Dr. Richard Sauerheber
(B.A. Biology, Ph.D. Chemistry, University of California, San Diego, CA)
Palomar College, 1140 W. Mission Rd., San Marcos, CA 92069
Email: firstname.lastname@example.org Phone: 760-744-2547
June 6, 2012
Response in Support of
Human Toxicity, Environmental Impact, and Legal Implications of Water Fluoridation
Declan Waugh, Enviro Management Services, 2012
First, it must be made clear that ingested fluoride ion does not decrease dental caries systemically. This has been amply demonstrated in the dental literature and the scientific literature
Hellwig and Lennon, Caries Research 38: 258, 2004; http://www.fluoride-class-action.com/wp-content/uploads/caries-research-systemic-versus-topical-fluoride.pdf; Zero, 1992; Rolla and Ekstrand, 1996; Featherstone,1999; Limeback,1999; Clarkson and McLoughlin, 2000 as reviewed in the 2006 National Research Council Report, http://www.nap.edu/openbook.php?record_id=11571&page=16
and in conclusions published by the U.S. Centers for Disease Control that systemic fluoride does not benefit teeth (Morbidity and Mortality Weekly Report, August, 2001). Moreover, not only does ingested fluoride not decrease caries, ingested fluoride cannot decrease caries, even topically, because fluoride that filters into saliva from the bloodstream (which averages 0.21 ppm in residents of 1 ppm fluoride water cities) is only approximately 0.02 ppm (NRC, 2006, p. 71), unable to influence teeth surfaces as can fluoride in pastes (1,500 ppm) and highly concentrated gels. This demonstrates that the process referred to was ‘water fluoridation’ to treat dental caries by taking fluoride ion internally through ingestion in humans squanders public funds.
Although many presume otherwise, the EPA does not regulate or promote the infusion of fluoride compounds into public water supplies (NRC, 2006, p.18). Instead, fluoride is correctly regarded by EPA as a contaminant in water that must be kept below estimated levels to help minimize the known pathologic effects of long-term ingestion of fluoride that is a listed toxic when not accompanied with calcium. The FDA correctly ruled in 1963 that fluoride is not a mineral nutrient and when added into water is an uncontrolled use of an unapproved drug. Synthetic industrial fluoride compounds lacking calcium have an LD50 in mammals of 125 mg/kg single oral dose (Merck Index, Rahway, N.J., 1976), while natural calcium fluoride is not a listed toxic, where calcium minimizes assimilation of fluoride from the GI tract and is the antidote to fluoride poisoning.
Ingested fluoride is now known to incorporate into the bloodstream by virtue of first forming the membrane lipid soluble agent hydrofluoric acid HF in the acidic stomach. HF is freely permeable across cells membranes, while the fluoride charged ion is not. After assimilation, at the alkaline pH of blood and interstitial fluid, HF largely re-dissociates to the free fluoride ion. The trace levels of HF that remain in blood can be calculated with the Henderson Hasselbach equation for an aqueous solution buffered at physiologic pH 7.4, an average blood fluoride level of 0.21 ppm, and the dissociation constant for the weak acid HF of 6 x 10-4, and is approximately 0.2 ppb HF. Although 1,000 times less concentrated than the free fluoride ion in blood, HF, being 1 million times more lipid soluble than fluoride ion, is the form by which fluoride enters intracellular fluid (Buzalaf, MA; Whitford, GM, Fluoride metabolism, Monographs in oral science 2011;22:20-36).
Fluoride indeed is known from biochemical measurements to incorporate into brain and other cells in man and animals and to alter intracellular structural components. In brain cells this was a chief concern to the NRC committee because brain functional alterations can be subtle and can go undetectable for long periods and are difficult to assess by experimental measurement. In fact, human controlled clinical drug testing trials, required by the Food Drug and Cosmetic Act for any chemical proposed to be used as an ingestible to be taken internally the US., do not evaluate brain impairment in data submitted to the FDA for drug approval. It is necessary thus to state clearly that there are no ‘robust’ studies on any ingestible fluoride compound in humans to this date.
We now have data unknown at the time water ‘fluoridation’ began. Fluoride incorporation into bone is permanent and irreversible, accumulating during lifetime consumption typically to levels that weaken bone, rendering bone more subject to fracture, where bone concentrations of 4,000 mg/kg lifetime in a 1 ppm treated city are more subject to fracture than at lower fluoride intake levels. Most disturbing, published only months ago at the Veterans Administration Health Care Center, Los Angeles, CA, PET scan direct observations proved that systemic fluoride incorporates into atherosclerotic plaque in coronary arteries of cardiovascular disease patients, the leading lethal disease entity in the U.S. (Yuxin, et.al., Nuclear Medicine Communications, January, 2012).
The NRC Report did not have the objective of evaluating water fluoridation per se and did not have the original intent of examining data published on safety and effectiveness, or lack thereof, for water fluoridation levels at the widely used concentration of 1 ppm compared to lower levels. However, much data published since 1993 were reviewed relevant to fluoridation, at 1 ppm as controls to compare effects found at 2–4 ppm and higher. The committee intention was to evaluate whether the EPA primary and secondary Maximum Contaminant Level interim assignments from 1984 were achieving their stated purpose in the U.S. NRC concluded unanimously, yes unanimously, that the MCL and SMCL must be lowered because current allowed levels are not protective of human health. This is because of the widely and conclusively documented adverse pathology in those exposed to 2 and 4 ppm fluoride in water, compared to lower levels (NRC, 2006, p. 6).
In full agreement with this consensus, the U.S. Health and Human Services recommended January, 2012 that water fluoride levels not exceed 0.7 ppm fluoride as a temporary measure until official regulations can be established. The motivation for this change is the glaring fact that as of 2004, 41% of U.S. children aged 12-15 have permanent abnormal tooth fluorosis, with its enamel hypoplasia that is difficult and expensive to restore.
It is appropriate now to grade the effectiveness and usefulness of the EPA regulations imposed in 1984 on the fluoride contaminant in drinking water. The MCL was set at 4 ppm to help minimize development of severe toxic effects in those exposed lifetime. The idea was to minimize severe bone fluorosis, a bizarre painful condition that causes a person to be unable to walk. The NRC reported that severe debilitating skeletal fluorosis cases in the U.S. are extremely rare and this particular adverse pathologic effect caused by fluoride was basically achieved. However, we now know that 4 ppm fluoride in water lifetime leads to 10,000-12,000 mg/kg fluoride levels in bone, severely weakening bone making bone more subject to fracture compared to consumption of water at lower fluoride levels. Because the U.S. now has 1/3 million cases of hip fractures in the U.S. elderly, it is appropriate that the NRC Committee request the MCL be lowered.
The failing grade for the MCL is also given due to the fact that severe dental fluorosis occurs in significant abundance in children exposed to 4 ppm fluoride in water. The severe form of dental fluorosis is a permanent toxic poisoning effect on the damaged teeth. The MCL, at the time of the NRC review, appeared to prevent the incidence in excess of the intended 15% amount, but this now may be a too low estimate of this condition in the U.S. Also, moderate fluorosis afflicts an enormous number of U.S. children currently, and it is necessary to understand that the NRC reviewed studies proving that this condition is not merely cosmetic, but harmful. Moderate fluorosis on front teeth is detrimental to one’s appearance and can affect one’s overall sense of well-being and likelihood of employability and is now known to be associated with systemic pathology. 50% of all ingested fluoride is retained permanently in bone lifetime, independent of water concentration consumed, and there is no concentration low enough at which tooth fluorosis from systemic fluoride can exist without concurrent massive accumulation of fluoride in bone. The vastly increased incidence of ‘moderate’ fluorosis with enamel hypoplasia (estimated in 2006 at 15% even at 2 ppm and far higher at 4 ppm) is itself an effect that should be restricted according to the original intent of the EPA MCL under auspices of the Safe Drinking Water Act.
Detailed well-controlled human clinical trials proved an elevated risk of nonvertebral fractures after only 4 years of exposure to drinking water with the MCL fluoride level of 4 ppm. Also there was consensus that fluoride can weaken bone and increase fracture risk in animals and man. The effect of fluoride on bone density observed in animal studies is fully consistent with the human evidence (p. 7). Thus the MCLG, which technically was intended to prevent any significant toxic effect in the exposed population, was never adequately low. The current MCL does not protect U.S. citizens from the substantial occurrence of fluoride-induced bone weakening and fracture or from permanent abnormal tooth fluorosis with its enamel hypoplasia, where the function of normal (non-fluoridated enamel hydroxyapetite) is to protect underlying dentin and pulp from cavitation and infection.
The SMCL was set by EPA decades ago at 2 ppm for the purpose of minimizing, not just sever toxicity, but any significant adverse effect on human health. In regards to the fluoride contaminant, a provisional effect chosen for this purpose was severe dental enamel fluorosis, to be maintained under 15% of the exposed population. Although this might have been achieved if fluoride exposures were limited to water intake alone, or might have been successful for healthy persons, this SMCL has failed. Fluoride in the U.S. from sources other than water account for 30% of total fluoride found in blood and add to the burden from fluoride in water, which is the major but not the only source. Also, many persons consume far more water than the National average, those who work outdoors in heavy labor such as field work, and athletes, and those with diabetes who consume twice as much water as normal. As a result, existing fluoride water levels have led to the endemic of enamel fluorosis of all forms that we now have in U.S. children. And as above, moderate fluorosis is a significant adverse effect and is in fact defined as the first visible sign of systemic fluoride poisoning, is a more appropriate SMCL endpoint.
Taken together the NRC could have been more adamant in requesting water fluoridation be halted. Abnormal permanent tooth fluorosis, objectionable, unsightly and costly to restore, increases in incidence in every city from fluoridation, without exception. But the NRC made it clear their stated purpose was not to evaluate fluoridation at levels less than 2 ppm because the actual purpose was to determine whether 2 ppm was an adequate level for the fluoride contaminant to prevent significant adverse pathology, so no request on water fluoridation was made. The NRC however is fully justified in concluding that the EPA standards must be lowered because the health of American citizens is now compromised by taking fluoride internally through ingestion, mostly from public water supplies, natural or by intentional infusion of industrial synthetic fluoride compounds. Since water fluoridation leads to 57-90% of the total fluoride concentration in the bloodstream, depending on the health of the consumer and on water hardness and other factors, many on the NRC committee have chosen to oppose fluoridation of public water supplies (personal communication, NRC committee member).
The claim that aluminum fluoride interaction studies have published contradictory findings is false. The presence of low level fluoride ion in water that also contains low levels of aluminum ion causes enhanced assimilation of aluminum. There is no doubt about this effect of fluoride on the uptake of aluminum which causes consistent, widely observed accumulation of aluminum in brain tissue with dramatic alterations in the structure of cellular components in brain:
Varner, 1998 http://www.actionpa.org/fluoride/aluminum.html ; Miu, 2003;
Bhatnager, 2002; Shivarajashankara, 2002 as reviewed in NRC, 2006, p. 218).
Because aluminum in the stomach at acidic pH competes with hydrogen ion for binding with fluoride, and because the association constant for aluminum fluoride is far greater than that for HF (also discussed in NRC,2006, p. 211), aluminum fluoride complexes form, which, being uncharged, are assimilated well. Free aluminum ion, not complexed with fluoride, is not assimilated significantly after ingestion. (In fact for this reason many cities infuse aluminum as an inexpensive method to clarify water supplies). Fluoridation of water that contains aluminum is a contraindication because of assimilation of aluminum that fluoride causes.
At the same time fluoride enhances aluminum uptake, aluminum itself also inhibits assimilation of fluoride. Aluminum lowers the free fluoride concentration in the gut, due to complexation, which interferes greatly with formation of HF. Normally at stomach pH, 50% of ingested fluoride ion is converted to HF (Sauerheber, submitted to Journal of Toxicology and Pharmacology, 2012), in agreement with data at a pH below and above this pH (NRC, 2006, p. 268), and HF is then freely assimilated. HF, not charged fluoride, freely permeates cell membranes (Buzalaf, 2011) and is the form by which fluoride gains entry into the blood. Charged fluoride ion is eliminated out the GI tract well. In the presence of aluminum found infused into public water supplies, little fluoride is converted to HF and the fluoride that is assimilated is mostly that complexed with aluminum. Most all fluoride would be assimilated, as HF, if aluminum is absent. So it is correct to state that fluoride enhances aluminum uptake (from zero) and that aluminum decreases fluoride assimilation (less than 100%), all at the same time. The presence of aluminum helps keep fluoride as the charge ion rather than HF, the assimilated form, while fluoride complexes significant aluminum, raising its assimilation from otherwise essentially zero. The effects are relative, and both are observed. There is no ‘contradictory’ data set.
Richard Sauerheber, Ph.D.