June 25, 2000

According to the directive of the Department of Health (DOH), this “systematic review of public water fluoridation” was restricted to the following five objectives or queries:

1. What effects does fluoridation have on the incidence of dental caries?
2. If these effects are beneficial, how do they compare with alternatives to fluoridation?
3. Does fluoridation result in an equitable reduction in caries across groups and different geographical locations?
4. Does water fluoridation have negative or adverse health effects?
5. Do natural and artificial water fluoridation differ in their effects?

Overview

In considering these objectives and the guidelines laid out for addressing them, one must bear in mind that the DOH is a long-time advocate of fluoridation and is unlikely to retreat from that position. Nevertheless, its stated goal for this report is to provide a sound scientific review to guide future decisions about fluoridation in the United Kingdom. Since the review is strictly limited to the above five objectives, can this goal be achieved?

From a scientific standpoint, the exclusion of animal and laboratory data from the review, as stated on page 80 of the report, places undue reliance on admittedly deficient epidemiological investigations that can only be as valid as the adequacy and completeness of the date included in them, no matter how sophisticated the statistical analyses might be. In terms of human population studies, the omission of all reference to unrefuted peer-reviewed reports of reversible adverse health effects of fluoridation points up a major defect in the review. By not citing pertinent experimental and clinical case-study data on the toxic properties and biomedical hazards of fluoridation, the review clearly has a serious major shortcoming.

Moreover, by not allowing examination of other admittedly important aspects of fluoridation, the DOH has been able to tailor the report to its own restricted views of the subject, thereby making the review very inadequate and misleading in its presentation.

Objective 1: What effects does fluoridation have on the incidence of dental caries?

In dealing with its primary objective, the review regrettably fails to cite findings of knowledgeable scientists and expert health researchers that contradict claims of significant caries reduction by water fluoridation. This oversight reflects an underlying major defect in the selection and interpretation of evidence. Recent fluoridation studies showing little or no reduction in tooth decay in permanent dentition of children are ignored. These investigations include large-scale and even whole-population surveys in such heavily fluoridated countries as Australia (1), Canada (2), New Zealand (3), and the United States (4-6). By omitting these studies, the review has not met its goal to provide an “expert scientific review” of fluoridation.

Contrary to the conclusions of the report, cessation of fluoridation does not necessarily cause an increase in tooth decay. In Holland, for example, caries rates continued to decline in cities after fluoridation was terminated in 1976 (7). In La Salud, Cuba, fluoridation was discontinued in 1990, but dental examinations in 1997 revealed that tooth decay among the children had continued to decline dramatically (8). A school mouth rinse program was offered as a possible explanation for the decline, but other recent research indicates that the anti-caries benefits of such programs are very small (9).

Equally disturbing is the failure of the review even to mention many of the fundamental defects and errors in the four primary North American fluoridation studies as well as in many of the lesser fluoridation studies that have been pointed out by Sutton (10), Diesendorf (11), Colquhoun (12), Ziegelbecker (13), and others (14).

For example, when fluoridation began in 1945 in Grand Rapids, Michigan, the 1944-45 base-line dental examinations were made of all children in 79 schools in Grand Rapids and in all schools in the control city of Muskegon, Michigan. Beginning in 1946, however, the teeth of the children in only 25 schools in Grand Rapids were examined, and essentially all the decline in tooth decay found after five years had already appeared in 1946, thus indicating that the reported reduction was simply an artifact resulting from biased sample selection. Moreover, Muskegon, with caries rates running about the same as in Grand Rapids, began fluoridating its water supply in 1951 and thereby ceased being a control. Comparisons with natural fluoride (1.3 ppm) Aurora, Illinois, were then introduced, but the reported decline in decay rates in Grand Rapids during the 1950s and 1960s were little different from those occurring in other nonfluoridated cities, e.g., in the State of New Jersey.

When the other three original fluoridation studies (Brantford, Ontario; Evanston, Illinois; and Newburgh, New York) along with many other later studies are examined closely, numerous related shortcomings are found (15). Thus, in the Newburgh study, the water supply of the control city in Kingston is comparatively soft and not like that of Newburgh which, at the time, had much more tooth-building calcium and magnesium than the water in Kingston. Moreover, in the ninth year of fluoridation in Newburgh, when the official investigators were claiming large reductions in tooth decay in Newburgh compared to Kingston, New York State Education Department dental examinations revealed a significantly greater need for dental repair in children in fluoridated Newburgh than in nonfluoridated Kingston (16). Since then, children’s caries rates have declined markedly in both cities, and today they are about the same or slightly lower for certain ages in Kingston, which remains unfluoridated. Failure to cite and consider these unrefuted criticisms is obviously a serious weakness or even a fatal flaw for the credibility of the review.

Similarly, it is an egregious omission for the review not to have dealt with the dubious origins and unscientific promotion of water fluoridation, which clearly fall under the perview of Objective 1. During the 1930s, when fluoridation was first proposed, the United States Public Health Service had collected data from hundreds of communities and counties in 26 states on the occurrence of dental caries as well as dental fluorosis among children in relation to natural fluoride levels in the drinking water (17).

From these data the occurrence and severity of the toxic (not merely “cosmetic”) effect of dental fluorosis in relation to increasing fluoride content of drinking water were clearly evident. Not so, however, with the findings on dental caries, which were highly variable. But by collecting data from 21 nonrandomly-selected cities in only four states it was possible to propose a highly questionable inverse relation between tooth decay and increasing fluoride (18).

For example, with 0.5-0.6 ppm fluoride in drinking water, children in Colorado had about the same number of carious permanent teeth per child (in the original surveys) as children of the same age in Illinois at 1.2 ppm. On the other hand, in Wisconsin, tooth decay with 0.5 ppm F in the water was twice as high as in Colorado with 0.5 ppm but nearly the same as in Ohio with only 0.1-0.2 ppm. With such gross inconsistencies, is it any surprise when data from over 130 surveys around the world are examined (19), no overall inverse correlation between tooth decay and natural fluoride in drinking water can be detected?

Further doubt about any significant anti-caries effect of water fluoridation can be seen in the fact that tooth decay rates in much of continental Europe are generally lower without fluoridation than in many fluoridated communities elsewhere. In Denmark the National Agency for Environmental Protection and in Sweden a special Fluoride Commission have recommended against fluoridation. The same is true for health and water authorities in Austria, Belgium, Finland, Germany, Italy, Norway, and other countries in Europe as well as China, India, and Japan in Asia. In this respect, their assessment agrees with that of scientists and other professionals in the U.S. Environmental Protection Agency based on their own independent study of the scientific literature (20).

Objective 2: How does fluoridation compare with other methods to reduce tooth decay?

With such a large body of current evidence indicating no significant reduction in dental caries in the permanent teeth of children in fluoridated communities compared to nonfluoridated communities, there is little point in trying to “compare” anti-caries effects of water fluoridation with other methods to reduce tooth decay. The beneficial effects of nutritionally sound anti-caries diets and the practice of good dental hygiene are of course well known.

Objective 3: Does fluoridation have equitable effects on caries reduction?

As with the previous objective, this question assumes there is a significant positive dental benefit from fluoridation. As already pointed out, a substantial body of contemporary evidence does not support this assumption. Along related lines, however, a recent comparison of Medi-Cal dental care costs for needy children in California during 1994 -1995 showed very little difference between fluoridated and nonfluoridated areas (21).

Objective 4: Does fluoridation have negative or adverse health effects?

Unfortunately, in addressing this topic, the review refers only to epidemiological data, and it does so with a marked bias toward exculpation, e.g., by mislabeling dental fluorosis essentially as a cosmetic and not a toxic effect and by excluding clearly relevant contrary evidence. Thus, by not considering all pertinent fluoridation-related findings on such concerns as hip fracture incidence and bone fragility among the elderly and post-menopausal women, osteosarcoma (bone cancer) among young males, earlier onset of menarche among females, and increased osteoarthritis, kidney failure, depressed thyroid function, and Down syndrome births to younger mothers, the review conveys a false sense of safety and fails to meet its goal of scientific credibility.

For example, by excluding important findings showing an association between fluoridation and osteosarcoma in young males (22), and by not including a recent incisive rebuttal (23) of the deficient epidemiological studies claiming to refute earlier research connecting higher rates of Down syndrome births to elevated levels of fluoride in drinking water in the North Central United States, the review clearly falls short of being objective and trustworthy.

With regard to other types of studies on human populations, numerous unrefuted reports of clinical investigations of neuromuscular, gastro-intestinal, urological, hypersensitivity, and other reversible toxic effects of 1-ppm fluoridated water clearly should have been included but were not. Peer-reviewed medical publications of such studies began to appear in 1955 and have been amply confirmed by competent laboratory data and follow-up by appropriate blind and double-blind procedures (24).

When these patients (35 years ago the writer was one of them) changed to distilled or other low-fluoride water for all drinking, beverages, and cooking, the symptoms dramatically disappeared without medication, only to return when consumption of fluoridated water was resumed. The exclusion of any consideration of these well-documented human case studies from the review is completely inexcusable.

Objective 5: Do natural and artificial fluoridation differ in effectiveness?

Like objectives 2 and 3, this question implicitly assumes that fluoridation effectively reduces tooth decay. As emphasized above, a substantial body of evidence now contradicts that assumption. In the review the only relevant study cited is an early one from artificially fluoridated Brantford and naturally fluoridated Stratford, Ontario, Canada. The reported findings from the 1940s and 1950s showing that artificial and natural fluoridation have similar caries-reducing effects in the two cities are accepted at face value. In fairness, however, serious inconsistencies and deficiencies in the data which cast doubt on the reliability of the study (10,15) should have been considered.

Another important aspect of this question is the difference between the chemical nature of artificial fluoridation as currently practiced and what was done previously. Today, industrial-grade fluorosilicic acid, H2SiF6, or its sodium salt, Na2SiF6, which are by-products from the manufacture of phosphate fertilizers, are generally used to fluoridate water supplies, whereas in the past, mainly sodium fluoride, NaF, was used. As bulk chemicals, H2SiF6 and Na2SiF6 are contaminated by significant amounts of toxic impurities such as arsenic, lead, and radioactivity.

Although a few laboratory studies have been conducted with reagent-grade H2SiF6 and Na2SiF6, the contaminated commercial-grade products used in fluoridation have not been tested. In the drinking water of rats, Na2SiF6 causes much more excretion of fluoride in the urine and less in the faeces than does NaF (25). Moreover, recent research not cited in the review has found that when fluorosilicates are used in water fluoridation, more children have blood-lead levels in excess of the current optimal maximum of 10 g/dL than with NaF fluoridation or no fluoridation (26).

Still another complication of artificial fluoridation that should be mentioned occurs with alum treatment of water to remove turbidity. Fluoride in millimolar amounts in water forms tight complexes with micromolar amounts of aluminum ions which appear to act as phosphate analogs with toxic physiological consequences, especially with disturbances of guanine nucleotide binding (G) proteins in various cells and tissues of the body (27).

Closing comments: Setting the record straight

From its inception, fluoridation has been fatally flawed with insurmountable problems and inconsistencies. Its underlying rationale - to reduce tooth decay by raising the fluoride content of drinking water to ten times the level generally found in uncontaminated surface waters - is plainly contradicted by the fact that, with adequate dental care and nutrition, and in the absence of cariogenic refined-food diets, low caries rates are found everywhere without appreciable fluoride in the water. In short, good, decay-resistant teeth do not require fluoride.

Also, from the very beginning, many of the toxic effects of excessive fluoride intake were well recognized. Even in the 1930s, when fluoridation was being proposed, a leading engineer of the American Water Works Association was recommending a maximum of only 0.1-ppm fluoride in finished water for an appropriate margin of safety (28). A tenfold higher level of 1 ppm, later recommended for fluoridation, was considered to be grounds for rejection of a water supply because of the harm it could cause, especially to babies and children.

Today we know even more how valid this concern was. The total fluoride intake of an infant, breast-fed by its mother as nature intended, is only about 0.01 mg per day (29). On the other hand, with formula prepared with fluoridated water the daily fluoride intake of a small baby even exceeds the currently recommended maximum of 0.05 mg/kg/body weight, thereby leading to dental fluorosis and other toxic effects.

We now also know there is very little systemic anti-caries effect from fluoride. Whatever anti-caries effect fluoride might have is today considered to be essentially topical. Thus, ingested fluoride or fluoridated water that is swallowed has very little demonstrable anti-caries benefit. But, along with other sources, it does cause disfiguring dental fluorosis, which now, on average, affects over 30 percent of children in fluoridated areas. The expensive dental costs for correcting objectionable dental fluorosis now exceed those of repairing cavities, and the increased costs of medical treatment resulting from illness caused by excessive fluoride intake through fluoridation can be even greater and certainly exceed the monetary outlays for fluoridation.

Finally, there is a very disturbing but not well-known parallel between the promotion of water fluoridation by health agencies and the one-time advocacy of the addition of tetraethyl lead (TEL) to motor fuel. In the late1920s and early 1930s, despite strong warnings of serious risks to public health in allowing more lead to enter the environment, U.S. Surgeon General Hugh Cumming, working closely with industrial promoters of TEL, gave favorable reports on the additive to British and other health ministries, assuring them of the safety of having lead in gasoline (30).

Later, the Kettering Laboratory in Cincinnati, also known for its extensive studies to “prove” the safety of water fluoridation, produced misleading data on human blood lead levels in the general U.S. population. Because of contaminated controls (Mexican Indians eating from lead-glazed pottery and cookware), these levels were subsequently found to be more than ten times higher than in non-exposed people. Today, with the phasing out of leaded gasoline since the late 1970s, blood levels in the U.S. have decreased by 75-80 percent, and a lead level of 10 g/dL is now considered a danger in children compared to 50 g/dL only 25 years ago. Thus, as our knowledge and understanding improve, our appreciation and recognition of environmental hazards also improve.

Unfortunately, as this review shows, this improvement has not happened widely enough with fluoridation. Public health authorities in the United States, Britain, and other English-speaking countries remain adamant in their outdated and incorrect views about fluoride and fail to recognize its potential for serious toxic effects on health and the environment. Just as with discoveries about the insidious nature of TEL, recognition of the magnitude of fluoride toxicity is bound to occur. But at present there is simply too much prestige and public confidence at stake for many health officials to admit that adding fluoride to public water supplies has been, in a way, as big a mistake as adding TEL to motor fuel, no matter how well intentioned.

Both fluoride and lead are persistent environmental pollutants, and, like lead, fluoride accumulates in the human body with disastrous consequences to health. Only by acknowledging and dealing honestly with this fact and its implications can this or any other review of fluoridation ever be considered an acceptable scientific document.

Albert W. Burgstahler, Ph.D.
Professor Emeritus of Chemistry
The University of Kansas
Lawrence, Kansas, USA

June 25, 2000

LITERATURE CITED

1. Diesendorf, M. A re-examination of Australian fluoridation trials. Search 1986;17:256-61.

2. Gray, A.S. Fluoridation: Time for a new base line? J Can Dent Assoc 1987; 53:763-5.

3. Colquhoun, J. Fluorides and the decline in tooth decay in New Zealand. Fluoride 1993; 26:125-34. Cf. Community Health Studies 1987; 11:85-9; 1988;12:187-91.

4. Hildebolt, C.F., Elvin-Lewis, M., Molnar, S., et al. Caries prevalences among geochemical regions of Missouri. Am J. Physical Anthropol 1989;78:79-92.

5. Yiamouyiannis, J. Water fluoridation and tooth decay: Results from the 1986-1987 National Survey of U.S. schoolchildren. Fluoride 1990;23:55-67.

6. Steelink, C. Letter. Chem & Eng News 17 July 1992:2-3. Cf. abstract of AAAS presentation: An analysis of the causes of tooth decay in children in Tucson, Arizona. Fluoride 1994;27:238.

7. Kalsbeek, H. Evidence of decrease in prevalence of dental caries in the Netherlands: An evaluation of epidemiological caries surveys on 4-6- and 11-15-year-old children, performed between 1965 and 1980. J Dent Res (Special Issue) 1982;61:1321-6. Cf. Kalsbeek, H., Kwant, G. W., Groeneveld, A., et al. Caries experience of 15-year-old children in the Netherlands after discontinuation of water fluoridation. Caries Res 1993;27:201-5. See also, Ziegelbecker, R. Letter. Fluoridation in Europe. Fluoride 1998;31:171-4.

8. Künzel, W. and Fischer, T. Caries prevalence after cessation of water fluoridation in La Salud, Cuba. Caries Res 2000;34:20-5.

9. de Liefde, B. A study of the chemical treatment of early caries of occlusal pits and fissures. NZ Dent J 1987;83:10-2. See also, de Liefde, B. The decline in caries in New Zealand over the past 40 years. NZ Dent J 1998;94:109-13.

10. Sutton, P.R.N. Fluoridation: Errors and Omissions in Experimental Trials. 2nd Ed. Melbourne Univ Press, 1960. (Includes replies to criticisms of first edition.)

11. Diesendorf, M. The mystery of declining tooth decay. Nature 1986; 322:125-9. Cf. Int J Clin Nutr Rev 1990; 10:292-303.

12. Colquhoun, J. Flawed foundation: A re-examination of the scientific basis for a dental benefit from fluoridation. Community Health Studies 1990;14:288-96. See also, Colquhoun, J. Why I changed my mind about water fluoridation. Persp Biol Med 1997;41:29-44.

13. Ziegelbecker, R. A critical review of the fluorine caries problem. Fluoride 1970;3:71-9. Cf. Open letter to Lord Jauncey. National Fluoridation News Winter 1983/84;29(4):3-4.

14. E.g., by Klerer, M. The fluoridation experiment. Contemporary Issues 1956;7:119-43; Schatz, A. and Martin, J.J. The failure of fluoridation in the United Kingdom. Pakistan Dent Rev 1972;22:3-7; Waldbott, G.L., Burgstahler, A.W., and McKinney, H.L. Fluoridation: The Great Dilemma. Coronado Press, Lawrence, Kansas, 1978, pp. 185-90; 357-8; Yiamouyiannis, J. Fluoride the Aging Factor, 3rd Ed. Health Action Press, Delaware, Ohio, 1993, Ch.14.

15. Sutton, P.R.N. The Greatest Fraud: Fluoridation. Kurunda Pty. Ltd., Lorne, Australia, 1996.

16. Letter of J.A. Forst, M.D. Cited on page 357 of Fluoridation: The Great Dilemma (ref. 14 above).

17. Dean, H.T., Distribution of mottled enamel in the United States. Pub Health Rep 1933;48:703-34. Messner, C.T., Galafer, W.M., Cady, F.C., and Dean, H.T. Dental survey of school children, ages 6-14 years in 1933-1934 in 26 States. Pub Health Bulletin No. 226, May 1936.

18. Dean, H.T., Arnold, F.A. Jr., and Elvove, E. Domestic water and dental caries. V. Additional studies of the relation of fluoride domestic waters to dental caries experience in 4,425 white children, aged 12 to 14 years, of 13 cities in 4 States. Pub Health Rep 1942;57:1155-79. (Includes data on 7,257 “selected 12-14 year-old white school children of 21 cities of 4 States”)

19. Ziegelbecker, R. Fluoridated water and teeth. Fluoride 1981;14:123-8. Ziegelbecker, R. and Ziegelbecker, R.C. WHO data on dental caries and natural fluoride levels. Fluoride 1993;26:263-6.

20. Statement: Why EPA’s headquarters union of scientists opposes fluoridation. Fluoride 1999; 32:179-86.

21. Yiamouyiannis, J.A. Dental costs not affected by fluoridation – large-scale tooth decay studies show lack of ‘beneficial’ effects. XXII ISFR Conference Abstracts. Fluoride 1998;31:S14.

22. Yiamouyiannis, J.A. Fluoridation and cancer: The biology and epidemiology of bone and oral cancer related to fluoridation. Fluoride 1993;26:83-96.

23. Takahashi, K. Fluoride-linked Down syndrome births and their estimated occurrence due to water fluoridation. Fluoride 1998;31:61-73.

24. Waldbott, G. L. The preskeletal phase of chronic fluoride intoxication. Fluoride 1998;31:13-20 plus list of his fluoride publications, pp. 21-5. Spittle, B. Allergy and hypersensitivity to fluoride. Fluoride 1993;26:267-73. See also relevant chapters in books by Waldbott et al. and by Yiamouyiannis in ref. 14 above.

25. Kick, C. H., Bethke, R. M., Edgington, B. H., et al. Fluorine in animal nutrition. Ohio Agricultural Experiment Station Bulletin 558, Nov. 1935.

26. Masters, R. D. and Coplan, M. J. Water treatment with silicofluorides and lead toxicity. Int. J Environ Studies 1999;56:435-49.

27. Strunecka, A. and Patocka, J. Pharmacological and toxicological effects of aluminofluoride complexes. Fluoride 1999;32-230-42.

28. Babbit, H.E., and Dolland, J.J. Quality of Water Supplies in Water Supply Engineering. 3rd Ed. McGraw-Hill, New York, 1939, page 454.

29. Dietary Reference Intakes: Calcium, Phosphorus, Magnesium, Vitamin D, and Fluoride. Institute of Medicine, National Academy of Sciences, Washington, D.C., 1997. For comment, see letters in Fluoride 1998;31:153-7; 1999;32:187-98.

30. Kitman, J. L. The secret history of lead. The Nation 20 March 2000:11-44.