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by Dr. J. William Hirzy
Senior Vice President, NTEU Chapter 280
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. For a history of how drinking
water fluoridation began, see "Fluoride, Teeth
and the Atomic Bomb", by investigative reporters
Joel Griffiths and Chris Bryson.
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
0.01mg/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).
* Read an interview with Dr. Hirzy
concerning the NTP's Fluoride Cancer study
* Read Dr. Hirzy's June 2000 Testimony to the US
Senate
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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>
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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. On-line at http//:www.rvi.net/~fluoride/naep.htm
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)
http://www.fluoridealert.org/hp-epa.htm
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