May 1, 1999
WHY EPA'S HEADQUARTERS UNION OF
SCIENTISTS OPPOSES FLUORIDATION
The following documents why our union, formerly National
Federation of Federal Employees Local 2050 and since April 1998 Chapter 280 of
the National Treasury Employees Union, took the stand it did opposing
fluoridation of drinking water supplies. Our union is comprised of and
represents the approximately 1500 scientists, lawyers, engineers and other
professional employees at EPA Headquarters here in Washington, D.C.
The union first became interested in this issue rather by
accident. Like most Americans, including many physicians and dentists, most of
our members had thought that fluoride's only effects were beneficial -
reductions in tooth decay, etc. We too believed assurances of safety and
effectiveness of water fluoridation.
Then, as EPA was engaged in revising its drinking water
standard for fluoride in 1985, an employee came to the union with a complaint:
he said he was being forced to write into the regulation a statement to the
effect that EPA thought it was alright for children to have "funky"
teeth. It was OK, EPA said, because it considered that condition to be only a
cosmetic effect, not an adverse health effect. The reason for this EPA position
was that it was under political pressure to set its health-based standard for
fluoride at 4 mg/liter. At that level, EPA knew that a significant number of
children develop moderate to severe dental fluorosis, but since it had deemed
the effect as only cosmetic, EPA didn't have to set its health-based standard
at a lower level to prevent it.
We tried to settle this ethics issue quietly, within the
family, but EPA was unable or unwilling to resist external political pressure,
and we took the fight public with a union amicus curiae brief in a lawsuit
filed against EPA by a public interest group. The union has published on this
initial involvement period in detail.1
Since then our opposition to drinking water fluoridation has
grown, based on the scientific literature documenting the increasingly
out-of-control exposures to fluoride, the lack of benefit to dental health from
ingestion of fluoride and the hazards to human health from such ingestion.
These hazards include acute toxic hazard, such as to people with impaired
kidney function, as well as chronic toxic hazards of gene mutations, cancer,
reproductive effects, neurotoxicity, bone pathology and dental fluorosis.
First, a review of recent neurotoxicity research results.
In 1995, Mullenix and co-workers2 showed that rats given
fluoride in drinking water at levels that give rise to plasma fluoride
concentrations in the range seen in humans suffer neurotoxic effects that vary
according to when the rats were given the fluoride - as adult animals, as young
animals, or through the placenta before birth. Those exposed before birth were
born hyperactive and remained so throughout their lives. Those exposed as young
or adult animals displayed depressed activity. Then in 1998, Guan and
co-workers3 gave doses similar to those used by the Mullenix research group to
try to understand the mechanism(s) underlying the effects seen by the Mullenix
group. Guan's group found that several key chemicals in the brain - those that
form the membrane of brain cells - were substantially depleted in rats given
fluoride, as compared to those who did not get fluoride.
Another 1998 publication by Varner, Jensen and others4
reported on the brain- and kidney damaging effects in rats that were given
fluoride in drinking water at the same level deemed "optimal" by
pro-fluoridation groups, namely 1 part per million (1 ppm). Even more
pronounced damage was seen in animals that got the fluoride in conjunction with
aluminum. These results are especially disturbing because of the low dose level
of fluoride that shows the toxic effect in rats - rats are more resistant to
fluoride than humans. This latter statement is based on Mullenix's finding that
it takes substantially more fluoride in the drinking water of rats than of
humans to reach the same fluoride level in plasma. It is the level in plasma
that determines how much fluoride is "seen" by particular tissues in
the body. So when rats get 1 ppm in drinking water, their brains and kidneys
are exposed to much less fluoride than humans getting 1 ppm, yet they are
experiencing toxic effects. Thus we are compelled to consider the likelihood
that humans are experiencing damage to their brains and kidneys at the
"optimal" level of 1 ppm.
In support of this concern are results from two epidemiology
studies from China5, 6 that show decreases in I.Q. in children who get more
fluoride than the control groups of children in each study. These decreases are
about 5 to 10 I.Q. points in children aged 8 to 13 years.
Another troubling brain effect has recently surfaced:
fluoride's interference with the function of the brain's pineal gland. The
pineal gland produces melatonin which, among other roles, mediates the body's
internal clock, doing such things as governing the onset of puberty. Jennifer
Luke7 has shown that fluoride accumulates in the pineal gland and inhibits its
production of melatonin. She showed in test animals that this inhibition causes
an earlier onset of sexual maturity, an effect reported in humans as well in
1956, as part of the Kingston/Newburgh study, which is discussed below. In
fluoridated Newburgh, young girls experienced earlier onset of menstruation (on
average, by six months) than girls in non-fluoridated Kingston.8
From a risk assessment perspective, all these brain effect
data are particularly compelling and disturbing because they are convergent.
We looked at the cancer data with alarm as well. There are
epidemiology studies that are convergent with whole-animal and single-cell
studies (dealing with the cancer hazard), just as the neurotoxicity research
just mentioned all points in the same direction. EPA fired the Office of
Drinking Water's chief toxicologist, Dr. William Marcus, who also was our local
union's treasurer at the time, for refusing to remain silent on the cancer risk
issue.9 The judge who heard the lawsuit he brought against EPA over the firing
made that finding - that EPA fired him over his fluoride work and not for the
phony reason put forward by EPA management at his dismissal. Dr. Marcus won his
lawsuit and is again at work at EPA. Documentation is available on request.
The type of cancer of particular concern with fluoride,
although not the only type, is osteosarcoma, especially in males. The National
Toxicology Program conducted a two-year study10 in which rats and mice were
given sodium fluoride in drinking water. The positive result of that study (in
which malignancies in tissues other than bone were also observed), particularly
in male rats, is convergent with a host of data from tests showing fluoride's
ability to cause mutations (a principal "trigger" mechanism for
inducing a cell to become cancerous) e.g.11a, b, c, d and data showing
increases in osteosarcomas in young men in New Jersey12 , Washington and Iowa13
based on their drinking fluoridated water. It was his analysis, repeated
statements about all these and other incriminating cancer data, and his requests
for an independent, unbiased evaluation of them that got Dr. Marcus fired.
Bone pathology other than cancer is a concern as well. An
excellent review of this issue was published by Diesendorf et al. in 1997.14
Five epidemiology studies have shown a higher rate of hip fractures in
fluoridated vs. non-fluoridated communities.15a, b, c, d, e. Crippling skeletal
fluorosis was the endpoint used by EPA to set its primary drinking water
standard in 1986, and the ethical deficiencies in that standard setting process
prompted our union to join the Natural Resources Defense Council in opposing
the standard in court, as mentioned above.
Regarding the effectiveness of fluoride in reducing dental
cavities, there has not been any double-blind study of fluoride's effectiveness
as a caries preventative. There have been many, many small scale, selective
publications on this issue that proponents cite to justify fluoridation, but
the largest and most comprehensive study, one done by dentists trained by the
National Institute of Dental Research, on over 39,000 school children aged 5-17
years, shows no significant differences (in terms of decayed, missing and
filled teeth) among caries incidences in fluoridated, non-fluoridated and
partially fluoridated communities.16 The latest publication17 on the fifty-year
fluoridation experiment in two New York cities, Newburgh and Kingston, shows
the same thing. The only significant difference in dental health between the
two communities as a whole is that fluoridated Newburgh, N.Y. shows about twice
the incidence of dental fluorosis (the first, visible sign of fluoride chronic
toxicity) as seen in non-fluoridated Kingston.
John Colquhoun's publication on this point of efficacy is
especially important.18 Dr. Colquhoun was Principal Dental Officer for
Auckland, the largest city in New Zealand, and a staunch supporter of
fluoridation - until he was given the task of looking at the world-wide data on
fluoridation's effectiveness in preventing cavities. The paper is titled,
"Why I changed My Mind About Water Fluoridation." In it Colquhoun
provides details on how data were manipulated to support fluoridation in
English speaking countries, especially the U.S. and New Zealand. This paper
explains why an ethical public health professional was compelled to do a 180
degree turn on fluoridation.
Further on the point of the tide turning against drinking
water fluoridation, statements are now coming from other dentists in the
pro-fluoride camp who are starting to warn that topical fluoride (e.g. fluoride
in tooth paste) is the only significantly beneficial way in which that
substance affects dental health.19, 20, 21 However, if the concentrations of
fluoride in the oral cavity are sufficient to inhibit bacterial enzymes and
cause other bacteriostatic effects, then those concentrations are also capable
of producing adverse effects in mammalian tissue, which likewise relies on
enzyme systems. This statement is based not only on common sense, but also on
results of mutation studies which show that fluoride can cause gene mutations
in mammalian and lower order tissues at fluoride concentrations estimated to be
present in the mouth from fluoridated tooth paste.22 Further, there were tumors
of the oral cavity seen in the NTP cancer study mentioned above, further
strengthening concern over the toxicity of topically applied fluoride.
In any event, a person can choose whether to use fluoridated
tooth paste or not (although finding non-fluoridated kinds is getting harder
and harder), but one cannot avoid fluoride when it is put into the public water
supplies.
So, in addition to our concern over the toxicity of
fluoride, we note the uncontrolled - and apparently uncontrollable - exposures
to fluoride that are occurring nationwide via drinking water, processed foods,
fluoride pesticide residues and dental care products. A recent report in the
lay media23 that, according to the Centers for Disease Control, at least 22
percent of America's children now have dental fluorosis, is just one indication
of this uncontrolled, excess exposure. The finding of nearly 12 percent
incidence of dental fluorosis among children in un-fluoridated Kingston New
York17 is another. For governmental and other organizations to continue to push
for more exposure in the face of current levels of over-exposure coupled with
an increasing crescendo of adverse toxicity findings is irrational and
irresponsible at best.
Thus, we took the stand that a policy which makes the public
water supply a vehicle for disseminating this toxic and prophylactically
useless (via ingestion, at any rate) substance is wrong.
We have also taken a direct step to protect the employees we
represent from the risks of drinking fluoridated water. We applied EPA's risk
control methodology, the Reference Dose, to the recent neurotoxicity data. The
Reference Dose is the daily dose, expressed in milligrams of chemical per
kilogram of body weight, that a person can receive over the long term with
reasonable assurance of safety from adverse effects. Application of this
methodology to the Varner et al.4 data leads to a Reference Dose for fluoride
of 0.000007 mg/kg-day. Persons who drink about one quart of fluoridated water
from the public drinking water supply of the District of Columbia while at work
receive about 0.01mg/kg-day from that source alone. This amount of fluoride is
more than 100 times the Reference Dose. On the basis of these results the union
filed a grievance, asking that EPA provide un-fluoridated drinking water to its
employees.
The implication for the general public of these calculations
is clear. Recent, peer-reviewed toxicity data, when applied to EPA's standard
method for controlling risks from toxic chemicals, require an immediate halt to
the use of the nation's drinking water reservoirs as disposal sites for the
toxic waste of the phosphate fertilizer industry.24
This document was prepared on behalf of the National
Treasury Employees Union Chapter 280 by Chapter Senior Vice-President J.
William Hirzy, Ph.D. For more information please call Dr. Hirzy at
202-260-4683. His E-mail address is hirzy.john@epa.gov
END NOTE LITERATURE CITATIONS
1. Applying the NAEP code of ethics to the Environmental
Protection Agency and the fluoride in drinking water standard. Carton, R.J. and
Hirzy, J.W. Proceedings of the 23rd Ann. Conf. of the National Association of
Environmental Professionals. 20-24 June, 1998. GEN 51-61.
2. Neurotoxicity of sodium fluoride in rats. Mullenix, P.J.,
Denbesten, P.K., Schunior, A. and Kernan, W.J. Neurotoxicol. Teratol. 17
169-177 (1995)
3. 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, Neurotoxicology and Teratology 20 537-542 (1998).
4. 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,
R.L. Brain Research 784 284-298 (1998).
5. Effect of high fluoride water supply on children's
intelligence. Zhao, L.B., Liang, G.H., Zhang, D.N., and Wu, X.R. Fluoride 29
190-192 (1996)
6. Effect of fluoride exposure on intelligence in children.
Li, X.S., Zhi, J.L., and Gao, R.O. Fluoride 28 (1995).
7. Effect of fluoride on the physiology of the pineal gland.
Luke, J.A. Caries Research 28 204 (1994).
8. 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).
9. Memorandum dated May 1, 1990. 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 ODW.
10. Toxicology and carcinogenesis studies of sodium fluoride
in F344/N rats and B6C3F1 mice. NTP Report No. 393 (1991).
11a. Chromosome aberrations, sister chromatid exchanges,
unscheduled DNA synthesis and morphological neoplastic transformation in Syrian
hamster embryo cells. Tsutsui et al. Cancer Research 44 938-941 (1984).
11b. Cytotoxicity, chromosome aberrations and unscheduled
DNA synthesis in cultured human diploid fibroblasts. Tsutsui et al. Mutation
Research 139 193-198 (1984).
11c. Positive mouse lymphoma assay with and without S-9
activation; positive sister chromatid exchange in Chinese hamster ovary cells
with and without S-9 activation; positive chromosome aberration without S-9
activation. Toxicology and carcinogenesis studies of sodium fluoride in F344/N
rats and B6C3F1 mice. NTP Report No. 393 (1991).
11d. An increase in the number of Down's syndrome babies
born to younger mothers in cities following fluoridation. Science and Public
Policy 12 36-46 (1985).
12. A brief report on the association of drinking water
fluoridation and the incidence of osteosarcoma among young males. Cohn, P.D.
New Jersey Department of Health (1992).
13. Surveillance, epidemiology and end results (SEER)
program. National Cancer Institute in Review of fluoride benefits and risks.
Department of Health and Human Services. F1-F7 (1991).
14. New evidence on fluoridation. Diesendorf, M., Colquhoun,
J., Spittle, B.J., Everingham, D.N., and Clutterbuck, F.W. Australian and New
Zealand J. Public Health. 21 187-190 (1997).
15a. Regional variation in the incidence of hip fracture:
U.S. white women aged 65 years and older. Jacobsen, S.J., Goldberg, J., Miles,
,T.P. et al. JAMA 264 500-502 (1990)
15b. Hip fracture and fluoridation in Utah's elderly
population. Danielson, C., Lyon, J.L., Egger, M., and Goodenough, G.K. JAMA 268
746-748 (1992).
15c. The association between water fluoridation and hip
fracture among white women and men aged 65 years and older: a national
ecological study. Jacobsen, S.J., Goldberg, J., Cooper, C. and Lockwood, S.A.
Ann. Epidemiol.2 617-626 (1992).
15d. Fluorine concentration is drinking water and fractures
in the elderly [letter]. Jacqmin-Gadda, H., Commenges, D. and Dartigues, J.F.
JAMA 273 775-776 (1995).
15e. Water fluoridation and hip fracture [letter]. Cooper,
C., Wickham, C.A.C., Barker, D.J.R. and Jacobson, S.J. JAMA 266 513-514 (1991).
16. Water fluoridation and tooth decay: Results from the
1986-1987 national survey of U.S. school children. Yiamouyiannis, J. Fluoride
23 55-67 (1990).
17. Recommendations for fluoride use in children. Kumar,
J.V. and Green, E.L. New York State Dent. J. (1998) 40-47.
18. Why I changed my mind about water fluoridation.
Colquhoun, J. Perspectives in Biol. And Medicine 41 29-44 (1997).
19. A re-examination of the pre-eruptive and post-eruptive
mechanism of the anti-caries effects of fluoride: is there any anti-caries
benefit from swallowing fluoride? Limeback, H. Community Dent. Oral Epidemiol.
27 62-71 (1999).
20. Fluoride supplements for young children: an analysis of
the literature focussing on benefits and risks. Riordan, P.J. Community Dent.
Oral Epidemiol. 27 72-83 (1999).
21. Prevention and reversal of dental caries: role of low
level fluoride. Featherstone, J.D. Community Dent. Oral Epidemiol. 27 31-40
(1999).
22. Appendix H. Review of fluoride benefits and risks.
Department of Health and Human Services. H1-H6 (1991).
23. Some young children get too much fluoride. Parker-Pope,
T. Wall Street Journal Dec. 21, 1998.
24. 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.
OTHER CITATIONS (This short list does not include the entire
literature on fluoride effects)
a. Exposure to high fluoride concentrations in drinking
water is associated with decreased birth rates. Freni, S.C. J. Toxicol.
Environ. Health 42 109-121 (1994)
b. Ameliorative effects of reduced food-borne fluoride on
reproduction in silver foxes. Eckerlin, R.H., Maylin, G.A., Krook, L., and
Carmichael, D.T. Cornell Vet. 78 75-91 (1988).
c. Milk production of cows fed fluoride contaminated
commercial feed. Eckerlin, R.H., Maylin, G.A., and Krook, L. Cornell Vet. 76
403-404 (1986).
d. Maternal-fetal transfer of fluoride in pregnant women.
Calders, R., Chavine, J., Fermanian, J., Tortrat, D., and Laurent, A.M. Biol.
Neonate 54 263-269 (1988).
e. Effects of fluoride on screech owl reproduction:
teratological evaluation, growth, and blood chemistry in hatchlings. Hoffman,
D.J., Pattee, O.H., and Wiemeyer, S.N. Toxicol. Lett. 26 19-24 (1985).
f. Fluoride intoxication in dairy calves. Maylin, G.A.,
Eckerlin, R.H., and Krook, L. Cornell Vet. 77 84-98 (1987).
g. Fluoride inhibition of protein synthesis. Holland, R.I.
Cell Biol. Int. Rep. 3 701-705 (1979).
h. An unexpectedly strong hydrogen bond: ab initio
calculations and spectroscopic studies of amide-fluoride systems. Emsley, J.,
Jones, D.J., Miller, J.M., Overill, R.E. and Waddilove, R.A. J. Am. Chem. Soc.
103 24-28 (1981).
i. The effect of sodium fluoride on the growth and
differentiation of human fetal osteoblasts. Song, X.D., Zhang, W.Z., Li, L.Y.,
Pang, Z.L., and Tan, Y.B. Fluoride 21 149-158 (1988).
j. Modulation of phosphoinositide hydrolysis by NaF and
aluminum in rat cortical slices. Jope, R.S. J. Neurochem. 51 1731-1736 (1988).
k. The crystal structure of fluoride-inhibited cytochrome c
peroxidase. Edwards, S.L., Poulos, T.L., Kraut, J. J. Biol. Chem. 259
12984-12988 (1984).
l. Intracellular fluoride alters the kinetic properties of
calcium currents facilitating the investigation of synaptic events in
hippocampal neurons. Kay, A.R., Miles, R., and Wong, R.K.S. J. Neurosci. 6
2915-2920 (1986).
m. Fluoride intoxication: a clinical-hygienic study with a
review of the literature and some experimental investigations. Roholm, K. H.K.
Lewis Ltd (London) (1937).
n. Toxin-induced blood vessel inclusions caused by the
chronic administration of aluminum and sodium fluoride and their implications
for dementia. Isaacson, R.L., Varner, J.A., and Jensen, K. F. Ann. N.Y. Acad.
Sci. 825 152-166 (1997).
o. Allergy and hypersensitivity to fluoride. Spittle, B.
Fluoride 26 267-273 (1993)
Up
Home Fluoride:
Protected Pollutant or Panacea?
Are the claimed benefits of ingesting fluoride over-rated
and the risks to our health and eco-system under-reported? Scientific
Abstracts
Bones | Calgary | Cavities | Fertility | Cancer | Health
risks | Neurological | Dental Fluorosis and Pictures
ISFR | Ethics | Tributes | Fraud | Authors | Deaths | Quotes
| Environment | Skeletal Fluorosis | Definitions
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