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-workers \2
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-workers \3 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 others \4 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 China\5,\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 Luke\7 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 study \10 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 Jersey
\12 , Washington and Iowa \13 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
publication \17 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 media\23, 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 York\17 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 0.001mg/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. Yiamouyannis, 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 1-16 (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)
For a history of how drinking water fluoridation began, see "Fluoride,
Teeth and the Atomic Bomb", by investigative reporters Joel
Griffiths and Chris Bryson, available on-line at
http://www.rvi.net/~fluoride
