. (See
abstract)
b) Nutritional Deficiencies (back to top)
Beary DF. (1969). The effects offluoride and low calcium on the physical properties of the
rat femur. The Anatomical Record 164: 305-316.
.
Jowsey J, et at. (1972). Effect of combined therapy with sodium fluoride, vitamin D and
calcium in osteoporosis. American Journal of Medicine 53(1):43-9.
Li G, Ren L. (1997). [Effects of excess fluoride on bone turnover under conditions of diet
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A BIblIography of Scientific Literature on Fluoride
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with different calcium contents] [Article in Chinese] Zhonghua Bing Li Xue Za Zhi 26
(5):277-80. (See abstract)
Likimani S, et al. (1992). The effects of protein -deficiency and fluoride on bone mineral
content of rat tibia. Calcified Tissue International 50(2):157-64. (See abstract)
Marier JR, et al. (1963). Accumulation of skeletal fluoride and its implications. Archives of
Environmental Health 6: 664-671.
Riggins RS, et al. (1976). The effect of fluoride supplementation on the strength of
osteopenic bone. Clinical Orthopaedics (114):352-7.
Riggins RS, et al. (1974). The effects of sodium fluoride on bone breaking strength.
Calcified Tissue Research 14: 283-289.
Teotia M, Teotia SP, Singh KP. (1998). Endemic chronic fluoride toxicity and dietary
calcium deficiency interaction syndromes of metabolic bone disease and defonnities in
India: year 2000. Indian Journal of Pediatrics 65(3):371-81. (See abstract)
ll. SKELETAL FLUOROSIS (back to top)
Note: Early symptoms of skeletal fluorosis may be misdiagnosed as a form of arthritis. Click here to
learn more.
Endemic Fluorosis (back to top)
Azar HA, et al. (1961). Skeletal fluorosis due to chronic fluoride intoxication. Annals of
Internal Medicine 55: 193-200.
Cao J, et al. (2003). Brick tea fluoride as a main source of adult fluorosis. Food and
Chemical Toxicology 41(4):535-42. (See abstract)
Choubisa SL, et al. (2001). Endemic fluorosis in Rajasthan. Indian Journal of
Environmental Health 43(4): 177-89. (See abstract)
Christie DP. (1980). The spectrum of radiographic bone changes in children with fluorosis.
Radiology 136(1):85-90. (See abstract)
Hileman B. (1988), Fluoridation of water. Questions about health risks and benefits remain
after more than 40 years. Chemical and Engineering News August 1. 26-42. (See excerpt)
Jolly SS, et al. (1973). Endemic fluorosis in Punjab: 1. skeletal aspect. Fluoride 6: 4-18.
Jolly SS, et al. (1971). Human fluoride intoxication in Punjab. Fluoride 4: 64-79.
Jolly SS. (1968). An epidemiological, clinical and biochemical study of endemic, dental and
skeletal fluorosis in Punjab. Fluoride 1(2): 65-75.
Juncos LI, Donadio JV Jr. (1972). Renal failure and fluorosis. Journal of the American
Medical Association 222(7):783-5. (See abstract)
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Kilborn LG, et al. (1950). Fluorosis with report of an advanced case. Canadian Medical
Association Journal 62: 135-141.
Krishnamachari KA. (1986). Skeletal fluorosis in humans: a review of recent progress in the
understanding of the disease. Progress in Food and Nutrition Sciences 10(3 -4):279-314.
(See abstract)
Krishnamachari KA, Krishnaswamy K. (1973). Genu val gum and osteoporosis in an area of
endemic fluorosis. The Lancet. 2(7834): 877-879. (See abstract)
Kumar SP, Harper RA. (1963). Fluorosis in Aden. British Journal of Radiology 36: 497-
502.
Latham MC, Grech P. (1967). The effects of excessive fluoride intake. American Journal of
Public Health 57: 651-660.
Lian ZC, Wu EH. (1986). Osteoporosis--an early radiographic sign of endemic fluorosis.
Skeletal Radiology 15(5):350-3. (See abstract)
Misra UK, et al. (1988). Endemic fluorosis presenting as cervical cord compression.
Archives of Environmental Health 43: 18-21.
Mithal A, et al. (1993). Radiological spectrum of endemic fluorosis: relationship with
calcium intake. Skeletal Radiology 22(4):257-61. (See abstract)
Pandit CG, et al. (1940). Endemic fluorosis in South India. Indian Journal of Medica I
Research 28: 533-558.
Pinet A, PinetF. (1968). Endemic fluorosis in the Sahara. Fluoride 1(2): 85-93.
Savas S, et al. (2001). Endemic fluorosis in Turkish patients: relationship with knee
osteoarthritis. Rheumatology International 21(1):30-5. (See abstract)
Shortt HE, et al. (1937). Endemic fluorosis in the Madras presidency. Indian Journal of
Medical Research 25: 553-568.
Siddiqui AH. (1970). Neurological complications of skeletal fluorosis with special reference
to lesions in the cervical region, Fluoride 3: 91-96.
Siddiqui AH. (1955). Fluorosis in Nalgonda district, Hyderabad-Deccan. British Medical
Journal ii (Dee 10): 1408-1413.
Singh A, et al. (1963). Endemic fluorosis. Epidemiological, clinical and biochemical study
of chronic fluoride intoxication in Punjab. Medicine. 42: 229-246.
Singh A, et al. (1961). Skeletal fluorosis and its neurological complications. Lancet 1: 197-
200.
Susheela AK, et al. (1993). Prevalence of endemic fluorosis with gastro-intestinal
manifestations in people living in some North-Indian villages. Fluoride 26(2): 97-104. (See
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A Bibliography of Scientific Literature on Fluoride
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abstract)
Teotia SPS, et al. (1976). Symposium on the Non-Skeletal Phase of Chronic Fluorosis: The
Joints. Fluoride 9(1): 19-24. (See paper)
UNICEF Water, Environment & Sanitation. (1999). Fluoride in water: An overview.
Waterfront December. (See report)
Wang Y, et al. (1994). Endemic fluorosis of the skeleton: radiographic features in 127
patients. American Journal of Roentgenology 162(1 ):93-8. (See abstract).
Zhavoronkov AA. (1977). [Non-skeletal forms offluorosis]. Arkh Patol. 39(3):83-91. (See
abstract)
See also:
Fluoride Action Network. (2002). Fluorosis in India: Recent Reports.
http://www.fluoridealert.orglfluorosis-india.htm
Industrial Fluorosis (back to top)
Camow BW, Conibear SA. (1981). Industrial fluorosis. Fluoride 14(4): 172-181. (See
study)
Czerwinski E, et al. (1988). Bone and joint pathology in fluoride-exposed workers. Archives
of Environmental Health 43(5):340-3. (See abstract)
Czerwinski E, Lankosz W. (1978). Skeletal changes in industrial and endemic fluorosis.
Fluoride 11(1):29-32. (See study).
Czerwinski E, Lankosz W. (1977). Fluoride-induced changes in 60 retired aluminum
workers. Fluoride 10(3): 125-136. (See study)
Derryberry OM, et at. (1963). Fluoride exposure and worker health. Archives of
EnvironmentalHealth 6: 503-514.
Franke J, et at. (1975). Industrial fluorosis. Fluoride 8(2): 61-83.
Grandjean P. (1982). Occupational fluorosis through 50 years: clinical and epidemiological
experiences. American Journal of Industrial Medicine 3(2):227-36. (See abstract)
Hodge HC, Smith FA. (1979). Occupational fluoride exposure. Journal of Occupational
Medicine 19: 12-39.
Kaltreider NL, et al. (1972). Health survey of aluminum workers with special reference to
fluoride exposure. Journal of Occupational Medicine 14(7): 531-541.
Moller PF, Gudjonsson SV. (1932). Massive fluorosis of bones and ligaments. Acta
Radiology 13:269-294.
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.
Roholm K. (1937). Fluoride intoxication: a clinical-hygienic study with a review of the
literature and some experimental investigations. H.K. Lewis Ltd, London.
Runge H, Franke J. (1989). Radiological modifications of the skeletal system among
aluminum smelter workers: A 15 year retrospective study. Fluoride 22: 157-164. (See
study)
Waldbott GL, Cecilioni VA. (1969). Neighborhood fluorosis. Fluoride 2(4): 206-213. (See
study)
Zhiliang Y, et al. (1987). Industrial fluoride pollution in the metallurgical industry in China.
Fluoride 20(3): 118-125. (See study)
Livestock Fluorosis (back to top)
Griffith-Jones W. (1977). Fluorosis in dairy cattle. The Veterinary Record 100: 84-89. (See
abstract)
Huffman WT. (1949). Effects on livestock of air contamination caused by fluoride fumes.
pp. 59-63. In: Air Pollution. Proceedings of the United States Technical Conference on Air
Pollution. McGraw-Hill Book Co, New York.
Krook L, Maylin GA. (1979). Industrial fluoride pollution. Chronic fluoride poisoning in
Cornwall Island cattle. Cornell Veterinarian 69(Suppl 8): 1-70. (See abstract)
. Lillie RJ. (1970). Air Pollutants Affecting the Performance of Domestic Animals: A
Literature Review. U.S. Dept. of Agriculture. Agricultural Handbook No. 380. Washington
D.C.
National Academy of Sciences. (1960). The fluorosis problem in livestock production.
Committee on Animal Nutrition, Agricultural Board. Washington DC.
Roholm K. (1937). Fluoride intoxication: a clinical-hygienic study with a review of the
literature and some experimental investigations. H.K. Lewis Ltd, London.
Schmidt HJ, Rand WE. (1952). A critical study of the literature on fluoride toxicology with
respect to cattle damage. American Journal of Veterinary Research 13: 39-48.
Shupe JL, Olson AE. (1971). Clinical aspects of fluorosis in horses. Journal of the
American Veterinary Association 158: 167-174. (See study)
Shupe JL, et al. (1963). The effect offluorine on dairy cattle n. Clinical and pathologic
effects. American Journal of Veterinary Research 24: 964-979.
Suttie JW. (1977). Effects offluoride on livestock. Journal of Occupational Medicine 19:
40-48.
. m. FLUORIDE & THE BRAIN (back to top)
Fluoride &.LearninglBehavior:
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.
Bhatnagar M, et al. (2002). Neurotoxicity offluoride: neurodegeneration in hippocampus of
female mice. Indian Journal of Experimental Biology 40: 546-54. (See abstract)
Calderon J, et al. (2000). Influence of fluoride exposure on reaction time and visuospatial
organization in children. Epidemiology 11(4): S153. (See abstract)
Calvert GM, et al. (1998). Health effects associated with sulfuryl fluoride and methyl
bromide exposure among structural fumigation workers. American Journal of Public Health
88(12): 1774-80. (See abstract)
Ekambaram P, Paul V. (2001). Calcium preventing locomotor behavioral and dental
toxicities of fluoride by decreasing serum fluoride level in rats. Environmental Toxicology
and Pharmacology 9(4):141-146. (See abstract)
Li XS. (1995). Effect of Fluoride Exposure on Intelligence in Children. Fluoride 28(4):189-
192. (See abstract)
Li Y, et al. (1994). [Effect of excessive fluoride intake on mental work capacity of children
and a preliminary study of its mechanism] Hua Hsi I Ko Ta Hsueh Hsueh Pao. 25(2): 188-
91. (See abstract)
Lin Fa-Fu; et al (1991). The relationship of a low-iodine and high-fluoride environment to
subclinical cretinism in Xinjiang. Iodine Deficiency Disorder Newsletter Vol. 7. No.3. (See
study)
. Long YG, et al. (2002). Chronic fluoride toxicity decreases the number of nicotinic
acetylcholine receptors in rat brain. Neurotoxicology and Teratology 24(6):751-7. (See
ab stract)
Lu Y, et al (2000). Effect of high-fluoride water on intelligence of children. Fluoride 33:74-
78. (See abstract I See study)
Mattsson JL, et al. (1988). Subchronic neurotoxicity in rats of the structural fumigant,
sulfuryl fluoride. Neurotoxicology and Teratology 10(2): 127-33. (See abstract)
Morgan L, et al (1998). Investigation of the possible associations between fluorosis,
fluoride exposure, and childhood behavior problems. Pediatric Dentistry 20: 244-252. (See
ab stract)
Mullenix P, et al. (1995).Neurotoxicity of Sodium Fluoride in Rats. Neurotoxicology and
Teratology 17: 169-177. (See abstract I See editorial discussing this study)
Paul V, et al. (1998). Effects of sodium fluoride on locomotor behavior and a few
biochemical parameters in rats. Environmental Toxicology and Pharmacology 6: 187-191.
(See abstract)
.
Schettler T, et al. (2000). Known and suspected developmental neurotoxicants. pp. 90-92.
In: In Harms Way - Toxic Threats to Child Development. Greater Boston Physicians for
Social Responsibility: Cambridge, MA. (See excerpt)
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Spittle B. (2000). Fluoride and Intelligence (Editorial). Fluoride 33: 49-52. (See editorial)
Xiang Q, et al. (2003). Effect of fluoride in drinking water on children's intelligence.
Fluoride 36: 84-94. (See abstract)
Yang Y, et al. (1994). [Effects of high iodine and high fluorine on children's intelligence
and the metabolism of iodine and fluorine]. Zhonghua Liu Xing Bing Xue Za Zhi.15(5):296-
8. (See abstract)
Zhang C, et al. (1999). [Effect of fluoride-arsenic exposure on the neurobehavioral
development of rats offspring] Wei Sheng YanJiu. 28(6):337-8. (See abstract)
Zhang Z, et at. (2001). [Effects of selenium on the damage ofleaming-memory ability of
mice induced by fluoride]. Wei Sheng Yan Jiu. 30(3): 144-6. (See abstract)
Zhang Z, et at. (1999). [Effect of fluoride exposure on synaptic structure of brain areas
related to leaming-memory in mice] [Article in Chinese]. Wei Sheng Yan Jiu 28(4):210-2.
(See abstract)
Zhao LB, et al (1996). Effect of high-fluoride water supply on children's intelligence.
Fluoride 29: 190-192. (See abstract)
Synergistic effects of Fluoride/Aluminum (back to top)
Allain P, et at. (1996). Enhancement of aluminum digestive absorption by fluoride in rats.
Research in Community Molecular Pathology and Pharmacology 91(2):225-31. (See
abstract)
Chase M. (1992). Rat studies link brain cell damage with aluminum and fluoride in water.
Wall Street Journal October 28: B6. (See article)
Strunecka A, Patocka J. (1999). Pharmacological and toxicological effects of
aluminofluoride complexes. Fluoride 32: 230-242. (See paper)
van der Voet GB, et at. (1999). Fluoride enhances the effect of aluminium chloride on
interconnections between aggregates of hippocampal neurons. Archives o/Physiology and
Biochemistry 107(1):15-21. (See abstract)
Varner JA, et al. (1998). Chronic Administration of Aluminum-Fluoride and Sodium-
Fluoride to Rats in Drinking Water: Alterations in Neuronal and Cerebrovascular Integrity.
Brain Research 784: 284-298. (See abstract I See condensed version of study I See media
report)
Varner JA, et al. (1997). Toxin-induced blood vessel inclusions caused by the chronic
administration of aluminum and sodium fluoride and their implications for dementia.
Annals o/the New YorkAcademy o/Science 825: 152-166. (See condensed version of
study)
Other (back to top)
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.
Chen J, et al. (2002). Studies on DNA damage and apoptosis in rat brain induced by
fluoride. Zhonghua Yu Fang Yi Xue Za Zhi. 36(4):222-224. (See abstract)
Chen J, et aI. (2002). Selective decreases of nicotinic acetylcholine receptors in PC12 cells
exposed to fluoride. Toxicology 183(1-3):235-42. (See abstract)
Du L. (1992). [The effect of fluorine on the developing human brain]. Chung-hua Ping Li
Hsueh Tsa Chih. 21(4):218-20. (See abstract)
Eisenbrandt DL, Nitschke KD. (1989). Inhalation toxicity of sulfuryl fluoride in rats and
rabbits. Fundamentals of Applied Toxicology 1989 Apr;12(3):540-57. (See abstract)
Guan ZZ, et aI (1998). Influence of chronic fluorosis on membrane lipids in rat brain,
Neurotoxicology and Teratology 20: 537-542. (See abstract)
Kay AR, et al. (1986). Intracellular fluoride alters the kinetic properties of calcium currents
facilitating the investigation of synaptic events in hippocampal neurons. Journal of
Neuroscience 6(10):2915-20. (See abstract)
Lakshmi Vani M, Pratap Reddy K. (2000). Effects offluoride accumulation on some
enzymes of brain and gastrocnemius muscle of mice. Fluoride 33: 17-26. (See abstract)
.
National Research Council. (1971). Effects of Fluoride on Human Health: Nervous System.
In: Fluorides. Committee on Biological Effects of Atmospheric Pollutants. National
Academy of Sciences. Washington, D.C. Chapter 9. (See excerpt)
Shashi A. (2003). Histopathological investigation of fluoride-induced neurotoxicity in
rabbits. Fluoride 36: 95-105. (See abstract)
Shashi A, et aI. (1994). Effect oflong-term administration offluoride on levels of protein,
free amino acids and RNA in rabbit brain. Fluoride 27: 155-159.
Shivarajashankara YM, et aI. (2002). Histological changes in the brain of young fluoride-
intoxicated rats. Fluoride 35(1): 12-21. (See study)
Shivarajashankara YM , et aI. (2002). Brain lipid peroxidation and antioxidant systems of
young rats in chronic fluoride intoxication. Fluoride 35: 197-203. (See abstract)
Trabelsi M, et al. (2001). Effect of fluoride on thyroid function and cerebellar development
in mice. Fluoride 34: 165-173. (See study)
IV. SILICOFLUORIDES & LEAD UPTAKE (back to top)
Masters R, et aI. (2000). Association of Silicofluoride Treated Water with Elevated Blood
Lead. Neurotoxicology 21(6): 1091-1099. (See abstract)
.
Masters RD, Coplan M. (1999). Water treatment with Silicofluorides and Lead Toxicity.
International Journal of Environmental Studies 56: 435-449. (See abstract)
For commentary, see:
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Coplan MJ, Masters RD. (2001). Silicofluorides and fluoridation. Fluoride 34(3): 161-220.
(See paper)
"Dartmouth researcher warns of chemicals added to drinking water." (March 15, 2001).
Dartmouth College News Accessible online at:
http://www.dartmouth.edu/-news/releases/marOl/fluoride.html
V. FLUORIDE & THE PINEAL GLAND (back to top)
Luke J. (1997). The Effect of Fluoride on the Physiology of the Pineal Gland. Ph.D. Thesis.
University of Surrey, Guildord. (See abstract)
Luke J. (2001). Fluoride Deposition in the Aged Human Pineal Gland. Caries Research
35:125-128. (See abstract)
VI. FLUORIDE & CANCER (back to top)
US National Toxicology Program's Bioassay
Bucher JR, et aI. (1991). Results and conclusions of the National Toxicology Program1s
rodent carcinogenicity studies with sodium fluoride. International Journal of Cancer 48
(5):733-7. (See abstract)
National Toxicology Program [NTP] (1990). Toxicology and Carcinogenesis Studies of
Sodium Fluoride in F344/N Rats and B6C3f1 Mice. Technical report Series No. 393. NllI
PubI. No 91-2848. National Institute of Environmental Health Sciences, Research Triangle
Park, N.C. (See executive summary I See study)
For commentary on NIP Study, see:
Calabrese E. (1991). Evaluation of the National Toxicology Program (NTP) Cancer
Bioassay on Sodium Fluoride. Commissioned by the East Bay Municipal Utility District.
Oakland, California. (See paper)
Connett P. (2000). Fluoride: A Statement of Concern. Waste Not #459. Canton NY. (See
excerpt)
Rirzy JW. (2000). Video-taped interview with Dr. J. William Rirzy, Senior Vice President,
EP A Headquarters Union. Interview by Michael Connett. July 3. (Read interview)
Lee JR. (1993). Fluoridation and Bone Cancer. Fluoride 26(2):79-82. (See paper).
Liteplo RG, et aI. (1994). Inorganic fluoride: Evaluation of risks to health from
environmental exposure in Canada. Journal of Environmental Science and Health. Part C,
Environmental Carcinogenesis & EcotoxicoJogy Reviews 12: 327-344.
Marcus W. (1995). Radio Interview with Dr. William Marcus, Senior Scientist, Office of
Drinking Water, EPA. Interview by Dr. Gary Null. March 10. (Read interview)
Marcus W. (1990). Memorandum from Dr. William Marcus,to Alan B. Hais, Acting
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Director Criteria & Standards Division ODW, US EPA. May 1, 1990. (See memo)
.
Marshall E. (1990). The Fluoride Debate: One More Time. Science January 10: 276-277.
(See article)
World Health Organization. (2002). Environmental Health Criteria 227: FLUORIDES.
World Health Organization, Geneva. (See excerpt)
Recent Epidemiological Studies on Fluoridation/Cancer (back to top)
Cohn PD. (1992). A Brief Report On The Association Of Drinking Water Fluoridation And
The Incidence of Osteosarcoma Among Young Males. New Jersey Department of Health
Environ. Health Service: 1- 17. (See Executive Summary)
Hoover RN, et al. (1991). Time trends for bone and joint cancers and osteosarcomas in the
Surveillance, Epidemiology and End Results (SEER) Program. National Cancer Institute.
In: Review of Fluoride: Benefits and Risks Report of the Ad Hoc Committee on Fluoride of
the Committee to Coordinate Environmental Health and Related Programs US Public
Health Service. pp Fl -F7.
Takahashi K, et al. (2001). Regression analysis of cancer incidence rates and water fluoride
in the U.S.A. based on IACMARC (WHO) data (1978-1992). International Agency for
Research on Cancer. Journalo/Epidemiology 11(4): 170-179. (See abstract)
.
Tohyama E. (1996). Relationship between fluoride concentration in drinking water and
mortality rate from uterine cancer in Okinawa prefecture, Japan. Journal 0/ Epidemiology 6
(4):184-191. (See abstract)
Yiamouyiannis JA. (1993). Fluoridation and cancer: The biology and epidemiology of bone
and oral cancer related to fluoridation. Fluoride 26(2):83-96.
See also:
National Cancer Institute (1989). Cancer Statistics Review, 1973-1987, Bethesda, MD:
National Institutes of Health. Publication No.90-2789.
US Department of Health and Human Services, (1991). Review offluoride: benefits and
risks. Report of the Ad Hoc Subcommittee on Fluoride. Washington, DC. (See synopsis)
Occupational Fluoride/Cancer (back to top)
Grandjean P, et al. (1992). Cancer incidence and mortality in workers exposed to fluoride.
Journal o/the National Cancer Institute 84(24):1903-9. (See abstract)
Grandjean P, et al. (1985). Mortality and cancer morbidity after occupational fluoride
exposure. American Journal o/Epidemiology 121: 57-64. (See abstract)
. Fluoride & Mutagenicity (back to top)
Aardema MJ, et al (1989). Sodium fluoride-induced chromosome aberrations in different
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stages of the cell cycle: a proposed mechanism. Mutation Research 223: 191-203. (See
abstract)
Albanese R. (1987). Sodium fluoride and chromosome damage (in vitro human lymphocyte
and in vivo micronucleus assays). Mutagenesis 2(6):497-9. (See abstract)
Bale SS, Mathew MT. (1987). Analysis of chromosomal abnormalities at anaphase-
telophase induced by sodium fluoride in vitro. Cytologia 52: 889-893. (See abstract)
Caspary WJ, et al (1987). Mutagenic activity offluorides in mouse lymphoma cells.
Mutation Research 187(3):165-80. (See abstract)
Chen J, et al. (2000). [Effects of selenium and zinc on the DNA damage caused by fluoride
in pallium neural cells of rats]. Wei Sheng Yan Jiu. 29(4):216-7. (See abstract)
Cole J, et al. (1986). The mutagenicity of sodium fluoride to L5178Y [wild-type and TK +/_
(3.7.2c)] mouse lymphoma cells. Mutagenesis 1(2):157-67. (See abstract)
Crespi CL, et al. (1990). Sodium fluoride is a less efficient human cell mutagen at low
concentrations. EnvironmentalMolecular Mutagenesis 15(2):71-7. (See abstract)
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Emsley J, et al (1981). An unexpectedly strong hydrogen bond: Ab initio calculations and
spectroscopic studies of amide-fluoride systems. Journal of the American Chemical Society
103: 24-28.
Gerdes RA, et al. (1971). The effects of atmospheric hydrogen fluoride upon Drosophila
melanogaster. n. Fecundity, hatchability and fertility. Atmospheric Environ. 5: 117-122.
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Hayashi N, Tsutsui T. (1993). Cell cycle dependence of cytotoxicity and clastogenicity
induced by treatment of synchronized human diploid fibroblasts with sodium fluoride.
Mutation Research 290: 293-302. (See abstract)
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Archives of Environmental Health 29:230-5. (See abstract)
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Khalil AM. (1995). Chromosome aberrations in cultured rat bone marrow cells treated with
inorganic fluorides. Mutation Research 343(1):67-74. (See abstract)
Kishi K, Ishida T. (1993). Clastogenic activity of sodium fluoride in great ape cells.
Mutation Research 301(3):183-8. (See abstract)
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Lithuanian populations: effects of occupational and environmental exposures. Mutation
Research 445: 225-229. (See abstract)
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Research 195(2): 127-36. (See abstract)
Meng Z, Zhang B. (1997). Chromosomal aberrations and micronuclei in lymphocytes of
workers at a phosphate fertilizer factory. Mutation Research 393: 283-288. (See paper)
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phosphate fertilizer factory. Mutation Research 334(2):243-6. (See abstract)
Mihashi M, Tsutsui T. (1996). Clastogenic activity of sodium fluoride to rat vertebral body-
derived cells in culture. Mutation Research 368(1):7-13 (See abstract)
Mohamed AH, Chandler ME. (1982). Cytological effects of sodium fluoride on mice.
Fluoride 15(3): 110-18. (See abstract)
Mohamed AH. (1977). Cytogenetic effects of hydrogen fluoride gas on maize. Fluoride 10
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Mukerjee RN, Sobels FH. (1968). The effect of sodium fluoride and idoacetamide on
mutation induction by X-irradiation in mature spermatozoa of drosophila. Mutation
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fluoride. Report of the Subcommittee on Health Effects of Ingested Fluoride. National
Academy Press, Washington, DC. (See chapter)
Pati PC, Bhunya SP. (1987). Genotoxic effect of an environmental pollutant, sodium
fluoride, in mammalian in vivo test system. Caryologia 40:79-87.
Ramesh N, et al. (2001). Low levels ofp53 mutations in Indian patients with osteosarcoma
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Toxicology, and Oncology 20(3):237-43.(See abstract)
Rivedal E, et al. (2000). Morphological transformation and effect on gap junction
intercellular communication in Syrian hamster embryo cells as screening tests for
carcinogens devoid of mutagenic activity. Toxicology In Vitro 14(2): 185-92. (See abstract)
Scott D, Roberts SA. (1987). Extrapolation from in vitro tests to human risk: experience
with sodium fluoride clastogenicity. Mutation Resear-eh 189(1):47-58. (See abstract)
Sheth FJ, et al. (1994). Sister chromatid exchanges: A study in fluorotic individuals of
North Gujurat. Fluoride 27: 215-219. (See abstract)
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the Society for Experimental Biology andMedicine 119:252-255. (See study)
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Tsutsui T, Suzuki N, Ohmori M. (1984) Sodium fluoride-induced morphological and
neoplastic transformation, chromosome aberrations, sister chromatid exchanges, and
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and unscheduled DNA synthesis in cultured human diploid fibroblasts induced by sodium
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Tsutsui T, Ide K, Maizumi H. (1984). Induction of unscheduled DNA synthesis in cultured
human oral keratinocytes by sodium fluoride. Mutation Research 140(1):43-8. (See
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abstract)
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Vll. FLUORIDE & THE THYROID (back to top)
For additional references onfluoride/thyroid, click here
Fluoride treatment for Hyperthyroidism
Galletti P, Joyet G. (1958). Effect of Fluorine on Thyroidal Iodine Metabolism in
Hyperthyroidism. Journal of Clinical Endocrinology 18: 1102-1110 (See study)
Goldemberg L. (1930). Compt Rend Soc Bioi (paris) 104: 1031.
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May W. (1935). [Antagonismus zwischen Jod und Fluor im Organismus] Klin Wochenschr
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May W. (1937). (Behandlung the Hyperthyreosen einschliesslich des schweren genuinen
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Schuld A. (1999). Fluoride-Iodine Antagonism: Some History. Parents of Fluoride
Poisoned Children, (See paper)
Stecher P, et al. (1960). The Merck Index of Chemicals and Drugs. Merck & Co., Inc,
Rathway NJ.
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Day TK, Powell-Jackson PRo (1972). Fluoride, Water Hardness, and Endemic Goitre.
Lancet 1:1135-1138. (See study)
Desai VK, et aI. (1993). Epidemiological study of goitre in endemic fluorosis district of
Gujarat. Fluoride 26: 187-90. (See excerpt)
Jooste PL. (1999). Endemic goitre in the absence of iodine deficiency in schoolchildren of
the Northern Cape Province of South Africa. European Journal of Clinical Nutrition 53
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(1):8-12. (See abstract)
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McKay FS. (1918). Progress of the year in the investigation of mottled enamel with special
reference to its association with artesian water. Journal of the National Dental Association
5:721-750.
Siddiqui AH. (1969). Incidence of simple goiter in areas of endemic fluorosis in NaIgonda
District, Andra Pradesh, India. Fluoride 2:200-205.
Steyn DG, et aI. (1955). Endemic Goitre in the Union of South Africa and Some
Neighbouring Territories. Union of South Africa. Department of Nutrition. (See excerpts)
Wespi HJ. (1954). Besteht ein Antagonismus zwischen Fluor und Jod? Praxis 43: 616-623.
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Zhao W, et aI. (1998). Long-term effects of various iodine and fluorine doses on the thyroid
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FluoridelIodine InteractionsCback to top)
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Guan ZZ, et aI. (1988). Synergistic action of iodine-deficiency and fluorine-intoxication on
rat thyroid. Chinese Medical Journal 101(9):679-84.
Lin Fa-Fu, et aI (1991). The relationship of a low-iodine and high-fluoride environment to
subclinical cretinism in Xinjiang. Iodine Deficiency Disorder Newsletter Vol. 7. No. 3.(See
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Minder W, GordonoffT. (1956). An antagonism between iodine and fluorine. Arch Intern
Pharma Codyn 107: 374-381.
Sidora YD, et al. (1983). [Indices of the pituitary-thyroid system in residents of cities with
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Steyn DG, et aI. (1955). Endemic Goitre in the Union of South Africa and Some
Neighbouring Territories. Union of South Africa. Department of Nutrition. (See excerpts)
Stole V, Podoba 1. (1960). Effect of fluoride on the biogenesis of thyroid hormones. Nature
188:855-856.
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Wilson RH, DeEds F. (1940). The synergistic action of thyroid on fluoride toxicity.
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Yang Y, et aI. (1994). [Effects of high iodine and high fluorine on children's intelligence
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8. (See abstract)
Zhao W, et al, (1998). Long-tenn Effects of Various Iodine and Fluorine Doses on the
Thyroid and Fluorosis in Mice. Endocrine Regulations 32(2):63-70. (See abstract I See
study)
For more references, see:
Schuld A. (2002). History of the fluoride/iodine antagonism. Parents of Fluoride Poisoned
Children. (See paper)
Other
Bachinskii PP, et at. (1985) Action of the body fluorine of healthy persons and
thyroidopathy patients on the function of hypophyseal-thyroid the system. Probl Endokrinol
(Mosk) 31(6):25-9. (See abstract)
BaIabolkin MI, et al. (1995). [The interrelationship of the thyroid and immune statuses of
workers with long-tenn fluorine exposure] [Article in Russian] Ter Arkh. 67(1):41-2. (See
abstract)
Bobek S, et al. (1976). Effect oflong-tenn fluoride administration on thyroid hormones
level blood in rats. Endocrinologia Experimentalis 10(4):289-95.(See abstract)
Kendall-Taylor P. (1972). Comparison of the effects of various agents on thyroidal adenyl
cyclase activity with their effects on thyroid honnone release. Journal of Endocrinology 54
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Hara K. (1980). [Studies on fluorosis, especially effects of fluoride on thyroid metabolism].
Koku Eisei Gakkai Zasshi. 30(1):42-57.
Hillman D, et aI. (1979). Hypothyroidism and anemia related to fluoride in dairy cattle.
Journal of Dairy Science 62(3):416-23. (See abstract)
Tokar VI, et aI. (1989). [Chronic effects of fluorides on the pituitary-thyroid system in
industrial workers]. Gig Tr ProfZabol (9): 19-22. (See abstract)
Trabelsi M, et aI. (2001). Effect of fluoride on thyroid function and cerebellar development
in mice. Fluoride 34: 165-173. (See study)
Yu YN. (1985). [Effects of chronic fluorosis on the thyroid gland]. Zhonghua Yi Xue Za
Zhi. 65(12):747-9.
VIII. FLUORIDE & the KIDNEYS (back to top)
Kidney damage in skeletal fluorosis (back to top)
Ando M, et aI. (2001). Health effects of fluoride pollution caused by coal burning. Science
of the Total Environment 271(1-3):107-16. (See abstract)
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Derryberry OM, et al. (1963). Fluoride exposure and worker health. Archives of
EnvironmentalHealth 6: 503-511.
Kumar SP, Harper RA. (1963). Fluorosis in Aden. British Journal of Radiology 36: 497-
502.
Shortt HE, et al. (1937). Endemic fluorosis in the Madras presidency. Indian Journal of
Medical Research 25: 553-568.
Siddiqui AH. (1955). Fluorosis in Nalgonda district, Hyderabad-Deccan. British Medical
Journal ii (Dec 10): 1408-1413.
Singh A, et al. (1963). Endemic fluorosis. Epidemiological, clinical and biochemical study
of chronic fluoride intoxication in Punjab. Medicine 42: 229-246.
Fluoride-Induced Nephrotoxicity (back to top)
Abdel-Latif, M:M, et al. (2003). Serum fluoride ion and renal function after prolonged
sevoflurane or isoflurane anaesthesia. Egyptian Journal of Anaesthesia 19: 79-83. (See
abstract I See study)
Arthaud LE, Loomis TA. (1975). The relationship of the total dose and duration of
methoxyflurane anesthesia to renal toxicity in Fischer 344 rats. Toxicology of Applied
Pharmacology 33: 176.
. Atkinson F, Hard GC. (1966). Chronic fluorosis in the guinea-pig. Nature July 23.429-430.
Banu Priya C, et al. (1997). Toxicity of fluoride to diabetic rats. Fluoride 30: 51-58. (See
abstract I See study)
Bond AM, Murray MM. (1952). Kidney function and structure in chronic fluorosis. British
Journal of Experimental Pathology 33: 168-176.
Borke JL, Whitford GM. (1999). Chronic fluoride ingestion decreases 45Ca uptake by rat
kidney membranes. Journal of Nutrition 129(6):1209-13. (See abstract I See study)
Cittanova ML, et al. (2002). Fluoride ion toxicity in rabbit kidney thick ascending limb
cells. European Journal of Anaesthesiology 19(5):341-9. (See abstract)
Cittanova ML, et al. (1996). Fluoride ion toxicity in human kidney collecting duct cells.
Anesthesiology 84(2):428-35. (See abstract)
Cousins MJ, et al. (1983). Anaesthesia and the kidney. Anesthesiology and Intensive Care
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Daston GP, et al. (1985). Toxicity of sodium fluoride to the postnatally developing rat
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Dote T, et al. (2000). Toxicokinetics of intravenous fluoride in rats with renal damage
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Environmental Health 73 Suppl:S90-2. (See abstract)
. Eisenbrandt DL, Nitschke KD. (1989). Inhalation toxicity of sulfuryl fluoride in rats and
rabbits. Fundamentals of Applied Toxicology 1989 Apr;12(3):540-57. (See abstract)
Goldberg ME, et al. (1996). Sevoflurane versus isoflurane for maintenance of anesthesia:
are serum inorganic fluoride ion concentrations of concern? Anesthesia and Analgesia 82
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Gottlieb LS, Trey C. (1974). The effects of fluorinated anesthetics on the liver and kidneys.
Annual Review of Medicine 25: 411-429. (See excerpt)
Greenberg SR. (1986). Response of the renal supporting tissues to chronic fluoride
exposure as revealed by a special technique. Urologia Internationa/is 41(2):91-4. (See
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Guan ZZ, et aI. (2000). Changed cellular membrane lipid composition and lipid
peroxidation of kidney in rats with chronic fluorosis. Archives of Toxicology 74(10):602-8.
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Jankauskas J. (1974). Effects offluoride on the kidney: A review. Fluoride 7: 93-105. (See
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Kessabi M, et al. (1985). Experimental acute sodium fluoride poisoning in sheep: Renal,
hepatic, and metabolic effects. Fundamentals of Applied Toxicology 7(2): 93-105. (See
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Kessabi M, et al. (1981). Comparison of sodium and stannous fluoride nephrotoxicity.
Toxicology Letters 7(6):463-7. (See abstract)
Kour K, Singh J. (1980). Histological findings in kidneys of mice following sodium
fluoride administration. Fluoride 13: 163-167. (See abstract)
Lantz 0, et aI. (1987). Fluoride-induced chronic renal failure. American Journal of Kidney
Disorders 10(2): 136-9. (See abstract)
Manocha SL, et al. (1975). Cytochemical response of kidney, liver and nervous system to
fluoride ions in drinking water. Histochemical Journal 7: 343-355. (See abstract)
Mazze RI. (1984). Fluorinated anesthetic nephrotoxicity: An update. Canadian Anaesthetic
Society Journal 31 :S 16-S22. (See abstract)
Mazze RI, et aI. (1977). Inorganic fluoride nephrotoxicity: prolonged enflurane and
halothane anesthesia in volunteers. Anesthesiology 46(4):265-71. (See abstract I See
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Mazze RI. (1976). Methoxyflurane nephropathy. Environmental Health Perspectives
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cell line NRK-52E. Biological and Pharmaceutical Bulletin 23(5):581-4. (See abstract)
. National Research Council. (1993). Effects of ingested fluoride on renal, gastrointestinal,
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45 Suppll :S32-40. (See abstract)
Partanen S. (2002). Inhibition of human renal acid phosphatases by nephrotoxic micromolar
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Reichle FM, Conzen PF. (2003). Halogenated inhalational anaesthetics. Best practice &
research. Clinical anaesthesiology 17(1):29-46. (See abstract)
Roman RJ, et al. (1977). Renal tubular site of action offluoride in Fischer-344 rats.
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Shashi A, et al. (2002). Toxic effects of fluoride on rabbit kidney. Fluoride 35(1): 38-50.
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Singer I, and Forrest IN. (1976). Drug-induced states of nephrogenic Diabetes Insipidus.
Kidney International 10:82-95.
Singh M, Kanwar KS. (1981). Effect of fluoride on tissue enzyme activities in rat:
Biochemical and histochemical studies. Fluoride 14: 132-141. (See abstract)
Taves DR, et al. (1972). Role of metabolism in the nephrotoxicity of methoxyflurane.
Toxicicology 0/ Applied Pharmacology 23 :795-796.
Thongboonkerd V, et al. (2002). Fluoride exposure attenuates expression of Streptococcus
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Tormanen CD. (2003). Substrate inhibition of rat liver and kidney arginase with fluoride.
Journal o/Inorganic Biochemistry 93(3-4):243-6. (See abstract)
Usuda K, et al. (1999). Usefulness of the assessment of urinary enzyme leakage in
monitoring acute fluoride nephrotoxicity. Archives o/Toxicology 73(6):346-51. (See
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nephrotoxicity. Archives o/Toxicology 72(2): 104-9. (See abstract)
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to rats in drinking water: Alterations in neuronal and cerebrovascular integrity. Brain
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Whitford GM, Stringer GI. (1978). Duration of the fluoride-induced urinary concentrating
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Kidney ailments heighten susceptibility to fluoride toxicity (back to top)
Amala I, et al. (1985). Effects offluoride on bone in Finland. Histomorphometry of cadaver
bone from low and high fluoride areas. Acta Orthopaedica Scandinavica 56(2): 161-6.
Banu Priya C, et al. (1997). Toxicity of fluoride to diabetic rats. Fluoride 30: 51-58. (See
abstract I See study)
Call RA, et al. (1965). Histological and chemical studies in man on effects of fluoride.
Public Health Reports 80: 529-538.
Gerster JC, et al. (1983). Bilateral fractures offemoral neck in patients with moderate renal
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Juncos LI, Donadio JV Jr. (1972). Renal failure and fluorosis. Journal of the American
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Kono K, et al. (1984). Urinary fluoride excretion in fluoride exposed workers with
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Linsman JF, McMurray CA. (1943). Fluoride osteosclerosis from drinking water. Radiology
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FluoridelKidney Stones - Association (back to top)
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Anasuya A, Rao BS. (1983). Effect of fluoride, silicon and magnesium on the mineralizing
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FluoridelKidney Stones - No association (back to top)
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Das TK, et al. (1994). Toxic effects of chronic fluoride ingestion on the upper
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Journal of Gastroenterology and Hepatology 7(4):355-9. (See abstract)
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Fluoride 35(1): 28-37. (See study)
Shayiq RM, et al. (1984). Alteration in gastric secretion of rats administered NaP. Fluoride
17: 178-182. (See abstract)
Sondhi H, et al. (1995). Intestinal effects of sodium fluoride in Swiss Albino mice. Fluoride
28: 21-24. (See abstract)
Spak CJ, et al. (1990). Studies of human gastric mucosa after application of 0.42% fluoride
gel. Journal of Dental Research 69(2):426-9. (See abstract)
.
Spak CJ, et al. (1989). Tissue response of gastric mucosa after ingestion of fluoride. British
Medical Journal 298(6689): 1686-7. (See study)
Susheela AK, et al. (1993). Prevalence of endemic fluorosis with gastro-intestinal
manifestations in people living in some North-Indian villages. Fluoride 26(2): 97-104. (See
abstract)
Susheela AK, et al. (1992). Fluoride ingestion and its correlation with gastrointestinal
discomfort. Fluoride 25(1): 5-22. (See abstract)
Susheela AK, Das TK. (1988). Chronic fluoride toxicity: a scanning electron microscopic
study of duodenal mucosa. Journal of Toxicology and Clinical Toxicology 26(7):467-76.
(See abstract)
Waldbott GW. (1977). Gastric ulcer and fluoride. Fluoride 10: 140-151. (See abstract)
Whitford GM, et al. (1997). Effects offluoride on structure and function of canine gastric
mucosa. Digestive Diseases and Sciences 42(10):2146-55. (See abstract)
x. FLUORIDE & REPRODUCTIVE SYSTEM (back to top)
.
Animals:
Araibi AA, et al. (1989). Effect of high fluoride on the reproductive perrormance of the
male rat. Journal of Biological Science Research 20: 19-30.
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Chinoy NJ, Patel TN. (2001). Efects of sodium fluoride and aluminium chloride on ovary
and uterus of mice and their reversal by some antidotes. Fluoride 34: 9-20. (See study)
Chinoy NJ, Sharma A. (2000). Reversal of fluoride-induced alteration in cauda epididymal
spermatozoa and fertility impairment in male mice. Environmental Sciences 7: 29-38. (See
abstract)
Crunoy NJ, Sharma A. (1998). Amelioration of fluoride toxicity by vitamin E and D in
reproductive functions of male mice. Fluoride 31: 203-216. (See abstract)
Chinoy NJ, et al. (1991). Microdose vasal injection of sodium fluoride in the rat.
Reproductive Toxicolology 5(6):505-12. (See abstract)
Chinoy NJ , Sequeira E. (1989). Effects of fluoride on the histoarchitecture of reproductive
organs of the male mouse. Reproductive Toxicolology 3(4):261-7. (See abstract)
Collins TF, et al. (2001). Multigenerational evaluation of sodium fluoride in rats. Food and
Chemical Toxicology 39(6):601-13. (See abstract)
Collins TF, et al. (1995). Developmental toxicity of sodium fluoride in rats. Food and
Chemical Toxicology 33(11 ):951-60. (See abstract)
Eckerlin RH, et al. (1988). Ameliorative effects of reduced food-borne fluoride on
reproduction in silver foxes. Cornell Veterinarian 78(4):385-91. (See abstract)
Elbetieha A, et al. (2000). Fertility effects of sodium fluoride in male mice, Fluoride 33:
128-134. (See abstract I See study)
Kour K, Singh J. (1980). Histological finding of mice testes following fluoride ingestion.
Fluoride 13: 160-162. (See abstract)
Ghosh D, et al. (2002). Testicular toxicity in sodium fluoride treated rats: association with
oxidative stress. Reproductive Toxicolology 16(4):385.(See abstract)
Guna Sherlin DM, Verma RJ. (2001). Vitamin D ameliorates fluoride-induced
embryotoxicity in pregnant rats. Neurotoxicology and Teratology 23(2): 197 -201. (See
ab stract)
Hiyasat AS. (2000). Reproductive Toxic effects of ingestion of sodium fluoride in female
rats. Fluoride 33(2): 79-84. (See study)
Hoffman DJ, et al. (1985). Effects of fluoride on screech owl reproduction: teratological
evaluation, growth, and blood chemistry in hatchlings. Toxicology Letters 26(1):19-24. (See
abstract)
Kumar A, Susheela AK. (1994). Ultrastructural studies of spermiogenesis in rabbit exposed
to chronic fluoride toxicity. International Journal o/Fertility andMenopausal Studies 39
(3):164-71. (See abstract)
National Research Council. (1993). Reproductive effects of fluoride. In: Health Effects of
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Ingested Fluoride. Report of the Subcommittee on Health Effects of Ingested Fluoride.
National Academy Press Washington, DC. (See chapter)
Narayana MY, et aI. (1994). Reversible effects of sodium fluoride ingestion on spermatozoa
of the rat. International Journal of Fertility andMenopausal Studies 39(6):337-46. (See
ab stract)
Narayana MY, Chinoy NJ. (1994). Effect of fluoride on rat testicular steroidogenesis.
Fluoride 27: 7-12. (See abstract)
Pattee OH, et aI. (1988). Effects of dietary fluoride on reproduction in Ea~tem Screech-
Owls. Archives of Environmental Contamination and Toxicology 17: 213-218. (See
ab stract)
Shashi A. (1990). Histopathological changes in rabbit ovary during experimental fluorosis.
Indian Journal of Pathology and Microbiology 33(2): 113-7. (See abstract)
Shashi A. (1990). Histopathological changes in rabbit testes during experimental fluorosis.
Folia Morphol (praha) 38(1):63-5. (See abstract)
Sprando RL, et aI. (1997). Testing the potential of sodium fluoride to affect
spermatogenesis in the rat. Food and Chemical Toxicology 3-5(9):881-90. (See abstract)
Susheela AK, Kumar A. (1991). A study of the effect of high concentrations of fluoride on
the reproductive organs of male rabbits, using light and scanning electron microscopy.
Journal of Reproductive Fertility 92(2):353-60. (See abstract)
Verma RJ, Sherlin DM. (2001). Vitamin C ameliorates fluoride-induced embryotoxicity in
pregnant rats. Human & Experimental Toxicology 20(12):619-23. (See abstract)
Zhao ZL, et al. (1995). The influence of fluoride on the content of testosterone and
cholesterol in rat. Fluoride 28: 128-130. (See abstract)
Humans:
Chinoy, NJ, Narayana MY. (1994). In vitro fluoride toxicity in human spermatozoa.
Reproductive Toxicology 8(2):155-9. (See abstract)
Freni SC. (1994). Exposure to high fluoride concentrations in drinking water is associated
with decreased birth rates. Journal of Toxicology and Environmental Health 42: 109-121.
(See abstract)
Kuznetsova LS. (1969). The effects of the various operations in the manufacture of
superphosphate on the sex organs of female workers. Gig Tr i Prof Zabo!. 13: 21-25. (See
discussion of study)
Neelam, K, et aI. (1987). Incidence of prevalence of infertility among married male
members of endemic fluorosis district of Andhra Pradesh. In: Abstract Proc Conf Int Soc
for Fluoride Res. Nyon, Switzerland.
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.
Ortiz-Perez D, et aI. (2003). Fluoride-induced disruption of reproductive hormones in men.
EnvironmentalResearch 93(1):20-30. (See abstract)
Susheela AK, Jethanandani P. (1996). Circulating testosterone levels in skeletal fluorosis
patients. Journal of Toxicology and Clinical Toxicology 34(2): 183-9. (See abstract)
Tokar VI, Savchenko ON. (1977). Effect of inorganic fluorine compounds on the functional
state of the pituitary-testis system. Prob/ Endokrinol (Mosk). 23(4):104-7. (See abstract)
x. FLUORIDE & THE IMMUNE SYSTEM
Gibson S. (1992). Effects of fluoride on immune system function. Complementary Medicine
Research 6: 111-113. (See excerpts)
Greenberg SR. (1982). Leukocyte response in young mice chronically exposed to fluoride.
Fluoride 15: 119-123. (See abstact)
Jain SK, Susheela AK. (1987). Effect of sodium fluoride on antibody formation in rabbits.
Environmental Research 44: 117-125. (See abstract)
Loftenius A, et al. (1999). Fluoride augments the mitogenic and antigenic response of
human blood lymphocytes in vitro. Caries Research 33:148-55. (See abstract)
.
Susheela AK, Jain SK. (1983). Fluoride-induced haematological changes in rabbits. Bulletin
of Environmental Contamination and Toxicology 30: 388-93. (See abstract)
Sutton P. (1991). Is the ingestion offluoride an immunosuppressive practice? Medical
Hypotheses 35: 1-3. (See paper)
Sutton P. (1987). Does fluoride ingestion affect developing immune system cells? Medical
Hypotheses 23: 335-336. (See paper)
Wilkinson PC. (1983). Effects of fluoride on locomotion of human blood.leucocytes in
vitro. Archives of Oral Biology 28: 415-8. (See abstract)
xu. ALLERGY /HYPERSENSITIVITY TO FLUORIDE (back to top)
Goldman D. (2001). Tacrolimus ointment for the treatment of steroid-induced rosacea: a
preliminary report. Journal of the American Academy of Dermatology 44: 995-8. (See
abstract)
Feltman R, Kosel G. (1961). Prenatal and postnatal ingestion offluorides - Fourteen years
of investigation - Final report. Journal of Dental Medicine 16: 190-99. (See excerpts)
Lewis A, Wilson CWo (1985). Fluoride hypersensitivity in Mains tap water demonstrated by
skin potential changes in guinea-pigs. Medical Hypotheses 16: 397-402. (See abstract)
. Shea 11, et al. (1967). Allergy to fluoride. Annals of Allergy 25:388-91. (See study)
Spittle B. (1993). Allergy and hypersensitivity to fluoride. Fluoride 26(4):267-73. (See
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paper)
Waldbott GL, Burgstahler AW, McKinney m... (1978). Fluoridation: The Great Dilemma.
Coronado Press, Inc., Lawrence, Kansas.
Zanfanga PE. (1976). Allergy to fluoride. Fluoride 9(1): 36-41. (See study)
Xill. DOWN'S SYNDROME (back to top)
Burgstahler A W. (1975). Editorial Review: Fluoride and Down's Syndrome (Mongolism).
Fluoride 8: 1-11, 120.
Erickson JD, et at. (1976). Water Fluoridation and Congenital Malformations: No
Association. Journal of the American Dental Association 93 (5): 981-984. (See abstract)
Needleman m.., et at. (1974). Fluoridation and the Occurrence of Down's Syndrome. New
England Journal of Medicine 291: 821-823.
Rapaport 1. (1961). A propos du mongolisme infantile. Dne deviation du metabolisme de
tryptophane provoquee par Ie fluor chez la drosophile. Bull. Acad Natl. Med (paris). 145:
450-453. (See discussion of Rapaport's research)
Rapaport 1. (1960). Oligophrenie mongolienne et ectodermoses congenitales. Ann.
Dermatol. Syphiligr. 87: 263-278.
Rapaport 1. (1959). Nouvelles recherches sur Ie mongolisme. A propos du role
pathogenique du fluor. Bull. Acad Nat. Med (paris). 143: 367-370.
Rapaport 1. (1957). Contribution a l'etude etiologique du mongolisme. Role des inhibiteurs
enzymatiques. Encephale. 46: 468-481.
Takahashi K. (1998). Fluoride-linked down syndrome births and their estimated occurrence
due to water fluoridation. Fluoride 31(2):61-73. (See paper)
Waldbott GL, Burgstahler AW, and McKinney m... (1978). Fluoridation: The Great
Dilemma. Coronado Press, Inc., Lawrence, Kansas. p. 212-219. (See excerpt)
Whiting P. (2001). Association of Down's syndrome and water fluoride level: a systematic
review of the evidence. BioMed Central Public Health 1 :6.(See study)
XIV. FLUORIDE & CARIES (Tooth Decay) (back to top)
Decline of Caries in Western Industrialized Societies (Irrespective of Fluoridation) (back to top)
Colquhoun 1. (1997). Why I changed my mind about Fluoridation. Perspectives in Biology
andMedicine. 41:29-44. (See paper)
DiesendorfM. (1986). The mystery of declining tooth decay. Nature 322: 125-129. (See
paper)
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Glass RL. (1981). Secular changes in caries prevalence in two Massachusetts towns, Caries
Research 15: 445-50. (See abstract) .
Gray AS. (1987). Fluoridation: time for a new base line? Journal of the Canadian Dental
Association 53: 763-5. (See abstract)
Haugejorden O. (1996). Using the DMF gender difference to assess the "major" role of
fluoride toothpastes in the caries decline in industrialized countries: a meta-analysis.
Community Dentistry and Oral Epidemiology 24(6):369-75. (See abstract)
KalsbeekH, Verrips GH. (1990). Dental caries prevalence and the use of fluorides in
different European countries. Journal of Dental Research 69(Spec Iss): 728-32. (See
abstract)
Leverett DR. (1982). Fluorides and the changing prevalence of dental caries. Science 217
(4554):26-30. (See abstract)
Marthaler TM, et al. (1996). The prevalence of dental caries in Europe 1990-1995. ORCA
Saturday afternoon symposium 1995. Caries Research 30(4):237-55. (See abstract)
Peters son GH, Bratthall D. (1996). The caries decline: a review of reviews. European
Journal of Oral Science 104(4(Pt 2)):436-43. (See abstract)
Reich E. (2001). Trends in caries and periodontal health epidemiology in Europe.
International Dental Journal 51(6 Suppll):392-8. (See abstract)
WHO (Online). WHO Oral Health Country/Area Profile Programme. Department of
Noncommunicable Diseases Surveillance/Oral Health. WHO Collaborating Centre, Malmo
University, Sweden. (See data)
Caries Decline in Belgium - (Unfluoridated Water, Fluoridated Salt):
Carvalho IC, et al. (2001). The decline in dental caries among Belgian children between
1983 and 1998. Community Dentistry and Oral Epidemiology 29(1):55-61. (See abstract)
Caries Decline in Denmark - (Unfluoridated Water, Unfluoridated Salt):
Petersen PE. (1992). Effectiveness of oral health care-some Danish experiences.
Proceedings of the Finnish Dental Society 88(1-2): 13-23. (See abstract)
Caries Decline in Finland - (Unfluoridated Water, Unfluoridated Salt):
Vehkalahti M, Rytomaa I, Helminen S. (1991). Decline in dental caries and public oral
health care of adolescents. Acta Odontologica Scandinavica 49(6):323-8. (See abstract)
Caries Decline in France - (Unfluoridated Water, Fluoridated Salt):
Obry-Musset AM. (1998). [Epidemiology of dental caries in children] [Article in French]
Arch Pediatr. 5(10): 1145-8. (See abstract)
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f\ tslollograpny ot :SclentItlc LIterature on .Fluoride
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Caries Decline in Germany - (Unfluoridated Water, Fluoridated Salt):
Gulzow HJ. (1990). [Preventive dentistry in the Federal Republic of Germany] [Article in
German] Oralprophylaxe. 12(2):53-60. (See abstract)
Caries Decline in Greece - (Unfluoridated Water, Unfluoridated Salt):
Athanassouli I, et al. (1994). Dental caries changes between 1982 and 1991 in children aged
6-12 in Athens, Greece. Caries Research 28(5):378-82. (See abstract)
Caries Decline in Iceland - (Unfluoridated Water, Unfluoridated Salt):
Einarsdottir KG, Bratthall D. (1996). Restoring oral health: On the rise and fall of dental
caries in Iceland. European Journal of Oral Science 104(4 ( Pt 2)):459-69, (See abstract)
Caries Decline in The Netherlands - (Unfluoridated Water, Unfluoridated Salt):
Truin GJ, et al. (1994). Caries prevalence in Belgium and The Netherlands. International
Dental Journal 44(4 Suppll):379-8. (See abstract)
Caries Decline in Norway - (Unfluoridated Water, Unfluoridated Salt):
Birkeland lM, Haugejorden O. (2001). Caries decline before fluoride toothpaste was
available: earlier and greater decline in the rural north than in southwestern Norway. Acta
Odontologica Scandinavica 59(1):7-13 (See abstract)
Kallestal C, et al. (1999). Caries-preventive methods used for children and adolescents in
Denmark, Iceland, Norway and Sweden. Community Dentistry and Oral Epidemiology 27
(2):144-51. (See abstract)
Caries Decline in Sweden - (Unfluoridated Water, Unfluoridated Salt):
Stecksen-Blicks C, Holm AK. (1995). Dental caries, tooth trauma, malocclusion, fluoride
usage, toothbrushing and dietary habits in 4-year-old Swedish children: changes between
1967 and 1992. International Journal of Paediatric Dentistry 5(3): 143-8:(See abstract)
Caries Decline in Switzerland - (Unfluoridated Water, Fluoridated Salt):
Menghini G, et al. (2003). [Caries prevalence among students in 16 Zurich districts in the
years 1992 to 2000 Schweiz Monatsschr Zahnmed 113 (3) :267 - 77. (See ab stract)
Marthaler TM. (1991). [School dentistry in Zurich Canton: changes as a result of caries
reduction of 80 to 85 percent] [Article in German] Oralprophy/axe. 13(4): 115-22. (See
abstract)
NIDR's National Survey of Dental Health in US (Largest dental survey conducted in US): (back to
!Qill
Brunelle, JA, Carlos JP. (1990). Recent trends in dental caries in U.S. children and the
effect of water fluoridation. Journal of Dental Research 69(Special edition): 723-727. (See
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paper)
. Heller KE, et al (1997). Dental caries and dental fluorosis at varying water fluoride
concentrations. Journal of Public Health Dentistry 57(3): 136-143. (See abstract)
Hileman B. (1989). New studies cast doubt on fluoridation benefits. Chemical and
Engineering News May 8. (See article)
Yiamouyiannis JA. (1990). Water fluoridation and tooth decay: Results from the 1986-87
national survey of U.S. schoolchildren. Fluoride 23: 55-67. (See paper)
Fluoridation Cessation Studies (back to top)
Burt BA, et al. (2000). The effects of a break: in water fluoridation on the development of
dental caries and fluorosis. Journal of Dental Research 79(2):761-9. (See abstract)
Kunzel W, et al. (2000). Decline in caries prevalence after the cessation of water
fluoridation in former East Germany. Community Dentistry and Oral Epidemiology 28(5):
382-389. (See abstract)
Kunzel W, Fischer T. (2000). Caries prevalence after cessation of water fluoridation in La
Salud, Cuba. Caries Research 34(1): 20-5. (See abstract)
Maupome G, et al. (2001). Patterns of dental caries following the cessation of water
. fluoridation. Community Dentistry and Oral Epidemiology 29(1): 37-47. (See abstract)
Seppa L, et al. (2000) Caries trends 1992-98 in two low-fluoride Finnish towns formerly
with and without fluoride. Caries Research 34(6): 462-8. (See abstract)
Critique of Early Fluoridation Trials (back to top)
Sutton P. (1960) Fluoridation: Errors and Omissions in Experimental Trials. Melbourne
University Press. Second Edition. (See report ).
Sutton P. (1996). The Greatest Fraud: Fluoridation. A Factual Book. Kurunda Pty, Ltd, PO
Box 22, Lome, Australia 3232.
Fluoride's Topical Vs. Systemic Effects (back to top)
Burt BA. (1999). The case for eliminating the use of dietary fluoride supplements for young
children. Journal of Public Health Dentistry 59: 269-74. (See abstract) .
Carlos JP. (1983). Comments on Fluoride. Journal of Pedodontics Winter: 135-136.
CDC. (2001). Recommendations for Using Fluoride to Prevent and Control Dental Caries in
the United States. Mortality andMorbidity Weekly Review 50(RR14):1-42. (See report)
. CDC (1999). Achievements in Public Health, 1900-1999: Fluoridation of Drinking Water to
Prevent Dental Caries. Mortality andMorbidity Weekly Review 48(41): 933-940. (See
report)
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Featherstone J.D.B. (1999) Prevention and reversal of dental caries: role oflow level
fluoride. Community Dentistry and Oral Epidemiology 27:31-40. (See abstract)
Featherstone, J.D.B. (2000). The Science and Practice of Caries Prevention. Journal of the
American Dental Association 131: 887-899. (See abstract)
Heifetz SB, Proskin HM. (1995). Serendipitous results ofa pilot study: precaution
indicated. Journal of Clinical Dentistry 6(1): 117-9. (See abstract)
Fejerskov 0, et al. (1981). Rational use of fluorides in caries prevention. Acta Odontologica
Scandinavica 241-249, (See abstract)
Leverett DH. (1991). Appropriate uses of systemic fluoride: considerations for the '90s.
Journal of Public Health Dentistry 51: 42-7. (See excerpt)
Levine, R.S., (1976). The action offluoride in caries prevention: a review of current
concepts. British Dental Journal 140: 9-14.
Locker, D. (1999). Benefits and Risks of Water Fluoridation. An Update of the 1996
Federal-Provincial Sub-committee Report. Prepared for Ontario Ministry of Health and
Long Term Care. (See report )
Limeback, H. (1999). A re-examination of the pre-eruptive and post-eruptive mechanism of
the anti-caries effects of fluoride: is there any caries benefit from swallowing fluoride?
Community Dentistry and Oral Epidemiology 27: 62-71. (See abstract)
Mirth DB et al. (1985). Comparison of the cariostatic effect of topically and systemically
administered controlled release fluoride in the rat. Caries Research 19: 466-74.
Fluoride and Pit & Fissure Decay: (back to top)
Journal of the American Dental Association. (1984). Preserving the perfect tooth. Editorial.
Vol. 108.
"It is estimated that 84% of the caries experience in the 5 to 17 year-old
population involves tooth surfaces with pits andfissures. AlthoughfIuorides
cannot be expected appreciably to reduce our incidence of caries on these
surfaces, sealants can. "
Gray AS. (1987). Fluoridation: time for a new base line? Journal of the Canadian Dental
Association 53: 763-5.
"The type of caries now seen in British Columbia's children of 13 years of age,
is mostly the pitandfissure type. Knudsen in 1940, suggested that 70 percent of
the caries in children was in pits and fissures. Recent reports indicate that
today, 83 percent of all caries in North American children is of this type. Pit
andfissure cavities aren't considered to be preventable by fluorides, they are
prevented by sealants. "
White B. (1993). Toward improving the oral health of Americans: an overview of oral
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health status, resources and care delivery. Public Health Reports 108(6): 657-672.
"Fluoridation and the use of other fluorides have been successful in decreasing
the prevalence of dental caries on the smooth surfaces of teeth. Unfortunately,
these efforts have much less effect on dental caries that occur in the pits and
fissures of teeth (particularly on the biting surfaces of teeth) where more than
85 percent of dental caries now occur. "
Pinkham JR, ed. (1999). Pediatric Dentistry Infancy Through Adolescence. 3rd Edition.
Philadelphia: WB Saunders Co.
"[EJnamel surfaces with pits andfissures receive minimal caries protection
from either systemic or topical fluoride agents. "
Fluoride & Baby Bottle Tooth Decay (back to top)
Barnes GP, et al. (1992). Ethnicity, location, age, and fluoridation factors in baby bottle
tooth decay and caries prevalence of Head Start children. Public Health Reports 107: 167-
73. (See abstract)
Shiboski CH, et al. (2003), The association of early childhood caries and race/ethnicity
among California preschool children. Journal of Public Health Dentistry 63(1):38-46. (See
abstract)
Von Burg MM, et al. (1995). Baby bottle tooth decay: a concern for all mothers. Pediatric
Nursing 21 : 515-519. (See abstract)
Elevated Fluoride Exposure Increases Tooth Decay (back to top)
Awadia AK, et al. (2002). Caries experience and caries predictors - a study of Tanzanian
children consuming drinking water with different fluoride concentrations. Clinical Oral
Investigations (2002) 6:98-103. (See abstract)
Budipramana ES, et al. (2002). Dental fluorosis and caries prevalence in the fluorosis
endemic area of Asembagus, Indonesia. International Journal of Paediatric Dentistry 12
(6):415-22. (See abstract)
Ekanayake L, Van Der Hoek W. (2002). Dental caries and developmental defects of enamel
in relation to fluoride levels in drinking water in an arid area of sri lanka. Caries Research
36(6):398-404. (See abstract)
Grobleri SR, et al. (2001). Dental fluorosis and caries experience in relation to three
different drinking water fluoride levels in South Mrica. International Journal of Paediatric
Dentistry 11(5):372-9. (See abstract)
Mann J,et al. (1990). Fluorosis and dental caries in 6-8-year-old children in a 5 ppm
fluoride area. Community Dentistry and Oral Epidemiology 18(2):77-9. (See abstract)
Mann J, et al. (1987). Fluorosis and caries prevalence in a community drinking above-
optimal fluoridated water. Community Dentistry and Oral Epidemiology 15(5):293-5. (See
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abstract)
. Ramseyer WF, et al. (1957). Effect of Sodium Fluoride Administration on Body Changes in
Old Rats. Journal of Gerontology 12: 14-19. (See excerpt)
.
.
RetiefDH, et al. (1979). Relationships among fluoride concentration in enamel, degree of
fluorosis and caries incidence in a community residing in a high fluoride area. Journal of
Oral Pathology 8: 224-36. (See abstract)
Roholm K. (1937). Fluoride intoxication: a clinical-hygienic study with a review of the
literature and some experimental investigations. H.K. Lewis Ltd, London: (See excerpts)
Teotia SPS, Teotia M. (1994). Dental caries: a disorder of high fluoride and low dietary
calcium interactions (30 years of personal research). Fluoride 27(2): 59-66. (See abstract)
See also:
Steelink C, (1992). Fluoridation Controversy. (Letter). Chemical Enginerering News July
27: 2-3.
Fluoride & Delayed Eruption of Teeth: (back to tot>)
Ainsworth NJ, (1933). Mottled teeth. British Dental Journal 55: 233-250.
Campagna L, et al. (1995). Fluoridated drinking water and maturation of permanent teeth at
age 12. Journal of Clinical Pediatric Dentistry 19(3):225-8. (See abstract)
Feltman R, Kosel G. (1961). Prenatal and postnatal ingestion of fluorides - Fourteen years
of investigation - Final report. Journal of Dental Medicine 16: 190-99.
Freitas JA, et al. (1971). Influence offluoridation in the chronology of eruption of
permanent teeth. Estomatologia e Cultura 5: 156-165.
Krook L, et al. (1983). Dental fluorosis in cattle. Cornell Veterinarian 73(4):340-62. (See
abstract)
Kunzel VW. (1976). [Cross-sectional comparison of the median eruption time for
permanent teeth in children from fluoride poor and optimally fluoridated areas] Stomatol
DDR. 5:310-21. (See abstract)
Lemmon JR. (1934). Mottled enamel of teeth in children. Texas State Journal of Medicine
30: 332-336.
Limeback, H. (2002). Systemic Fluoride: Delayed Tooth Eruption and DMFT vs Age
Profiles. abstract presented at IADR/AADR/CADR 80th General Session. San Diego,
California. March 6-9. (See abstract)
Roholm K. (1937). Fluoride intoxication: a clinical-hygienic study with a review of the
literature and some experimental investigations. HK. Lewis Ltd, London. (See excerpts)
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Virtanen n, et aI. (1994). Timing of eruption of permanent teeth: standard Finnish patient
documents. Community Dentistry and Oral Epidemiology 22(5 Pt 1 ):286-8. (See abstract)
See also:
Nadler GL. (1998). Earlier dental maturation: fact or fiction? Angle Orthod. 68(6):535-8.
(See abstract)
xv. DENTAL FLUOROSIS (back to top)
Mechanism of Action (back to top)
Aoba T, Fejerskov O. (2002). Dental fluorosis: chemistry and biology. Critical Review of
Oral Biology andMedicine 13(2):155-70. (See abstract)
DenBesten PK, et al. (2002). Effects offluoride on rat dental enamel matrix proteinases.
Archives of Oral Biology 47(11):763-770. (See abstract) .
DenBesten P (1999). Biological mechanism of dental fluorosis relevant to the use of
fluoride supplements. Community Dentistry and Oral Epidemiology 27,41-7. (See abstract)
Everett ET, et al. (2002). Dental Fluorosis: Variability among Different Inbred Mouse
Strains. Journal of Dental Research 81(11):794-8. (See abstract)
Matsuo S, et al. (1998). Mechanism of toxic action of fluoride in dental fluorosis: whether
trimeric G proteins participate in the disturbance of intracellular transport of secretory
ameloblast exposed to fluoride. Archives of Toxicology 72(12):798-806. (See abstract)
Ouyang W, et al. (2000). [Effect caused by uptake of different levels of calcium to enamel
fluorosis in rats] [Article in Chinese]. Zhonghua Kou Qiang Yi Xue Za Zhi. 35(1):47-9. (See
ab stract)
Current Rates of Dental Fl uorosis (back to top)
Clark DC. (1994). Trends in prevalence of dental fluorosis in North America. Community
Dentistry and Oral Epidemiology 22: 148-52. (See abstract)
Griffin SO, et al. (2002). Esthetically objectionable fluorosis attributable to water
fluoridation. Community Dentistry and Oral Epidemiology 30(3): 199-209. (See abstract)
Heller KE, et al (1997). Dental caries and dental fluorosis at varying water fluoride
concentrations. Journal of Public Health Dentistry 57(3) 136-143. (See abstract)
Lalumandier JA, et al (1995). The prevalence and risk factors of fluorosis among patients in
a pediatric dental practice. Pediatric Dentistry 17:1, 19-25. (See abstract)
Leverett D. (1986). Prevalence of dental fluorosis in fluoridated and nonfluoridated
communities--a preliminary investigation. Journal of Public Health Dentistry 46(4): 184-7.
(See abstract)
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McDonagh M, et al. (2000). A Systematic Review of Public Water Fluoridation. (liThe
York Review. ") NHS Center for Reviews and Dissemination. University of York.
September 2000. (See report)
Rozier RG. (1999). The prevalence and severity of enamel fluorosis in North American
children. Journal of Public Health Dentistry 59(4):239-46. (See abstract)
Tabari ED, et al. (2000). Dental fluorosis in permanent incisor teeth in relation to water
fluoridation, social deprivation and toothpaste use in infancy. British Dental Journal 189
(4): 216-220. (See abstract)
Williams JE, et al. (1990), Community Water Fluoride Levels, Preschool Dietary Patterns,
and The Occurrence of Fluoride Enamel Opacities. Journal of Pub Health Dentistry 50:276-
81. (See abstract)
Dental fluorosis more prevalent among African-Americans (back to top)
Butler WJ, et al. (1985). Prevalence of dental mottling in school-aged lifetime residents of
16 Texas communities. American Journal of Public Health 75(12):1408-12. (See abstract)
Kumar N, Swango P A. (2000). Low birth weight and dental fluorosis: is there an
association? Journal of Public Health Dentistry 60(3): 167-71. (See abstract)
Kumar N, Swango PA. (1999). Fluoride exposure and dental fluorosis in Newburgh and
Kingston, New York: policy implications. Community Dentistry and Oral Epidemiology 27
(3): 171-80. (See abstract)
Heller KE, et al. (2000). Water consumption and nursing characteristics of infants by race
and ethnicity. Journal of Public Health Dentistry 60(3): 140-6.(See abstract)
PerceptionslPsychological Effects of Dental Fluorosis (back to top)
Chikte UM, et al. (2001). Perceptions of fluorosis in northern Cape communities. South
African Dental Journal 56(11):528-32. (See abstract)
Griffin SO, et al. (2002). Esthetically objectionable fluorosis attributable to water
fluoridation. Community Dentistry and Oral Epidemiology 30(3): 199-209. (See abstract)
Jones J, Glasser G. (2002). The Psychological Impact of Dental Fluorosis. National Pure
Water Association. Wakefield, UK. (See paper)
McKnight CB, et al. (1998). A pilot study of esthetic perceptions of dental fluorosis vs.
selected other dental conditions. ASDC Journal of Dentistry for Children 65(4):233 -8, 229.
(See abstract)
Milsom KM, et al. (2000). A comparison of normative and subjective assessment of the
child prevalence of developmental defects of enamel amongst 12-year-olds living in the
North West Region, UK. Public Health. 114(5):340-4. (See abstract)
Rahmatulla AH. (1995). Clinical evaluation of two different techniques for the removal of
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fluorosis stains. Egyptian Dental Journal 41(3): 1287-94. (See abstract)
. Riordan Pl (1993). Perceptions of dental fluorosis. Journal of Dental Research 72(9): 1268-
74.(See abstract)
Rodd lID, Davidson LE. (1997). The aesthetic management of severe dental fluorosis in the
young patient. Dental Update 24(10):408-11. (See abstract)
Spencer AJ, et al. (1996). Water fluoridation in Australia. Community Dental Health 13
(Suppl 2):27-37. (See excerpt)
Welbury RR, Shaw L. (1990). A simple technique for removal of mottling, opacities and
pigmentation from enamel. Dental Update 17(4):161-3. (See abstract) .
Dental fluorosis & Bone fracture (back to top)
Alarcon-Herrera MT, et al. (2001). Well Water Fluoride, Dental fluorosis, Bone Fractures
in the Guadiana Valley of Mexico. Fluoride 34(2): 139-149.(See study)
Fluorosis & Caries (back to top)
Awadia AK, et al. (2002). Caries experience and caries predictors - a study of Tanzanian
children consuming drinking water with different fluoride concentrations. Clinical Oral
Investigations (2002) 6:98-103. (See abstract)
.
Budipramana ES, et al. (2002). Dental fluorosis and caries prevalence in the fluorosis
endemic area of Asembagus, Indonesia. International Journal of Paediatric Dentistry 12
(6):415-22. (See abstract)
Ekanayake L, Van Der Hoek W. (2002). Dental caries and developmental defects of enamel
in relation to fluoride levels in drinking water in an arid area of sri lanka. Caries Research
36(6):398-404. (See abstract)
Grobleri SR, et al. (2001). Dental fluorosis and caries experience in relation to three
different drinking water fluoride levels in South Mrica. International Journal of Paediatric
Dentistry 11(5):372-9. (See abstract)
Ibrahim YE, et al. (1997). Caries and dental fluorosis in a 0.25 and a 2.5 ppm fluoride area
in the Sudan.International Journal of Paediatric Dentistry 7(3): 161-6. (See abstract)
Mann J,et al. (1990). Fluorosis and dental caries in 6-8-year-old children in a 5 ppm
fluoride area. Community Dentistry and Oral Epidemiology 18(2):77-9. (See abstract)
Mann J, et al. (1987). Fluorosis and caries prevalence in a community drinking above-
optimal fluoridated water. Community Dentistry and Oral Epidemiology 15(5):293-5. (See
abstract)
.
Roholm K. (1937). Fluoride intoxication: a clinical-hygienic study with a review ofthe
literature and some experimental investigations. H.K. Lewis Ltd, London. (See excerpts)
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Teotia SPS, Teotia M. (1994). Dental caries: a disorder of high fluoride and low dietary
calcium interactions (30 years of personal research). Fluoride 27(2): 59-66. (See abstract)
Risk Factors for Fluorosis (back to top)
Angmar-Mansson B, Whitford GM. (1990). Environmental and physiological factors
affecting dental fluorosis. Journal of Dental Research 6(Spec Iss): 706-13. (See abstract)
Behrendt A, Oberste V, Wetzel WE. (2002). Fluoride concentration and pH of iced tea
products. Caries Research 36(6): 405-410. (See abstract)
Bentley EM, et al. (1999). Fluoride ingestion from toothpaste by young children. British
Dental Journal 186(9):460-2. (See abstract)
Burt BA. (1999). The case for eliminating the use of dietary fluoride supplements for young
children. Journal of Public Health Dentistry 59: 269-74. (See abstract)
Clark DC, et al. (1994). Influence of exposure to various fluoride technologies on the
prevalence of dental fluorosis. Community Dentistry and Oral Epidemiology 22: 461-4.
(See abstract)
Fein NJ, Cerklewski FL. (2001). Fluoride content of foods made with mechanically
separated chicken. Journal of Agricultural Food Chemistry 49(9):4284-6. (See abstract)
Fomon SJ, Ekstrand J, Ziegler EE. (2000). Fluoride intake and prevalence of dental
fluorosis: trends in fluoride intake with special attention to infants. Journal of Public Health
Dentistry 60(3): 131-9. (See abstract)
Fomon SJ, Ekstrand J. (1999). Fluoride intake by infants. Journal of Public Health
Dentistry 59(4):229-34. (See abstract)
Griffin SO, et al. (2002). Esthetically objectionable fluorosis attributable to water
fluoridation. Community Dentistry and Oral Epidemiology 30(3): 199-209. (See abstract)
Heilman JR, et al. (1999). Assessing fluoride levels of carbonated soft drinks. Journal of the
American Dental Association 130(11): 1593-9. (See abstract)
Kiritsy MC, et al. (1996). Assessing fluoride concentrations of juices and juice-flavored
drinks. Journal of the American Dental Association 127(7):895-902. (See abstract)
Levy SM, Guha-Chowdhury N. (1999). Total fluoride intake and implications for dietary
fluoride supplementation. Journal of Public Health Dentistry 59: 211-23. (See abstract)
Levy SM, et al. (1995). Sources of fluoride intake in children. Journal of Public Health
Dentistry 55(1):39-52. (See abstract)
Lewis DW, Limeback H. (1996). Comparison of recommended and actual mean intakes of
fluoride by Canadians. Journal of the Canadian Dental Association 62: 708-715. (See
abstract)
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.
Mascarenhas AK. (2000). Risk factors for dental fluorosis: a review of the recent literature.
Pediatric Dentistry 22(4):269-77. (See abstract)
Mascarenhas AK, Burt BA. (1998). Fluorosis risk from early exposure to fluoride
toothpaste. Community Dentistry and Oral Epidemiology 26(4):241-8. (See abstract)
Massier M, Schour I. (1952). Relation of endemic dental fluorosis to malnutrition. Journal
of the American Dental Association 44: 156-165. (See excerpt)
Murray MM, Wilson DC. (1948). Fluorosis and nutrition in Morocco. British Dental
Journal 84: 97.
Pendrys DG. (2000). Risk of enamel fluorosis in nonfluoridated and optimally fluoridated
populations: considerations for the dental professional. Journal of the American Dental
Association 131: 746-55. (See abstract)
Pendrys DG, Katz RV. (1998). Risk factors for enamel fluorosis in optimally fluoridated
children born after the US manufacturers' decision to reduce the fluoride concentration of
infant formula. American Journal of Epidemiology 148: 967-74. (See abstract) .
Pendrys DG, et al. (1994). Risk factors for enamel fluorosis in a fluoridated population.
American Journal of Epidemiology 140: 461-71. (See abstract)
Turner SD, et al. (1998). Impact of imported beverages on fluoridated and nonfluoridated
. communities. General Dentistry 46(2):190-3. (See abstract)
Level of fluoride in infant-formula made with fluoridated water is 100 times higher
than fluoride level found in women's breast milk:
Institute of Medicine. (1997). Dietary Reference Intakes for Calcium,
Phosphorus, Magnesium, Vitamin D, and Fluoride. Standing Committee on the
Scientific Evaluation of Dietary Reference Intakes, Food and Nutrition Board.
National Academy Press.
XVI. FLUORIDE: NOT an ESSENTIAL NUTRIENT (back to top)
National Research Council (1993). Health Effects ofIngested Fluoride. National Academy
Press, Washington DC. See page 30. (See report)
XVll. SOURCES OF FLUORIDE EXPOSURE (back to top)
Behrendt A, Oberste V, Wetzel WE. (2002). Fluoride concentration and pH of iced tea
products. Caries Research 36(6): 405-410. (See abstract)
Bentley EM, et al. (1999). Fluoride ingestion from toothpaste by young children. British
Dental Journal 186(9):460-2. (See abstract)
.
Burgstahler AW, et al. (1997). Fluoride in California wines and raisins. Fluoride 30: 142-
146. (See abstract)
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.
Department of Health & Human Services (DHHS). (1991). Review of Fluoride: Benefits
and Risks. Report of the Ad Hoc Committee on Fluoride. Page 17.
DiesendorfM, Diesendorf A. (1997). Suppression by medical journals of a warning about
overdosing formula-fed infants with fluoride. Accountability in Research 5:225-237.
Farkas CS. (1975). Total fluoride intake and fluoride content of common foods: a review.
Fluoride 8: 98-105. (See abstract)
Fein NJ, Cerklewski FL. (2001). Fluoride content of foods made with mechanically
separated chicken. Journal of Agricultural Food Chemistry 49(9):4284-6. (See abstract)
Fomon SJ, Ekstrand J, Ziegler EE. (2000). Fluoride intake and prevalence of dental
fluorosis: trends in fluoride intake with special attention to infants. Journal of Public Health
Dentistry 60(3): 131-9. (See abstract) .
Fomon SJ, Ekstrand J. (1999). Fluoride intake by infants. Journal of Public Health
Dentistry 59(4):229-34. (See abstract)
Kiritsy MC, et al. (1996). Assessing fluoride concentrations of juices and juice-flavored
drinks. Journal of the American Dental Association 127(7):895-902. (See abstract)
Levy SM, et al. (1995). Sources offluoride intake in children. Journal of Public Health
Dentistry 55(1):39-52. (See abstract)
Lung SC, et al. (2003). Fluoride concentrations in three types of commercially packed tea
drinks in Taiwan. Journal of Exposure Analysis and Environmental Epidemiology 13(1):66-
73. (See abstract)
Mascarenhas AK. (2000). Risk factors for dental fluorosis: a review of the recent literature.
Pediatric Dentistry 22(4):269-77. (See abstract)
Mascarenhas AK, Burt BA. (1998). Fluorosis risk from early exposure to fluoride
toothpaste. Community Dentistry and Oral Epidemiology 26(4):241-8. (See abstract)
Marier JR. (1977). Some current aspects of environmental fluoride. Science of the Total
Environment 8(3):253-65. (See abstract)
.
Marier J, Rose D. (1977). Environmental Fluoride. National Research Council of Canada.
Associate Committe on Scientific Criteria for Environmental Quality. NRCC No. 16081.
(See report).
Marier J, Rose D. (1966). The Fluoride Content of Some Foods and Beverages - a Brief
Survey Using a Modified Zr-SP ADNS Method. Journal of Food Science 31: 941-946. (See
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abstract & excerpt)
. Pang D, et al. (1992). Fluoride intake from beverage consumption in a sample of North
Carolina children. Journal of Dental Research 71: 1382-1388.
Prival M, Fisher F. (1974). Adding fluorides to the diet. Environment 16(5): 29-33.
Stannard JG, et al. (1991). Fluoride levels and fluoride contamination of fruit juices.
Journal of Clinical Pediatric Dentistry 16(1):38-40. (See abstract)
Turner SD, et al. (1998). Impact of imported beverages on fluoridated and nonfluoridated
communities. General Dentistry 46(2): 190-3. (See abstract)
Warnakulasuriya S, et al. (2002). Fluoride content of alcoholic beverages. Clinica Chimica
Acta 320(1-2):1-4. (See abstract)
XVllI. NUTRITONAL DEFICIENCIES EXACERBATE FLUORIDE'S TOXICITY (back to top)
Agency for Toxic Substances and Disease Registry (ATSDR) (1993). Toxicological Profile
for Fluorides, Hydrogen Fluoride, and Fluorine (F). U. S. Department of Health & Human
Services, Public Health Service. ATSDR/TP-91/17. (See report)
.
Antonyan OA. (1980). Lipid peroxidation in fluorosis and the protective role of dietary
factors. Zh Eksp KlinMed. 20(4): 381-388. (See abstract)
Chen YC, et al. (1997). Nutrition survey in dental fluorosis-afflicted areas. Fluoride 30
(2):77-80. (See abstract)
Ekambaram P, Paul V. (2001). Calcium preventing locomotor behavioral and dental
toxicities of fluoride by decreasing serum fluoride level in rats. Environmental Toxicology
and Pharmacology 9(4):141-146. (See abstract)
Krishnamachari KA, Krishnamachari K. (1973). Genu valgum and osteoporosis in an area
of endemic fluorosis. The Lancet 2(7834):877-879. (See abstract)
Li G, Ren L. (1997). [Effects of excess fluoride on bone turnover under conditions of diet
with different calcium contents] Zhonghua Bing Li Xue Za Zhi. 26(5):277-80. (See abstract)
Lin Fa-Fu, et al (1991). The relationship of a low-iodine and high-fluoride environment to
subclinical cretinism in Xinjiang. Iodine Deficiency Disorder Newsletter. Vol. 7. No. 3.(See
study)
Marier J, Rose D. (1977). Environmental Fluoride. National Research Council of Canada.
Associate Committe on Scientific Criteria for Environmental Quality. NRCC No. 16081.
(See report).
.
Massier M, Schour I. (1952). Relation of endemic dental fluorosis to malnutrition. Journal
of the American Dental Association 44: 156-165. (See excerpt)
Ouyang W, et al. (2000). [Effect caused by uptake of different levels of calcium to enamel
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fluorosis in rats] [Article in Chinese]. Zhonghua Kou Qiang Yi Xue Za Zhi. 35(1):47-9. (See
abstract)
Roholm K. (1937). Fluoride intoxication: a clinical-hygienic study with a review of the
literature and some experimental investigations. H.K. Lewis Ltd, London.
Suttie JW, Faltin EC. (1973). Effects of sodium fluoride on dairy cattle: influence of
nutritional status. American Journal of Veterinary Research 34: 479-483.
Tazhibaev ShS, et al. (1987). [Modifying effect of nutrition on the mutagenic activity of
phosphorus and fluorine compounds]. Vopr Pitan. (4):63-6. (See abstract)
Teotia SPS, TeotiaM. (1994). Dental caries: a disorder of high fluoride and low dietary
calcium interactions (30 years of personal research). Fluoride 27(2): 59-66. (See abstract)
Teotia M, Teotia SP, Singh KP. (1998). Endemic chronic fluoride toxicity and dietary
calcium deficiency interaction syndromes of metabolic bone disease and deformities in
India: year 2000. Indian Journal of Pediatrics 65(3):371-81. (See abstract)
Teotia SPS, et al. (1984). Environmental Fluoride and Metabolic Bone Disease, An
Epidemiological Study (Fluoride and Nutrition Interactions) Fluoride 17(1): 14-22.
Zhao W, et al. (1998). Long-term effects of various iodine and fluorine doses on the thyroid
and fluorosis in mice. Endocrine Regulations 32(2):63-70. (See abstract
See also:
Susheela AK, Bhatnagar M. (2002). Reversal of fluoride induced cell injury through
elimination offluoride and consumption of diet rich in essential nutrients and antioxidants.
Molecular and Cellular Biochemistry 234-235(1-2):335-40. (See abstract)
XIX. ACUTE TOXICITY of FLUORIDE (back to top)
Akiniwa, K. (1997). Re-Examination of Acute Toxicity of Fluoride. Fluoride 30: 89-104.
(See paper)
Gleason MN, Gosselin RE, Hodge HC, Smith RP. (1969). Clinical Toxicology of
Commercial Products. 3rd Ed. Williams & Wilkins, Baltimore.
Hodge HC, Smith FA. (1965). Fluorine Chemistry Vol. IV. Academic Press, New York.
Waldbott GW. (1979). Editorial: Anoter Fluoride Fatality - A Physician's.Dilemma.
Fluoride 12(1): 55-57. (See paper)
See also:
Carton R. (1994). Middletown Maryland: Latest City to Receive Toxic Spill ofPluoride in
their Drinking Water. The Townsend Letter for Doctors and Patients. October 15. 1124.
(See paper)
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xx. SYSTEMIC FLUORIDE NEVER APPROVED BY FDA (back to top)
. Food& Drug Administration. (2000). Letter from Melinda K. Plaisier, Associate
Commissioner for Legislation, FDA, to Congressman Ken Calvert. Dec 21,2000. (See
letter)
Kelly JV. (2000). Letter to Senator Robert Smith, Chairman of Environment and Public
Works Committee, U.S. Senate, August 14, 2000. (See letter)
XXI. ALTERNATIVES TO FLUORIDE (back to top)
Xylitol
Alanen P, et al. (2000). Sealants and xylitol chewing gum are equal in caries prevention.
Acta Odontologica Scandinavica 58(6):279-84. (See abstract)
Alanen P, et al. (2000). Xylitol candies in caries prevention: results of a field study in
Estonian children. Community Dentistry and Oral Epidemiology 28(3):218-24. (See
abstract)
Autio IT. (2002). Effect ofxylitol chewing gum on salivary Streptococcus mutans in
preschool children. ASDC Journal of Dentistry for Children 69(1 ):81-6, 13. (See abstract)
Calamari SE, et al. (1997). Effects ofxylitol, sorbitol and fluoride mouthrinses on glucose
. clearance in adolescents. Acta Odontologica Scandinavica 10(1):25-36. (See abstract)
Edgar WM. (1998). Sugar substitutes, chewing gum and dental caries--a review. British
Dental Journal 184(1):29-32. (See abstract)
Gales MA, Nguyen TM. (2000). Sorbitol compared with xylitol in prevention of dental
caries. Annals of Pharmacotherapy 34(1):98-100. (See abstract)
Hayes C. (2001). The effect of non-cariogenic sweeteners on the prevention of dental
caries: a review of the evidence. Journal of Dental Education 65(10): 1106-9 .(See abstract)
Hildebrandt GH, Sparks BS. (2000). Maintaining mutans streptococci suppression with
xylitol chewing gum. Journal of the American Dental Association 131 (7): 909-16. (See
abstract)
Honkala S, et al. (1999). Use ofxylitol chewing gum among Finnish schoolchildren. Acta
Odontologica Scandinavica 57(6):306-9. (See abstract)
Hujoel PP, et al. (1999). The optimum time to initiate habitual xylitol gum-chewing for
obtaining long-term caries prevention. Journal of Dental Research 78(3):797-803. (See
abstract)
.
Isokangas P, et at. (2000). Occurrence of dental decay in children after maternal
consumption of xylitol chewing gum, a follow-up from 0 to 5 years of age. Journal of
Dental Research 79(11): 1885-9. (See abstract)
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.
Isokangas P, et al. (1993). Long-term effect ofxylitol chewing gum in the prevention of
dental caries: a follow-up 5 years after termination of a prevention program. Caries
Research 27(6):495-8. (See abstract)
Lynch H, Milgrom P. (2003). Xylitol and dental caries: an overview for clinicians. Journal
of the Californian Dental Association 31(3):205-9. (See abstract)
Machiulskiene V, et al. (2001). Caries preventive effect of sugar-substituted chewing gum.
Community Dentistry and Oral Epidemiology 20 29(4):278-88. (See abstract)
Makinen KK, et al. (1998). Physical, chemical, and histologic changes in dentin caries
lesions of primary teeth induced by regular use of polyol chewing gums. Acta Odontologica
Scandinavica 56(3): 148-56. (See abstract)
Makinen KK, et al. (1998). A descriptive report of the effects ofa 16-month xylitol
chewing-gum programme subsequent to a 40-month sucrose gum programme. Caries
Research 32(2):107-12. (See abstract)
Makinen KK, et al. (1996). Conclusion and review of the Michigan Xylitol Programme
(1986-1995) for the prevention of dental caries. International Dental Journal 46(1):22-34.
(See abstract)
.
Makinen KK, et al. (1996). Polyol-combinant saliva stimulants and oral health in Veterans
Affairs patients--an exploratory study. Special Care in Dentistry 16(3): 104-15. (See
abstract)
Petersson LG, et al. (1991). Caries-preventive effect of dentifrices containing various types
and concentrations offluorides and sugar alcohols. Caries Research 25(1):74-9. (See
abstract)
Rekola M. (1986). Changes in buccal white spots during 2-year consumption of dietary
sucrose or xylitol. Acta Odontologica Scandinavica 44(5):285-90. (See abstract)
Roberts MC, et al. (2002). How xylitol-containing products affect cariogenic bacteria.
Journal of the American Dental Association 133(4):435-41. (See abstract)
Scheie AA, Fejerskov DB. (1998). Xylitol in caries prevention: what is the evidence for
clinical efficacy? Oral Disease 4(4):268-78. (See abstract)
Scheinin A, et al' (1993). Xylitol-induced changes of enamel microhardness paralleled by
microradiographic observations. Acta Odontologica Scandinavica 51(4):241-6. (See
abstract)
Scheinin A, et al. (1985). Collaborative WHO xylitol field studies in Hungary. VII. Two-
year caries incidence in 976 institutionalized children. Acta Odontologica Scandinavica 43
(6):381-7. (See abstract)
.
Simons D, et al. (2002). The effect of medicated chewing gums on oral health in frail older
people: a I-year clinical trial. Journal of the American Geriatric Society 50(8):1348-53.
(See abstract)
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Simons D, et al. (1999). The effect ofxylitol and chlorhexidine acetate/xylitol chewing
gums on plaque accumulation and gingival inflammation. Journal of Clinical
Periodontology 26(6):388-91. (See abstract)
Soderling E, et al. (2000). Influence of maternal xylitol consumption on acquisition of
mutans streptococci by infants. Journal of Dental Research 79(3):882-7. (See abstract)
Soderling E, et al. (1991). Long-term xylitol consumption and mutans streptococci in
plaque and saliva. Caries Research 25(2):153-7. (See abstract)
Soderling E, Scheinin A. (1991). Perspectives on xylitol-induced oral effects. Proceedings
of the Finnish Dental Society 87(2):217-29. (See abstract)
Steinberg LM, et al. (1992). Remineralizing potential, antiplaque and antigingivitis effects
ofxylitol and sorbitol sweetened chewing gum. Clinical Preventive Dentistry 14(5):31-4.
(See abstract)
Tanzer JM. (1995). Xylitol chewing gum and dental caries. International Dental Journal 45
(1 Suppl 1):65-76. (See abstract)
Trahan L, et al. (1996). Emergence of multiple xylitol-resistant (fructose PTS-) mutants
from human isolates of mutans streptococci during growth on dietary sugars in the presence
ofxylitol. Journal of Dental Research 75(11): 1892-900. (See abstract)
XXII. REVIEWS of the SCIENTIFIC LITERATURE (back to top)
Agency for Toxic Substances and Disease Registry (ATSDR) (1993). Toxicological Profile
for Fluorides, Hydrogen Fluoride, and Fluorine (F). U.S. Department of Health & Human
Services, Public Health Service. ATSDR/TP-91/17. (See report)
American Dental Association. (1999). Fluoridation Facts. (See report)
CDC. (2001). Recommendations for Using Fluoride to Prevent and Control Dental Caries in
the United States. Mortality and Morbidity Weekly Review 50(RR14): 1-42. (See report )
CDC (1999). Achievements in Public Health, 1900-1999: Fluoridation of Drinking Water to
Prevent Dental Caries. Mortality andMorbidity Weekly Review 48(41): 933-940 October
22, 1999. (See report)
Colquhoun J. (1997). Why 1 changed my mind about Fluoridation. Perspectives in Biology
andMedicine 41:29-44. (See report)
Connett P, et al. (2001). Fluoridation: Time for a Second Look? Rachel's Environment and
Health News May 10. No. 724. (See report)
Connett P. (2000). Fluoride: A Statement of Concern. Waste Not #459. Canton NY. (See
report)
Department of Health and Human Services. (1991). Review of fluoride: benefits and risks.
Report of the Ad Hoc Subcommittee on Fluoride. Washington, DC. (See synopsis)
http://www . slweb. org/bibliography .html
8/21/2003
.
.
.
A Bibliography of Scientific Literature on Fluoride
Page 53 of 54
DiesendorfM, et al. (1997). New evidence on fluoridation. Australian & New Zealand
Journal of Public Health 21: 187-190. (See report)
DiesendorfM. (1995). How science can illuminate ethical debates: a case study on water
fluoridation. Fluoride 28: 87-104. (See report)
DiesendorfM, Sutton P. (1986). Fluoride: New Grounds for Concern. The Ecologist 16(6).
(See report)
Environment Canada. (1993). Inorganic Fluorides: Priority Substances List Assessment
Report. Government of Canada, Ottawa. (See report)
Greater Boston Physicians for Social Responsibility. (2000). Known and suspected
developmental neurotoxicants. pp. 90-92. In: In Harms Way - Toxic Threats to Child
Development. Greater Boston Physicians for Social Responsibility: Cambridge, MA. (See
excerpt)
Hileman B. (1988). Fluoridation of water. Questions about health risks and benefits remain
after more than 40 years. Chemical and Engineering News August 1, 1988,26-42. (See
report)
Hirzy JW. (1999). Why EPA's Headquarters Professionals' Union Opposes Fluoridation.
National Treasury Employees Union Chapter 280. May 1. (See report)
Limeback H. (2000). Why I am now officially opposed to adding fluoride to water. (See
report)
Liteplo RG, et al. (1994). Inorganic fluoride: Evaluation of risks to health from
environmental exposure in Canada. Journal of Environmental Science and Health. Part C,
Environmental Carcinogenesis & Ecotoxicology Reviews 12: 327-344.
Locker D. (1999). Benefits and Risks of Water Fluoridation. An Update of the 1996
Federal-Provincial Sub-committee Report. Prepared for Ontario Ministry of Health and
Long Term Care. (See report)
Mancuso N, et al. (1997). Natick Fluoridation Study Committee Report. (See report)
Marier J, Rose D. (1977). Environmental Fluoride. National Research Council of Canada.
Associate Committe on Scientific Criteria for Environmental Quality. NRCC No. 16081.
(See report).
McDonagh M, et al. (2000). A Systematic Review of Public Water Fluoridation. (liThe
York Review. ") NHS Center for Reviews and Dissemination. University of York.
September 2000. (See report I See peer review of study I See letter from Chair of Advisory
Board)
National Research Council. (1993). Health effects of ingested fluoride. Report of the
Subcommittee on Health Effects of Ingested Fluoride. National Academy Press,
Washington, DC. (See report)
http://www . slweb .org/bibli ography .html
8/21/2003
.
.
.
A Bibliography of Scientific Literature on Fluoride
Roholm K. (1937). Fluoride intoxication: a clinical-hygienic study with a review of the
literature and some experimental investigations. H.K. Lewis Ltd, London.
Schmidt TC. (2000). Fluoride's Effect on Bone - and some related considerations.
JohnLeeMD.com. March 12. (See report)
Taskforce on Fluoridation. (1997). The Lord Mayors Taskforce on Fluoridation - Final
Report. (Brisbane, Australia). (See report)
World Health Organization. (2002). Environmental Health Criteria 227: FLUORIDES.
World Health Organization, Geneva. (See report)
(back to top)
http://www.slweb.org/bibliography .html
Page 54 of 54
8/21/2003
..
\
PRESSRElEASE
Natioal r~ol FMmi E~ (1.oaJ20SQ) · P.a. Bel76011.~ D.tlOOI3 .ptlone: (202) 110-2313
· fa: (202) "'-113'
For 1.....~Mtc lef H
~
Contact:
July 7,1997
J. William Hlrzy. Ph. D.
Senior V.P. NFFE. Local 2050
(202) 260-2383
(202) 401-3139
PMnet
fa:
EPA SCIENTISTS :raKE STAN!) AGAINST FLUORIDATIO:t-l
WedneSlkry, 2 Ju(y 1997 1100 member NFFE (1oca12050) USEPA sdentists,
toxicologists, engineers and attorneys who assess scientific data for-ME.E
DRINKlNG WATER ACT standards. etk_ unanimously went on record
against the practice of drinking water fluorida.tion.
National Federation of Federal Employees (Local 2050) issued the statement:
.
"Our members' review of the body of c::vidence over the last eleven
years. including animal and human epidemiological studies.
indicate a causal link between f1uorid~fluorid.a.rlon and cancer,
genetic damage. neurological impairment. and bone pathology. Of
panicular concern are epidemiological studies linking fluoride
exposure to l~red IQin children".
.
"As the professionals who are charged with assessing the safety of
drinking water, we conclude that the health and ~lfare of the
public is not served by the addition of this substance (fluorides) to
the drinking water".
For more information on USEPA Union. Local 2050 statement contact:
J. William Hirzy, Ph. D., Senior V.P., NFFE Local 2050. (202) 260-2383.
TOXICOLOGICAL PROFILE FOR
FLUORIDES, HYDROGEN FLUORIDE,
AND FLUORINE
Prepared by:
Clement International Corporation
Under Contract No. 205-88-0608
Prepared for:
Agency for Toxic Substances and Disease Registry
U.S. Public Health Service
April 1993
112
2. HEALTH EFFECTS
2 . 6 ImERACTIOlfS WIm OTBBR CBBIaCALS
The absorption of fluoride from the gastrointestinal tract of humans
and/or animals is affected by the presence of several minerals including
calcium, magnesium, phosphorus, and aluminum (Rao 1984). These effects are
discussed in Section 2.8. No reliable data on interactions that exacerbate
negative effects of fluoride were located.
2.7 POPULATIONS THA'l' ARB tJIn1SUALLY SUSCBP'l'IBLE
Existing data indicate that subsets of the population may be unusually
susceptible to the toxic effects of fluoride and its compounds. These
populations include the elderly, people with deficiencies of calcium,
magnesium, and/or vitamin C, and people with cardiovascular and kidney
problems.
Because fluoride is excreted through the kidney, people with renal
insufficiency Would have impaired renal clearance of fluoride (Juncos and
Donadio 1972). Fluoride retention on a low-protein, low-calcium, and low-
phosphorus diet was 65% in patients with chronic renal failure, compared with
20% in normal subjects (Spencer et al. 1980a). Serum creatinine levels were
weakly correlated (r=O.35-0.59) with serum fluoride levels (Hanhijarvi 1982).
People on kidney dialysis are particularly Susceptible to the Use of
fluoridated water in the dialysis machine (Anderson et al. 1980). This is due
to the decreased fluoride clearance combined with the intravenous exposure to
large amounts of fluoride during dialysis. Impaired renal clearance of
fluoride has also been found in people with diabetes mellitus and cardiac
insufficiency (Hanhijarvi 1974). People over the age of 50 often have
decreased renal fluoride clearance (Hanhijarvi 1974). This may be because of
the decreased rate of accumulation of fluoride in bones or decreased renal
function. This decreased clearance of fluoride may indicate that elderly
people are more susceptible to fluoride toxicity.
Poor nutrition increases the inCidence and severity of dental fluorosis
(Murray and Wilson 1948; Pandit et al. 1940) and skeletal fluorosis (Pandit et
al. 1940). Comparison of dietary adequacy, water fluoride levels, and the
incidence of skeletal fluorosis in several villages in India suggested that
vitamin C deficiency played a major role in the disease (Pandit et al. 1940).
Calcium intake met miniDIUDI standards, although the source was grains and
vegetables, rather than milk, and bioavailability was not determined. Because
of the role of calcium in bone formation, calcium deficiency would be expected
to increase Susceptibility to effects of fluoride. No studies in humans
supporting this hypothesis were located. Calcium deficiency was found to
increase bone fluoride levels in a twO-week study in rats (Guggenheim et al.
1976) but not in a lO-day study in monkeys (Reddy and Srikantia 1971). Guinea
pigs administeted fluoride and a low-protein diet had larger increases in bone
fluotide than those given fluoride and . control diet (Parker et .1. 1979).
Bone changes in monkeys follOwing fluoride treatment appear to be more marked
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Fax Transmission
Pinellas County Utilities Administration
14 South Ft. Harrison Ave., 5th Floor
Clearwater, FL 33756
Phone: 727-464-3438
Fax: 727-464-4152
To:
Betty Taylor
Fax No.~ 726-0423
From:
Pick Talley
DIrector of Utilities
Pages: 1 (Including Cover)
Subject: Fluoride Compound
Date: 8/19/03
Dear Ms. Taylor:
Because we have not yet begun an engineering study on the exact compound or in
what quantities it will be used in the Pinellas County public water supply, we cannot
provide the exact compound and its properties to you at this time.
We can say, however, that the compound that is most used in large applications
such as fluoridation of water is hydrofluorosilic add.
We will be happy to provide detailed infonnation to~u a:td the general public just
as soon as it becomes available.
Esteemed Voices have, for 50 years, warned
the American public that water fluoridation
has dangerous long-term consequences to health:
William Marcus, Ph.D., D.A.B.T. (Toxicology), fonner U.S. EPA, Senior Science AcMsor, Office of Drinking Water..
Albert W. Burgstahler, PILD. (Organic Chern, Environ. Fluoride)
Robert J. Carton, Ph.D. (ErNiron. Sciences and Risk Assessment).
Paul Connett, Ph.D. (Environmental Chemistry and Toxicology).
Richard Foulkes, M.D., fmr. Consult. to Health Minstr., BC, Canada
J. William Hrzy, Ph.D. (Chern and Risk Assess) Sr.VP, NFFE,EPA
Robert L. Isaacson, Ph.D. (Neurobeh8\lioral Science). Dist.
Prof. Da\Ad C. Kennedy, D.D.S., Inter. Acad. Oral Meet and Toxicology.
Harold D. Kletschka, M.D., F.A.C.S.(inr. Chair. of Bio-Medicus,lnc)
Lennart Krook, D.V.M., Ph.D. (pathology) Cornell Univ.and NYSC.
Richard A. Kunin, MD., Pres., Soc. for orthomotecuia Hlth.Medicine
Gene W. NfIer, Ph.D. (Biochemistry and Toxicology).
Phyllis Mullemy, Ph.D. Owmacology and Neumtoxicology)
John Colquhoun, BDS, MPhlL Ph.D., DipEd., Prin. Dent. Ofc. NZ.
John A.Yiamouyiannis, Ph.D. (Biochemistry)
A. K. Susheela, Ph.D., F.A.Sc., F.A.M.S. Qfistocryochemistry)
Benedict J. Gallo, Ph.D.(Botany). Research Mcrobiologist.
Norman R Mancuso,Ph.D. (Chemistry) Apollo Project Scientist.
Andrew Bema-lficks, Hazardous Substance Engineer, Cal EPA.
Jason Kupperschmidt, B.C. (Chem. Engr)
Rudolph Ziegelbecker, Ph.D. (phys.) Inst. of En\Aron Hlth.Austria
M.A. Krikker M.D., Hemochromatosis Found, Albany, N.Y.
Dean Burk, Ph.D. (Biochemistry) former Senior Chemist and
Director Cytochemistry Section, National Cancer Institute.
Harold Warner, Prof Of Research; Chief, Biomedical Engineer Div.
Sheila L. M. Gibson, M.D., B.Sc., M.F. Horn. (Research Physician)
James B. Patrick, Ph.D. (Chemistry) , Antibiotics Research.
I. R B. Mann, Senior Lecturer in ErNiron. Studies, U. of Auckland.
Bruce J. Spittle, Ph.D., Psycho. Med., U. of Otago Med. Sch., NZ
George L. Waldbott, MD., lIadr. Inter Soc for FI. Res. and j. Fluoride
Alfred Taylor, Ph.D, Research Scientist, Clayton Fnd. Biochem. Inst.
Ludwik Gross, M.D, 1inr Chief of Cancer Res. Vetrans Admin, N.Y.
Dr. Daniel laskin, Chf. Diagnostician, Columbia Sch of Dental Surg.
Geoffrey E. Smith, L.D.S., RC.S. Dental Surgeon.
Philip R- N. Sutton, D.D.Sc., L.D.S., F.RA.C.D.S.
Brian A. Dementi- Ph.D. (Biochemistry and Toxicology)
John P. Flaherty, Chief Justice, Supreme Court of Pennsylvania
Simon Beisler, M.D., Chief of Urology, Roosevelt Hosp. N.Y.
Fred Squier, M.D., Head of Oral Surgery, Lenox Hill Hasp. N.Y.
John Garlock, M.D., Consulting Surgeon, ML Sinai Hasp. N.Y.
Monday. Augusl18, 2003 America Online: V0n34 Page: 1
.
~
Edgar A. Lawrence, M.D., Dir. of Medicine, Lenox HII
Girard F. Oberrender, M.D., Dir. ofOtolaryugology, Lenox HII
Frederick B. Ex ner, M.D. Fellow ofthe Am. Coli. Of Radiology.
Charles C. Bass, M.D., Dean Emeritus, Tulane Univ. Mad. Sch.
Alton Ochsner, M.D., head, Dept of Surgery, Tulane Univ. Med. Sch.
Alfred I Murray, M.S.T. (Chemistry).
Mark Diesendorf, Ph-O. (INUthematics).
John J. Miller, Ph.D. (Biochemistry)
Paull-L Phillips, Ph.D. (Biochemistry)
Kaj Roholm, M.D., Ph.D. (Biochemistry)
Hubert A. Arnold, Ph.D. (Math) UCDavis
James W. Benfield, A.B., D.D.S., F.A.C.D.
Eugene Peterson, Ph.D. (Chem.Engr.) UCB.
Cornelius Steelink, Prof Erner. Chern.
John Thomson, Ph.D. (Biochemistry)
D. Skinner, B. Sc., MD. C.A.F.C.1.
Richard Manus, Ph.D. (physics) UCBerkely
Laura Nader, Ph.D. (Anthropology)UCB
D. W. Hanson, Ph.D. (Chern. Engr.)UCB
C. J; King, Ph.D. (Chern. Engr.)UCB
J. B. Neilands, Ph.D. (Biochemistry)UCB
Giovanni Ames, Ph.D. (Biochem.) UCB John R. Lee, M.D. (Physician)
J. C. Smart, Ph-D. (Chemistry) UCB
Gerard F. Judd, Ph.D. (Chemistry)
Gerson Jacobs, MD.
Michael F. Ziff, 0.0.5..
Harvey Petraborg, MD.
Robert I H. Mick, D.D.S. E. R- Cooper, M.D.
C. T. Betts, D.D.S.
I E. Waters, D.D.S.
Allen London, D.D.S.
Edward A. Mclaughlin, M.D.
Philip E. Zafagna, M.D.
George W. Heard, D.D.S.
Charles Dillon, D.D.S., L.D.
S. Leslie A. Russell, D.M.D. (dentist)
Casimir R. 5 heft: , D.D.S.
Jonathan Fonnan, M.D.
Ross Pringle, D.D.S.
A. B. MacWhimiie, D.D.S.
A.C. Baumann, D.D.S.
Kirk Youngman, D.M.D.
L. A. Alesen, M.D.
Paul W. Sheeran, D.M.D.
Thomas F. Evans, D.D.S.
Robert Davis, D.D.S.
William I Filante, MD.
Monday, AugU8l18, 2003 ArMric:a 0.._: V0n34 "-: 2
Joyal W. Taylor, D.D.S.
Michael Ohnstad, D.D.S.
Sheridan B. Mianasen, D.D.S
Scott McAdoo, D.D.S.
Tony Lees, B.D.S. Dentl Surgn
Frederick W. Howe, D.D.S.
Ellsworth D. Foreman, D.M.D.
Robert D. Stephan, D.D.S.
Carl Mestman, D.D.S.
Hans Moolenburgh, M.D.
Peter Mansfield, M.D.
William F. Corell, M.D.
F. Logan Stanfield, M.D.
Julian Whitaker, MD.
Robert C. Atkins, M.D.
James A. Paar, M.D.
Kemieth H. Rudolph, M.D.
Jonathan Wright M.D.
John McDougall, MD.
Steven M. Rachlin, M.D.
John R. Ulliendahl, Jr. D.D.S.
Hal A. Huggins, D.D.S.
Herbert H. Robinson, D.D.S.
James P. Hammond, MD.
Philip Sukel, D.D.S.
Deloss E. Winkler, Ph.D. (Chern.)
Andrew Weil, UD, Health Advocate
Thomas M. DeStefimo, A.B., D.D.S.
Harlee S.Strauss, Ph.D. (Molecular Biology)
GeoflTey Dobbs, Ph.D. (Botony) A.R.C.S.
Frederick I. Scott, B.E., M.S., Chern. Engr.
Thomas D. Hinesly, Prof. of Soil Ecology
Roy E. Hanford, MD. (phys. and Surgeon)
Stanley Monteith, MD., ret. Ortho. Surgeon.
G. A. Samotjoi, Ph.D. (Chemistry) UCB
Henry Cheung, Ph.D. (Chern. Engr.)Alexis T Bell, Ph.D. (Chem. Engr.)UCB
. Above affiliations are listed for identifications purposes only and do not ~ instiution endorsement
, Monday. August 18, 2003 _ Onm.: Von:W Page: 3
Water fluoridation uses fertilizer manufacturing waste products
Page lof2
. . . ~ . . . . . . . .
"The largest production of the acid [water fluoridation chemicals]
is as a byproduct of phosphate fertilizer manufacture."
One of several companies, Lt;.l, sells fluoride to municipalities. Read about LCI's
recommended uses of fluoride. Here are some excerpts from their web page.
Founded in 1983, LCI LTD started as a supplier of fluorides to municipalities for
fluoridation of their potable water systems.
In 1993, LCI purchased a Hydrofluoric Acid plant, Norfluor, S.A. de C.V. in Juarez,
Mexico. Today, LCI offers a wide range of specialty fluorides for water fluoridation and
industrial applications.
Properties
It is a 20 to 35 percent aqueous solution. It is a colorless to straw yellow,
transparent, fuming, corrosive liquid. It has a pungent odor and irritating action on
the skin.
Manufacture
Fluorosilicic acid (Hydrofluorosilicic acid) is manufactured by two different processes,
resulting in products with different characteristics. The largest production of the
acid is as a byproduct of phosphate fertilizer manufacture. A smaller amount is
produced from HF and silica resulting in a purer product at slightly higher strength.
[Editor: this is an EXACT quote from their web page, as of September 15, 1999]
Uses:
. Sterilization of equipment
. Electroplating
. Tanning of animal hides
. Ceramics and Glass: Glass etching .
. Commercial Laundry: As a neutralizer for alkalis
. Hardening of Cement
. Oil well acidizing
. Rust and Stain removal for textiles
. Wood preservative
. Water fluoridation
http://www.nofluoride.com/lci_fluoride_mfg.htm
2/17/02
Water fluoridation uses fertilizer manufacturing waste products
..
#
Manufacture
Sodium Fluoride is made by neutralizing Hydrofluorosilicic acid with caustic soda
(NaOH).
Uses:
. Commercial Laundry. Laundry souring agent
. Manufacture of vitreous enamels
. Manufacture of coated papersWood preserative
. Water fluoridation
copyrighted material (if any) property of LeI
http://www.nofluoride.com/lci_fluoride_mfg.htm
Page 2 of2
2/17/02
, MSDS FSA printable
Page 1 of 4
CARGILL
FERTILIZER
8813 HIGHWAY 41 SOUTH
RIVERVIEW, FLORIDA 33569
EMERGENCY TELEPHONE - CHEMTREC 1-800-424-9300
MATERIAL SAFETY DATA SHEET
Revised 11/26/01
http://www.cargillfertilizer.com/MSDS/msdsfsap.htm
3/10/02
r MSDS FSA printable
Page 2 of 4
http://www.cargillfertilizer.com/MSDS/msdsfsap.htm
3/1 0/02
MSDS FSA printable
Page 3 of4
http://www.cargillfertilizer.comlMSDS/msdsfsap.htm
3/10/02
r MSDS FSA printable
Page 4 of 4
11sECTION XII ECOLOGICAL INFORMATION
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http://www.cargillfertilizer.comlMSDS/msdsfsap.htm
3/10/02
Derailed Baltimore Train Carrying Fluorosilicic Acid
Page 1 of7
. #
.A
I.;
Fluoride Action
Network
Derailed Baltimore Train Carrying
F1uorosilicic Acid
Fluoride Action Network
Derailed Baltimore Train Carrying Fluorosilicic Acid
.l!mtlrrW.r~_SP1L--"Buming cars in rail tunnel resist control" July 20, 2001
"The most dangerous of the train's load of chemicals, according to experts, is
fluorosilicic acid - and there was no indication it was leaking. But fIrefIghters
not determine whether fIre was burning near it, because the acid was being carried
far ahead in cars 29 and 30."
Associated Press -- "Derailed Chemical Train in Baltimore Still Bums" July 19,
2001
- "City Health Commissioner Peter Beilenson said he was most concerned about
hydrochloric acid and fluorosilicic acid, two of at least six hazardous chemicals on
board the train. "
http://www.fluoridealert.org/news/maryland/train.htm
2/17/02
Derailed Baltimore Train Carrying Fluorosilicic Acid
. ,
Page 2 of7
W(,)fldN~\\!~ -- "List of Chemicals on Derailed Train" July 18, 2001
Chemicals included in the cargo manifest of the train involved in Wednesday's
derailment in Baltimore:
-Hydrochloric acid, a metal cleaner. Not combustible, but highly corrosive. If
inhaled, can cause a burning sensation, cough, labored breathing, shortness of
and sore throat. On contact with skin or eyes, can cause severe bums.
-Glacial acetic acid, a glass solvent Flammable. If inhaled, can cause sore
cough, burning sensation, headache, dizziness, shortness of breath, labored
breathing. On contact with skin or eyes, can cause pain, redness and severe bums.
-Fluorosilicic or hydrofluoric acid, used to fluoridate water. Not combustible,
corrosive. If inhaled, can cause a burning sensation, cough and shortness of breath.
On contact with skin or eyes, can cause pain, redness, blisters and severe bums.
-Propylene glycol, a deicing fluid. Combustible. Can cause redness and pain in
eyes.
- Tripropylene, a lubricant similar to pain thinner.
-Ethyl hexyl phthalate, used to make flexible products like PVC piping.
Combustible. If inhaled, can cause cough or sore throat.
Baltimore Sun
July 20, 2001
Burning cars in rail tunnel resist control
By David Michael Ettlin
Sun Staff
ht1P~!Lw~:W:,S!J._tlSP.QU]~Un~w_sn~~b~1::~_.nHtlmin2Ql~!12Q_._~tQry:l
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Baltimore fIrefighters waged a cautious second-day attack yesterday on a
nightmarish railroad tunnel fire that shut downtown businesses, knotted traffIc,
freight service along the East Coast and Midwest and disrupted e-mails and cell
phone service.
Temperatures in the century-old Howard Street Tunnel rose as high as 1,500
Fahrenheit - hot enough to cause some of the CSX rail cars to glow, according to
Battalion Chief Hector L. Torres, a Fire Department spokesman. "You're talking
about metal glowing," he said. "The tanks are too hot to off-load. We have to
the frre under control. "
http://www.fluoridealert.org/news/maryland/train.htm
2/17/02
Derailed Baltimore Train Carrying Fluorosilicic Acid
, ,
Page 3 of7
Sections of the 60-car freight train had been burning inside the 1.7 -mile tunnel
about 3:15 Wednesday afternoon, and fIrefighters could not predict when they
extinguish the fIre and remove all the cars - 31 of them loaded with a variety of
chemicals and goods.
Unable to reach the fIre from the tunnel's ends, the Fire Department changed
and came in from the top - through a manhole entrance near Howard and Lombard
streets.
While Baltimore officials and National Transportation Safety Board investigators
focused on the train and frre, repair crews descended under street beds to reroute
fIber optic cables running through the tunnel.
The cable damage had an impact well beyond Baltimore, from inoperable cell
phones in suburban Maryland, to corporate Web pages that couldn't be updated in
Manhattan, to e-mail crashes in Mrica.
Meanwhile, a water main break linked to the frre forced the closure of two
office towers and obstructed traffic, shutting down Howard Street.
The Orioles canceled a doubleheader yesterday.
Amid the frrefighting battle and downtown chaos, officials said the investigation
could take up to 15 months, and repairs likely will be long and costly. But they
thankful that there had been few injuries and no catastrophe.
"As terribly inconvenient as this has been, in many ways we've been lucky there
wasn't a serious explosion or widespread contamination," said Gov. Parris N.
Glendening after touring the accident site near Oriole Park at Camden Yards in
afternoon.
It appeared that the frre began as cars on the 4,000-foot-Iong CSX freight train
derailed at 3:07 p.m. Wednesday. A ruptured tanker car carrying a flammable
chemical leaked and fueled an underground inferno about 30 feet below the water
main that broke, according to a CSX offIcial inspecting the damage.
Firefighters described a scene of intense heat and dark. "It's just like walking into
oven. The smoke is so thick you can't even see your hand in front of your face,"
one firefIghter, his face covered in black soot.
All he could see inside the tunnel, the fIrefighter said, was the glowing metal of
tanker cars. "It was a deep orange, like a horseshoe just pulled out of the oven."
In the alternative frrefIghting plan, taken up about noon, a 5-inch-diameter hose
fed into the manhole on Lombard Street near Howard Street. FirefIghters walked
the southern end of the tunnel, connected hoses to the line from above and used a
cascade of water to significantly lower the temperatures over the next few hours.
The tactic enabled frrefighters to close in on still-burning cars, and investigators to
begin unraveling the accident.
http://www.fluoridealert.orglnews/marylandltrain.htm
2/17/02
. ,
Derailed Baltimore Train Carrying Fluorosilicic Acid
Page 4 of7
Mayor Martin O'Malley, asked about costs of the frrefighting, cleanup and repairs,
said, "We're not really counting dollars now. All we're counting is the number of
in the tunnel and the number of brave men and women who are going in there to
fight this frre."
Five cars from the end of the train were detached and towed out of the tunnel
9 a.m. - an empty covered hopper, three empty gondolas, and a charred boxcar
coat of golden yellow paint was largely burned black. Its cargo - bales of pulp
- smoldered during hours of unloading by a backhoe.
Last night, crews were trying to remove the next cars in line on the northbound
- a chain of four tanker cars hauling thousands of gallons of chemicals. One of
car No. 53, was found by frrefighters and a Maryland Department of the
Environment's hazardous materials team to be "leaking along the seams," said
spokesman John Verrico.
The 20,OOO-gallon tanker car was loaded with hydrochloric acid. About a quarter
it was estimated to have spilled - some seeping into storm sewer drains inside the
tunnel and carried into the Inner Harbor.
Near the Light Street Pavilion at Harborplace, the Coast Guard used floating
to protect the waters from the flow, which contained "soot and ash and petroleum
and traces of the tripropylene," Verrico said. The flow was discovered quickly
enough to prevent a fish kill, officials said.
Fixing the acid leak proved difficult. The adjacent tank car, No. 52, "burnt up to a
husk," V errico said. It contained the tripropylene, a highly flammable petroleum
compound used in the manufacture of some plastics.
"It's speculating for me to say this, but that's probably what was fueling the fire to
bum so hot and so long," V errico said. "The heat situation is making it damn near
impossible for us to remove the hazardous chemicals," he said.
Tripropylene produces irritating, but not highly toxic, fumes when it bums, and
MDE sampling found no hazardous compounds in the smoke coming from the
tunnel, Verrico said.
The cars just north of No. 52 contained plywood and were burning, and "all of the
next several cars have either wood products or rolls of paper in them," Verrico
"We know that at least three or four of them are involved in the fire and there may
more beyond that, but we can't get there to find out."
Firefighters couldn't neutralize the acid leak in the normal way, by spreading an
alkaline chemical to neutralize it. In the presence of heat, the combination would
have been explosive.
Nor could they pump out the chemical. "That tank is too hot," Verrico said. The
plastic pumps that have to be used to pump acid chemicals would have melted.
To cool the acid, frrefighters opened the manhole cover and sprayed the leaking
http://www.fluoridealert.orglnews/maryland/train.htm
2/17/02
Derailed Baltimore Train Carrying Fluorosilicic Acid
, ,
Page 5 of7
with water for about two hours.
Late yesterday afternoon, a vacuum hose was lowered through the manhole and
contractors hired by CSX began to pump the hydrochloric acid from car 53 and an
adjacent car, 54, which was not leaking, into tanker trucks. The operation was
continuing late last night, authorities said.
At a news conference last night, National Transportation Safety Board member
Hammerschmidt gave an account of the accident based on data from sensors and
interviews with crew members.
His chronology began at 3:04 p.m. Wednesday with the locomotives 100 yards
of the tunnel entrance.
The train's emergency braking activated at 3:07 p.m., and the crew was unable to
reset the air brakes, he said. The locomotives were about a half-mile from the
tunnel's northern end.
Unable to contact radio dispatchers, the crew used a cell phone to call a supervisor
and report there had been a problem.
At 3:15 p.m., they shut down the leading two locomotives and then uncoupled the
third from the train cars to drive out and get away from fumes in the tunnel. The
engines left the tunnel at 3:27 p.m., sensors showed.
The crew said they reached the dispatcher from outside the tunnel about 3:25 p.m.,
then noticed minutes later that the fumes were not dissipating - and appeared to be
smoke - and alerted a dispatcher.
According to the train crew, Hammerschmidt said, city fIre personnel arrived at
p.m. and were given the train's cargo manifest - although the Fire Department has
said it was notified at 4:15 p.m.
By the time frrefIghters were arriving, the situation was beyond control deep in the
tunnel.
FirefIghters from Engine 13 and Truck 16 arrived fIrst and saw smoke floating
the tunnel's northern opening. The engineer and conductor told frre officials the
might be carrying hazardous materials, and thought there was a frre but didn't
where.
The fIrefighters marched into the black smoke. But after only a few steps into the
tunnel, the frrefighters said they could not see.
"I couldn't see my hand in front of my face," said frrefIghter Daniel MacFarlane.
"I just didn't want to die," said Capt James Smith.
Firefighter Jim McCafferty worried about getting lost and never being found.
http://www.fluoridealert.orglnews/maryland/train.htm
2/17/02
Derailed Baltimore Train Carrying Fluorosilicic Acid
J ,
Page 60f7
Wednesday night, the ftreftghters tried another mission into the tunnel. They
into the back of a flatbed CSX truck and rode in reverse toward the train. They'd
drive a few feet, get out and walk, scouting the terrain to make sure the truck
run into the train.
But even on the truck, they were nervous. "CSX guys told us the tires might
in the heat," MacFarlane said. "That meant we couldn't get out."
Yesterday, investigators reported fmding 800 feet of rail that had spread apart
and under some of the rear cars. But they had not determined what caused the
derailment, ruptured the tanker car or ignited the ftre.
The governor stopped by the Camden Yards end of the tunnel for a quick tour and
meeting with the mayor in late afternoon, but chose not to climb down to the CSX
tracks.
"The last thing they need is an elected official trying to get into the tunnel, so I
go in there," Glendening said. "These men and women here just lived through
something extraordinary and we have to remember what they've done."
State officials said they considered asking the federal government to declare the
a disaster area but realized that it does not meet the qualiftcations.
"Mter this is over, we'll sit down for some hard discussion of recouping this cost.
This is a very expensive operation," Glendening said. "In the long term, "we may
seek federal assistance to repair the tunnel."
By evening, frreftghting had ceased while contractors tried to remove the cars
with hazardous chemicals.
Fire officials explained it was too dangerous for their men to work in the tunnel
the cars were gone.
The number of ftreftghters on the scene was reduced to 50 from the city
one-third of the overnight high of 150 from both the city and Baltimore County.
With the 800 feet of track spread and unusable, the contractors laid down
track last night. They were slowed late last night in trying to remove derailed car
loaded with a relatively non-toxic plastic compound called ethyl hexyl phthalate,
because its enormous weight seemed to move the temporary track.
The most dangerous of the train's load of chemicals, according to experts, is
fluorosfiicic acid - and there was no indication it was leaking. But frreftghters
not determine whether frre was burning near it, because the acid was being carried
far ahead in cars 29 and 30.
"If it gets hot, fluorosilicic acid can release hydrofluorisilicic acid, and that's
extremely toxic," said Melanie Lesko, a chemistry professor at Texas A&M
University at Galveston.
http://www.fluoridealert.orglnews/maryland/train.htm
2/17/02
. Derailed Baltimore Train Carrying Fluorosilicic Acid
, .
Page 70f7
At three schools near the north end of the tunnel - Mount Royal Elementary,
T. Washington and Samuel C. Taylor - "there have been some complaints of smell
and smoke," Verrico said.
"We've gone in and tested. ... There's no trace of any chemical. There is a slight
of smoke," he said.
V errico said fIrefighters were concerned about the health of residents in some
apartment buildings near the north end of the tunnel, where the smoke was heavy.
"They're going to be continuously checking on the residents of those buildings,
especially the elderly," he said.
The accident also postponed two games between the Baltimore Orioles and Texas
Rangers - cancellations that Joe Foss, chief operating officer for the Orioles, said
the team about $3 million in concession spending, tickets and parking.
Sun staff writers contributing to this article included Tim Craig, Heather Dewar,
Stacey Hirsh, Stephen Kiehl, Robert Little, Jon Morgan, Erika Niedowski,
Ratner, Del Quentin Wilber and Kimberly A. C. Wilson.
Copyright ~ 2001, The Baltimore Sun
http://www.fluoridealert.orglnews/maryland/train.htm
2/17/02
'\
Communities which have Rejected Fluoridation Since 1990 '
Compiled by Maureen Jones & Fluoride Action Network "In' about 600A. of 2000 referenda held in the U.S. since
1950, fluoridation has been voted down." - Zev Ramba, Washington Bureau Editor of AGD Impact (the publication ofthe
Academy of General Dentistry). Quoted in the ~hemical & Eneineerina News (81H88).
"Avoid a referendum. The s1atistics are that 3 out of 4 fluoridation referenda fail."- Susan Allen, RDH, BS Fluoridation
Coordinator, Public Health Dental Program, State Hea"h Office, Florida. May 7, 1990. (See letter)
"The fact that nearly 3 out of every 5 communities which vote on the issue have rejected fluoridation, year after
year, does in all likelihood represent a collective judgment on the part of the public that, when all things are
considered,f1uoridation is not an acceptable public health measure." - Ec/oNard Groth III, PhD Dissertation, 'Stanford
University, May 1973
Bums Lake. British Columbia. Canada June 25, 2003
Dutton-Dunwich. Ontario. Canada June 2003
West Elein. Ontario. Canada June 2003
Seauim. Washinaton State May 7, 2003
York. Nebraska May 6, 2003
Canton. New York February 18, 2003
Shaler. Pennsvlvania February 11, 2003
Billinas. Montana November 5,2002
Kalisoell. Montana November 5, 2002
Washoe County. Nevada November 5,2002
Methuen. Massachusetts November 5, 2002
Reddina. California November 5, 2002
Wats omA lie. California November 5,2002
Texarkana. Arkansas November 5, 2002
Ashdown. Arkansas November 5, 2002
Oneida. New York August 6, 2002
Franklin. North Carolina May 2002
Plain,,;ne. Massachusetts April 1, 2002
Monroe. Louisiana February 26, 2002
Colorado Sprines. Colorado January16, 2002
Kennewick. Washinaton January 15, 2002
Benninton. Vermont January 8, 2002
Lanai. Hawaii January 2002
Cobalt. Ontario December 11, 2001
Erie. Colorado November 2001
Modesto. California November 7, 2001
Worcester. Massachusetts November 7, 2001
Flaestaff. Arizona November 7, 2001
Sutherlin. Oreaon November 7, 2001
KamlooDS. British Columbia October 13,2001
White Salmon. Washinaton September 2001
Goldendale. Washinaton September 2001
Bishopville. South Carolina June 2001
Harper. Kansas May 31, 2001
Brewster. Massachusetts May 15, 2001
McPherson. Kansas April 3, 2001
Norrideewock. Maine MayS, 2001
Blue River, Wisconsin February 2001
Sunday, June 28, 2003 Amerlce Online: Von34 Pege: 1
Willamina. Orecon January 2001
Ithaca. New York. November 7,2000
Sookane. Washinaton November 7, 2000
Brattleboro. Vermont November 7,2000
Wenatchee. Washinaton November"t, 2000
Shawano. Wisconsin November 7, 2000
Nibly City, Utah November 7, 2000
Hyrum City" Utah November 7, 2000
Providence City, Utah November 7, 2000
Smithfield City, Utah November 7,2000
Logan City, Utah November 7, 2000
River Heights, Utah November 7,2000
Peauannock. New Jersev November 7,2000
Ozark. Missouri November 7,2000
Wooster. Ohio November 7, 2000
Sauamish. British Columbia October 16,2000
Woodside. Califomia September 2000
Ste. Gene\Aeve. Missouri August 8, 2000
Winfield, Kansas March 6, 2000
Wilmington, Massachusetts February 15, 2000
Santa Barbara, California November 23,1999
Johnstown, New York November 19,1999
Tooele, Utah November 2, 1999
Wichita, Kansas October 26, 1999
Boca Raton, Florida October 25, 1999
EI Ca~on, Califomia April 27, 1999
Escondida. California April 7, 1999
Helix Water District, California April 7, 1999
Lakeside Water District', Califomia April 6, 1999
Hutchinson, Kansas March 30,1999
RivenAew Water District, Califomia March 24,1999
La Mesa. California March 9, 1999
Santa Cruz, California March 4, 1999 ...banned
Bremerton, California February 2, 1999
Olympia, Washington December 15, 1999
Seward, Nebraska November 3, 1998
Whitehorse, Yukon Territory, Canada July 28,1998... quit after 30 years
Grand Island, Nebraska May 13, 1998... quit
Norfolk, Nebraksa May 13, 1998
North Platte, Nebraska May 13, 1998
Washington, Missouri April 7, 1998
Kitmat, British Columbia, Canada March 1998... quit
Hot Springs, Arkansas February 1998
Ridgefield, Oregon December 22,1997
Largo, Florida July 15, 1997
Clearwater, Florida July 15, 1997
North Redington Beach, Florida July 15, 1997
Amsterdam, New York May 21, 1997
Suisun City, California May 1, 1997
Yardly, Pennsylvannia April 16, 1997
Village ofOrfordville, Wisconsin December 9,1996
Westem Nassau County, New York November 21, 1996... quit after 23 years
Kelowna, British Columbia, Canada November 16, 1996... quit after 42 years
Gothenberg, Nebraska December 1996
Bloomer, Wisconsin November 6, 1996
Kodiak, Alaska July 12, 1996
Carle Place, New York February 1, 1996... quit
Sunday. June 29. 2003 Amerlce Online: Von34 hge: 2
~
Winter Springs, Florida January 10, 1996
Pasco, Florida December 14, 1995
York, PennsylvanniaJuly 29, 1995
Thurmont, Maryland February 3, 1994
Albany, New York December 8, 1994
Middletown, Maryland November 1993... quit
Samia, Ontario,. Canada January 30, 1993
Barnstable, (Cape Cod) Massachusetts November4,1993
Wagoner, Oklahoma June 17,1993
Redwood Valley, California February 6,1993,
Los Altos Hills (purissima) California 1993 ,
Campbell River, British COlumbia, Canada April 1993... quit after 33 years
Port Hardy, British Columbia, Canada November 1993... quit after 19 years
Squamish, British Columbia, Canada November 1993... quit after 20 Yflars
Fort Smith, Arkansas November 3, 1992
Milltown, Wisconsin October 17, 1992
Bellingham, Washington May 19, 1992
COmox/COurtenay, British COlumbia, Canada February 1992
Palm Beach County, Florida October 22, 1991
Ketchikan, Alaska October 2, 1991
Suffolk COunty, New York August 15, 1991
Da\lis, California December 14, 1990... 5th rejection
Morgan Hill, California March 7, 1990... quit
I '
H
Fluoride Action Network I 802-859-3363 I info@ftuoridealert.ora
Sunday, Juna 28, 2003 America Online: Von34 Paga: 3
Fluoridation and Cancer
Fluoride added to public water supplies may be linked to
cancer, suggests two new studies,.
"The likelihood of fluoride acting' as a genetic ca use of cancer
requires consideration," writes Takahashi and colleagues in '
the July 2001 Journal of Epidemiologyl who found that 23 of
36 cancer sites (63.9%) were associated positively with
fluoridation status, using World Health Organization data and
the US Fluoridation Census.
, Some studies, e.g., Hoover (1976) and Knox (1985) claim
no credible fluoridation/cancer association exists. However,
Takahashi and co-authors found the Hoover/Knox assessments
flawed, and explain why in their paper.
The authors report that the National Cancer Institute
provided epidemIological evidence of a relation between cancer
incidence and water fluoridation in 1987. These findings
provoked a 1990 National1bxicology Program (NTP) study
I that determined fluoride could be a cancer-causing agent
because four male rats out of 261 developed osteosarcoma (a
rare bone cancer).
The NTP study "supplied a detailed description of the
toxicology of fluoride. not only in terms of osteosarcoma. but
also lesions in the oral mucosa, thyroid gland. skin and
uterus...(which) prompted us to re-test the hypothesis of an
epidemiological association between water fluoridation and
cancer incidences...." wrote Takahashi who found fluoridation'
status positively correlates to cancers of the oral cavity,
pharynx, colon, rectum, hepato-bilary and urinary organs and
I bone cancer in males.
.Such a broad spectrum association has never been
observed for any particular known carcinogen, but it may be
reasonable for fluoride, because of its st1"Ong ~Iectronegtltive
nature," the authors explain.
After ten years of water fluoridation, children aged 7-18 in
Newburgh, New York, had more cortical bone defects than the
non-fluoridated control city, Kingston. And more osteosarcoma
occurred in young males in fluoridated portions of New Jersey.
.....these two facts may be connected pathophysiologically,"
Takahashi reports.
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Takahashi urges researchers worldwide to "further assess
fluoride as a genetic cause of cancers. . .and stop the application
off1uoride for prevention of teeth caries (cavities) if this indeed
presents as a risk factor for cancer."
In ano~her study,2 Ramesh and colleagues, "propose that high
fluoride bone content might have been one of the major factors
causing osteosarcoma," in the Journal of Environmental
Pathology 1b%icology and Oncology, 2001, Vol. 20, issue 3.
Ramesh, et a1. analyzed bone samples of 20 Indian
osteosarcoma patie~ts."The very high levels of fluoride
accumulation in the, bone samples of (2 Indian osteosarcoma
patients) in which p53 gene mutation have also been detected
suggest possible adverse effects of fluoride on the DNA of the
osteosarcoma patients," Ramesh and colleagues write.
Mutations in the p53 pnes are the most commonly observed
genetic alterations in human cancer. Ramesh concludes that
"fluoride probably causes mutations in p53."
"These new findings raise important questions about
potential harm from water fluoridation, especially when
coupled with the current recogrJtion that ingesting fluoride
does not reduce tooth decay but has caused a massive increase
in disfiguring dental fluorosis," says lawyer Paul Beeber,
President, New York State Coalition Opposed to Fluoridation.
The NYS Coalition Opposed to Fluoridation consists of
scientists, physicians, dentists, legislators. lawyers,
environmentalists, university professors, other professionals,
and concerned citizens who volunteer their efforts to inConn
thepublicaboutfluorid~uoridation~scientiftcallysupported
harmful dental, systemic and cumulative effects, to balance '
the usually pro-fluoridation opinion that's reported by
mainstream media.
(1) http://www.ncbi.nim.nih.gov/entrezlquery.fcgi?
cmd..Retrieve&db=PubMed&IisCulds=1l512573&dopt=Abstract
(2) http://www.ncbi.nlm.nih.gov/entrezlquery.fcgi?
cmd:Retrieve&db=PubMed&list_uids=11797833&dopt.=Abstract
For more Information, contact
Paul Beeber, President
New York State Coalition Opposed to Fluoridation
516-378.7309
Email: nyscot@aol.com
Website: http://www.orgsites.com/ny/nyscof
Paul Connett, PhD, Professor of Chemistry, St. Lawrence
University in Canton, New York, ggvideo@northnet.org,
Fluoride Action Network
http://www.fluoridealert.org/f-bonecancer.htm
TOWNSEND LEn'ER for DOCTORS. PATlENTS - JUNE 2002
The Phosphate Fertilizer Industry: An Environmental Overview
Page 1 ofl
In 1995. the TaJ1JjJHT.rib.lIIlC summcd up thc situation liS follows:
"The l],S. dell1and tor tluorine. which was 400.000 tons. is expected to jump 25 percent by next year.., Even though
600.000 tons or fluorine are contained in the 20 million tons of phosphate rock mined in Florida. thc tluorine market has
becn inaccessiblc because thc,'Jluorine is tied up with silica. a hard. glassy materia1."
Of course. not all of the phosphate industry's tluoridt' wasle is disposed of in the ponds. As not~d earlier. the phosphate industry has round
at least one regular eonsumcr of its silieotluorides: municipal water-treatment facilities,
According to recent ~StiIJ.111!(;~, the phosphate industry sells approximately 200,000 .tons of silicolluoridcs (l;ydrotluorosilicic acid & sodium
'silicolluoride) to US communities each year for use as II water tluoridation agent (Coplan & Masters 20(1).
6) Fluoridation: "An idelll solution to a long-standing problem"? (hack lo top)
In J 983. Rebecca Hanmer. the Deputy Assistant Administrator for Water at the US Environmental Protection Agency. described the policy
of using the phosphate industry's silico!1uorides for tluoridation as follows:
"In regard to the useofllllosilicie acid as the source oftluoride for tluoridation. this agencv regards such use as an ideal
solution to a long standing problem. By recovering by-product tluosilicic acid fromlertilizer manufacturing, water and air
polllllion are minimized. and water authorities have a low-cost source of tluoride available \0 them" (~cclettc-,,)
Another EPA ot1icial. l)L_L_\".lilli.ll}JJ)-lirzy. the current Senior Vice-President of EPA Headquarters Union. recently cxpressed a different
view on the matter. According to Hirzy:
'''If this Sill IT gets out into the air. it's a pollutant: ifit gets into the river. it's a pollutant: ifit gets into the lake it's a
pollutant: but ifit goes right into your drinking water system. it's not a pollutant. That's amazing.., There's got to be a
better way to manage this stuff' (Hirzy 2(00),
7) Recent Findings 011 Silicolluol'idl'S (back 1<> \('1'1
Adding to Hirzy's. and the EFAJil1iq.l1:s. concerns are three recent findings,
First and fort'most are two recent studies reporting a relationship betv..'ecn water treated with silicolluorides and elevated levels oflead in
children's blood (Masters & Coplan 1999,2(00), The authors ofthese studies speculate that the silicolluoride complex may increasethc
uptake oflead (derived from other environmental sources. such as lead paint) into the bloodstream,
The second finding is the recent. and quite remarkable conc.;ssioll from the EPA. that despite 50 years of\vater lluoridation. the EPA has
110 chronic health studies on silicotluorides, All safety studics on nuolide to date have been conducted using pharmaceutical-grade sodium
lluoride, not industrial-grade silicolluorides, A silnjlar L'9L1c.c.ssiol1 has also been obtained from the respective authorities in England,
httn:/ /www.fluoridealert.onl/nhosnhateloverview.htm
8/6/03
August 9, 2003
Dear Commissioners:
My name is:
Betty Taylor
34 Crane Drive
Safety Harbor, Florida 34695
Please consider the following recent facts regarding the use of fluoride or rather,
fluorosilicic acid in our drinking water. People with weak immune systems,
children and the elderly will be adversely atTected first. Many of these people are
unable to convey their message to you in person. It is very expensive and dangerous
to add fluoride to our drinking water. Supplements are abundantly available to
those who choose to use it. Here are a few of the newest updated facts on
fluorosilicic acid.
DEFLUORIDATION AND UNICEF
"UNICEF works closely with the Government and other partners in defluoridation
programmes in India ... to provide fluoride-safe water in all areas affected." "UNICEF
has also sponsored research and development on the use of activated alumina for removal
of fluoride from water." Why is this happening in other countries concerned for their
health and not our country?
As other cities and most of Europe learn the new facts regarding it's toxicity, they are
removing the chemical from their drinking water. Lawsuits have taken place in different
areas of our country and are listed in a document I have presented to the Commissioners
entitled, The Fluoride Fiasco by, By Gary Null, Ph.D.
The Fluoridation Fiasco
By Gary Null, Ph.D.
'This document contains 20 pages of informative information regarding. fluoride. Please
make special note of page 7 regarding Skeletal Fluorosis, page 8, Bone fractures, and
page 9, Fluoride Poisoning and toxic spills.
Page 7
Skeletal Fluorosis- " Wh~n fluoride is ingested, approximately 93% of it is absorbed into
the bloodstream. A good part of the material is excreted, but the rest is deposited in the
bones and teeth, and is capable of causing a crippling skeletal fluorosis. . This is a
condition that can damage the musculoskeletal and nervous systems and result in muscle
wasting, limited joint motion, spine deformities, and calcification of the ligaments, as
well as neurological deficits."
Pages 9 and 10
Note the states aCf0SS the country with health problems resulting from mishaps with
fluoride and the resulting lawsuits attributed to such.
Many cities across the United States and Canada have removed fluoride recently
from their drinking water: Some after more than 42 years.
(partial list)
Year 2003- York, Nebraska
Shaler, Pennsylvania
Dutton-Dunwich, Ontario, Canada
Canton, New York
Burns Lake, British Columbia, Canada
West Elgin, Ontario, Canada
Year 2002- Billings, Montana
Methuen, Massachusetts
Texarkana, Arkansas
Franklin, North Carolina
Washoe County, Nevada
Redding, California
Oneida. New York
Monroe, Louisiana
Take a look right here in Plant City at the Coronet Company! Check the
background on the investigations on the concerns of the phosphates and fluoride
polluting tile surrounding ground and the cases of cancer in the immediate area!
BIOEFFECTS
EFFECTS OF FLUORIDE ON DEVELOPMENT OF BONE
TAKEN FROM FDA SITE ONLINE
"Various kinds of toxicity have been attributed to ingestion of fluoride, including
dental fluorosis, bone fracture, reproductive, renal, gastrointestinal, and
immunological toxicities; genotoxicity; and carcinogenicity."
Prominent Researcher Apologizes for Pushing Fluoride
by Barry Forbes
The Tribune, Mesa Arizona
Sunday, December 5,1999
The President of the Canadian Association for Dental Research, Hardy Limeback,
states:
"The vast majority of aU fluoride additives come from Tampa Bay, Florida
smokestack scrubbers. The additives are a toxic byproduct of the super-phosphate
fertilizer industry." "Tragically, that meaDS we're not just dumping toxic fluoride
into our drinking water. We're also exposing innocent, unsuspecting people to
deadly elements of lead, arsenic and radium, all of them carcinogenic. Because of
the cumulative properties of toxins, the detrimental effects on human health are
catastrophic."
Please take a good careful look at the facts and make an important decision based
on what is right for everyone's overall health. Ask why. we would use fluoride if it is
a toxic chemical and why Organizations such as UNICEF are removing it for health
reasons in other countries and not ours. Many parts of Europe have long ago
removed fluoride from their drinking water.
Fluorosilicic acid
Is toxic at very low levels
Causes bone cancer, osteoarthritis and fluorosis of the teeth
Comes from industrial waste -'- Phosphates
Fluoride additives are a toxic byproduct of the super-phosphate fertilizer
industry
CDC-
Found many toxic chemicals in peoples blood
Study on HUMAN EXPOSURE TO TOXIC CHEMICALS
EPA-
Has no information on health effects of chronic ingestion of (fluorosilicic acid)SiF-
treated water. What is the purpose of adding a chemical to our drinking water that has
not been evaluated fully and is believed to be toxic?
Thank you,
Betty Taylor
Defluoridation and UNICEF
UNICEF has worked closely with the Government and other partners in defluoridation prograrrmes in '...dia. w here excessive fluor.ide has been know n
for many years to exist in IWCh of the nation's groundwater. In the 19BOs, UN~supportedthe Government's Technology Mssion in the effort to
identify and address the fluoride problem: the Government subsequently launched a massive programme. still under way, to provide fluoride-safe
water in all the areas affected.
Over the past fIVe years. UNICEF's focus in the India progrElmme has been on strengthening the systems for monitoring water quality. facilitating water
treatment by households. and advocating alternative water supplies w hen necessary. Education - both of households and cOlT1'TlUnities - is key to the
strategy. A number of demonstration projects have been initiated in fluorosis-affected areas. with the emphasis currently on introducing household
defluoridation. UNICEF has also sponsored research and, developmer;rt on the use of activated l!!!';Irinafor. removal of fluoride from water.
Since fluoride must now be considered an issue of w orldw ide importance. the years of experience in Riia should help UNICEF and its partners
provide four types of assistance towards an eventual solution:
A'omoting a better understanding of the problem and its impact on chftdren;
Raising the awareness of relevant governments and the public on the fluoride issue in particular and the importance in general of monitoring water
quality;
Demonstrating. through pilot projects. the efficacy of low -cost fluoride removal technologies;
Strengthening community and government capacity for fluorosis prevention. including a credible system for risk assessment that comprises both water
quaflty monitoring and health monitoring.
Notes:
'Fluorine and fluorides'. Environmental Health Criteria 36, IPCS International A'ograrrme on Cherrieal Safety. WHO, 1984. The WHO guideline values for
fluoride in drinking water were reevaluated in 1996. without change. and the issue is currently under further review.
Prevention and control of fluorosis in India, Rajiv Gandhi National Drinking Water Mssion, 1993.
'Endemic fluorosis in Mexico', Auoride. vol. 30. no. 4.1997.
Data from a national research project under the eighth FIVe-Year Economic and Social Development Ran. 1995.
'Auorine and fluorides', see note 1 above.
Information supplied by UNICEF India.
I Home I About WES I Publications I Online Services I Contacts I
Thul8day. June 12. 2003 America Online: Von34 Page: 1
, Fluorosis worldwide
The latest information show s that fluorosis is endemic in at least 25 countries across the globe (see map). The total IlUrmer of people affected is not
known, but a conservative estimate would number in the tens of nillions. n 1993,15 of ndia's 32 states were identified as endenic for f1uorosis~. In
Mexico, 5 million people (about 6% of the population) are affected by fluoride in groundwate@. Fluorosis is prevalent in some
parts of central and western China, and caused not only by drinking fluoride in groundwater but also by breathing airborne'
fluoride released from the burning of fluoride-laden coal~. Worldwide, such instances of industrial fluorosis are on the rise.
..
Ulumrit"S with t'1ldmlk lltlOo'051$ due. to ~s.flUIJride ill dmJA:ilfg lVlner
Thursday, June 12, 2003 America Online: V0n34 Page: 1
" Study to Address Cancer, Bone Problems, & Other Health Concerns Near Coronet Phosp... Page 1 of 5
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Section: Pol1utiolll'!~ws > phosphate IndustT\
Study to Address Cancer, Bone Problems, &
" ' Other Health Concerns Near Coronet
Phosphate
Note from FAN: We are honored to note that the Tampa Tribune cites the Fluoride Action
Network, along with the Environmental Protection Agency & Ag~ncy for Toxic Substances &
Disease Registry, as references for technical infonnation used in this report. See:
http://pasco.tbo.com/pascoIMGA32CLH2ID.html
The Tampa Tribune
Sunday 13 Ju~v 2003
Ulhaf Lies Beneath Affects Rising Homes
by Deborah Alberto
(See originalilJ~ljQfl
,
PLANT CITY - Carl Crowell isn't sure what caused his prostate cancer, and he can't say why
many of his neighbors have been stricken with other forms of the disease.
Public health agencies don't know either. But they are trying to determine whether pollution
from a phosphate plant and old landfills could be linked to illness in Crowell's neighborhood
and another Plant City community about two miles away.
Crowell, 7], isn't pointing a finger of blame. But he wonders why the city would consider a
plan to create Plant City's largest development - 2,600 houses - between the neighborhoods
being studied by health otlicials.
It's a question some city officials are asking, too.
..... nG. ");igl;
~
"Are we going to develop an area where we have to warn people that [living there] may be
hazardous to your health?" Plant City Commissioner Richard Glorioso said.
The state has unearthed no definitive evidence that cancer rates in the communities are higher
than state averages. But officials are concerned the complaints - including bone impairnlents,
bad teeth and cancer - are coming from areas near the Coronet Industries phosphate processing
plant, where they have found elevated levels of cancer-causing substances in groundwater and
soil. The plant is just south of the] ,300 acres on which Sunrise Homes proposes to build the
Lakeside Station development. The development would be on land owned by Gregg Enterprises
- formerly Consolidated Minerals Inc.
When state investigators checked out health complaints, residents "pointed out almost every
house as having people currently sick with cancer or people who have died in the last few years
of cancer - often both husband and wife, and sometimes children," says a report written by Beth
Copeland andShaun Crawford of the Florida Department of HeaIth.
That report helped persuade the U.S. Agency for Toxic Substances and Disease Registry on
Friday to authorize the Health Department to further study the effects ofthe plant and
surrounding properties on the residents' health.
The agency, an ann of the federal Centers for Disease Control and Prevention,could have a
report ready by March, said John Steward, the agency's petition coordinator.
Oflicials first want to find out whether people were exposed to toxic substances, Steward said.
An exposure investigation, sometimes part of the process, involves testing for the presence of
chemicals in blood, hair or urine.
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8/1/03
, Study to Address Cancer, Bone Problems, & Other Health Concerns Near Coronet Phosp... Page 2 of ~
"There's enough information to suggest there is a potential for people becoming exposed to
those [contaminants] in the past. currently or in the future," he said.
The Health Department's recommendation focused much of its attention on Coronet, which
processes phosphate for use in animal feed supplements.
State health officials said their initial findings - carcinogens in groundwater at Coronet, air
quality problems and a history of pollution at the site - merit further investigation.
In a report to the federal agency June 18, the' Health Department said a community spokesman
repOJ;ted that 36 people living in a neighborhood of about 500 northwest of Coronet have died
of cancer in the past few years. A spokesmaii' for the community of about 200 residents to tbe
east said 98 people there have died from cancer. No time period was given.
The state has not verified the numbers, however, and state cancer statistics for the ZIP codes
atTected show rates consistent with state averages.
Some residents have told the state their illnesses might be attributed to pollution from Coronet
or possibly waste burning on adjacent dumps from the late 1950s to the late 1960s.
The old landfills - on the Lakeside Station site - would be developed as a park. Much of the
property intended for the housing development also was mined for phosphate until the 1930s.
Cancer Clusters
Cancer clusters, concentrated areas where the disease occurs in an abnormally high percentage
of the population, as the community complaints suggest, are often difticult to verify even after
extensive investigation.
Jim Baker, Coronet's environmental manager, said he is uncomfortable commenting on the
Health Department's report because it is preliminary.
Arsenic, cadmium, chromium, lead and gross alpha radiation were found in high concentrations
from 1998 through 2002 on Coronet's land, the state report says. All are carcinogens.
FI uoride - also found in groundwater at the plant - can cause bone problems in high
concentrations, health officials said. The amounts reported at Coronet far exceed state and
federal guidelines.
The community east of Coronet gets its water from private wells, and those living northwest of
the plant are on city water. Health ofticials are concerned not only with the drinking water but
also general exposure to toxic substances in air emissions or from children playing in ditches
tlooded with contaminated \\-'lIter.
Some symptoms reported by people south of U.S. 92 and west of Park Road and also in the
community east of Coronet off Wiggins Road are consistent with effects caused by high levels
of fluoride, said Copeland, a community involvement specialist with the state Health
Department.
City officials are considering a land-use change that would designate the industrially zoned
property for mixed-use residential development. That would allow Sunrise Homes to build a
community complete with commercial businesses, light industrial businesses and a school.
City commissioners plan to discuss ordinance changes that would make way for the
development at an 8 a.m. workshop Monday before taking it to a public hearing at 7:30 that
night.
History Of Poll ution
Consolidated Minerals sold the Coronet plant to Japanese investors in 1993 but still owns much
of the surrounding property. Coronet has changed ownership many times, and pollution from
http://www.fluoridealert.org/pollution/l 589 .html
8/1/03
Study toAddress Cancer, Bone Problems, & Other Health Concerns Near Coronet .Phosp.... .Page 3 ot5
the plant was documented as early as the 1960s.
Plant owners were sued in federal court in the 1960s by citrus growers who claimed dust from
Coronet ruined their crops. They were awarded $200,000 in damages.
Coronet has been been under county scrutiny since at least the late 1990s due to air pollution
and hydrofluoric acid spills that caused water contamination.
Also included in the health otTicials' rep~rt in June to the federal toxic substance' agency were
results of tests at the Coronet plant site conducted by the state Department of Environmental
Protection. Levels of several toxic substances exceeded safety guidelines.
Each time the region experiences heavy rain, settling ponds at the plant release arsenic and
other toxic substances into nearby English Creek.
Coronet Industries is under orders from the state to make sure the spills stop. When the
di scharges occur, the toxic water tlows into the creek and eventually into the Alafia River.
Initially, Coronet agreed to enlarge its ponds, which would eliminate surface water discharges.
But Baker said that plan was ditched in favor of a' . more proactive" strategy that involves
treating the water. He said negotiations with the state are under way, and' 'there has been no
defi niti ve treatment yet."
Coronet also is trying to avoid a shutdown by the Hillsborough County Environmental
Protection Commission for air emissions violations.
The plant has a lengthy history of emissions violations, and the environmental commission has
required the owners to bring the plant up to standards to eliminate toxic emissions by 2005.
"We completed a self-audit, which is being used as a too] to assist in compliance with air
pollution," Baker said. The plan involves upgrades to facilities at the plant.
Mixed Reactions
Glorioso said the state health report' 'raises grave concerns" about developing the area. Mayor
Bill Dodson also expressed concerns about potential environmental problems on the property
but changed his mind in May when county environmental onicia]s said it was safe to build
there.
But Commissioner Mike Sparkman, who has lived in Plant City all of his life, doesn't "fee]
there is a problem as it relates to most of the property."
"I used to do a lot of dove hunting out there," he said. "It's some beautiful property."
Sunrise Homes commissioned several environmental studies on the land proposed for
development. The tirst study showed elevated levels of arsenic and other metals but was
inaccurate because of turbidity in collected samples, said Bob App]eyard, Sunrise's land
manager. Subsequent studies indicated the property was safe for development, he said.
Appleyard said tests for gamma radiation, which provide an idea of radon concentrations, were
conducted. "The levels of gamma radiation are not at all something we are uncomfortable
with," he said.
The state Health Department's reports shouldn't be taken lightly, though, Appleyard said. "We,
more than anyone, want to know more:"
"We all know Coronet is a polluter," but that doesn't mean toxic substances on the company's
property atTected outlying areas, s~lch as the Lakeside Station site, he said.
Jim Shimberg JT., the attorney for Gregg Enterprises, owner of the property to be developed,
http://www .fluoridealert.org/pollution/1589 .html
8/1/03
Study to Address Cancer, Hone Problems, is!. other Health t;oncerns Near t;oronet PbOSp... page"" or :)
called the state report "a little misleading and inaccurate."
He used the developer's studies as he unsuccessfully tried topersuade federal ,health officials to
not order a further health assessment.
"We've got a lot of time and money invested in this," he said. He could not estimate the cost of
the development but. said" hundreds of thousands" of dollars have been spent.
Runoff Stays On Property'
I.
He, said the runot;ffrom the land where dev~opment is proposed does not travel into the
communities reporting health problems.
"The stonnwater on Gregg's property stays in lakes and a discharge pond on property," he said.
Shimberg added, however. that if there is a serious public health concern, "we want to know
about it."
To date, the only testing done outside Coronet land was on 13 wells southeast of the plant. That
testing was done under the direction of the state Department of Environmental Protection, and it
revealed slightly elevated levels of arsenic in one of the wells.
Fluoride also was found in some wells. health officials said.
. .
Because so little testing has been done, health otlicials have no way of knowing whether the
contaminants are atfecting neighboring areas.
"What bothers me the most is what I don't know," said Crawford, an environmental scientist
and health assessor with the Florida Department of Health.
Coronet reported four discharges into English Creek from December 1997 to April 1998, a total
of about 150 million gallons of water contaminated with arsenic.
Another discharge in September 200 I totaled 178 million gallons of contaminated water,
according to the state.
Runotf from the old landfills on the proposed Lakeside Station development crosses over Park
Road into the community northwest of Coronet, contributing to severe tlooding, according to
the Health Departrnenfs report.
"Ifthere was, or is, contamination, tlooding from rainfall could have carried it further into the
community," the report said.
County officials said the water with extremely high levels of contaminants is confined to the
Coronet plant property. The highly contaminated water was found beneath a leaky tank, said
Sam E1rabi, an engineer with Hillsborough's environmental commission.
"That water is not leaving the site," he said.
State otlicials said the jury is out, however, as to which way groundwater is tlowing.
"We're waiting on an assessment from [Coronet] to discern exactly how the groundwater is
tlowing," said Bill Kelsey, a hydrogeologist with the state environmental department.
Ifs not just water that worries health otlicials,
Dust and particulates generated by the plant have sparked enforcement action by the county.
The plant has a lengthy history of emissions violations, and Hillsborough'senvironmental
http://www .fluoridealert.orglpollution/15 89 .html
8/1/03
Study to Address cancer, Hone l'TOOlemS, is[, Uther l1ea.ltn concerns Near coronet l'nosp... l'age::> or::>
commission required the owners to bring the plant up to standards to eliminate toxic emissions
by 2005 or face being shut down.
The process Coronet uses to make its animal food supplements produces dust particles and a
noxious gas called hydrotluoric acid gas, which, if released untreated, can kill plants and rust
metal, Hillsboroughenvironmental officials said.
Some residents question whether the lack oflife and vegetation in ponds at the Plant City Golf
Course, owned by Coronet, signals the presence of such emissions.
Baker said one pond on the course that looked particularly bad was not one ofthe factory's
monitoring ponds.
"I'm not a biologist, so I can't comment on the status of the pond," he said.
Now that health officials are investigating, residents want questions like that answered.
Corey Bradley was a promising young college student when he was diagnosed with colon
cancer. He died at age 22.
His mother, Dorothy, has wondered for years whether some sort of environmental contaminants
might have contributed to his death. -
"It really bothered me," she said. "He was so young. How could he have caught something like
that?"
* Researcher Jody Habayeb contributed to this report. Reporter Deborah Alberto can be reached
at (813) 754-3763
See also:
Horid~J)~arlmenl of Health's Preliminary R~ort on Coronet (submitted 10 A TSQR)
Public Health Concerns Tru11lR Other Priorities In Plant City
Ihe PhOlijJhale Fertilizer Industrv: An Elivironmental Overview
Fluoride Action Network I 802-859-3363 I inforij)tluoridealert.org
http://www.fluoridealert.org/pollution/I589 .html
8/1/03
,Flonda Vepartment or 11.ealID .t'reummary 11.ealID Kepon on \.,oronet mausmes - .t'age ';J
. .
Page 9.
Florida Department of Health Preliminary Health Report on CQr.9JlelJQdJI.~tries
Plant City, Florida. June 18, 2003.
(To see the Tampa Tribune article discussing this report, c/ic:..ILb?fe)
. .
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http://www.fluorideaction.orglphosphate/coronet/page9.htm
8/1/03
Ost1997 AR
page 1 01 1
BIOEFFECTS
Effects of Fluoride on Development of Bone
Key words: fluoride, bone strength, bone density, radiographic testing, mechanical testing, tech support,
~~ 'I
Various kinds of toxicity have been attributed to ingestion of fluoride, including dental fluorosis; bone
fracture; reproductive, renal, gastrointestinal, and immunological toxicities; genotoxicity; and
carcinogenicity. In 1990, a study by the PHS National ToxicologyPrograrn (NTP) found equivocal
I evidence of carcinogenicity associated with fluoride ingestion, based ona small number of
osteosarcomas in male rats. In response to this finding, a subcommittee of the PHS Committee to
Coordinate Environmental Health and Related Programs (CCEHRP) conducted a thorough review of the
benefits and risks of water fluoridation and other sources of fluoride. The committee issued a report in
1991 recommending further study related to various regulatory requirements for fluoride.. Regarding
fluorides effects on bone, CCEHRP recommended research to (1) determine the risk factors associated
with the development of fluoride-associated osteosarcoma, and (2) further elucidate the mechanisms of
fluoride action on bone at the molecular and physical chemical levels.
A collaborative study between CFSAN and CDRH was undertaken in response to the CCEHRP
recommendations. The objective was to determine the levels of fluoride in the plasma, urine, and bone
of rats at various stages of development and to characterize the bone strength for those rats. For each
category of rat (male/female and pregnant/not pregnant at various stages--neonatal, weanling, and adult),
I five fluoride levels were studied (Oto 250 ppm in drinking water). CFSAN determined the fluoride
content of one femur from each rat and CDRH conducted radiographic and mechanical testing on the
contralateral femora to assess the effects of treatment on bone strength. For the' radiographic, imaging
part of the study, computerized tomography testing was performed to measure bone density in the mid-
diaphyseal and distal sections of the bone. This enabled study of the effects of treatment on both cortical
and trabecular bone. Plain-film radiographs of each bone were also made for a collaborative study with
the University of Chicago using fractal analysis to estimate bone strength. Results from these imaging
studies will be compared with results from mechanical (bending) tests on the bones to determine (1) the
developmental effects of fluoride on bone strength, and (2) the correlation between bone density, fractal
dimension and bone strength. Testing has been completed by DMMS and DECS, and the data are being
analyzed.
Impact: The Environmental Protection Agency (EP A) regulates fluoride levels in drinking water and
FDA regulates fluoride intoothpaste, other dental products (e.g., composite fillings and dental cements),
bottled water, water used in food processing, infant formula, and dietary supplements. This study will
provide FDA (and possibly EPA) with additional data to address regulatory concerns identified in the
CCEHRP report on the benefits and risks of fluoride. The part of the study examining correlation
between mechanical and radiographic test data may be of use to CDRH, CDER, CBER, and perhaps
others with respect to evaluating imaging devices used to predict fracture risk, bone substitute materials,
drugs used to treat or prevent osteoporosis, and methods for storing bone and bone marrow for
transplant.
~_.....~....,-~---.-
."" .._. ~ ..,..l>l!'1..._,....______.1Il:. " ......._...
IH~Jl1Jil IPJ~yJOJt~ lli~~11 [CQmm~DJ~l
http://www.fda.gov/cdrh/ost/rpt97/0STI997ARll.HTML
6/12/03
Prominent researcher apologizes for pushing,
fluoride
Barry Forbes ,I ..
The, Tribune, Mesa, AZ
Sunday, December 5,1999
"Whyd you do it, Doc? Whyd you toss the fluoride folks overboard?" I had just tracked down Dr.
Hardy Limeback, B.Sc., Ph.D in Biochemistry, D.D.S., head of the Department of Preventive
Dentistry for the University of Toronto, and president of the Canadian Association for Dental
Research.
(Whew.)
Dr. Limeback is Canada's leading fluoride authority and, until recently, the country's primary promoter
of the controversial additive. In a surprising newsmaker interview this past April, Dr. Limeback
announced.a dramatic change of heart. "Children under three should never use fluoridated
toothpaste," he counseled. "Or drink fluoridated water.
And baby formula must never be made up using Toronto tap water. Never."
Why, I wondered? VVhat could have caused such a povverful paradigm shift?
"It's been building up for a couple of years," Limeback told me during a recent telephone interview.
"But certainly the crowning blow was the realization that \He have been dumping contaminated
fluoride into water reservoirs for half a century. The vast majority of all fluoride additives come from
Tampa Bay, Florida smokestack scrubbers. The additives are a toxic byproduct of the super-
phosphate fertilizer industry."
"Tragically," he continued, "that means we're not just dLmping toxic fluoride into our drinking water.
We're also exposing innocent, lI'lSuspecting people to deadly elements of lead, arsenic and radium,
all ofthem carcinogenic. Because of the ClI11ulative properties oftoxins, the detrimental effects on
human health are catastrophic."
A recent study at the University of Toronto confirmed Dr. Limeback's 'JIIOrst fears. "Residents of cities
that fluoridate have double the fluoride in their hip bones vis-a-vis the balance of the population.
Worse, \He discovered that fluoride is actually altering the basic architecture of human bones."
Skeletal fluorosis is a debilitating condition that occlJ's when fluoride accumulates in bones, making
them extremely weak and brittle. The earliest symptoms? "Mottled and brittle teeth," Dr. Limeback
told me. "In Canada we are now spending more money treating dental fluorosis than we do treating
cavities. That includes my own practice."
One of the most obvious living experiments today, Dr. Limeback believes, is a proof-positive
Sunday, June 29, 2003 America Online: Y0n34 Pege: 1
comparison between any two Canadian cities. "Here in Toronto 'He've been fluoridating for 36 years.
Yet Vancouver - which has never fluoridated ~ has a cavity rate 10'Her than Toronto's."
And, he pointed out, cavity ~~tes are low all across the industrialized world - including Europe, which
is 98% fluoride free. Low because of improved standards of living, less refined sugar, regular dental
checkups, flossing and frequent brushing. Now less than 2 cavities per child Canada-wide, he said.
"1 don't get it, Doc. Last month, the Centers for Disease Control (CDC) ran a. puff piece all across
America saying the stuff was better than sliced bread. What's the story?" "Unfortunately," he replied,
"the CDC is basing its position on data that is 50 years old, and questionable at best. Absolutely no
one has done research on f1uorosilicates, which is the junk they're dUllJping into the drinking water."
"On the other hand," he added, "the evidence against systemic fluoride in-take continues to pour in."
"But Doc, the dentists."
"1 have absolutely no training in toxicity," he stated firmly. "Your well-intentioned dentist is simply
I following 50 years of misinformation from public health and the dental association. Me, too.
Unfortunately, we were wrong."
Last week, Dr. Hardy Limeback addressed his faculty and students at the University of Toronto,
Department of Dentistry. In a poignant, memorable meeting, he apologized to those gathered before
him. "Speaking as the head of preventive dentistry, I told them that I had unintentionally mislead my
colleagues and my students. For the past 15 years, I had refused to study the toxicology information
that is readily available to anyone. Poisoning our children was the furthest thing from my mind."
"The truth," he confessed to me, "was a bitter pill to swallow. But swallow it I did."
South of the border, the paradigm shift has yet to dawn. After half a century of delusion, the CDC,
American Dental Association and Public Health stubbornly and skillfully continue to manipulate public
opinion in favor of fluoridation.
Meantime, study after study is delivering the death knell of the deadly toxin. Sure, fluoridation will be
around for a long time yet, but ultimately its supporters need to ready the life rafts. The poisonous
waters of doubt and confusion are bound to get choppier.
"Are lawsuits inevitable?" I asked the good doctor. "Remember tobacco," was his short, succinct
reply.
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The Fluoridation Fiasco
by Gary Null, Ph.D.
There's nothing like a glass of cool, clear water to quench one's thirst. But the next time
you or your child reaches for one, you might want to question whether that water is in fact,
too toxic to drink. If your water is fluoridated, the answer may well be yes.
For decades, we have been told a lie, a lie that has led to the deaths of hundreds of
thousands of Americans and the weakening of the immune systems of tens of millions
more. This lie is called fluoridation. A process we were led to believe was a safe and
effective method of protecting teeth from decay is in fact a fraud. In recent years it's been
shown that fluoridation is neither essential for goOd health nor protective of teeth. What it
does is poison the body. We should all at this point be asking how and why public health
policy and the American media continue to live with and perpetuate this scientific sham.
How to Market a Toxic Waste
"We would not purposely add arsenic to the water supply. And we would not purposely
add lead. But we do add fluoride. The fact is that fluoride is more toxic than lead and just
slightly less toxic than arsenic."]
These words of Dr. John Yiamouyiannis may come as a shock to you because, if you're
like most Americans, you have positive associations with fluoride. You may envision tooth
protection, strong bones, and a government that cares about your dental needs. What you've
probably never been told is that the fluoride added to drinking water and toothpasteis a
crude industrial waste product of the aluminum and fertilizer industries, and a substance
toxic enough to be used as rat poison. How is it that Americans have learned to love an
environmental hazard? This phenomenon can be attributed to a carefully planned marketing
program begun even before Grand Rapids, Michigan, became the first community to
officially fluoridate its drinking water in 1945.2 As a result of this ongoing campaign,
nearly two-thirds of the nation has enthusiastically followed Grand Rapids' example. But
this push for fluoridation has less to do with a concern for America's health than with
industry's penchant to expand at the expense of our nation's well-being.
The first thing you have to understand about fluoride is that it's the problem child of
industry. Its toxicity was recognized at the beginning of the Industrial Revolution, when, in
the 1850s iron and copper factories discharged it into the air and poisoned plants, animals,
and people.3 The problem was exacerbated in the 1920s when rapid industrial growth meant
massive pollution. Medical writer Joel Griffiths explains that "it was abundantly clear to
both industry and government that spectaClilar U.S. industrial expansion - and the economic
and military power and vast profits it promised - would necessitate releasing millions of
tons of waste fluoride into the environment. ,,4 Their biggest fear was that "if serious injury
to people were established, lawsuits alone could prove devastating to companies, while
public outcry could force industry-wide government regulations, billions in pollution-
control costs, and even mandatory changes in high-fluoride raw materials and profitable
technologies. ,,5
http://www.tldp.com/issue/157-8/157fluor.htm
8/1 0/03
.l-Cl.~C k VJ. kJ.
At first, industry could dispose of fluoride legally only in small amounts by selling it to
insecticide and rat poison manufacturers.6 Then a commercial outlet was devised in the
1930swhen a connection was made between water supplies bearing traces of fluoride and
lower rates of tooth decay. Griffiths writes that this was not a scientific breakthrough, but
rather part of a "public disinformation campaign" by the aluminum industry "to convince
the public that fluoride was safe and good. " Industry's need prompted Alcoa-funded
scientist GeraldJ. Cox to announce that "The present trend toward complete removal of
fluoride from water may need some reversal. ,,7 Griffiths writes: '
"The big news in Cox'sannouncement was that this 'apparently worthless by-product' had
not only been proved safe (in low doses), but actually beneficial; it might reduce cavities in
children. A proposal was in the air to add fluoride to the entire nation's drinking water.
While the dose to each individual would be low, 'fluoridation' on a national scale would
require the annual addition of hundreds of thousands of tons of fluoride to the country's
drinking water.
"Government and industry - especially Alcoa - strongly supported intentional water
fluoridation...[it] made possible a master public relations stroke - one that could keep
scientists and the public off fluoride's case for years to come. If the leaders of dentistry,
medicine, and public health could be persuaded to endorse fluoride in the public's drinking
water, proclaiming to the nation that there was a 'wide margin of safety,' how were they
going to turn around later and say industry's fluoride pollution was dangerous?
"As for the public, if fluoride could be introduced as a health enhancing substance that
should be added to the environment for the children's sake, those opposing it would look
like quacks and lunatics....
"Back at the Mellon Institute, Alcoa's Pittsburgh Industrial research hlb, this news was
galvanic. Alcoa-sponsored biochemist Gerald J. Cox immediately fluoridated some lab rats
in a study and concluded that fluoride reduced cavities and that 'The case should be
regarded as proved.' In a historic moment in 1939, the first public proposal that the U.S.
should fluoridate its water supplies was made - not by a doctor, or dentist, but by Cox, an
industry scientist working for a company threatened by fluoride damage claims. ,,8
Once the plan was put into action, industry was buoyant. They had finally found the
channel for fluoride that they were looking for, and they were even cheered on by dentists,
government agencies, and the public. Chemical Week, a publication for the chemical
industry, described the tenor of the times: "Allover the country, slide rules are getting warm
as waterworks engineers figure the cost of adding fluoride to their water supplies." They are
riding a trend urged upon them, by the U.S. Public Health Service, the American Dental
Association, the State Dental Health Directors, various state and local health bodies, and
vocal women's clubs from coast to coast. It adds up to a nice piece of business on all sides
and many firms are cheering the PHS and similar groups as they plump for increasing
adoption of fluoridation. ,,9
Such overwhelming acceptance allowed government and industry to proceed hastily,
albeit irresponsibly. The Grand Rapids experiment was supposed to take 15 years, during
which time health benefits and hazards were to be studied. In 1946, however, just one year
into the experiment, six more U.S. cities adopted the process. By 1947,87 more
communities were treated; popular demand was the official reason for this unscientific
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The general public and its leaders did support the cause, but only after a massive
government public relations campaign spearheaded by Edward L. Bernays, a nephew of
Sigmund Freud. Bernays, a public relations pioneer who has been called "the original spin
doctor, " 10 was a masterful PR strategist.. As a result of his influence, Griffiths writes,
"Almost overnight...the popular image of fluoride - which at the time was being widely sold
as rat and bug poison - became that of a beneficial provid~ of gleaming smiles, absolutely
safe, and good for children, bestowed by a benevolent paternal government. Its opponents
were permanently engrav~ 'on the public mind as crackpOts and right-wing loonies."}}
Griffiths explains that while opposition to fluoridation is usually associated with right-
wingers, this picture is not totally accurate. He provides an interesting historical perspective
on the anti-fluoridation stance:
"Fluoridation attracted opponents from every point on the continuum of politics and
sanity. The prospect of the government mass-medicating the water supplies with a well-
known rat poison to prevent a nonlethal disease flipped the switches of delusionals across
the country - as well as generating concern among responsible scientists, doctors, and
citizens.
"Moreover, by a fortuitous twist of circumstances, fluoride's natural opponents on the left
were alienated from the rest of the opposition. Oscar Ewing, a Federal Security Agency
administrator, was a Truman "fair dealer" who pushed many progressive programs such as
nationalized medicine. Fluoridation was lumped with his proposals. Inevitably, it was
attacked by conservatives as a manifestation of "creeping socialism," while the left rallied to
its support. Later during the McCarthy era, the left was further alienated from the opposition
when extreme right-wing groups, including the John Birch Society and the Ku Klux Klan,
raved that fluoridation was a plot by the Soviet Union and/or communists in the government
to poison America's brain cells.
"It was a simple task for promoters, under the guidance of the 'original spin doctor, I to
paint all opponents as deranged - and they played this angle to the hilt....
"Actually, many of the strongest opponents originally started out as proponents, but
changed their minds after a close look at the evidence. And many opponents came to view
fluoridation not as a communist plot, but simply as a capitalist-style con job of epic
proportions. Some could be termed early environmentalists, such as the physicians George
L. Waldbott and Frederick B. Exner, who first documented government-industry complicity
in hiding the hazards of fluoride pollution from the public. Waldbott and Exner risked their
careers in a clash with fluoride defenders, only to see their cause buried in toothpaste
ads." II
By 1950, fluoridation's image was a sterling one, and there was not much science could
do at this point. The Public Health Service was fluoridation's main source of funding as well
as its promoter, and therefore caught in a fundamental conflict of interest. 12 If fluoridation
were found to be unsafe and ineffective, and laws were repealed, the organization feared a
loss of face, since scientists, politicians, dental groups, and physicians unanimously
supported it. 13 For this reason, studies concerning its effects were not undertaken. The
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Oakland Tribune noted this when it stated that "public health officials have often suppressed
scientific doubts" about fluoridation. 14 Waldbott sums up the situation when he says that
from the beginning, the controversy over fluoridating water supplies was "a political, not a
scientific health issue. "IS
The marketing of fluoride continues. In a 1983 letter from the Environmental Protection
Agency, then Deputy Assistant Administrator for Water, RebecCa Hammer, writes that the
EP A "regards [fluoridation] as an ideal environmental solution to a long-~tanding problem.
By recovering by-product fluosilicic acid from fertilizer manufacturing, water and air
pollution are minimized and water utilities have a low~st source offluoride available to
them.,,16 More recently, a 1992 policy statement from the Depa~ent of Health and Human
Services says, "A recent comprehensive PHS review of the benefits and potential health '
risks of fluoride has concluded that the practice of fluoridating community water supplies is
safe and effective." 17
Today, nearly 250 million people worldwide drink fluoridated water, including about 130
million Americans in 9600 communities. Out of the 50 largest cities in the US, 41 have
fluoridated water. 18
To help celebrate fluoride's widespread use, the media recently reported on the 50th
anniversary offluoridation in Grand Rapids. Newspaper articles titled "Fluoridation: a
shining public health success,,19 and "After 50 years, fluoride still works with a smile,,20
painted glowing pictures of the practice. Had investigators looked more closely, though,
they might have learned that children in Muskegon, Michigan, an unfluoridated "control"
city, had equal drops in dental decay. They might also have learned of the other studies that
dispute the supposed wonders of fluoride.
The Fluoride Myth Doesn't Hold Water
The big hope for fluoride was its ability to immunize children's developing teeth against
cavities. Rates of dental caries were supposed to plummet in areas where water was treated.
Yet decades of experience and worldwide research have contradicted this expectation
numerous times. Here are just a few examples:
In British Columbia, only 11% of the population drinks fluoridated water, as opposed to
40-70% in other Canadian regions. Yet British Columbia has the lowest rate of tooth decay
in Canada. In addition, the lowest rates of dental caries within the province are found in
areas that do not have their water supplies fluoridated.21
According to a Sierra Club study, people in unfluoridated developing nations have fewer
dental caries than those living in industrialized nations. As a result, they conclude that
"fluoride is not essential to dental health. ,,22
In 1986-87, the largest study on fluoridation and tooth decay ever was performed. The
subjects were 39,000 school children between 5 and 17 living in 84 areas around the
country. A third of the places were fluoridated, a third were partially fluoridated, and a third
were not. Results indicate no statistically significant differences in dental decay between
fluoridated and unfluoridated cities.23
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A World Health Organization survey reports a decline of dental decay in western Europe,
which is 98% unfluoridated. They state that western Europe's declining dental decay rates
are equal to and sometimes better than those in the U.S.24 '
A 1992 University of Arizona study yielded surprising results when they found that "the
more fluoride a child drinks, the more cavities appear in the teeth.,,2S
Although aU Native American reservations are fluorida~, children living there have
much higher incidences of-dental decay and other oral health problems than do children
living in other U.S. communities.26
In light of all the evidence, fluoride proponents now make more modest claims. For
example, in 1988, the ADA professed that a 40- to 600.10 cavity reduction could be achieved
with the help of fluoride. Now they claim an 18- to 25% reduction. Other promoters
mention a 12% decline in tooth decay.
And some former supporters are even beginning to question the need for fluoridation
altogether. In 1990, a National Institute for Dental Research report stated that "it is likely
that if caries in children remain at low levels or decline further, the necessity of continuing
the current variety and extent offluoride-based prevention programs will be questioned. ,,27
Most government agencies, however, continue to ignore the scientific evidence and to
. market fluoridation by making fictional claims about, its benefits and pushing for its
expansion. For instance, according to the U.S. Department of Health and Human Services,
"National surveys of oral health dating back several decades document continuing decreases
in tooth decay in children, adults and senior citizens. Nevertheless, there are parts of the
country and particular populations that remain without protection. For these reasons, the
U.S. PHS...has set a national goal for the year 2000 that 75% of persons served by
community water systems will have access to optimally fluoridated drinking water;
currently this figure is just about 60%. The year 2000 target goal is both desirable and yet
challenging, based on past progress and continuing evidence of effectiveness and safety of
this public health measure." 17
This statement is flawed on several accounts. First, as we've seen, research does not
support the effectiveness of fluoridation for preventing tooth disease. Second, purported
benefits are supposedly for children, not adults and senior citizens. At about age 13, any
advantage fluoridation might offer comes to an end, and less than 1 % of the fluoridated
water supply reaches this population.28 And third, fluoridation has never been proven safe.
On the contrary, several studies directly link fluoridation to skeletal fluorosis, dental
fluorosis, and several rare forms of cancer. This alone should frighten us away from its use.
Biological Safety Concerns
Only a small margin separates supposedly beneficial fluoride levels from amounts that
are known to cause adverse effects. Dr. James Patrick, a former antibiotics research scientist
at the National Institutes of Health, describes the predicament:
"[There is] a very low margin of safety involved in fluoridating water. A concentration of
about 1 ppm is recommended...in several countries, severe fluorosis has been documented
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from water supplies containing only 2 or 3 ppm. In the development of drugs...we generally
insist on a therapeutic index (margin of ~afety) of the order of 100; a therapeutic index of2
or 3 is totally unacceptable, yet that is what has been proposed for public water supplies.n29
Other countries argUe that even 1 ppm is not a safe concentration. Canadian studies, for
example, imply that children under three should have no fluoride whatsoever. The Journal
of the Canadian Dental Association states that "Fluoride supplements should not be
recommended for children less than 3 years old. .030 Sin~ these supplements contain the
same amount of fluoride as water does, they are basically saying that children under the age
of three shouldn't be drinking fluoridated water at all, under any circumstances. Japan has
reduced the amount of fluoride in their drinking water to one-eighth of what is
recommended in the U.S. Instead of 1 milligram per liter, they use less than. 15 hundredths,
of a milligram per liter as the upper limit allowed. 31
Even supposing that low concentrations are safe, there is no way to control how much
fluoride different people consume, as some take in a lot more than others. For example,
laborers, athletes, diabetics, and those living in hot or dry regions can allbe expected to
drink more water, and therefore more fluoride (in fluoridated areas) than others.32 Due to
such wide variations in water consumption, it is impossible to scientifically control what
dosage of fluoride a person receives via the water supply. 33
Another concern is that fluoride is not found only in drinking water; it is everywhere.
Fluoride is found in foods that are processed with it, which, in the United States, include
nearlyall bottled drinks and canned foods.34 Researchers writing in The Journal of Clinical
Pediatric Dentistry have found that fruit juices, in particular, contain significant amounts of
fluoride. In a recent study, a variety of popular juices and juice blends were analyzed and it
was discovered that 42% of the samples examined had more than I pprn' of fluoride, with
some brands of grape juice containing much higherlevels - up to 6.8 ppm! The authors cite
the common practice of using fluoride-containing insecticide in growing grapes as a factor
in these high levels, and they suggest that the fluoride content of beverages be printed on
their labels, as is other nutritional information.35 Considering how much juice some
children ingest, and the fact that youngsters often insist on particular brands that they
consume day after day, labeling seems like a prudent idea. But beyond this is the larger
issue that this study brings up: Is it wise to subject children imd others who are heavy juice
drinkers to additional fluoride in their water?
Here's a little-publicized reality: Cooking can greatly increase a food's fluoride content.
Peas, for example, contain 12 micrograms of fluoride when raw and 1500 micrograms after
they are cooked in fluoridated water, which is a tremendous difference. Also, we should
keep in mind that fluoride is an ingredientin pharmaceuticals, aerosols, insecticides, and
pesticides.
And of course, toothpastes. It's interesting to note that in the 1950s, fluoridated
toothpastes were required to carry warnings on their labels saying that they were not to be
used in areas where water was already fluoridated. Crest toothpaste went so far as to write:
"Caution: Children under 6 should not use Crest." These regulations were dropped in 1958,
although no new research was available to prove that the overdose hazard no longer
existed. 36
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Today, common fluoride levels in toothpaste are l000ppm. Research chemist Woodfun
Ligon notes that swallowing a small amount adds substantially to fluoride intake. 36 Dentists
say that chit dren commonly ingest up to 0.5 mg of fluoride a day from toothpaste. 36
This inevitably raises another issue: How safe is all this fluoride? According to scientists
and informed doctors, such as Dr. John tee, it is not safe at all. Dr. Lee first took an anti-
fluoridation stance back in 1972, when as chainnan of an environmental health committee
for a local medical society, he was asked to state their position on the subject. He stated that
after investigating the references given by both pro- and ~-fluoridationists, the group
discovered three important things:
"One, the claims of benefit of fluoride, the 6()O.Io reduction of cavities, was not established
by any of these studies. Two, we found that the investigations into the toxic side effects of
fluoride have not been done in any way that was acceptable. And three, we discovered that
the estimate of the amount of fluoride in the food chain, in the total daily fluoride intake"
had been measured in 1943, and not since then. By adding the amount of fluoride thatwe
now have in the food chain, which comes from food processing with fluoridated water, plus
all the fluoridated toothpaste that was not present in 1943, we found that the daily intake of
fluoride was far in excess of what was considered opti~a1."31 .
What happens when fluoride intake exceeds the optimal? The inescapable fact is that this
substance has been associated with severe health problems, ranging from skeletal and dental
fluorosis to bone fractures, to fluoride poisoning, and even to cancer.
Skeletal Fluorosis
When fluoride is ingested, approximately 93% of it is absorbed into the bloodstream. A
good part of the material is excreted, but the rest is deposited in the bones and teeth,37 and
is capable of causing a crippling skeletal fluorosis. This is a condition that can damage the
musculoskeletal and nervous systems and result in muscle wasting, limited joint motion,
spine deformities, and calcification of the ligaments, as well as neurological deficits. 38
Large numbers of people in Japan, China, India, the Middle East, and Mrica have been
diagnosed with skeletal fluorosis from drinking naturally fluoridated water. In India alone,
nearly a million people suffer from the affii cti on. 39 While only a dozen cases of skeletal
fluorosis have been reported in the United States, Chemical and Engineering News states
that "critics of the EPA standard speculate that there probably have been many more cases
of fluorosis - even crippling fluorosis - than the few reported in the literature because most
doctors in the U.S. have not studied the disease and do not know how to diagnose it. ,,40
Radiologic changes in bone occur when fluoride exposure is 5 mglday, according to the
late Dr. George Waldbott, author of Fluoridation: The Great Dilemma. While this 5 mglday
level is the amount of fluoride ingested by most people living in fluoridated areas,41 the
number increases for diabetics and laborers, who can ingest up to 20 mg offluoride daily. In
addition, a survey conducted by the Department of Agriculture shows that 3% of the U.S.
population drinks 4 liters or more of water every day. If these individuals live in areas
where the water contains a fluoride level of 4 ppm, allowed by the EP A, they are ingesting
16 mglday from the consumption of water alone, and are thus at greater risk for getting
skeletal fluorosis.42
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Dental Fluorosis
According to a 1989 National Institute for Dental Research study, 1-2% of children living
in areas fluoridated at 1 ppm develop dental fluorosis, that is, permanently stained, brown
mottled teeth. Up to 23% of children living in areas naturally fluoridated at 4 ppmdevelop
severe dental fluorosis.43 Other research gives higher figures. The publication Health
Effects of Ingested Fluoride, put out by the National Academy of Sciences, reports that in
areas with optimally fluoridated water (1 ppm, either natural or added), dental fluorosis
levels in recent years ranged from 8 to 51 %. Recently, a prevalence of slightly over 80%
was reported in children 12-14 years old in Augusta, Georgia.43
Fluoride is a noteworthy chemical additive in that its officially acknowledged benefit and
damage levels are about the same. Writing in The Progressive, science journalist Daniel
Grossman elucidates this point: "Though many beneficial chemicals are dangerous when
consumed at excessive levels, fluoride is unique because the amount that dentists
recommend to prevent cavities is about the same as the amount that causes dental
fluorosis. ,,44 Although the American Dental Association and the government consider
dental fluorosis only a cosmetic problem, the American Journal of Public Health says that
"...brittleness of moderately and severely mottled teeth may be associated with elevated
caries levels. ,,45 In other words, in these cases the fluoride is causing the exact problem that
it's supposed to prevent. Yiamouyiannis adds, "In highly naturally-fluoridated areas, the
teeth actually crumble as a result. These are the first visible symptoms of fluoride
poisoning. ,,46
Also, when considering dental fluorosis, there are factors beyond the physical that you
can't ignore - the negative psychological effects of having moderately to severely mottled
teeth. These were recognized in a 1984 National Institute of Mental Health panel that
looked into this problem. 44
A telling trend is that TV commercials for toothpaste, and toothpaste tubes themselves,
are now downplaying fluoride content as a virtue. This was noted in an article in the
SarasotalFlorida ECO Report, 47 whose author, George Glasser, feels that manufacturers are
distancing themselves from the additive because offears oflawsuits. The climate is ripe for
these, and Glasser points out that such a class action suit has already been filed in England
against the manufacturers offluoride-containing products on behalf of children suffering
from dental fluorosis.
Bone Fractures '
At one time, fluoride therapy was recommended for building denser bones and
preventing fractures associated with osteoporosis. Now several articles in peer-reviewed
journals suggest that fluoride actually causes more harm than good, as it is associated with
bone breakage. Three studies reported in The Journal of the American Medical Association
showed links between hip fractures and fluoride.48-50 Findings here were, for instance, that
there is "a small but significant increase in the risk of hip fractures in both men and women
exposed to artificial fluoridation at 1 ppm."51 In addition, the New England Journal of
Medicine reports that people given fluoride to cure their osteoporosis actually wound up
with an increased nonvertebral fracture rate.52 Austrian researchers have also found that
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fluoride tablets make bones more susceptible to fractures.53 The U.S. National Research
Council states that the U.S. hip fracture rate is now the highest in the world. 54
Louis V. Avioli, professor at the Washington University School of Medicine, says in a
1987 review of the subject: "Sodium fluoride therapy is accompanied by so many medical
complications and side effects that it is hardly worth exploring in depth as a therapeutic
mode for postmenopausal osteOporosis, since it fails to decrease the propensity for hip
fractures and increases the incidence of stress fractures in the extremities. ,,54
..,
Fluoride Poisoning
In May 1992,260 people were poisoned, and one man died, in Hooper Bay, Alaska, after
drinking water contaminated with 150 ppm offluoride. The accident was attributed to poor'
equipment and an unqualified operator. 55 Was this a fluke? Not at all. Over the years, the
CDC has recorded several incidents of excessive fluoride permeating the water supply and
sickening or killing people. We don't usually hear about these occurrences in news reports,
but interested citizens have learned the truth from data obtained under the Freedom of
Information Act. Here is a partial list of toxic spills we have not been told about:
July 1993 - Chicago, TIlinois: Three dialysis patients died and five experienced toxic
reactions to the fluoridated water used in the treatment process. The CDC was asked to
investigate, but to date there have been no press releases.
May 1993 - Kodiak, Alaska (Old Harbor): The population was warned not to consume
water due to high fluoride levels. They were also cautioned against boiling the water, since
this concentrates the substance and worsens the danger. Although equipment appeared to be
functioning normally, 22-24 ppm of fluoride was found in a sample. '
July 1992 - Marin County, California: A pump m8Ifunction allowed too much fluoride into
the Bon Tempe treatment plant. Two million gallons of fluoridated water were diverted to
Phoenix Lake, elevating the lake surface by more than two inches and forcing some water
over the spillway.
December 1991 - Benton Harbor, Michigan: A faulty pump allowed approximately 900
gallons of hydrofluosilicic acid to leak into a chemical storage building at the water plant.
City engineer Roland Klockow stated, "The concentrated hydrofluosilicic acid was so
corrosive that it ate through more than two inches of concrete in the storage building." This
water did not reach water consumers, but fluoridation was stopped until June 1993. The
original equipment was only two years old.
July 1991 - Porgate, Michigan: After a fluoride injector pump failed, fluoride levels reached
92 ppm and resulted in approximately 40 children developing abdominal pains, sickness,
vomiting, and dianhea at a school arts and crafts show.
November 1979 - Annapolis, Maryland: One patient died and eight became ill after renal
dialysis treatment. Symptoms included cardiac arrest (resuscitated), hypotension, chest pain,
difficulty breathing, and a whole gamut of intestinal problems. Patients not on dialysis also
reported nausea, headaches, cramps, diarrhea, and dizziness. The fluoride level was later
found to be 35 ppm; the problem was traced to a valve at a water plant that had been left
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open all night. 55
Instead of addressing fluoridation's problematic safety record, officials have chosen to
cover it up. For example, the ADA says in one booklet distributed to health agencies that
"Fluoride feeders are designed to stop operating when a malfunction occurs... so prolonged
over-fluoridation becomes a mechanical impossibility.,,56 In addition, the information that
does reach the population after an accident is woefully inaccurate. A spill in Annapoli,s,
Maryland, placed thousands at risk, but official reports reduced the number to eight. 57
Perhaps officials are afraid they will invite more lawsuits like the one for $480 million by
the wife of a dialysis patient who became brain-injured as the result of fluoride poisoning.
Not all fluoride poisoning is accidental. For decades, industry has knowingly released '
massive quantities of fluoride into the air and water. Disenfranchised communities, with
people least able to fight back, are often the victims. Medical writer Joel Griffiths relays this
description of what industrial pollution can do, in this case to a devastatingly poisoned
Indian reservation:
"Cows crawled around the pasture on their bellies, inching along like giant snails. So
crippled by bone disease they could not stand up, this was the only way they could graze.
Some died kneeling, after givingbirth to stunted calves. Others kept on crawling until, no
longer able to chew because their teeth had crumbled down to the nerves, they began to
starve...." They were the cattle of the Mohawk Indians on the New York-Canadian St. Regis
Reservation during the period 1960-1975, when industrial pollution devastated the herd-
and along with it, the Mohawks' way oflife....Mohawk children, too, have shown signs of
damage to bones and teeth. ,,58
Mohawks filed suit against the Reynolds Metals Company and the Aluminum Company
of America (Alcoa) in 1960, but ended up settling out of court, where they received
$650,000 for their cows. 59
Fluoride is one of industry's major pollutants, and no one remains immune to its effects.
In 1989, 155,000 tons were being released annually into the air,60 and 500,000 tons a year
were disposed of in our lakes, rivers, and oceans.61
Cancer
Numerous studies demonstrate links between fluoridation and cancer; however, agencies
promoting fluoride consistently refute or cover up these findings.
In 1977, Dr. John Yiamouyiannis and Dr. Dean Burk, former chief chemist at the
National Cancer Institute, released a study that linked fluoridation to 10,000 cancer deaths
per year in the U.S. Their inquiry, which compared cancer deaths in the ten largest
fluoridated American cities to those in the ten largest unfluoridated.cities between 1940 and
1950, discovered a 5% greater rate in the fluoridated areas.62 The NCIdisputed these
'findings, since an earlier analysis of theirs apparently failed to pick up these extra deaths.
Federal authorities claimed that Yiamouyiannis and Burk were in error, and that any
increase was caused by statistical changes over the years in age, gender, and racial
composition. 63
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In order to settle the question of whether or not fluoride is a carcinogen, a Congressional
subcommittee instructed the National Toxicology Program (NTP) to perform another
investigation.64 That study, due in 1980, was not released untii 1990. However, in 1986,
while the study was delayed, the EP A raised the standard fluoride level in drinking water
from 2.4 to 4 ppm.65 After this step, some of the government's own employees in NFFE
Local 2050 took what the Oakland Tribune termed the "remarkable step of denouncing that
action as political. ,,66
When the NTP study results became known in early 1990, union president Dr. Robert
Carton, who works in the EPA's Toxic Substances Division, published a statement. It read,
in part: "Four years ago, NFFE Local 2050, which represents all 1100 professionals at EPA
headquarters, alerted then Administrator Lee Thomas to the fact that the scientific support
documents for the fluoride in drinking water standard were fatally flawed. The fluoride
juggernaut proceeded as it apparently had for the last 40 years - without any regard for the
facts or concern for public health.
"EPA raised the allowed level of fluoride before the results of the rat/mouse study
ordered by Congress in i977 was complete. Today, we find out how irresponsible that
decision was. The results reported by NTP, and explained today by Dr. Yiamouyiannis, are,
as he notes, not surprising considering the vast amount of data that caused th~ animal study
to be conducted in the first place. The results are not surprising to NFFE Local 2050 either.
Four years ago we realized that the claim that there was no evidence that fluoride could
cause genetic effects or cancer could not be supported by the shoddy document thrown
together by the EP A contractor.
"It was apparent to us that EP A bowed to political pressure without having done an in-
depth, independent analysis, using in-house experts, of the currently existing data that show
fluoride causes genetic effects, promotes the growth of cancerous tissue, and is likely to
cause cancer in ~umans.IfEPA had done so, it would have been readily apparent - as it was
to Congress in 1977 - that there were serious reasons to believe in a cancer threat.
"The behavior by EP A in this affair raises questions about the integrity of science at EP A
and the role of professional scientists, lawyers and engineers who provide the interpretation
of the available data and the judgements necessary to protect the public health and the
environment. Are scientists at EP A there to arrange facts to fit preconceived conclusions?
Does the Agency have a responsibility to develop world-class experts in the risks posed by
chemicals we are exposed to every day, or is it permissible for EPA to cynically shop
around for contractors who will provide them the 'correct' answers?,,67
What were the NTP study results? Out of 130 male rats that ingested 45 to 79 ppm of
fluoride, 5 developed osteosarcoma, a rare bone cancer. There were cases, in both males and
females at those doses, of squamous cell carcinoma in the mouth.68 Both rats and mice had
dose-related fluorosis of the teeth, and female rats suffered osteosclerosis of the long
bones.69
When Yiamouyiannis analyzed the same data, he found mice with a particularly rare
form of liver cancer, known as hepatocholangiocarcinoma. This cancer is so rare, according
to Yiamouyiannis, that the odds of its appearance in this study by chance are 1 in 2 million
in male mice and 1 in 100,000 in female mice.39 He also found precancerous changes in oral
squamous cells, an increase in squamous cell tumors and cancers, and thyroid follicular cell
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tu~ors as a result of increasing levels of fluoride in drinking water.70
A March 13, 1990, New York Times article commented on the NTP findings: "Previous
animal tests suggesting that water fluoridation might pose risks to humans have been widely
discounted as technically flawed, but the latest investigation carefully weeded out sources
of experimental or statistical error, many scientists say, and cannot be discounted. ,,71 In the
same article, biologist Dr. Edward Groth notes: "The importance of this study...is that it is
the first fluoride bioassay giving positive results in which the latest state-of-the-art '
procedures have been rigorously applied. It has to be taken seriously." 71 '
On February 22, 1990, the Medical Tribune, an international medical news weekly
received by 125,000 doctors, offered the opinion of a federal scientist who preferred to
remain anonymous:
"It is difficult to see how EP A can fail to regulate fluoride as a carcinogen in light of what
NTP has found. Osteosarcomas are an extremely unusual result in rat carcinogenicity tests.
Toxicologists tell me that the only other substance that has produced this is radium....The
fact that this is a highly atypical form of cancer implicates fluoride as the cause. Also, the
osteosarcomas appeared to be dose-related, and did not occur in controls, making it a clean
study. ,,72
Public health officials were quick to assure a concerned public that there was nothing to
worry about! The ADA said the occurrence of cancers in the lab may not be relevant to
humans since the level of fluoridation in the experimental animals' water was so high?3 But
the Federal Register, which is the handbook of government practices, disagrees: "The high
exposure of experimental animals to toxic agents is a necessary and valid method of
discovering possible carcinogenic hazards in man. To disavow the findings of this test
would be to disavow those of all such tests, since they are all conducted according to this
standard.,,73 As a February 5, 1990, Newsweek article pointed out, "such inegadosing is
standard toxicological practice. It's the only way to detect an effect without using an
impossibly large number of test animals to stand in for the humans exposed to the
substance." 74 And as the Safer Water Foundation explains, higher doses are generally
administered to test animals to compensate for the animals' shorter life span and because
humans are generally more vulnerable than test animals on a body-weight basis.75
Several other studies link fluoride to genetic damage and cancer. An article in Mutation
Research says that a study by Proctor and Gamble, the very company that makes Crest
toothpaste, did research showing that 1 ppm fluoride causes genetic damage?6 Results were
never published but Proctor and Gamble called them "clean," meaning animals were
supposedly free of malignant tumors. Not so, according to scientists who believe some of
the changes observed in test animals could be interpreted as precancerous.77 Yiamouyiannis
says the Public Health Service sat on the data, which were finally released via a Freedom of
Information Act request in 1989. "Since they are biased, they have tried to cover up harmful
effects," he says. "But the data speaks for itself Half the amount of fluoride that is found in
the New York City drinking water causes genetic daniage. ,,46
A National Institutes of Environmental Health Sciences publication, Environmental and
Molecular Mutagenesis, also linked fluoride to genetic toxicity when it stated that "in
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cultured human and rodent cells, the weight of evidence leads to the conclusion that fluoride
exposure results in increased chromosome aberrations." 78 The ,result of this is not only birth
defects but the mutation of normal cells into cancer cells. The Journal of Carcinogenesis
further states that "fluoride not only has the ability to transfonn nonnal cells into cancer
cells but also to enhance the cancer-causing properties of other chemicals.,,79
Surprisingly, the PHS put out a report called Review of fluoride: benefits and risks, in
which they showed a substantially higher incidence of bone cancer in young men exposed
to fluoridated water compared to those ,who were not. The New Jersey Department of '
Health also found that the risk of bone cancer was about three times as high in fluoridated
areas as in nonfluoridated areas. 46
Despite cover-up attempts, the light of knowledge is filtering through to some
enlightened scientists. Regarding animal test results, the director of the U.S. National
Institute of Environmental Health Sciences, James Huff, does say that "the reason these
animals got a few osteosarcomas was because they were given fluoride...Boneis the target
organ for fluoride. ,,80 Toxicologist William Marcus adds that "fluoride is a carcinogen by
any standard we use. I believe EP A should act immediately to protect the public, not just on
the cancer data, but on the evidence of bone fractures, arthritis, mutagenicity, and other
effects. ,,81
The Challenge of Eliminating Fluoride
Given all the scientific challenges to the idea of the safety offluoride, why does itremain
a protected contaminant? As Susan Pare of the Center for Health Action asks, ". ..even if
fluoride in the water did reduce tooth decay, which it does not, how can the EPA allow a
substance more toxic than Alar, red dye #3, and vinyl chloride to be injected purposely into
drinking water?,,82
This is certainly a logical question and, with all the goOd science that seems to exist on
the subject, you would think that there would be a great deal of interest in getting fluoride
out of our water supply. Unfortunately, that hasn't been the case. As Dr. William Marcus, a
senior science advisor in the EPA's.Office of Drinking Water, has found, the top
governmental priority has been to sweep the facts under the rug and, if need be, to suppress
truth-tellers. Marcus explains83 that fluoride is one of the chemicals the EPA specifically
regulates, and that he was following the data coming in on fluoride very carefully when a
determination was going to be made on whether the levels should be changed. He
discovered that the data were not being heeded. But that was only the beginning of the story
for him. Marcus recounts what happened:
"The studies that were done by Botel Northwest showed that there was an increased level
of bone cancer and other types of cancer in animals....in that same study, there were very
rare liver cancers, according to the board-certified veterinary pathologists at the contractor,
Botel. Those really were very upsetting because they were hepatocholangeal carcinomas,
very rare liver cancers;...Then th~~ were several other kinds of cancers that were found in
the jaw and other places.
"I felt at that time that the reports were alarming. They showed that the levels of fluoride
that can cause cancers in animals are actually lower than those levels ingested in people
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(who take lower amounts but for longer periods of time).
"I went to a meeting that was held in Research Triangle Park, in April 1990, in which the
National Toxicology Program was presenting their review of the study. I went with several
colleagues of mine, on,e, of whom was a board-certified veterinary pathologist who
originally reported hepatocholangeal carcinoma as a separate entity in rats and mice. I asked
him ifhe would look at the slides to see if that' really was a tumof or if the pathologists at
Botel had made an error. He told me after looking at the slides that, in fact, it was correct.
"At the meeting, every one of the cancers reported by the contractor had been
downgraded by the National Toxicology Program. I have been in the toxicology business
looking at studies of this nature for nearly 25 years and I have neve,r before seen every
single cancer endpoint downgraded.... I found that very suspicious and went to see an
investigator in the Congress at the suggestion of my friend, Bob Carton. This gentleman and
his staff investigated very thoroughly and found out that the scientists at the National
Toxicology Program down at Research Triangle Park had been coerced by their superiors to
change their findings. ,,83
Once Dr. Marcus acted on his findings, something ominous started to happen'in his life:
"...I wrote an internal memorandum and gave it to my supervisors. I waited for a month
without hearing anything. Usually, you get a feedback in a week or so. I wrote another
memorandum to a person who was my second-line supervisor explaining that if there was
even a slight chance of increased cancer in the general population, since 140 million people
were potentially ingesting this material, that the deaths could be in the many thousands.
Then I gave a copy of the memorandum to the Fluoride Work Group, who waited some
time and then released it to the press.
"Once it got into the press all sorts of things started happening at EP A. I was getting
disciplinary threats, being isolated, and all kinds ofthingswhich ultimately resulted in them
firing me on March 15, 1992.,,83
In order to be reinstated at work, Dr. Marcus took his case to court. In the process, he
learned that the government had engaged in various illegal activities, including 70 felony
counts, in order to get him fired. At the same time, those who committed peIjury were not
held accountable for it. In fact, they were rewarded for their efforts:
"When we finally got the EP A to the courtroom. ..they admitted to doing several things to
get me fired. We had notes ofa meeting...thatshowed that fluoride was one of the main
topics discussed and that it was agreed that they would fire me with the help of the
Inspector General. When we got them on the stand and showed them the memoranda, they
finally remembered and said, oh yes, we lied about that in our previous statements.
"Then...they admitted to shredding more than 70 documentS that they had in hand-
Freedom of Information requests. That'sa felony.... In addition, they charged me with
stealing time from the government. They...tried to show...that I had been doing private work
on government time and getting paid for it. When we came to court, I was able to show that
the time cards they produced were forged, and forged by the Inspector General's staff....,,83
For all his efforts, Dr. Marcus was rehired, but nothing else has changed: "The EPA was
ordered to rehire me, which they did. They were given a whole series of requirements to be
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rCl.!5Iti.1.... V.1-".1
met, such as paying me my back pay, restoring my leave, privileges, and sick leave and
annual leave. The only thing they've done is put me back to work. They haven't given me
any of those things that they were required to do. ,,83 ..
What is at the core of such ruthless tactics? John Yiamouyiannis feels that the central
concern of government is to protect industry, and that the motivating force behind fluoride
use is the need of certain businesses to dump their toxic waste products somewhere. They
try to be inconspicuous in the disposal process and not ma~~ waves. "As is nonnal, the
solution to pollution is dilu~on. You poison everyone a littl,e bit rather than poison a few
people a lot. This way, peopl~ don't Ialow what's going on':I,46
Since the Public Health Service has promoted the fluoride myth for over 50 years, they're
concerned about protecting their reputation. So scientists like Dr. Marcus, who know about
the dangers, are intimidated into keeping silent. Otherwise, they jeopardize their careers. Dr.
John Lee elaborates: "Back in 1943, the PHS staked their professional careers on the
benefits and safety of fluoride. It has since become bureaucratized. Any public health
official who criticizes fluoride, or even hints that perhaps it was an unwise decision, is at
risk oflosing his career entirely. This has happened time and time again. Public health
officials such as Dr. Gray in British Columbia and Dr. Colquhoun in New Zealand found no
benefit from fluoridation. When they reported these results, they immediately lost their
careers.... This is what happens - the public health officials who speak out against fluoride
are at great risk oflosing their careers on the spot. ,,31
Yiamouyiannis adds that for the authorities to admit that they're wrong would be
devastating. "It would show that their reputations really don't mean that much.... They don't
have the scientific background. As Ralph Nader once said, if they admit they're wrong on
fluoridation, people would ask, and legitimately so, what else have they not told us right?,,46
Accompanying a loss in status would be a tremendous loss in revenue. Yiamouyiannis
points out that "the indiscriminate careless handling of fluoride has a lot of companies, such
as Exxon, U.S. Steel, and Alcoa, making tens of billions of dollars in extra profits at our
expense.... For them to go ahead now and admit that this is bad, this presents a problem, a
threat, would mean tens of billions of dollars in lost profit because they would have to
handle fluoride properly. Fluoride is present in everything from phosphate fertilizers to
cracking agents for the petroleum industry. ,,46
Fluoride could only be legally disposed of at a great cost to industry. As Dr. Bill Marcus
explains, "There are prescribed methods for disposal and they're very expensive. Fluoride is
a very potent poison. It's a registered pesticide, used for killing rats or mice.... If it were to
be disposed of, it would require a class-one landfill. That would cost the people who are
producing aluminum or fertilizer about $7.000+ per 5000- to 6000-gallon truckload to
dispose of it. It's highly corrosive. ,,83
Another problem is that the U.S: judicial system, even when convinced of the dangers, is
powerless to change policy. Yiawouyiannis tells of his involvement in court cases in
Pennsylvania and Texas in which, while the judges were convinced that fluoride was a
health hazard, they did not have the jurisdiction to grant relief from fluoridation. That would
have to be done, it was ultimately found, through the legislative process.46 Interestingly, the
judiciary seems to have more power to effect change in other countries. Yiamouyiannis
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states that when he presented the same technical evidence in Scotland, the Scottish court
outlawed fluoridation based on the evidence.46
Indeed, most of western Europe has rejected fluoridation on the grounds that it is unsafe.
In 1971, after 11 years'oftesting, Sweden's Nobel Medical Institute recommended against
fluoridation, and the process was banned. The Netherlands outlawed the practice in 1976,
after 23 years of tests. France decided against it after consulting With its Pasteur Insti~te64
and West Germany, now Germany, rejected the practice because the recommended dosage
of 1 ppm was "too close to the dose at which long-term damage to the human body is to be
expected. ,,84 Dr. Lee sums it up: "All of west em Europe, except one or two test towns in
Spain, has abandoned fluoride as a public health plan. It is not put in the water anywhere.
They all established test cities and found that the benefits did not occur and the toxicity was
evident. ,,31
Isn't it time the United States followed western Europe's example? While the answer is
obvious, it is also apparent that government policy is unlikely to change without public
support. We therefore must communicate with legislators, and insist on one of our most
precious resources - pure, unadulterated drinking water. Yiamouyiannis urges aU American
people to do so, pointing out that public pressure has gotten fluoride out of the water in
places like Los Angeles; Newark and Jersey City in New Jersey; and Bedford,
Massachusetts.46 He emphasizes the immediacy of the probleIIl: "There is no question with
regard to fluoridation of public water supplies. It is absolutelyunsafe...and should be
stopped immediately. This is causing more destruction to human health than any other
single substance added purposely or inadvertently to the water supply. We're talking about
35,000 excess deaths a year... 10,000 cancer deaths a year... 130 million people who are
being chronically poisoned. We're not talking about dropping dead after drinking a glass of
fluoridated water.... It takes its toll on human health and life, glass after glass. ,,46
There is also a moral issue in the debate that has largely escaped notice. According to
columnist James Kilpatrick, it is "the right of each person to control the drugs he or she
takes." Kilpatrick calls fluoridation compulsory mass medication, a procedure that violates
the principles of medical ethics.13 A recent New York Times editorial agrees:
"In light of the uncertainty, critics [of fluoridation] argue that administrative bodies are
unjustified in imposing fluoridation on communities without obtaining public consent....
The real issue here is not just the scientific debate. The question is whether any
establishment has the right to decide that benefits outweigh risks and impose involuntary
medication on an entire population. In the case of fluoridation, the dental establishment has
made opposition to fluoridation seem intellectually disreputable. Some people regard that as
tyranny. ,,85
Correspondence:
Gary Null, PhD
P. O. Box 918
Planetarium Station
New York, New York 10024 USA
212-799-1246
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rl1~t: 11 VI ~1
References
1. Dr. John Yiamouyiannis, in interview with Gary Null, 3/10/95. His
statement is referenced in the Clinic~l Toxicology of Commercial
Products, Fifth Ed., Williams and Wilkins.
2. Joel Griffiths, "Fluoride: Commie Plot or Capitalist Ploy," Covert
Action, Fall 1992, Vol. 42, p. 30.
I "
3. Ibid., p. 27.
4. Ibid., p. 28.
5. Ibid.
6. McNeil, The Fight for Fluoridation, 1957, p. 37.
7. Griffiths, op. cit., p. 28.
8. Griffiths, op. cit.
9. G.L. Waldbott et al., Fluoridation: The Great Dilemma, Lawrence, XS,
Coronado Press, 1978, p. 295.
10. Paul Farhi, Washington Post, 11/23/91.
11. Griffiths, op. cit., p. 63.
12. Longevity Magazine, pp. 7-89.
13. The Morning Call, 2/7/90
14. Science, 1/90.
15. Waldbott, op. cit., p. 255.
16. Letter, Rebecca Hammer, 3/83.
17. U.S. Dept. of Health and Human Services, "Policy statement on
community water fluoridation," July 22, 1992, Washington, D.C.
18. Chemical and Engineering News, 8/1/88, p. 29; Amer. J. Pub. Health,
editorial, 5/89, p. 561; J.A. Brunelle and J.P. Carlos, "Recent trends in
dental caries in U.S. children and the effect of water fluoridation,"
2/90, p. 276.
19. Los Angeles Times. 1/ 26/95..
20. The Chicago Tribune, 1/26/95.
21. A.S. Gray, Canadian Dental Association Journal, October 1987, pp.
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763.
22. Letter, Sierra Club to Wm. K. Reilly, EPA, 7/21/89.
23. John Yiamouyiannis, Fluoride, 1990, Vol. 23, pp. 55-67.
24. Center for Health Action, 3/30/90.
25. Clinical Pediatrics, Nov. 1991.
26. ADA News, 10/17/94.
27. Chemical and Engineering News, 8/1/88, p.31.
28. Waldbott, op. cit., p. xvii.
29. Statement by Dr. James Patrick before Congressional Subcommittee,
8/4/82.
30. Journal of the Canadian Dental Association, Vol. 59, Apr. 1993, p.
334.
31. Gary Null interview with Dr. John Lee, 3/10/95.
32. F. Exner and G. Waldbott, The American fluoridation experiment, 1957,
p. 43.
33. Federal Register, 12/24/75.
34. Chemical and Engineering News, 8/1/88, p. 33.
35. Jan G. Stannard et al., "Fluoride levels and fluoride contamination
of fruit juices," The Journal of Clinical Pediatric Dentistry, Vol. 16,
No.1, 1991, pp. 38-40.
36. Waldbott, op. cit., pp. 307-308.
37. Chemical and Engineering News, 8/1/88, p. 49.
38. New York State Coalition Opposed to Fluoridation, release, 11/89.
39. Gary Null interview with Dr. John Yiamouyiannis 4/28/90.
40. Chemical and Engineering News, 8/1/88, p. 36.
41. Waldbott, op. cit., p. 38.
42. F. Exner andG. Waldbott, op. cit., pp. 42-43.
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43. Schenectady Gazette Star, 8/5/89.
44. Daniel Grossman, "Fluoride's Revenge,"
The Progressive,
Dec. 1990, pp. 29-31.
"
45. American Journal qf Public Health, 12/85.
41"
46. Gary Null interview with Dr. John Yiamouyiannis, 3/10/95.
47. George Glasser, "Dental Fluorosis - 1;\ Legal Time Bomb!"
Sarasota/Florida ECO Report, Vol. 5, No.2, Feb. 1995, pp. 1-5.
48. JAMA, Vol. 264, July 25, 1990, pp. 500
49. Cooper et al., JAMA, Vol. 266, July 24, 1991, pp. 513-14.
50. Christa Danielson et al., "Hip fractures 'and fluoridation in Utah's
elderly population," JAMA, Vol. 268, Aug. 12, 1992, pp. 746-48'.
51. Ibid~, p. 746.
52. New England Journal of Medicine, Vol. 322, pp. 802-809.
53. Journal of Bone and Mineral Research, 11/94.
54. u.S. National Research Council, Diet and Health, Washington, D.C.,
National Academy Press, 1989, p. 121.
55. "Middletown, Maryland latest city to receive toxic spill of fluoride
in their drinking water," report by Truth About Fluoride, Inc., in
Townsend Letter for Doctors, 10/15/94, p. 1124.
56. Reprinted by M. Bevis, "Morbidity associated with ingestion/dialysis
of community water fluoride," CDC, Dental Div., 6/11/92, distributed by
Safe Water Foundation of Texas.
57. Townsend Letter for Doctors, 10/94, p. 1125.
58. Janet Raloff, "The st. Regis Syndrome," Science News, July 19, 1980,
pp. 42-43; reprinted in Griffiths, op. cit., p. 26.
59. Robert Tomalin, "Dumping grounds," Wall Street Journal, Nov. 29,
1990; reprinted in Griffiths, Ope cit.
60. "Summary review of health effects associated with hydrogen fluoride
acid related compounds," EPA Report Number 600/8-29/002F, Dec. 1988, pp.
1- .
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61. John Yiamouyiannis, Lifesaver's Guide to Fluoridation, Delaware,
Ohio, Safe Water Foundation, 1983,. p. 1.
62. John Yiamouyiannis and Dean Burk, "Fluoridation of public water
systems and cancer" geath rates in humans," presented at the 57th annual
meeting of the (\IDerican society of Biological Chemists, and published in
Fluoride, Vol. 10, No.3, 1'977, pp. 102-103.
I
63. National Institute of Dental Research, "Fluoridation of water and
cancer: a review of the epidemiological efficiency," 1985, pp. 10-13.
64. New York state Coalition Opposed to Fluoridation.
65. Newsday, 2/27/90.
66. Oakland Tribune, 2/16/90.
67. NFFE Local 2050, 3/90.
68. Washington Post, 2/20/90.
69. The Lancet, 2/3/90.
70. Center for Health Action.
71. M.W. Browne, The New York Times, 3/13/90.
72. Medical Tribune, 2/22/90.
73. New York state Medical News, 3/90.
74. S. Begley, Newsweek, 2/5/90.
75. Safe Water Foundation, 3/4/90.
76. Mutation Research, Vol. 223, pp. 191-203.
77. Joel Griffiths, Medical Tribune, 2/22/90.
78. Environmental and Molecular Mutagenesis, Vol. 21, pp. 309-318.
79. Journal of Carcinogenesis, Vol. 9, pp. 2279-2284.
80. Mark Lowey, "Scientists question health risks of fluoride," Calgary
Herald, calgary, Alberta, Canada, Feb. 28, 1992; in Griffiths, op. cit.,
p. 66.
81. Griffiths, op. cit., p. 66.
82. Center for Health Action, 3/90.
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83. Gary Null interview with Dr. William Marcus, 3/10/95.
84. Longevity Magazine, 7/89.
85. The New York Times, 3/13/90.
Gary Null, PhD, award winning investigative reporter, has authored 50 books on health and
nutrition, as well as numerous articles publislled in leading magazines. Dr. Null holds a PhD
in human nutrition and pub~ic health science from the Unioll Graduate School. Former
publisher of Natural Living Newslettet, the current Gary Null's Natural Living Journal
reports on healthy alternatives in today's medicine, nutrition and lifestyle choices, ten times
a year, and is available by calling 516-547-7177. Null hosts a nationally syndicated radio
show, Natural Living, from New York City. Call ~12-799-1246 for a radio listing in your
area.
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FLUOROSILICIC ACID ICSC: 1233
October 1995
Hexafiuorosilicic acid
Dihydrogen hexafluorosilicate
Fluosilicic acid
Hydrosilicofluoric acid
m B
..,1
CAS # 16961~34 F sH 2Si
RlECS # W8225000 Molecular mass: 144.1
UN # 1778
Ee# OO~11~0-5
TYPES OF
HAZARD ,
EXPOSURE ACUTE HAZARDS I SYMPTOMS PREVENTION
FIRE FIGHTING .
FIRE Not combustible. Gives off irritating or toxic fumes (or gases) in a fire.
FIRST AID I
In case of fire in the surroundings: all extinguishing agents allowed.
EXPLOSION
EXPOSURE
AVOID ALL CONTACTI
IN ALL CASES CONSULT A DOCTOR!
Inhalation Corrosive. Burning sensation. Cough. Shortness of breath.
Ventilation, local exhaust, or breathing protection.
Fresh air, rest. Half-upright position. Refer br medical attention.
Skin Corrosive. Pain. Blisters.
Protective glows. Protective clothing.
Remove contaminated clothes. Rinse skin YMh plenty of water or shower. Refer for medical attention.
Eyes Corrosive. Redness. Pain. Severe deep bums.
Face shield, or eye protection in combination with breathing protection.
First rinse with plenty of water for sewral minutes (rerTlOW contact lenses if easily possible), then take to a doctor.
Ingestion Corrosive. Abdominal cramps. Buming sensation. Vomiting.
Do not eat, drink, or smoke during work.
Rinse mouth. Do NOT induce wmiting. Refer for medical attention.
Sunday, July 27, 2003 Americe Online: V0n34 Page: 1
SPILLAGE DISPOSAL PACKAGING & LABELLING
Collect leaking and spilled liquid in sealable iron containers as far as possible. Absorb remaining liquid in sand or inert
absorbent and remove to safe place (extra personal protection: complete protective clothing including selkontained breathing
apparatus).
Q Symbol
R: 34
S: 1/2-26-27-45
UN Hazard ClasS: 8
UN Pack Group: II
Unbreakable packaging; put breakable packaging into closed unbreakable container. Do not transport with food and feedstuffs.
EMERGENCY RESPONSE STORAGE
Separated from strong bases, food and feedstufS. Well closed.
IM'PORTANT DATA
PHYSICAL STATE; APPEARANCE:
FUMING COLOURLESS LIQUID, WllH PUNGENT ODOUR.
CHEMICAL DANGERS:
The substance decomposes on heating or on burning producing toxic fumes of lIuoride. The solution in water is a strong acid,
it reacts violently with bases and is corrosive. Reacts with water or steam to produce toxic and corrosive fumes. Attacks glass
and stoneware. This substance (anhydrous fonn) dissociates almost instantly into silicon tetralluoride and corrosive and toxic
hydrogen lIuoride.
OCCUPATIONAL EXPOSURE LIMITS:
lLV (as F): ppm; 2.5 mglm 3 (as TWA) (ACGIH 1995-1996).
ROUTES OF EXPOSURE:
The substance can be absorbed into the body by inhalation of its aerosol and by ingestion.
INHALATION RISK:
No indication can be given about the. rate in which a harmful concentration in the air is reached on evaporation of this
substance at 20oC.
EFFECTS OF SHORT-TERM EXPOSURE:
Corrosive. The substance is corrosive to the eyes, the skin and the respiratory tract. Corrosive on ingestion. Inhalation of the
vapour ofthis substance may cause lung oedema (see Notes). The effects may be delayed. Medical observation is indicated.
EFFECTS OF LONG-TERM OR REPEATED EXPOSURE:
The substance may have effects on the bones and teeth, resulting in fluorosis.
PHYSICAL PROPERTIES
Boiling point: decomposes
Melting point: see Notes
Relative density (water = 1): see Notes
Solubility in water: miscible
ENVIRONMENTAL DATA
SundBY. July 71. 2003 AmerIca OnD...: V0n34 Page: 2
NOTES .'
Marketed as aqueous solution only. Density of61% solution at 250C is 1.46, and density of 300" solution at 17.50C is 1.27.
60-70% solution solidifies at about 190C, fanning a crystalfine dihydrate. The symptoms of lung oedema often do not become
manifest until a few hours haw passed and they are aggravated by physical efbrt. Rest and medcal observation are therefore
essential. Immediate administration of an appropriate SpraYI by a doctor or a person authorized by him/her, should be
considered.
,..
IPCS
International
Prograrrme on
..,
.t.(d '- #. ~ r""
~I/( "'\ r: . f .......'
~~IH <<@\ \!y
Chemical Safety ~ ~ UNEP
Programme on Chemical Safety and the European Comrrission
.
Prepared in the context of cooperation betw een the International
@IPCS1999
J. 0.51;; J. VJ.. ~
.f"lC'I;o~.
qft,1
,Sf
...,~~
UNITED STATES ENVIRONMENTAL PROTECTION AGENCY
NATIONAL RISK MANAGEMENT RESEAACHl.ABOAATORY
CiNCINNATI. OH 45a8
',,, '
" ~o\'ember I ~I 2000
OF~1Ct or
AE$'€Af!CM MC>CJeVflOPlEt4T
Roger D. Masters
Research ProfeSsor of GOVCf'l'Ul'lenl
Dartmouth College
Department of Government
6108 Silsby Hall
Hanover, New Hampshire 03755~3S4i
Dtar Professor Masters:
We have received your lcuer dated Septmlber 27, 2000,fequesting empirical s.ci~ntific
data we may have on the health effects of nuosilicic acid or sodium silicofluoride and manganese
neurotoxicity.
To ansv..er yaur first question on whether we have in our possession empirical scientific
dau on the effects of fluosilieie acid or sodium s.ilieofiuoride Oon health fl..'ld behavior, aur answer
is no.. Health e1Tects research is primaril)' conducted by our National Heahh and Environmental
Effects RC$CUch LaboraLOl)' (NHEERL), We have contacted ow colleagues at ~HEERL and
lhey report that with the exception cr some acute toxicity data. they were unable to find any
informalion on the drCCL~ of silicofluorides on health and behavior,
In anJv.'cr to your question on empirical inro~tion we rna)' have cn manganese
neurotoxicit)',l'Hf..ERL scientists forv."8J"d.ed to us several manuscriptS with reference sections
th.u c:onl$in informluion (Ill the neurotoxicity of manganese:. T'hesc are enclosed for your
information.
I apologize for the delay in responding to your request and hope you tlndthe enclosed
information usefuL
Sincerely,
a~t ~.~
Roben C. Thurnau, Chief
Treatment Teclu1ology Evaluation Branch
Water Supply and Water Resou.rccsDi\'tsion
EnclosUfeS
http://www.fluorideaction.org/images/letters/epa-masters.jpg
8/2/03
Dartmouth College - Darbnouth researcher warns ot cnem.tcaIS aaaea toanmong water -... rilg~ 1 01 ~
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Dartmouth researcher warns of chemicals
adde~, ~o drinking water
"
~, II
MARCH 15,2001 -In a recent artide in the journal NeuroToxicology, a
research team led by Roger D. Masters, Dartmouth College Research
Professor and Nelson A Rockefeller Professor of Government Emeritus,
reports evidence that public drinking water treated with sodium silicofluoride or
f1uosilicic acid, known as silicofluorides (SiFs), is linked to higher uptake of
lead in children.
Sodium fluoride, first added to public drinking water in 1945, is now used in
less than 10% of fluoridation systems nationwide, according to the Center for
Disease Control's (CDC) 1992 Auoridation Census. Instead, SiF's are now
used to treat drinking water delivered to 140 million people. VVhile sodium
fluoride was tested on animals and approved ,for human consumption, the
same cannot be said for SiFs.
Masters and his collaborator Myron J. Coplan, a consulting chemical engineer,
formerly Vice President of Albany International Corporation, led the team that
has now stucled the blood lead levels in over 400,000 children in three
different samples. In each case, they found a significant link between SiF-
treated water and elevated blood lead levels.
'We should stop using silicofluorides in our public water supply until we know
what they do," said Masters. Officials at the Environmental Protection Agency
have told Masters and Coplan that the EPA has no information on health
effects of chronic ingestion of SiF-treated water.
In their latest study published in a special December 2000 issue of
Neuro Toxicology, Masters, Coplan and their team analyzed data on blood
levels from more than 150,000 children ages 0 to 6. These tests were part of a
sample collected by the New York State Department of Children's Health,
mostly from 1994 to 1998 in comparable non-fluoridated and SiF-treated public
drinking water in communities with populations of similar size. Socia-economic
and demographic risk factors for high blood lead were also considered using
information from the 1990 U.S. Census. The researchers found that the
greatest likelihood of children having elevated blood lead levels occurs when
they are exposed both to known risk factors, such as old house paint and lead
in soil or water, and to SiF-treated drinking water.
"Our research needs further laboratory testing," added Masters. "This should
have the highest priority because our preliminary findings show correlations
between SiF use and more behavior problems due to known effects of lead on
brain chemistry." Also requiring further examination is German research that
shows SiFs inhibit cholinesterase, an enzyme that plays an important role in
regulating neurotransmitters.
"If SiFs are cholinesterase inhibitors, this means that SiFs have effects like the
chemical agents linked to Gulf War Syndrome, chronic fatigue syndrome and
other puzzling conditions that plague millions of Americans," said Masters. 'We
need a better understanding of how SiFs behave chemically and
physiologically. "
http://www.dartmouth. edu/-news/releases/200 1/marO 1/fluoride.html
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8/2/03
Dartmouth College - uanmoum researcner warns 01 cnermccus ilUU~ w WUllUl1~ w~c. - ,... racc. VI..
Currently, a bill before the New Hampshire House of Representatives would
impose more stringent testing on fluoridating chemicals added to public
drinking water. On March 7, 2001, Masters and Coplan testified in favor of the
bill, HB 754, The Fluoride Product Quality Control Act, at a public hearing.
Masters contends that bill's requirement for testing the silicofluorides is vital but
needS 'to be complemented by further research on neurotoxicity and behavior.
Masters and Coplan note that their recent studies contain the most extensive
empirical evidence of the health and behaviotal costs of these chemicals. "If
further research confirms our findings," Masters added, ''this may ~II be the
worst environmental poison sinCe leaded gasoline."
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http://www.dartmouth.edu/-news/releases/2001/mar01/fluoride.html
8/2/03
Dartmouth University Study (Sept '99) links fluoridation with high lead levels in children. Page 1 of 6
Dartmouth University Study
Links Fluoridation with High Lead Levels in Children
Although the dangers of lead poisoning have been known for years, substantial numbers of
children continue to suffer from blood lead above danger level of IO/-lgldL. The problem is
especially serious because lead poisoning is associated with higher rates of learning
disabilities, hyperactivity, substance abuse and crime.
Newly published research at Dartmouth College has uncovered an unsuspected factor that
increases vulnerability to environmental lead exposure. Analyzing a major survey of over
280,000 Massachusetts children, a team headed by Prof. Roger D. Masters has identified
chemicals widely used in treating public water supplies [Editor: WATER
FLUORIDATION] that apparently increase children's absorption of lead.
Plenary Address to
Annual Conference of the Association for Politics and the Life Sciences
Sept. 2, 1999
Poisoning the Well:
Neurotoxic Metals, Water Treatment, and Human Behavior
Roger D. Masters
Department of Government, Dartmouth College
Foundation for Neuroscience and Society
Summary: Heavy metals compromise normal brain development and neurotransmitter
function, leading to long-term deficits in learning and social behavior. At the individual
level, earlier studies revealed that hyperactive children and criminal offenders have
significantly elevated levels of lead, manganese, or cadmium compared to controls; high
blood lead at age seven predicts juvenile delinquency and adult crime. At the environmental
level, our research has found that environmental factors associated with toxicity are
correlated with higher rates of anti-social behavior.
F or the period 1977 to 1997, levels of violent crime and teenage homicide were significantly
correlated with the probability of prenatal and infant exposure to leaded gasoline years
earlier. Across all U.S. counties for both 1985 and 1991, industrial releases of heavy metals
were -- controlling for over 20 socio-economic and demographic factors -- also a risk-factor
for higher rates of crime. Surveys of children's blood lead in Massachusetts, New York, and
other states as well as NHANES III and an NIJ study of 24 cities point to another
environmental factor: where silicofluorides are used as water treatment agents, [also
know as water fluoridation] risk-ratios for blood lead over 1O/-lgldL are from 1.25 to 2.5,
with significant interactions between the silicofluorides and other factors associated with
lead uptake. Communities using silicofluorides also report higher rates of learning
disabilities, ADHD, violent crime, and criminals who were using cocaine at the time of
arrest.
Research conducted with Myron J. Coplan (Intellequity, Natick, MA) and Brian Hone under
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grants from the Office of Criminal Enforcement, Forensics and Training, Environmental
Protection Agency, the Earhart Foundation, and the Rockefeller Center for the Social
Sciences, Dartmouth College
I. Heavy metals, Neurotransmitter deregulation, and Anti-social Behavior
A. Toxic heavy metals such as lead, manganese and cadmium, combined with prenatal or
neonatal developmental insults, dietary deficits, and stress, damage the brain structures and
down-regulate essential neurotransmitters. Previous research in this area has found:
1. Because lead and other toxic metals are retained in bone and astroglial cells
in the brain, uptake during fetal development and early childhood has long-
lasting effects on development and behavior.
2. Among the toxic effects of lead is a reduction of dopamine function (which
disturbs the behavioral inhibition mechanisms in the basal ganglia) and
glutamate (which plays an essential role in the long term learning associated
with the hippocampus).
3. Manganese can downregulate serotonin function, reducing sociability and
increasing aggressiveness or depression.
B. Prior research at the individual level showed that the uptake of heavy metals is associated
with higher levels of learning disabilities, hyperactivity, substance abuse, violent crime, and
other forms of anti-social behavior.
1. In seven different samples of prison inmates, violent offenders had
significantly higher levels of lead, cadmium, or manganese in head hair than
non-violent offenders or controls.
2. In two prospective studies, high lead levels at age 7 (one measuring lead in
blood, the other bone lead) predicted juvenile delinquency and adult crime.
3. A substantial proportion of individuals diagnosed with ADD/ADHD are
likely to have dangerously high levels of lead, manganese, or cadmium in
bodily tissues.
4. Because alcohol, cocaine and other drugs temporarily restore
neurotransmitter functions that are abnormal, substance abuse may often be
crude self-medication in response to the effects of toxicity. For example,
because lead downregulates dopamine and cocaine is a non-selective dopamine
reuptake inhibitor, lead toxicity could increase the risk of cocaine abuse.
II. Heavy Metals, Blood Lead and Crime
A. Our own research shows that, for all U.S. counties, communities with industrial releases
of lead or manganese had, controlling for socio-economic and demographic factors, higher
violent crime rates in 1991. The comparable multiple regression analysis for 1985 replicates
this finding.
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B. Across the U.S., rates of violent crime and drug use have fallen continuously since 1993.
This effect may be explained by long-term benefits of the ban on leaded gasoline in the
1970's. The delay reflects the years needed before the appearance of teenage cohorts that
had not been exposed to leaded fumes during fetal development and early childhood.
1. Leaded gasoline was worse than lead toxicity in paint or water, since aerosol
lead is absorbed 40-50% whereas only 5-15% of ingested lead is retained in the
body.
2. Leaded gasoline sales from 1950 to 1980 are highly correlated with the
overall violent crime rate 18 years or later (r = .902 or higher).
3. The effect confirmed by correlating leaded gasoline sales from 1950 to 1980
with homicides by teenagers aged 14 to 17, which drop more sharply after 1993
than those by older offenders.
4. The negative effects of leaded gasoline on impulse control are also suggested
by the high correlation (r = .811) between leaded gas sales between 1949 and
1993 and the contemporary year's sales of hard liquor -- a pattern that is not
found for the consumption of beer or wine.
III. Water Treatment Procedures, Lead toxicity and crime.
A. The agent used to fluoridate public water supplies was shifted from sodium fluoride
(NaP) to fluosilicic acid (H2SiF6) or sodium silicofluoride (Na2SiF6) -- the silicofluorides
(SiP) -- on the basis of questionable biochemical assumptions and without adequate testing.
1. Although virtually all studies of fluoridation have continued to use NaP, over
90% of Americans drinking fluoridated are exposed to supplies treated with
SiP.
2. Although it is claimed that SiF is completely dissociated after injection in
water supplies, this assumption is inconsistent with published research and is
highly unlikely under the actual conditions of water treatment.
B. Because sodium fluoride and silicofluorides have very different biological effects,
undissociated SiP residues may be dangerous.
1. As early as 1935, animal studies showed that excess fluoride derived from
SiF is excreted through the kidneys, whereas fluoride residues from NaF are
more likely to be excreted in feces (indicating more active fluorine transport
across the gut-blood barrier after exposure to SiP).
2. Recent research on dental preparations shows that SiP compounds may be as
much as 19 times more biologically active than NaP.
3. Through one of several plausible mechanisms, SiP treated water can increase
the transport of heavy metals across the gut-blood and blood-brain barriers,
increasing rates of toxic uptake and behavioral dysfunction.
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IV. Communities using SiF have higher levels of lead in children's blood and higher rates
of anti-social behavior than locations with nonfluoridated or NaP treated water.
A. In Massachusetts, communities using SiP to fluoridate have higher rates of children with
over 1O/-lg/dL of blood lead and higher rates of crime. Average levels oflead in children's
blood were: H2SiF6 = 2.78 /-lg/dL; Na2SiP6 = 2.66 /-lg/dL; NaP = 2.07 /-lg/dL; non-
fluoridated = 2.02 /-lg/dL.
1. Within Massachusetts, those communities where the EP A reported lead
levels in water over 15ppb, this effect was more pronounced: H2SiP6 = 3.27
/-lg/dL; Na2SiF6 = 4.38 /-lg/dL; NaP = 1.90 /-lg/dL; non-fluoridated = 2.18
/-lg/dL.
2. These effects were confirmed in a matched sample of 30 SiF and 30 non-SiP
suburban middle-class communities: 1.94% of children exposed to SiF treated
water had blood lead over IO/-lg/dL, whereas on 0.76% of children not so
exposed had blood lead over this level (risk ratio = 2.55).
3. Rates of crime were also higher in Massachusetts communities using SiF
fluoridation.
4. Similar effects were confirmed in rural counties in six additional states
(Georgia, Wisconsin, Texas, Illinois, Alabama, and North Carolina).
B. Among 30,000 criminals in 24 cities studied by NIJ, those living where SiF is in water
were more likely to have been using cocaine at the time of their arrest (H2SiF6 = 44%;
Na2SiF6 = 43%; non-fluoridated = 32%).
1. There was no comparable difference for other drugs whose usage is not
associated with chemicals influenced by lead toxicity.
2. Crime rates in the cities using SiP were significantly higher than in non-
fluoridating cities (H2SiP6 = 1486 per 100,000; Na2SiP6 = 1480 per 100,000;
non-fluoridated = 1100 per 100,000), as were rates of death from alcoholism
(H2SiP6 = 56.1 per 100,000; Na2SiF6 = 53.8 per 100,000; non-fluoridated =
44.1 per 100,000).
C. Geographic analysis of data from NHANES III shows that in counties where over 90% of
the children receive SiF treated water, average blood lead is 5.1 /-lg/dL, compared to
3.7/-lg/dL where less than 10% of the children are exposed (risk ratio = 1.38). This effect is
highly significant (p < .0001) both for children 3-5 and for those 5-17.
1. Minorities are especially at risk. In high SiP exposure counties, blood lead
levels average 6.26 /-lg/dL among Black children, 4.86 /-lg/dL among Mexican-
Americans, and 3.05 /-lg/dL among Whites; in low SiP exposure counties,
Blacks average 4.37/-lg/dL, Mexican-Americans 3.86/-lg/dL, and Whites
2.03/-lg/dL (risk ratios between 1.26 and 1.50). For both 3-5 and 5-17 age-
groups, the interaction effect between a child's race and SiP exposure as factors
in higher blood lead is highly significant (p < .0001).
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2. Although NHANES III data also shows some benefits of fluoridation on
lower tooth decay, these effects are weaker and are not found among White
children aged 5-17. Moreover, lower rates of caries are not found among
children 15-17 (perhaps because fluoride can slow tooth eruption, which could
lead to misleading data when comparisons match age for children of different
races).
D. A preliminary survey of high school nurses and administrators in sixteen comparable
middle sized New York cities shows higher rates of ADHD cases treated with medication
and higher rates of learning disabilities in communities using SiP (risk ratio = 1.38).
V. Conclusion: the need to integrate neurotoxicology, environmental research and the
study of human behavior.
A. The brain is the most sensitive chemical organ in the body. While
discussions of toxins heretofore focused on cancer and disease, ADD/ ADHD,
alcoholism, substance abuse, and crime need to be studied in terms of the latest
biology and neuroscience of early development and brain function.
B. The effects of toxic heavy metals are consistent with the perspective of
Darwinian medicine: since lead and manganese are widely found in soils but
uptake depends on dietary deficits in calcium and other key elements, for most
of hominid evolution the effects discussed above would only have occurred in
time of dietary shortfall, when increased male-male conflict was not necessarily
mal-adaptive.
C. In contemporary society, these effects take on a different character.
Environmental pollution and dangerous water treatment procedures are human
activities whose results are both economically costly and morally unjust.
Innocent children should not be poisoned by public water supplies.
Contact: Roger D. Masters, Nelson A. Rockefeller Professor of Government
Emeritus
Foundation for Neuroscience and Society, Dartmouth College
(603646 1029).
The Authors
Roger D. Masters is Nelson D. Rockefeller Professor Emeritus in the Dartmouth College
Department of Government. He heads the Dartmouth Foundation for Neuroscience and
Society. For several decades he has researched the causes of violence and other
dysfunctional human behavior such as ADD, ADHD, drug abuse and the like. His
viewpoint, which has been published widely, is that toxins in the environment have subtle
effects on brain and neural functions which are ultimately manifested in behaviors which
many social scientists and politicians prefer to attribute to social dynamics.
Myron 1. Coplan is retired Vice President of Albany International Corp., a registered
Professional Chemical Engineer and a private consultant in Chemical Engineering dba
Intellequity. His fields include water chemistry and the treatment of water and waste-water
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via membranes. He has consulted to the phosphate fertilizer industry and has first-hand
knowledge of processes bearing on the production of fluoridating agents.
For over two years RDM and MJC have been collaborating in a study of the blood lead of
children and related behavioral outcomes with which elevated blood lead have been
associated. Under an EPA grant (Criminal Enforcement Branch) RDM and MJC have also
been studying aspects of criminal behavior, particularly violent crime and drug use. Their
work was also supported in part by a grant from the Earhart Foundation. Several
publications have been accepted by peer-reviewed journals and others are in preparation.
Parts of their work was presented at a New York Academy of Medicine symposium on
Environmental Toxins and Children's Health and Behavior in May 1999. They were also
invited participants at a Workshop on Alzheimer's Disease in February 1999 at the NIEHS
in Raleigh.
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Excerpt from "Truth Decay" by Robert & Kerrie Broe--www.tuberose.com
Fluoride
Sodium fluoride is the most violent protoplasmic poison known to science. The National Library of Medicine's computerized data
service on toxic substances rates fluorides 4-5 (very toxic-extremely toxic) on a scale of five. Scheele discovered fluorine in 1771, but
Moissan did not produce it in gaseous elemental purity unti11886. Fluoride is added to the water supply of most American cities for the
purpose of dental hygiene. The reader will be amazed to fmd out that such a result is not only unlikely but the reverse of the actual
outcome. The U.S. has been fluoridating drinking water for so many decades that people hardly think about it. Very few articles appear
about fluoridation in newspapers and magazines anymore. At least chlorine will evaporate from a glass of water if you let it sit for an
hour or so. Not so with fluoride. Even cooking, food processing, filtration, or digestion will not remove fluoride. Fluoride goes right
up the food chain. It accumulates in fat cells when ingested or absorbed through the skin or mucous membranes. Fluoride drops, tablets,
and vitamins are more likely to damage children's teeth than to prevent cavities, according to mainstream dental groups such as the
Canadian Dental Association and the Western Australia Health Department's Dental Service. Both organizations have stopped recom-
mending regular fluoride supplementation.
In the past, the American Dental Association (ADA), the American Medical Association (AMA) and the World Health Organization
(WHO) have all endorsed fluoridation, and many established scientific bodies have declared that its advantages are not debatable. But,
recently, the tide has been changing, and what the fluoride promoters will not reveal to their targeted legislators, City Council members,
County Commissioners, or even their unsuspecting well-intended supporters: The July 2000, peer-reviewed cover story of the Journal
of the American Dental Association (JADA) clarifed for every dentist in America that ingestion of fluoride does not provide any
significant reduction in the incidence oftooth decay--that any beneficial dental effect is as a result oftopical application directly
to the tooth.
The American Dental Association and the American Academy of Pediatrics have revised their reconunendations for controlled-dose
fluoride which restricts a doctor from prescribing fluoride to a child of 6 months to 3 years of age to 0.25 milligrams per day, the
amount found in one cup of fluoridated water, and none to an infant-meaning that, as a public policy, fluoridation mass medicates
at a higher expected dosage than a doctor in a non-fluoridated conununity can prescribe. The August 17,2001 Morbidity and Mortality
Weekly Report (MMWR) from the Centers for Disease Control and Prevention (CDC) despite its touting of fluoridation, included: "The
prevalence of dental caries in a population is not inversely related to the concentration of fluoride in enamel, and a higher concentration
of enamel fluoride is not necessarily more efficacious in preventing dental caries." In short, dental cavities are not a result of a lack
of fluoride exposure, and more fluoride is not better in the prevention of tooth decay.
In a Congressional investigation by the House Committee on Science, the Environmental Protection Agency (EPA), the CDC, National
Sanitation Foundation, and the Food and Drug Administration (FDA), all replied to inquiries that they have no scientific studies on the
actual fluorine-bearing substances used in 90% of the nation's fluoridaiton programs. The FDA, in a December 2000 conununi-
cation, stated that "Fluoride, when used for the diagnosis, cure, mitigation, treatment, or prevention of disease in man or animal is a drug
that is subject to Food and Drug Administration regulation." and that "No fluoride substance intended to be ingested for the purpose
of reducing tooth decay has ever been approved for safety and effectiveness."
On June 29, 2000, at the u.s. Senate Congressional Hearing on Arsenic, Radon, and Fluoride, held by the subcommittee on Fisheries,
Wildlife, and Water, 1. Willam Hirzy, Ph.D. testified on behalf of the union (that consists of and represents all of the toxicologists,
biologists, chemists, physicians, statisticians, epidemiologists, attorneys, engineers, scientists, and other professionals at the U.S. Envi-
ronmental Protection Agency, Washington, D.C.), calling for a moratorium on all fluoridation. In his testimony to Congress, Hirzy
cited scientific evidence that the union of scientists have in their possession, and court fmdings in three different states, whose conclu-
sions have never been overturned on the merits, that found, with reasonable certainty (Le. beyond speculation and guess), and by
preponderance of the evidence, including the testimony of experts learned in the field, that fluoride in public water supplies causes or
contributes to the cause of cancer, genetic damage, intolerant reactions, chronic toxicity, dental fluorosis, bone pathology and
neurological injury in humans, and that fluoride in public water supplies aggravates malnutrition, iodine deficiencies and other
existing illnesses.
Before fluoridation's implementation in 1945 and popular acceptance in 1950, sodium fluoride, a by-product of aluminum manufac-
ture, was known as an intractable industrial pollutant. Waterworks engineers warned that water containing 1 part-per-million
(ppm) fluoride is contaminated. The devilish plot to put fluoride in drinking water has been backed in Washington since an ex-
employee of the Aluminum Company of America was made Secretary of the Public Health Administration. Fluoride is a very
toxic substance, which is why it is the active ingredient in a number of pesticides. Two grams of fluoride is enough to kill an adult,
and 500 mg. is enough to kill a child. A tube of toothpaste can have as much as 1,500 mgs., and fluoride gel contains up to 6,000 mgs.
In the U.S., people have died, and many have become sick, when faltering fluoridation equipment has pumped excess fluoride into the
water. Poor nutrition exacerbates the toxic effects of fluoride exposure, which is one reason why it's wrong to target poor conununities
with fluoridation (poor nutrition is more prevalent in low income conununities).
Critical Condition 216
Subsets ofthe population may be unusually susceptible to the toxic effects of fluoride and its compounds. These populations include the
elderly, people with deficiencies of calcium, magnesium and/or vitamin C, and people with cardiovascular and kidney problems. Ninety-
eight percent of Western Europe has rejected water fluoridation. This includes Austria, Belgium, Denmark, Finland, France, Germany,
Italy, Luxembourg, Netherlands, Norway, and Sweden. The predominant reason for Europe's rejection is the belief that public drinking
water is not the appropriate vehicle with which to deliver medication to a population. Fluoride is not an essential nutrient, which means
that no human disease (including dental decay) has ever been linked to a fluoride deficiency. Fluoridation adds between 0.1 and 1.6
parts per billion (ppb) arsenic to drinking water, and therefore violates the EPA's Maximum Contaminant Level Goal for arsenic-
which is 0 ppb. When water fluoridation began 50 years ago, it was believed that fluoride needed to be ingested in order to be effective.
This is no longer the view of the dental establishment, which now generally concedes that fluoride's benefits are derived primarily from
topical application. No fluoride products designed for ingestion have ever been approved as safe or effective by the U.S. Food and Drug
Administration (FDA). Fluoridated water can appropriately be classified as an unapproved prescription drug. Fluoride is ineffective
at preventing the most common type of dental decay-pits andjissures. Pit & fissure decay-which is the decay found in the crevices
ofthe chewing surfaces-accounts for upwards of 85% of dental decay now experienced in the U.S. Despite the fact that nearly all large
U.S. cities have been fluoridated for decades, dental decay is currently rampant in virtually all poor urban areas. Routinely prescribed
to U.S. children who don't drink fluoridated water (starting with toothless six month olds), fluoride supplements were never tested for
safety and efficacy by the ED.A. These supplements comprise one category of many different medications the FDA officially
"grandfathered" in, (they were sold before drug testing was required by law). Current research shows that many of the old fluoride
studies were flawed. Fluoride's benefits are merely topical, not systemic, as was once thought.
Moreover, ingested fluoride can result in unwanted side effects, including dentalfluorosis (spotted, stained, or pitted teeth). BrianA.
Burt of the University of Michigan School of Public Health states that "fluoride supplements should no longer be used for young
children in North America...the risks of using supplements in infants and young children outweigh the benefits." Euan Swan,
author of the Canadian Dental Association's (CDA) new fluoride supplement guidelines, said, "The evidence supporting the effective-
ness of dietary fluoride supplements is relatively weak. There's better evidence indicating that they contribute to dental fluorosis."
"The notion that systemic fluorides are needed in nonfluoridated areas is an outdated one that should be abandoned altogether," says
Canada's leading fluoride authority, Hardy Limeback, head of the Department of Preventive Dentistry at the University of Toronto and
past president of the Canadian Association for Dental research. He says, "We are now spending more money treating dental fluorosis
than we would spend treating new decay if water fluoridation was halted."
Forms of Fluoride
There are five forms of fluoride that are often discussed and sometimes get confused. First, there is elemental fluorine, which is a gas
and the most reactive element in the periodic table. It reacts with every other element except three of the noble gases. It even reacts with
asbestos. Free fluorine is not produced in nature. Fluorine is not put in our drinking water! Fluorine is found in the form of hydrogen
fluoride, another gas. It etches glass. It dissolves in water to form a weak acid. It is a pollutant emitted by metal smelters, the oil
industry, ceramic and brick industries, coal fired power stations, incinerators, and a number of other industries. It's been responsible for
many deaths in air pollution incidents. Then there is the fluoride ion. The fluoride ion cannot be placed in a bottle by itself. It is a
negative ion; it must be accompanied by positive ions. Negative ions are formed when metals react with non-metals (fluorine is a non-
metal). When this happens, the metal transfers one or more of its electrons (negative particles) to the non-metal. The result is a
positively charged metal ion and a negatively charged ion. In the solid form, these positive ions and negative ions appear in a tidy three-
dimensional arrangement. This internal arrangement gives rise to the crystalline shape of these substances. For example, table salt has
crystals in the shape of a cube. When these substances (salts) are dissolved in water the positive ions and negative ions separate.
Sodium chloride is very soluble in water; calcium fluoride is far less soluble. Ten percent of the water fluoridated in the U.S. is
fluoridated with sodium fluoride. Complex ions are positive metal ions that are surrounded by negative ions or neutral molecules that
have a stronger bonding than simply electrostatic attraction. Thus they have different properties from the parent ions. Thus, (AIF4-) has
different properties from the parent Al3 + ion and the F - ions. It is this ability of the fluoride ion to form complexes with so many ions,
including a lot of toxic ones, and others that are needed by the body, which might help to explain why this umeactive species (in the
chemical sense) can be so biologically active and dangerous. Another form of fluoride that we meet is hexafluoro silicic acid (H2SiF 6)
and its sodium salt sodium fluorosilicate (Na2SiF6). These substances are used to fluoridate 90% of the fluoridated water in the U.S.
They are waste products from the superphosphate industry. Pro-fluoridation people claim that when these substances are diluted and
dissolved in water, they completely dissolve into Si02 and fluoride ion.
This is disputed, as there are still some silicon fluoride complexes left when the water reaches our taps. These complexes facilitate the
uptake of lead into the blood. Over 50% of the communities in the United States use fluorosilicic acid or sodium fluorosilicate to
fluoridate drinking water. Neither the EPA nor the Centers for Disease Control and Prevention can provide one safety study proving the
product is safe for long-term, low-level consumption. Not one clinical study with animal models has ever been done with the
products. Interestingly, all the people who say this product is 'safe' have no concept of how it is produced. The last form of fluoride that
we meet is the organofluoride group. These are compounds which have fluorine covalently bonded to carbon atoms.
217 Fluoride
One of the organofluorines, which you have probably handled, is the plastic PTFE. This is poly tetrafluoro ethylene, used in non-stick
frying pans. It consists of long chains of carbon attached to itself with two fluorines attached to each carbon. It is very stable and
resistant to chemical attack.
Fluorine is frequently added to pharmaceuticals. These drugs, when they are metabolized, break down in the body and produce fluoride
ion. The net result is that these drugs carry fluoride into very sensitive places, like the brain, where it can cause problems. Little
investigation has been done on this aspect of organofluorines. There are other organofluorines that are very toxic in their own right- the
toxicity has nothing to do with the fluoride ion itself; or the formation of the fluoride ion. Substances like fluorocitrate are very toxic
because they bind to an enzyme involved in sugar metabolism, and they don't let go-they block it-they prevent it from handling the
citrate, and it usually changes into something else. This rather unreactive chemical species called fluoride ions can interfere with
biological systems in three profound ways: a) by forming hydrogen bonds with key groups in proteins and nucleic acids, b) can complex
with metal ions like aluminum, beryllium, lead and carbon) can interfere with enzymes that use magnesium ions as a co-factor. For
many enzymes, magnesium helps to align the enzyme with the substrate it is working on, and fluoride can interfere with this alignment.
We're swallowing more fluoride each day with every glass of water. Since 1945, when fluoride was first put into the municipal water
system in Newburgh, New York, 75% of the United States water supply has been fluoridated. Other countries are taking a suspicious
look at fluoride. Sweden abandoned fluoridation on the reconunendation of a special fluoride commission. Denmark, Holland, Finland,
France, Germany and Japan have also rejected it, citing public health concerns. Plans to make fluoridation mandatory in Britain were
suspended in 1998 after the British Home Secretary intervened and urged the Health Secretary to review the negative evidence. Dis-
reputable and power-hungry persons in high places have been know to experiment with fluoride to see if it "could not be used to
subjugate the people of a whole community more quickly than fighting them into submission," according to William Guy Carr, a
retired commander from the Royal Canadian Navy.
Fluoride In Toothpaste
Contrary to its public image as a benign substance used solely to reduce tooth decay, fluoride is extremely corrosive, more toxic than
lead and just slightly less toxic than arsenic. Sodium fluoride, the active ingredient in most brands of toothpaste, was originally sold as
a rat poison. If a three-year-old ate half a tube of the toothpaste, it could kill him. "Fluoridated toothpaste contains 1,000-2,000
mgs. of fluoride. Fluoridated drinking water contains one to four parts per million. Fluoride is absorbed through mucous mem-
branes in the mouth. A child may not consume the whole tube, but smaller amounts daily are certainly a hazard to anyone. It is
estimated that children swallow or absorb approximately 1 mg. of fluoride at each brushing with such toothpaste. In 1987 the
Journal of Pediatrics issued a warning that children should use no more than "one-third of one pea-sized dollop of toothpaste" when
brushing their teeth. Allowing for the 4 ppm standard to which the EPA has raised fluoride, and based upon accurate water consumption
figures, approximately 50% of children under five are receiving a daily dose of fluoride known to cause skeletal fluorosis. Is the
possible saving of 0.8% of one tooth surface over a seventeen-year period worth the risk of skeletal fluorisis, cancer or AIDS? Imple-
mentation of sound nutritional principles, removal of pollutants that reduce natural inununity and appropriate health education proves
more effective in resolving the problems of tooth decay along with many other modem degenerative diseases.
Just as you lock your doors against unwanted intrusion, you must take the necessary steps to protect yourselves from this daily poison-
ing. It will have to be done by you. No one else will do it for you. Terry Leader, a dental hygienist from Long Island, witnessed, in
1969, a child given topical fluoride, who then went into convulsions and died in the dentist's chair. She pleads: "I just wish
parents would read before they subject their children to something so dangerous. It's not going to save them money. Good oral
hygiene prevents tooth decay; fluoride doesn't. The mystique behind many 'miracle' drugs is the belief that, like heat-seeking
missiles, they will zoom right to the enemy symptom and zap it neatly out of existence. So with fluoride, our bodies should deliver all
the fluoride directly to our teeth where it will supposedly harden the enamel and form an indestructible barrier to tooth decay. Such
magical thinking bears little relationship to biochemical reality.
Fluoride In Water
Corporations have a lot invested in fluoridation, which allows them to dispose of industrial pollution via dilution. Today, the most
conunon product used for fluoridation is hydrofluosilicic acid, which is not a natural substance but a waste product coming straight from
the scrubbers of the phosphate fertilizer industry. When phosphate is mined, they have to get rid of the attached fluorine or it would kill
the plants. So they put the phosphate through a sulfuric acid wash to separate the fluorine out into what is called hazardous waste liquor.
The fluorine is captured by a scrubber system since they can't let it go out into the air because it would kill all the plants and animals
around. If they had to dispose of this liquor as hazardous industrial waste, it would cost them $1.40 a gallon or more neutralize it-
depending on how much cadmium, lead, uranium, and arsenic are also present. They don't want to pay that, so instead they call it a
product and we pay them approximately 3 cents a gallon to dump in our water. Data collected in the largest survey to date-of over
39,000 American schoolchildren ages 5 to 17 in 84 conununities, showed that children living in fluoridated areas had tooth decay rates
nearly identical with those living in non-fluoridated areas.
Critical Condition 218
The cells that produce the collagen matrix that forms enamel are poisoned to the point that they can no longer produce opalescent pearl-
like enamel. Fluorotic enamel is irregular in texture, porous, chalky white to brown in color and brittle. In severe cases, the enamel
forms incompletely and corners easily break off the teeth. Even proponents of fluoridation acknowledge that fluorosis increases with
the level of fluoride in the water. Currently, an estimated 22% of American children exhibit the symptoms of fluorosis. This is not just
a cosmetic flaw; it's proof of the fact that the body has been overdosed with fluoride and has not been able to handle it. Bottle-fed babies
(whose formula is made with fluoridated water) are most likely to develop dental fluorosis. Mother's milk has virtually no fluoride
present. Those children who are deficient in protein, calcium, magnesium, phosphorous, and vitamin C are especially vulnerable to
fluoride poisoning. The accumulation of fluoride is greatly increased if the person has impaired kidney function. In short, the weakest
members of our society, the undernourished and the underfed, are the very children that fluoridation was to allegedly benefit. In some
poorer communities, as much as 80% of the children have fluorosis. But don't assume that if your child is healthy and well nourished,
he or she runs no risk. Look at the toothpaste, and read the directions-Children 2 to 6 years: To minimize swallowing, use a pea-sized
amount, and supervise brushing and rinsing until good habits are established." Tempted by bubble-gum flavors and artificial sweeten-
ers, a child can easily ingest more than the recommended amount. Studies show that children under four inadvertently swallow 50% to
100% of the toothpaste they put in their mouths, simply because they lack a fully developed gag reflex. The American Dental
Association will not give toothpaste its seal of approval unless it includes fluoride.
Dental fluorosis is just the first, visible evidence of much more serious changes in the body. When fluoride accumulates at high
concentrations in the bones, they become weak and brittle. Victims of this debilitating condition, called skeletal fluorosis can only
hobble forward, stiff and hunched. The osteoarthritis that afflicts many people in this country may actually be a misdiagnosed stage of
skeletal fluorosis. Recent studies have linked fluoride to an increased incidence of hip fractures, damage to the central nervous
system, and cancer. In China, researchers correlated dental fluorosis with a 10 point reduction in I.Q. Low levels of fluoride in the
drinking water of test animals produced pathological changes in the brain similar to those in humans with Alzheimer 's disease. Another
study demonstrated how fluoride interferes with the brain's pineal gland and inhibits its production of melatonin. What will happen
when the first generation of fluoride-fed children turns 70, after accumulating this poison over a lifetime in their bones? Cavities are
not life-threatening, but fluoridation comes with real risks and negligible benefits. Even if you believe in the value of fluoride, no
one should be allowed to use our drinking water as a delivery system. A lot of people consider Vitamin C beneficial, but so far it doesn't
flow out of the tap. Water is our most precious resource, and we have no business adding anything to it, other than what's necessary to
make it safe to drink. It is our responsibility to maintain this gift, as pure and pristine as possible, for each and every person to enjoy. In
1990, Dr. William Marcus, chief toxicologist for the EPA's Office of Drinking Water, was disturbed to find data from a study reporting
specific fluoride-related cancers altered or omitted in the final National Toxicology Program report.
When he demanded an independent review of the raw data, he was fired. Later, an investigation by the Senate Environment and Public
Works Committee corroborated his charges and produced evidence that government scientists had been pressured to portray fluoride
more positively. Because fluorine is the most negatively charged and interactive element of all, it bonds with practically everything and
does not exist separately in nature, despite its rank as the 13th most abundant element in the earth's crust. But most of it stays buried
there, unless it is mined and brought to the surface or created as a by-product of various manufacturing processes. Fluorine is kind of
a bully; it aggressively seeks out other electrons and is prized for its ability to disrupt and reconfigure other molecular bonds. One
reason people have been reluctant to. expose the problems of fluoride is that it cuts across so many industries. In its various forms,
fluoride is used to etch glass, ceramics and computer chips; refine petroleum products; separate out heavy metal and power rockets. Our
air is contaminated by fluoride emissions from the production of iron, steel, copper, aluminum and plastics. Fluoride is one of the
world's most widely used pesticides. If you walk past a house tented for termites, they're probably spraying sulfuryl fluoride (Vikane)
to kill the bugs.
Fluorinated Drugs
Many psychoactive drugs are fluorinated. The fluorine atom is attached to the active ingredients in many drugs in order to allow them
to penetrate into the brain or other targeted organs more easily. Because the fluoride enhances the penetrating power of the active
ingredient, less of the active ingredient needs to be made, and the manufacturer can save money. But the side effects of all the fluoride-
containing medications is scarcely ever discussed as a general health issue. The primary ingredients of most psychoactive drugs
suppress enzyme production, and the fluorine ion is also an enzyme inhibitor. The one particular side effect common to almost all
fluorinated drugs, which is mentioned in the Physician's Desk Reference, is memory loss. These drugs, including Prozac (jIuoxetene)-
and Paxil-antidepression drugs, contain three Fluorine atoms in each molecule that quickly kill the brain-issued enzymes that
normally maintain mood stability. Prozac and Paxil contain the fluoride containing Fluorophenyl compounds and are also known to
cause liver disease. Organic fluoride compounds undergo extensive transformation in the liver, and in many instances the resulting
metabolites may have higher activity and/or greater toxicity than the original compound. Prozac has caused hepatitis and has also been
shown to promote tumors in the liver. Rophypnol (flunitrazepam, or "Roofies,")-the date rape drug-is fluorinated Valium, which is
about 20-30 times more potent than Valium alone. Phen-Fen (Fenfluramine) a weight-loss drug, fluorinated corticosteroids and
fluorinated psychoactive drugs all contain fluoride. In 2000, a U.S. district judge approved a $3.75 billion national settlement of health
claims stemming from Fen-Phen. More than 9,000 lawsuits have been filed against American Home Products, maker of Fenfluramine.
People taking such drugs might exceed 5 mgs. in just one prescribed application.
219
Fluoride
We are essentially putting psychoactive drugs into the water supply. If you go in for surgery, you'll usually be given a fluoride-based
anesthetic because fluoride is virulent enough to throw you into an inunediate coma. Sevoflurane, one of many fluorinated agents used
in anesthesia, such as florinated Halothane, is thought to be responsible for renal failure. Hydrogen fluoride is the only toxic element
in the nerve gas Sarin (1500 times more poisonous than cyanide) used in the Japanese subway attack. On August 8th, 2001, Baycol-
a cholesterol-lowering drug taken by 700,000 Americans-was pulled off the market. It had been linked to 31 U.S. deaths. Bayer AG,
the maker of the drug, would not disclose the total number of deaths worldwide. Scientists have found that all fluoride compounds
interfere with thyroid hormones. Numerous congenital abnormalities have been reported due to first trimester exposure to
Fluconsazole, a systemic anti-fungal agent. There have been numerous fluorinated drugs removed from the market recently. Most have
been shown to cause serious adverse cardiac effects, probably due to fluoride's adverse effects on thyroid hormone activity.
Fluoride in the Food Chain
So now we have fluoride in our water, which means we're mass-medicating the population, although we can't control the dose because
everyone drinks varying amounts. Back when safety levels in the water were set at 1 ppm, there was basically no other source. Since
then, fluoride has been added to toothpaste, mouth rinses and dental floss. Dentists treat the teeth topically with fluoride, and doctors
prescribe fluoride supplements. And, of course, if fluoride is in the water, it's in the food chain. Food is irrigated, washed, and
processed with fluoridated water; we're consuming much more fluoride than we think. Independent lab reports show high levels in
common products: .98 to 1.2 ppmin Coca-Cola, 1 ppminMinute Maid orange juice, 2.1 ppm in Fruit Loops, 10ppmin Wheaties, 6.8
ppm in Gerber s white grape juice which is often used as a sweetener in baby foods. Grapes are commonly sprayed with an insecticide
that contains fluoride. A 1996 study published in the Journal of the American Dental Association warned parents to limit their children's
intake of juices due to excessive fluoride content. In fact, according to a 1993 government survey, children in non-fluoridated commu-
nities are already receiving at least 3 times the amount of fluoride recommended for total consumption, while children in fluoridated
communities are receiving 4.6 to 7 times the recommended amount. The National Research Council of Canada has done extensive
research on the many environmental sources of fluorides and the multiple avenues by which they enter the human food chain.
Most packaged foods are processed with fluoridated water, and many fruits and vegetables contain fluorides in pesticide and
fertilizer residues. When fluoridation fIrst began, exposure to fluoride from sources other than fluoridated water was minimal, but today
that is not the case. People now receive fluoride from a whole host of sources, including pesticide residues, fluoridated dental
products, mechanically de-boned meat, fluoride air pollution, and processed foods & beverages prepared with fluoridated water (soda,
juice, beer, cereal, etc). It has now reached the point where most people receive the "optimal" 1 mg./day of fluoride without ever
drinking a glass of fluoridated water. Foods such as sardines, tea, lettuce, spinach, and others have particularly high fluoride con-
tents. If fluoride is ingested, even though a person is eating a nutritious diet and taking the best supplements in the world, all the good
nutrition is rendered almost completely ineffective, and development or advancement of degenerative disease will ensue. The
hannfu1 effects of fluoride have been known for over one hundred years. How much more evidence is needed before we, the victims,
stop this behavior modifIcation program, being literally forced down out throats? Some beer-drinking men consume over six liters
of fluoridated water a day from beer alone.
Fluoride in Nature
In any case, fluoride is unavoidable in the diet, since it is the thirteenth most abundant element and is extremely reactive, forming
many compounds available to the human body. Fluorine occurs in nature as calcium fluoride. Sodium fluoride is an industrial waste
product from the aluminum and phosphate fertilizer industries. Since the 1920s and 1930s, it has been sold as a potent roach and
rat killer. Sodium fluoride (NaF), is over five hundred times more soluble than calcium fluoride (CaF). It requires eighty times
more CaF 2 to kill a rat than N aF. Fluoridation critics never accepted the transfonnation of sodium fluoride from dangerous chemical to
benign cavity fighter.
Fluoride in Industry
The fIrst fluoride compound purposely put in the public water was sodium fluoride, a toxic by-product of the aluminum industry.
During World War II, as Alcoa accelerated production to meet the need for more warplanes, they produced more of this pollutant and
faced mounting damage claims. Eager to put a positive spin on fluoride, the U.S. Public Health Service-then under the conunand of
Treasury Secretary Andrew Mellon, a founder and major stockholder of Alcoa-sent a company employed dentist out West to investigate
certain towns where fluoride occurs naturally in the water. This dentist observed that the inhabitants had fewer cavities than average,
although they also had stained and eroded teeth. In 1939, a scientist funded by Alcoa solved the disposal problem when he proposed
adding fluoride to drinking water to reduce tooth decay. Then in the 1940s the unimpeded production of fluoride became a matter of
national security-fluoride was the key substance used to separate the uranium isotope to build the atomic bomb. Millions of tons
of fluoride were required. In 1944, according to declassifIed documents, an accident at a DuPont plant in New Jersey producing
fluoride for the Manhattan Project released large quantities into the atmosphere. Crops were poisoned, animals were crippled, and
people were sickened. The fluoride even etched windows in the local school. Scientists scrambled to gloss over the adverse effects in the
interests of the war effort. Defense contractors and the government needed to create public support for fluoride and protect themselves
from liability as well.
Critical Condition
220
Fluoride's Effects on Physiology
The average consumer of fluoridated water is usually not aware that sodium fluoride, or hydrofluosilicic acid, is rated as more toxic
than lead in chemistry indices and only slightly less toxic than arsenic. Fluoride is not an essential nutrient and, according to the
National Academy of Sciences, has never been shown to be necessary for human life. Drs. Roger Berry and Wilfred Trillwood at
Oxford United Hospitals, concluded that sodium fluoride kills human cells at 1/20 the strength of fluoridated drinking water.
Biochemical research has established that chemical poisons like fluoride form hydrogen bonds with protein amide groups together.
Thus, since DNA strands are connected by hydrogen bonds, fluoride will damage chromosomes. General Chemistry, McQuarrie and
Rock, Univ. Cal., 1984, discusses fluorine: "Because its electro-negativity is higher than that of any other element, fluorine occurs
with a positive oxidation state in any compound." Thus, fluorine is the most reactive element known to chemists, and its greatest
affinity is for calcium.
An article in Nature, The International Journal of Science, Jan. 15, 1987, let the cat out of the bag, further exposing the fluoridation
fiasco. It published university studies showing that water boiled in an aluminum utensil for 10 minutes acquired 0.2-ppm of
aluminum, which is a cause of Alzheimer's disease. If water is fluoridated at Ippm, in ten minutes, 200 ppm of Aluminum are
released-l,OOO times more aluminum! Fluorine may cause irreversible loss of potassium from the human red cell. Fluorine
increases excretion of iron-thus leading to anemia. Even at 10 mg. per liter, fluorine causes anemia, lymphocytosis and leukope-
nia. Blood levels of vitamin B12 are lowered. Damaging effects of fluorine may be found in the stomach, duodenum, small
intestines, liver, spleen, lungs, brain, pancreas, adrenals and thyroid.
Fluorine causes liver and muscle glycogen depletion as well as lactic acid accumulation, with increased blood sugar. Especially
serious damage occurs in the spinal cord, with neurological symptoms following. The pituitary gland takes up several times as much
fluorine as any other soft tissue, which is especially dangerous because the pituitary is the master gland of the endocrine system.
Fluorine may cause anoxia in newborns and shorten their survival. Fluoride inhibits neuromuscular activity. Human Biochem-
istry, Orten and Neuhause, 9th Ed., tells us, "Calcium is needed by all cells. It is required for physiologic balance."
A particular and important effect of the calcium ion is on nervous tissue. If the ionic calcium of the blood falls, the nervous system
becomes hyperirritable. "Calcium is the main structural mineral in the body. Osteoporosis is a result of calcium loss in the
skeleton. During the last trimester of pregnancy, between 200 and 300 mg. of calcium are deposited every day in the skeleton of the
fetus. Pregnant women are given synthetic prenatal vitamins with added fluoride. Anyone with a calcium deficiency can experi-
ence muscle spasms and convulsions. Also, the tissue levels of two poisonous metals, lead and cadmium, increase, and blood clotting
is adversely affected causing thrombosis and embolism. Oxygen deprivation in heart muscle is increased, with calcium deficiency
causing arhythmias.
Fluoride is a mutagen. Rats dosed with fluoride had a statistically significant increase in bone tumors. Fluoride-dosed rats had tumors
of the thyroid, oral cavity and rare tumors of the liver. Female infertility is associated with elevated levels of fluoride (>3 ppm). One
ppm. of fluoride in water facilitates the uptake of aluminum into the brain of rats, producing the type of brain tangles (amyloid deposits)
that are associated with Alzheimers disease and other types of dementia. Fluoridated water was associated with elevated levels oflead
in children's blood. Lead is associated with a variety of neurological problems, including reduced intelligence, aggression and hyperac-
tivity. Recently released reports by the New York State Department of Public Health and an expert panel appointed by the U.S. Surgeon
General dispute the American Dental Association's blanket claim that there are no adverse health effects from fluoridation. Fluoridation's
effectiveness may be less than earlier studies had indicated, according to a new study by the National Institute for Dental Research. The
largest study in the fifty years since fluoridation of U.S. water supplies began covers almost 40,000 children, aged 5 to 17, in 84 areas
across the country. The Journal of the American DentalAssociation, Vol. 23,1936, pp. 569-570, states. "There is an increasing amount
of evidence of the injurious effects of fluorine, especially the chronic intoxication resulting from the ingestion of minute amounts of
fluorine over long periods of time." It adds: "Toxicity data suggests that fluorine, lead and arsenic belong to the same group, as far
as the ability to cause some symptoms of toxicity in minute dosage is concerned." Small daily doses oflead or arsenic are believed to
be harmful. Fluoride is in the same category.
The U.S. Department of Agriculture in 1939 surveyed and reported on the effects of fluoride. Fluorine was shown to be the cause ofa
disfiguring dental disease known as mottled enamel or fluorosis. Fluorine interferes with the normal process of calcification of
teeth during the process of their formation, so that affected teeth, in addition to being unusually discolored and ugly in appearance,
are structurally weak and deteriorate early in life. For this reason, it is especially important that fluorine be avoided during the
period of tooth formation, from birth to the age of 12 years. Pediatricians report that over 30% of U.S. children have some degree
of noticeable dental fluorosis, or mottling of the teeth from exposure to excessively high levels of fluoride. There is an almost
infinite array of fluoride-based toothpastes, mouthwashes, dentifrices, tablets and vitamins on pharmacy shelves, many of which warn
(in very tiny print) that they should not be used if the fluoride concentration in drinking water exceeds 0.7-ppm. The sources of
fluorine intoxication are...(among others)...drinking water containing 1 ppm or more of fluorine." It is estimated that approximately
40 million Americans suffer from arthritis, the most common type being osteoarthritis. Fluoride stimulates abnormal bone develop-
ment. High dose fluoride treatment increases bone mass, but the newly formed bone is structurally unsound. Thus, instead of
reducing hip fracture, high doses of fluoride increase hip fracture.
221 fluoride
Kyphosis (skeletal fluorosis spinal curvature) was very prevalent among a community whose drinking water contained 7.4 ppm fluo-
ride. It's alarming to learn of these adverse effects of fluoride at 1.1 parts per million when the Environmental Protection Agency raised
the safe level for fluoride up to 4.0 parts per million. Who is being protected, the people or the fIrms that sell fluoride and the
manufacturers who produce fluoride as a by-product they can't get rid of? Yes, the fluoride producers cannot dispose of this waste
product unless all of us drink a little bit each day.
Thyroid Dysfunction
Up until the 1950s, European doctors used fluoride to reduce the activity of the thyroid gland for people suffering from overactive
thyroid (hyperthyroidism). The daily dose of fluoride which people are now receiving in fluoridated communities (1.6 to 6.6 mg/day)
actually exceeds the dose of fluoride found to depress the thyroid gland (2.3 to 4.5 mg/day). Hypothyroidism is currently one of the
most common medical problems in the u.S. Synthroid, the drug doctors prescribe to treat hypothyroidism, was the fourth most
prescribed drug in the U.S. in 2000. Symptoms of hypothyroidism include depression,jatigue, weight gain, muscle andjoint pains,
increased cholesterol levels and heart disease. From a recent University of York report, considered the "fInal word on fluoridation," it
was shown that symptoms described in the literature on fluoride's adverse health effects are identical to those observed in thyroid
dysfunction, and the condition known as dental fluorosis is a direct result of fluoride-induced iodine deficiency during the time of
enamel fonnation. It showed an increase in thyroid cancers in the fluoridated areas when compared to non-fluoridated areas. In China,
where entire villages are being relocated due to fluoride contamination, fluoride is being openly acknowledged as the cause of thyroid
cancer, Kaschin-Beck disease, and iodine deficiency. It has been established since the 1930s that the thyroid hormones control tooth
eruption. Fluoridation delays the eruption of teeth because of its hypothyroid effect. Dental fluorosis is a sign of thyroid dysfunc-
tion. Any anti-thyroid substance administered during the time of enamel fonnation will produce the effects seen in dental fluorosis.
Fluorides actually cause cavities.
There are countless papers-some of them found in the York Report--clearly state that the dental defects seen in fluorosis predispose
the teeth to caries. Hyperthyroidism, caused after iodine was added to public water supplies in the early 1920s, led to the use of
fluorides as anti-thyroid medication. Fluorides are the worst endocrine disruptor imaginable. What was once known as fluoride-
iodine antagonism can now be explained in detail by thousands of papers showing the fluoride power on G-protein activation. The
biochemical activity of fluoride mimics TSH (thyroid-stimulating-hormone) on G-protein activation-molecular on/off switches by
which all thyroid hormone activity is regulated. Three-quarters of the world's population is suffering from iodine deficiency in areas
which are identical to endemic fluorosis areas. Tooth decay is an epidemic in certain U.S. populations, whether or not they live in
fluoridated cities. Eighty percent of decay occurs in 25% of the population, most of them poor and minorities. Well-meaning, but
misguided dentists and hygienists are still pushing to get more of the U.S. fluoridated by the year 20 I 0, primarily because they believe
it will help poor children who suffer every year from needless dental pain that interferes with their eating, learning, and sleeping. One
problem is that dentists want more money to actually treat poor children. Well-nourished children who practice good dental hygiene
usually have less decay.
Pol itics and Suppression of Truth
When the fluoridation campaign began, it was determined that the optimal dose was I milligram per day, which translates to 1 part per
million (ppm) in the water supply (assuming an individual drinks 1 liter of water a day). Officials concurred that concentrations of2
ppm would not be acceptable because that would produce too many cases of dental fluorosis. But over the decades the maximum
allowable contaminant level (fluoride is classifIed as a contaminant by the EPA), inched up to 2.4 ppm. Then in 1985 when the EPA
increased the allowance to 4 ppm, something unprecedented occurred. The union representing employees at EPA headquarters in
Washington D.C.-some 1500 scientists, engineers and other professionals-revolted against their own management and fIled an amicus
curiae brief in court to support a lawsuit brought by the National Resources Defense Council against the EPA. As the brief stated, in
their professional opinion, allowable fluoride levels should have been reduced rather than raised. They alleged that evidence of adverse
effects was manipulated or ignored in order to arrive at a preordained political conclusion. Why was this allowed when the Federal
Register of November 14, 1985, stated that the Office of Drinking Water received 11 out of 12 studies confIrming the carcinogenicity
(cancer-causing potential) of fluoride during a comment period on the safe allowable levels of fluoride in drinking water? An article
titled "Chronic Fluorine Intoxication" in a 1943 issue of the Journal of the American Medical Association (JAMA) declared, "Fluo-
rides are general protoplasmic poisons, probably because of their capacity to modify the metabolism of cells by changing the
permeability of the cell membrane and by inhibiting certain enzyme systems."
Slander and smear campaigns have been commonplace in the frenzy of the fluoridation wars. The late Dr. John A. Yiamouyiannis, a
biochemist and former biochemical editor of the prestigious Journal of the Chemical Abstracts Service, the world's largest chemical
infonnation center, was removed from his post in 1969 when he began to publish articles critical of fluoridation. Since thousands
of articles routinely passed through his hands, many of which showed the negative effects of even miniscule amounts of fluoride on
enzyme function and the immune system, he began to question its use for human conswnption. He says he was told by his editor-in-
chief at the time, Dr. Russell Rowlett, that the Chemical Abstracts Service's federal funding ($1.1 million) was injeopardy and that if
Yiamouyiannis did not "cease and desist" in his attack of fluoridation, he would be fired. When Yiamouyiannis did not comply,
he was put on probation and ultimately forced to resign.
Critical Condition 222
He continued to be an outspoken critic of fluoridation until the time of his death, and wrote a paper saying the NIDR data show no
difference in decay rates between areas with fluoridated and unfluoridated water supplies. Research scientists have produced a
report saying the same data, showing 18% less decay in the fluoridated areas, a difference they call significant, but which is far below
the 40 to 60% reduction claimed by the ADA.
In the summer of 1988, an article in the 100,000-member American Chemical Society's trade journal Chemical and Engineering News,
examined the evidence on safety and effectiveness of fluoride and found many unresolved questions: "If the lifeblood of science is open
debate of evidence, scientific journals are the veins and arteries of the body scientific. Yet journal editors often have refused, for
political reasons, to publish information that raises questions about fluoridation." Submissions critical of fluoridation are re-
turned as "inappropriate for publication." The bulk of the social science literature on fluoridation is scientifically proven and
indeed scientifically unquestionable. The many studies that fall into this category make no examination of the scientific evi-
dence, but rely entirely on the endorsements of dental and medical authorities. Those promoting fluoridation have had almost
exclusive access to the resources of authority, even while claiming that scientific truth was their strongest plank and that opponents to
fluoridation are spurred by personal or political motivation. Therefore, opposition to fluoridation has always been treated as an
anomaly, to be explained away as the activity of fringe groups and "quacks."
The problem began in 1950 when key public health and professional bodies such as the United States Public Health Service and the
ADA came out supporting fluoridation; Almost overnight, the scientific issues were treated as closed. Fluoridation was considered
scientifically proven and, furthermore, criticisms of fluoridation were treated as political rather than scientific. Opponents were
classified as cranks rather than as rational critics. The climate is the same today. The combination of direct attacks on public
opponents of fluoridation, fears about loss of grants, and the general labeling of them as ignorant and misguided, combine to discourage
scientists from doing research or speaking out on the issues. The relative lack of open opposition, in turn, encourages a perception of
the fringe nature of critics. The pro- fluoridationists, through their control over dental and medical associations, their control over health
authorities, and their influence over editorial policy of journals and publishers, have exerted power to stop expression of anti-
fluoridation views by professionals. Nevertheless, not all critics of fluoridation have been effectively silenced.
Brian Dementi, toxicologist at the Virginia State Department of Health, discussed in his 1981 report, Fluoride in Drinking Water, the
many scientific papers showing fluoride to be both mutagenic and carcinogenic. Dementi contends that there has not been nearly
enough research done to warrant the claim that fluoridation is absolutely safe. He concludes, "The weight of the evidence from
studies on mutagenic effects of fluoride indicates that the substance is mutagenic (causes mutations) at low concentrations." He adds
that "there appears to be virtually no margin of safety for fluoride of the nature generally sought after or required for exposures to
toxic substances." Dementi's report includes a 1969 study that shows an average 48% reduction in the activity of the enzyme succinic
dehydrogenase in the kidneys of golden hamsters that drank water containing I-ppm sodium fluoride. He discusses a study done in
1975, in which monkeys exposed to fluoride at the I-ppm level for 18 months exhibited cytochemical changes in their kidneys.
A 1979 report stated, "The available evidence suggests that some patients with long-term renal failure are being affected by
drinking water with as little as 2-ppm fluoride." In Dementi's report, which was deleted from Virginia Health Department files
because it was "too old," Dementi chronicles the research onjluoride mutagenesis. He writes that in 1977 researchers observed
leucocytes in cows suffering fromjluorosis (a systemic poisoning caused by excessive fluoride which can lead to severe crippling). The
chromosomal aberration rate was over twice that of controls. The authors concluded, "These data suggest that inorganic fluor
compounds represent a potential genetic hazard to mammals." Similarly, another 1977 study by a team who added sodium fluoride
to drinking water at various concentrations and noticed the effects on mouse cells (bone marrow and spermatocytes), showed "statisti-
cally significant increases in chromosomal aberrations in both types of cells even at drinking water levels as low as I-ppm sodium
fluoride." Dementi states, "Any perturbation of this complex system must be viewed, a priori, as cause for concern."
The largest epidemiological study ever done on fluoridated water and carcinogenicity was conducted in 1977 by Yiamouyiannis and Dr.
Dean Burk, retired head of cytochemistry at the National Cancer Institute, in which they monitored cancer rates over a twenty-year
period in ten fluoridated American cities and ten non-fluoridated ones. After controlling for population differences in age, race and sex,
the researchers found an increased cancer mortality rate in persons over age forty-five in fluoridated cities. The study was
validated in three courts of law in the U.S. Further studies on DNA and DNA-repair systems have shown that fluoride inhibits or
interferes with the ability of DNA to repair itself, thus providing a clue as to how fluoride might exert a carcinogenic impact on
human cells. The New Jersey Department of Health had conducted a study and found the incidence of osteosarcoma to be significantly
higher in fluoridated communities versus non-fluoridated ones.
The New Jersey findings supported similar ones by larger national studies and by the National Toxicology Program. In a 1989 Medical
Tribune, a weekly publication for health professionals revealed that a panel appointed to study the issue in 1983 by C. Everett Koop,
then surgeon general, also raised questions about health effects. All mention of those issues was edited out of the panel's final
report. The omission of health concerns from the panel's final report is "shocking," charged Robert Carton, an EPA scientist and
president of the union that represents the agency's scientific staff. The immune system, the body's National Guard, so to speak, using
white blood cells, is disrupted and rendered much less effective from the effects of fluoride.
223
Fluoride
These white blood cells are calcium dependent. One consequence is hypersensitivity or "allergy" which will bring increased, more
severe or longer-lasting colds, flus and other ills. Since studies have revealed that fluoride, taken over a long period of time, breaks
down the immune system, some researchers feel that it is therefore conducive to AIDS. The Cape Cod News, August 20, 1986,
observed that the three longest fluoridated areas in the U.S.-New York, Washington D.C. and San Francisco-are the most prolific
with AIDS. Los Angeles and San Antonio, on the other hand, have never been fluoridated, and this plague has been miniscule in these
cities." Though these two cities have large homosexual communities, AIDS isn't as prevalent. Dean Burk, Chief Chemist Emeritus
at U.S. Cancer Institute, states, "In point offact, fluoride causes more cancer death, and causes it faster than any other chemical."
(Fluoride and Cancer," Congressional Record H7176-6, July 21, 1975, by Dean Burk and lA. Yiamouyiannis).
Several studies, including one carried on over a period of years at the University of Wisconsin and published in 1963, show that
fluoridated areas have an exceptional number of stillbirths. Scientists know that fluoride passes through the placenta. Dr. Ionel
Rapaport, University of Wisconsin, "carried out two studies showing that mongolism, a birth defect characterized by mental and
physical retardation, occurs more often in areas where there is a relatively high fluoride content in the water." According to the
Grand Rapids Press, July 28, 1955, following widely publicized fluoridation experiments in Grand Rapids, Michigan: "Deaths rose
sharply after four years of fluoridation which began in 1945. Deaths from cancer, heart disease, intracranial (brain) disease,
diabetes and hardening of the arteries increased 25 to 50 percent over those in Michigan as a whole." The J.A.M.A. for Feb. 10,
1961 states, "Fluorine also tends to accumulate in the bones, leading to hyper-calcification and brittleness. Ligaments and
tendons also become calcified. Serious symptoms may ensue, such as loss of mobility of joints, easy fracture and pressure on the
spinal cord. Other defects include baldness in young men, anemia and decreased blood clotting power. In women, painful men-
struation, lowered birth rate, high incidence of fracture, thyroid alterations and liver damage."
When one drinks sodium fluoride (NaF) in water, they excrete calcium fluoride (CaF2) in their urine. This calcium was stolen from
the body. In 1936, fifty percent of Americans were calciwn deficient. The AMAjournal of the same year reported that out of 4,000
persons checked in at a New York hospital, only two were not suffering from calciwn deficiency. The situation is worse today. Fluoride
in drinking or cooking water can disrupt the enzymatic activity of proteins. Dr. John Yiamouyiannis (Fluoride The Aging Factor,
Health Action Press, 1983) observed, "If the shape (or confonnation) of the protein is greatly distorted by fluoride, the body's immune
system will no longer be able to recognize the protein and will attempt to destroy it."
The summer 1959 issue of Clinical Physiology reported on page 96, a study done by experimental embryologist James D. Eberrt and
published in Scientific American March 1959. It relates: "...he found that sodium fluoride in low concentrations blocked, almost
completely, the regions destined to form heart muscle but left the developing brain and spinal cord intact." He correlated this with the
high incidence of ventricular septal defect, which was relatively uncommon before the 1950s, and fluoridation. Most of the
advanced Western European countries have banned fluoridation or given it up. The United States is the most fluoridated country,
and it has the highest tooth decay rate in the world! So is fluoridation the "biggest hoax ever inflicted on humanity" or a modem
miracle opposed by a small, ignorant minority?
Non-fluoridated toothpaste is available at your local health food store or co-op. Children and parents who are truly concerned about
their children can refuse fluoride "swish" programs in public schools. The Union of Scientists and professionals at EPA headquarters
has voted to oppose fluoridation and has called upon Congress to issue a "national moratoriwn" on the sixty year old policy. The
toxicity of fluoride is so great and the purported benefits associated with it are so small-if there is any at all-that requiring every man,
woman and child in America to ingest it criminal behavior on the part of the government.
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FLUORIDE FACTS
. . like lead even in minute doses,
FACT #1 FI~ is mor:e toXIC than . lead, and Just .tdr.n I.e. proc:Jucee 8bnOI'm8t
accumulates in and II dam&glr'lg to brainlminc1, $WeIOPfT18t1l of chi ,
behavior in animals and reduCeS fQ in hUmanS.
.. . f . ,---W'NI and la 'inked to increaeed cancer
FACT fI2 FluoridatiOn 18' cancer-caueang. ~...,.'" ..,....1. ~ . nee Advisor at the Office of
rates in rat8. mie81 and hUmans ~ Dr. William Marcu8. SeniOr $Cje 'de'8 a carcinogen
Drinking W.er. stated unequivocally in hie May Day MemO that fl\JOO I .
Fun text of the memo available 800-728-3833
FACT t3 Numerous studieI.includirig four ~ilh8d in the Journal of ~ ~ Medc8I
AsSOCiation 8inc;e. 1990, h8v8 b.I'\d that hip fractUre rates are sub.tantiaUyhigher in people
residing in flUOlid8fed communities .
FACT 14, Oentat fluorosis, the firet vilibleliQn of ftUoridepoisonlng, atrectsfrom" ,to 51'4 Of
th. children dri~ng fluoridated water and has subste'"ttially in~ ~ tne.'a.t. 40. years .
Dental fluoroeis Is more than cosmetic damage with psychological harm. It t8 .Isoindicative of
neurological impairment (Se4Hef. C 3 Dr. U)
FACT #5 Allot the recent IIII'ge-scale 8tUdles on fluoridation and tooth decay show that
fluoridation does not reduce tooth decay . Studies from New Zealand, Can8da, Europe. ~ the
US have confirmed no difference in decay rates for permanent teeth of residents of fluoridated
va. non...ft~ communities. '
FACT 18 FtuorkJe drops and tabllQ .... nQt approved by the U.S. Food and Drug
Admini8tr8tion,..'18f8'oreffective . Inge8tedftuoride has no d.,tedable effect on deCay rat...
Fluoridetabteta,and 'drops have been 8hoY.n to bein~ive in reducing tooth decay and to
cause skin ' . '
eruptions, game, di.e., headache, and waakness - which dieappeal' \\tIen fluoride use is
discontlrlued.. 88 well as dental fluorosis, a f*lT**lt clsftgurement.
FACT #7 ~Iuoride causes Iodine deftclency \\t\tch can result in hypothYfOidi8m and frequently in .
hyperthyroid."" '. Fluorides were prescribed to patients urer'N"1g trom hyperthyroidism a, anti..
thyroid medicatIOn prior to 1950. FluorIde~. may eXacerbate Iodine ~~. During
pregnancyi ~. iodine requlrementl ..at their Peak. 1he fetus is espttCially vulnerable. Even
a slightly under'fuActioning thyroid gln:t am result in loss of tQ in the nev.fxm.
The fOllOwing waming is tequJted an a(I fIuoritJated toothpaste by the FDA since April 011997
~ue to ~ lB. nu~ d calls to the PoIaon ConttoI Centets for children who bfJcame acutely
iH from in(JeSted Huoride. The", 1$ apptOKlm_teIy 1 milligram of tluodde In a pea sized drop of
toothpaste.
WARNING: Keep out or teaCh 01 Children under I.,..,. of age. In caee of aeel."
overdoR. ... prvfeuionIII..... or contact a polson control center IrnmedJattfy.
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REFERENCES:
Fact 11 NeuratOJddty and InteIIIgenQe ,
Rtts:
A) Chronic AdminiltrltlOn 01 Alumlnum-F1UOl1de or ~ to RIta
In Drtnklng water. AltenllonS in NtutOf\II8ftCI ~ 1IUgIIY,
JA Varner. KF Jensen. W HoNIlh. RL tss,eson.. 8rIin ReseW! Vol. 784. PP
2,..2881-
B) lnftuence of ~Ic ~ on membt8f\81p1ds In ,.. bnIIn. ZZ.
GullO. Y.N. Wang, K.Q. x..o. C.Y. 081, Y.H. Chen. J.L Uu, P. Sindelat end
G. OIIIner. Ne~ and TnlOIOgY 20 537-142 (1888).
C) Mullenix. P.J.. Del....... P.K.. 8chUnIor. A. and KefMn. W.J..
Neuroto)dc:lty of SodIum Auortde In Rats, N.~ end TnlOIOgY,
VOl. 17, No.2. pp. 1.117, 1.
(0) Efftd of tuoride on the phySIOlOgy of the pin'" gland. Luke, JA,
CMes R~ 21 204 (11M).
{
Chilchn:
E) U, X8: Zhi. ~L: Gao. RO Etfedl of tIUOttd. eJCPOI'R on lnteIlIgenOe In
children. Fluoride 28:4. pp. 1.102 (1885)
F) ZhIG, L8; liang, D; W WU Lu-U8ftg !tfed$ of. high tIuOfIde......
supply on chitdten'S intellgenC8. FJuoctde val. 28:4 pp. 11001121.
F.ct G Fluodde Is cancer oaustnu, CInC* p.omoting:
A) carcinogenesis, Vol. 8, pp. 22N-22M (1818)
8) SocIum Fluoftde: individuII...... tumor pathology tltM (r1D],
Batt... Memorial InItIIUte,FebrUary 23,1_
C) Sodium Fluortde: indlvidUlI anlrMI tumor petboIogY tIIlIt pNceJ.
BIttel. MemoMllmtltute, April 11. 1.
D) Dr. WIn MaftlUS, May C8y Memo dllCU_eeI In Lancet 31, pIIQ8 737 <1*>
E) RtWIew of AuortcIe: Ben'" andAllb, U. S. PubIIe Health Service,
pp. F1-F1 (1.1) ,
F) FluOf1de VOl. 21, pp. 13-88 (1882) Fluoride Is en eQUtvOCll ClIfdnOgen
G) A Brief Report on the AIIOdItiOn of Ofinkino water Flucwldltlon end
the InddenCe of Osteosarcoma III10fIg Young Males, New Jeqey DepMment of
Health, NcMNnber 1002 .
H) FIuofIde. the Aging Factor. ....... Ac:don PntIS, pp. 72-10 (1183>
Fact tl3 Hip hdutt inCI'8ase InUd to Wlter ftuotIdelewelS
A)JaeobS8n SJ, GaIdb8Ig J. ..... TP, Btody .lA, et II. RegiOn8I ~
In the Incidence of hip fnlCtwa: U.S. while women IQ8d 15 yua and '
older. ...... Vol. 284. pp. 5OQ.502 (1880)
B) Cooper e, \Nlckhem CAC, 8IIrkCl'DJR, and JacobNn SJ; Wetertluortdatlon
_nd hipfnldure pelt"'. .lAMA VOl. 2M. pp. 51s.5t~. 1.1
C) Danielson C, Lyon tL. Egger M. and Goodenough GK. ttp fnIClurw n
fluoridation in UWI'$ eldertf poputIItion. JAMA Vol. zee. pp.748-748
(1t12)
0) Joumel of the AmedCan ~ AIIoddon Vol. m, pp. n6-m (1_>
E) Jac:obIen SJ, GoIdtlerO.lt COoperC, and L.odCWaOd SA. The _odaUon
betWeen weter fktoridItiOrt Ind hiP fnIC&ure wnong white women end men Iged
e5 years and Older: A nIIon8I ecolOgIC stucty. Ann EpIdemioI t8t2:
2:$17-.
F) Sodra MFR, Cleft UK. J8nnIu8Ch UL. and web Re, A prospeotM study of
bone mit1et8I content and frac:lure In communIiH wIh diffellltl'ltilll ftUOltde
expoauIW. Am J EpIdemioI1.t; 133.e.eo
G) K..... C. FlUOltdelIn DctnkklO water. Paper pretented at the WorUhoP
ora 0IinIdnu 'Mar Fluoride intIuenCe on Hip Fr1IdurW.... Bone HNIIh.
April 10. 1881. BethUd8. Md.
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, H) May, OS and W\IIOn MG. Hip fracturelln rNtlon to wat.r ftUOf1detlon;
an ecoIagic analysis. PreMnt8d at the WorkShOP Of\ Oftnlllng WfJ.er FIuoftde
Influence 01' Hip FI'8CtUr&s 1M Bone Health. ApfiI1D, 1981, Beth... Md.
Fact t4 AuoridltiOn inC:tHaM deIUI tIuOfOSiS. NOTE: TNlr.dls no
longer being contested.
A) ScIenc:e Vol. 217. pp.2t-30 (1082)
8) Joumel of the Arneric:an I)enlal A8IOCiltiol1 Vol. 101. pp. 5&-" <1 Q84>
C) Journal of pubic HMIlh DentiStry Vol. .e, pp. 184-117 <,->
O} HeIIIth Eft'eds d Ingested FIuOrfd.. NaUOnaJ Rtselrd- COunCil. pege 37
(1i83)
E) Wall StnMt Journal Dee 21, 1098 some YOUng ChIdren Gel Too Much
Fluoride by ral'll P..ur-Pope
The Center for 0is8M8 control estHnatH 22'" of Amerkan c:tIIdrwn have
dental fIiIlO.- due to excM1I fluoride intake
Fad t5 Tooth deCaY II1d dental C8r'e eo:s15 are not reduced. There are no
bfOaC-bIsed blinded stucIft of anlm.. or human$ whICh have fNer found ·
signitlc8f'tt reduction in tooth decay nItes of pennanent teeth in
ftUOltd8ttd .....
Al Colcwhoun. J. Child Dent8I HNlth otfferenoes In New ZMtInd. CommunItY
Health Stuclln Vol. 11:2, pp. 85-90 (1.7)
B) Journal of the C8nedian Oet*I Auoc.iatlon. Vol. 53, pp. Je3.7e5 (1987)
C) Fluoride Vol. ~. pp. &U7 (1Q8O)
0) Calfornla Department fA"""" recorOs of actual DentICat cotto
Unpublished research forWrit of Mandat.. Citizens AQ'" FIuoftdIUon va.
Altomey Gen..... Den Lungren 1/1.
e) CoIqut\OUn. J. fnauence of aodII daU and ftUortdatIOn on child dental
health Community on 0181 EpIdemIoI Vol. 13, pp. 31..1. 1885
F) Gray. A8 FluotIdlllOn T'1rne fat . New sue UM J Canadian Dent. AsIOC.
Vol. 10, ,., .
G) YIImOUYlannls. J "NationallnstlUte Dtnt8I ReINI'Ch study IIhoWI no
relattonshlp betMeft fluoddaton and tooth decay rate- American laborltOr)
511_
Fact" Fluoride df'G1)5 and tablets Ire not FDA appwed or proven
.ft....
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A) Letter from Frank R. Fuzlri. ChIef, Presot1pUon Drug CornI*rJCI. Food
and Drug Mmlnl8trdon to New ~ Asaemblyman Jahn Kelty CJuM 8.
1_>
B) PreYenting Tooth Decay: R...... from. Four-V. NtIIIonII Study, Robert/
WoochJohn$On FoundItion. $peCMII Report number, pp. '8. (Feb. 1883>
C) community DentIItry MId 0ftII EpkIemioIOQY. Vol. 11. pp. 88-82 (1"1)
O} 1092 PhySiCli.... Desk Retecence. pege 2273.
FACT", FkIOIkte causes iodine detIdenCy which OIn ....In
hypothyroidilm and oocasiomdy in hyperthyroIdllm.
A) GIIeIi PM. Joy<<, G - "EtfeQ of fluoItne On ThyroId8IlodIfte .....boIln.ln
HypMh)roidIIm- J am EndOCfinot 18:1102.'110 (1858)
8) GtII8lU (1_> PIe 0.8 to 4.5 F. dIIIIy to ...... tu1fIfIng from
Graves' dII..... In tIlOte ItudIeI thew...~ iOdine
deCAlned from 1.1 to e.7 ugldl. b8SiO met8boIIo _ fram +3"" to +~.
C) M". W - "8eMndIUng der HypothyreClMn elnIChIle8IId1 die lIChwenIn
genulnen MOrbuS 8utdow mil fItuCX'" I<In WodMInIChr 18:'. 584 (1837)
0) MIy trMled 1.1S1 hypedhyrOld pIIiInts _etrecIWeIy_ wti18 ynrs
with etther sodium ftuoride or .~ne ('Panllnon").
E) GoIIItt.etYOn Mundy - "EIntIUII van Fluor unci Jod auf den SloftwecbMI.
insbeSOndere euf ell $d1iktdrQSe" Mln:h Med woc:MnIChttft 105:2M-247 (1813)
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.- ---....-~- .- -
...------
:l-.
. e50
30 ~..cs \fMlled \n 8lLClIS& of
F) GOr1IIZe."~ ~ == ::'lning tuoridt. ........- ~~e
p8l\efU _~......- ;"'.-.--lIhip (I- L,DW-lodine anY r'IU'.... '~-:= REpORT
G) Un f.-Fu ... . "The twPJuvn-" '" XinJ'llng" UNICEF Aro PROJECT
Envif'onl'Mnt to SubcllnIcIt Crelin~ ~ (t.1)
100 NeWSlett8r. v..... 7 Nun1t* . ZhenO X _ ~ e.tfec;1.S of
H) Zheo W. ZhU H, Yu Z. AoId I<. ~Thyroid and ftuOrOSAIln MIG8.
variOUS Iodine and FtuOf1ne I)u8e$ on
EndDCI' Regul 32(2):~70 (1181)
Want more scientific information about
fluoride? Find it on the net.
Http://vNIW.nofluoride.eom
Http://WWW.flUOridatiOn.com
Intemational SOCIetY for Fluoride Research
http://WWW.ftuortde-joUmal.com
cadVialon of Canada
http://WWW.cadvisiOn.comItluoride
Fluoride I,sues
http://wNW.sonic.netl-kryptoxlftuoride.htm
Dental. Fluorosis:
http://WWW.inter-vieW.net/-sherrell
lAOMT Risk Assessment for ingested ftuorkSe
h1tP:/Iwww.SaveTeeth.org
Zero Waste America
http://WYNI.zerowasteamerica.orglFluoride.htm
The Preventive Dental Health Association's
http://emporium.tumpike.netlPIPDHNftuoride/blunder.htm
Stop FluoridatiOn USA
http://home.cdsnet.netl-ftuoride
HISTORY OF FLUORIDE - IODINE ANTAGONISM
httf):/IWNW. bruha.oomIftuorldelhtrnllhistory_th.htm
SYMPTOMS/ASSOCIATIONS FLUORIDE POISONING - HYPOTHYROIDISM
http://vNIW.bruha.comIftuolidelhtrnVSymptoms_hypo_f.htm
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Fluoridation History
. Used in the United States for over 50
years
. January 25,1945
- Grand Rapids, Michigan
. By 1960, tooth decay rates had
decreased by 560/0 in fluoridated areas
,_' ,,'s ;/o,,!!! lillo/Unli! Cup\IIO'11I I')')') \1 \\ L:I'-k\ DD~ \11)11
",111\\11:11 Cl'lllCI Ic)! FIIIIII'ic!:ilioll 1\>/ s~ RC'l,II<It\IIIIO'IIt.C, !l"ll\ c:d
2
Status in the United States
. 162 million U.S. residents benefit
trom fluoridation*
. Pinellas County has the largest water
system in Florida and the Eastern US
without water fluoridation
*U5 Centers for Disease Control & Pre~ention Division of
Oml Hea/th - Fluoridation Census 2000
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