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Fluoride, Cancer
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Does water fluoridation + have negative side effects?
+ A critique of the York + Review
+ Objective 4, Sections + 9.1 to 9.6 : CANCER STUDIES
+ by Peter Meiers, Saarbruecken, Germany
+ (October 30, 2000)

(Note by Andrew Saul: + Fluoridation of water owes its continued existence more to politics than to + science. If safety and effectiveness are truly considered, fluoride + would be questionable even as a prescription drug. But to freely add it + to public water supplies, often without any public vote whatsoever, is far + beyond questionable. Mr. Meiers' discussion of the dangers of fluoride + is important reading.)

The National Health + Service (NHS) Centre for Reviews and Dissemination at the University of York + recently released a review perceived to be "the final word on + fluoridation" [McDonagh et al. 2000]. To judge from the course of a + discussion about the layout of this York + review [Schuld 2000], the result was to be expected: benefits (though smaller + than previously claimed) with regard to caries prophylaxis, at the cost of + some "cosmetic defects" (dental fluorosis), no harm to general + health. This report is just one of many made in the past apparently aimed at + giving support to preoccupied views of the proponents of fluoridation. Like + other sections, the evaluation of the fluoridation-cancer link in this report + is far from presenting "a summary of the best available and most + reliable evidence on the safety and efficacy of water fluoridation". Not + only did the York + team disregard all relevant experimental data (a prerequisite to decide what + effects of fluoride should be looked for), it also, quite obvious to anyone + knowing the relevant literature, distorted facts to make its point.

This is not a new + experience. Fears of undesired effects of the controversial "public + health measure" have never been taken serious by its promoters. Even + though animal experimentation on fluoride and cancer, performed long before + any fluoridation experiment was started in the United States [Meiers 1984, + 1986], could have given reason for concern, investigations into possible + fluoride effects on human cancer victims were not initiated by promoters of + the measure prior to any fluoridation efforts nor in the course of the first + experimental trials, but by opponents whose charges posed a threat to the + continuing supply of public funds and thus necessitated appropriate replies + [American Dental Association 1952]. For example, at government hearings in + 1952, Taylor + [1952] presented evidence that fluoride shortens the lifespan of cancer-prone + mice. Perkins [1952] speculated on this basis that people in fluoridated + cities might die of cancer at an earlier age because of their fluoride + exposure: If a person would die of cancer at the age of 80, 70, 60, 50, or 40 + on a water intake free from fluorine, the same per-son would die at the age + of 65.6, 57.4, 49.2, 41, or 32.8 years, respectively, on a water intake + containing approximately 1 ppm of sodium fluoride.

Relative to the city of + Grand Rapids, fluoridated since January 1945, Perkins wrote:
+ "The vital + statistics provided by the health authorities of that city to the United + States Public Health Service and published in ´Vital Statistics of the United + States´, Part II, Table 14, for the year 1945 (the year fluoridation was + installed in Grand Rapids) show that 252 persons died of cancer. Four years + later, the same sources showed that the deaths in that city from cancer + totaled 349. This is an increase of approximately 39 percent in cancer deaths + during the first five years of fluoridation in Grand Rapids. It is significant that the + records for the five years previous to the adoption of fluoridation showed an + actual decrease in the cancer death rate of approximately 6 + percent."

It was these claims that + prompted Swanberg [1953] to evaluate the cancer data of Grand + Rapids and to compare them with cancer mortality data for the United States + as a whole. The York Committee describes this study [Section 9.4] as showing + that "The death rate from cancer in the study area decreased during the + study period whereas the death rate from cancer in the whole of the US (the + control area) increased over the same period" and excludes it from the + main analysis because the "whole of the US includes areas with fluoride + in the water supplies and so [is] not a suitable control area". While + this was a wise decision [see Ziegelbecker 1987] the team did not realize, + apparently, that the Swanberg study actually revealed something quite + different from the author's conclusion: the number of cancer deaths per + 100,000 residents per year increased in Grand Rapids + as it did in the U.S.A. + (Fig.1, upper graph). As to the large rise during the years of World War II + and the decrease afterwards, Swanberg explains that "it is known that in + the early forties there was a migration away from Grand Rapids toward the center of war + industries. After 1945 there was a migration back" which fact is + illustrated in the lower graph of Fig.1 (data taken from Swanberg´s + publication). If this migration involved just the younger residents it led to + a relative increase of the fraction of older people "per 100,000 + residents" during the years of war, thus increasing the crude cancer + death rate. Though Swanberg, editor of the journal that published his study, + gave the full set of data, he selected for his conclusion those data points + appropriate to show a decrease in cancer death rate after the start of + fluoridation:

"The death rate from + cancer in Grand Rapids + in 1944, the year before fluoridation was adopted, is given as 206.2 per + 100,000 population. In 1952, after 8 years of fluoridation, the cancer death + rate was 185.3 per 100,000, a decrease of 10 per cent. In the 9-year period + between 1944 and 1952 in the United + States as a whole, the cancer death rate + rose from 124 per 100,000 population in 1944 to 143.9 per 100,000 in 1952, an + increase of 16 per cent."

The York review committee either did not + realize this fraud or it chose to mention the unjustified conclusions of the + author to put some undeserved weight to other studies which apparently found + a decrease in cancer death rates after fluoridation started.

Likewise, the York team used a very + special approach to evaluate data from the Newburgh-Kingston study by + Schlesinger et al. [1956]. Table 12 in the Schlesinger et al. publication + lists the number of cancer deaths per 100,000 people in fluoridated Newburgh + and the non-fluoridated control city of Kingston for 1942 to 1954, an up and + down so that hardly any difference can be ascertained between the two cities + (Fig. 2). Yet, the York review team [see App. C10, p. 196] excerpted from + this list data for 1944 (219.0 for Newburgh vs. 169.0 for Kingston) and the + last year reported (221.2 for Newburgh, 264.4 for Kingston) when the number + of cancer deaths was in favor of fluoridated Newburgh (while in 1952, for + example, it was lower in Kingston). With this data selection the York team created the picture that cancer mortality went + way up in non-fluoridated Kingston, while it + remained nearly unchanged in fluoridated Newburgh.

Several studies published + after the 1956 Newburgh-Kingston "final report" focused on possible + effects of natural fluoride waters on the incidence or mortality of cancer + and revealed some major shortcomings. They were essentially static (comparing + data of just one year) as opposed to the time-trend analyses quoted above. + Further-more, the concentration of natural fluoride varies (even in one and + the same water supply), and so does the num-ber of registered water supplies + within each municipality [Heasman and Martin 1962; Glattre and Wiese 1979]. + Therefore, it seems to make no sense to compare areas with a water fluoride + level of 0.06-0.10 mg/l to areas with 0.11-0.5 mg/l, as Glattre and Wiese do, + nor to arrange fluoride cities into groups based on a difference of one + hundredth mg/l (i.e. 0,5-0,99 vs.1 mg/l and more) as Kinlen [1974, + 1975] does. Where more than one water source supplies a local authority some + authors calculated "weighted means" [Chilvers and Conway 1985]. On this basis, the latter + authors found some of the areas used by Kinlen [1974, 1975] to be + misclassified (see also Heasman and Martin 1962; Nixon and Carpenter 1974). + While these facts should have been reason enough to exclude the Kinlen paper + from the main analysis in the York review, his method of standardization + should have given it the final blow. But as to the Standard population used + by Kinlen the York team claims: "Not stated" (Appendix C10, p. + 191). The Kinlen paper has appendices, among them Appendix B which reads:

"The method for + obtaining the ratios shown in table I was to calculate for each sex and each + age group the number of cases that would be expected in the population in + question in each fluoride category if the total number of cases in all areas + combined was distributed uniformly." That means, he pooled the groups to + calculate his "expected" cancer deaths and thus used a reference + population partly exposed to the variable to be tested! While the York team excluded the + Swanberg study on this basis, it did ignore the same mistake made by + Kinlen.

In case fluoride + increases the number of deaths, inclusion of exposed people in the reference + population would raise the number of (speculative) "expected" + deaths in the groups to be examined (depending on population structure). As + Standardized Mortality Ratios (SMR´s) are calculated by dividing the number + of observed cancer deaths per 100,000 people (O) by the number of + "expected" cancer deaths per 100,000 people (E), the SMR (O:E) + becomes the lower the higher the "expected" (E) rate. This kind of + SMR calculation applied in time-trend studies to populations of different + size and structure (fluoridated vs. non-fluoridated cities) using a shifting + refer-ence population (USA 1950, 1960, 1970 as the standard for the + corresponding census years) creates the artifact of decreasing cancer death + rates in fluoridated cities.

An example: In a hypothetical + population with no change both in population structure and the number of + cancer deaths during 1950 to 1970, applying U. S. data in 1950 by age, gender + and race to calculate the number of deaths expected for 1950 in that + population, and likewise U.S. data in 1960 and 1970 for those respective + years, will result in an increasing number of expected deaths in the time + span 1950 to 1970, since cancer death rates rose in the U.S. during that + time. As the number of deaths expected in the hypothetical population will + increase, i.e. "E" becomes higher, the O:E ratio (SMR) becomes + lower. Thus one will be able to show that the cancer death rates decreased in + that population (while, as presupposed above, nothing happened at all with + the actual rates). What a large increase in cancer death rates would be + required just to balance the misleading SMR calcu-lations for the + hypothetical population if it were exposed to a carcinogen to be evaluated!

This is why the + re-analyses by Smith [1980] as well as Kinlen and Doll [1981] of the + Yiamouyiannis and Burk [1977] study on the fluoridation-cancer link are + useless. Of these, the Smith paper got a high ranking according to the York validity checklist + for it "did not include the error in the NCI data" (Section 9.1.1) – + which isn´t true, of course. After all, how can one expect the York committee members + to know the details of that year-long discussion of the 20-cities study to + evaluate properly the relevance of Smith´s re-analysis?

As the Grand Rapids and + Newburgh/Kingston data show, there are large fluctuations of cancer death + rates over time in individual cities so that it isn´t appropriate to select + just two data points for statistical evaluation, but the best approach would + be to make a linear regression analysis to compare rates before and after + fluoridation started. As differences might be small it seems to be a good + idea to pool the data of several fluoridated cities and to compare them to a + set of non-fluoridated ones.

In 1975, Yiamouyiannis + and Burk reported to the U.S. Congress that a set of 20 U.S. central cities + had almost identical cancer mortality rates (cancer deaths per 100,000 people + per year) between 1940 and 1950, but that since fluoridation started (in + 1952-1956) in a group of ten of these cities their cancer death rate + increased faster than that of the ten cities remaining non-fluoridated (Fig. + 3). The study was later published in the Journal "Fluoride" + [Yiamouyiannis and Burk 1977] and caused quite a stir.

Early in 1976, a + representative of the National Cancer Institute (NCI) claimed in a letter to + Congressman Delaney that the NCI´s re-analysis showed that the increase was + entirely due to changes in the age, race and sex structure of the population + in question [Fredrickson 1976]. While refusing congressional requests for + detailed data (weighted or unweighted rates used? Which reference population? + etc.), the NCI clandestinely has passed this data on to other scientists + [Yiamouyiannis 1977] who reported them as their "independent analysis" + [Doll and Kinlen 1977; Oldham and Newell + 1977]. However, the NCI data submitted contained two characteristic errors + reproduced in both papers: (A) The non-white females, age 65-74 in 1970, in + the non-fluoridated population should be 46.1 (not 51.1; thousands) so that + the total population becomes 7342.7 (thousands) instead of 7347.7. As a + result the expected number of cancer deaths in non-fluoridated cities in 1970 + is 12,384 (instead of 12,407). (B) Total cancer deaths in the non-fluoridated + cities in 1970 should be 14,272 (and not 14,487) [Kinlen and Doll, 1977; Oldham and Newell 1979]. The Smith [1980] paper + eliminated error (B) of the NCI data, but still contains error (A).

However, the main point + of disagreement between the statisticians is that whereas Burk and his group + derived putative "observed Cancer Death Rates" (CDRo) by linear + regression analysis of all available and pertinent data, i.e. the crude CDR´s + characterizing the observation period of 1953 to 1968, and extrapolation to + 1950 and 1970, other investigators have taken reported or pericensal CDRo + figures for 1950 and 1970. "If, as they say, only the censal or + pericensal data for 1950 or 1970 ought to be taken into account, the + association between fluoridation and cancer is wiped away by adjustment. If + instead, as we insist, the intermediate data for 1953 through 1968 must be + used, a large association remains, notwithstanding adjustment" [Graham + et al. 1987]. Neither regression analysis of cancer death rates + [Mahoney et al. 1991] nor calculation of intercensal population by + interpolation of data acquired in census years [Cohn 1992] seem to be + unacceptable methods. Furthermore, a look at age-specific cancer mortality + data for the twenty cities, unfortunately only available for 1970, indicates + a higher cancer mor-tality at an earlier age in the fluoridated group (Fig. + 4). The difference is obvious in these large populations even though people + in non-fluoridated cities are exposed to fluoride from sources other than + drinking water (tablets, drops, mouthwashes, topical applications, canned + foods prepared in fluoridated cities, etc.).

While epidemiologists + hitherto essentially looked for evidence in human populations of a per se + carcinogenic effect of fluoride, substantiated by more recent in-vitro + experiments [Tsutsui et al. 1984; Jones et al. 1988; Lasne et al. 1988], the + question raised by Perkins in 1952 relative to the promoter effects of + fluorides has still not been addressed, neither by health officials in + general nor by the York team. Humans today are exposed to not one but many + different carcinogenic agents (including chemicals, viruses, ionizing + radiation) which interact in very intri-cate ways. Fluoride is known to + inhibit some enzymes and to activate others. Fluoride inhibits the enzymatic + deacetylation of N-Hydroxy-Acetylaminofluorene [Irving 1966] and thus leaves more of the + substrate for a sulfotransferase enzyme that builds the ultimate carcinogen + from that compound. Fluoride activation of dimethyl-nitrosamine demethylase + in liver microsomes [Dophuoc et al. 1981, 1983] increases the carcinogenic + potential of dimethylnitrosamine. It has no obvious influence on the + oxidative activation of the ubiquitous carcinogenic hy-drocarbon + benzo(a)pyrene in vitro [Dophuoc et al. 1981, 1983], yet addition of fluoride + to the food of experi-mental animals injected with this compound leads to + increased incidence of malignant tumors [Tannenbaum and Silversone 1949]. + Likewise, skin cancer induced in animals by skin painting with benzo(a)pyrene + becomes ear-lier visible and leads to earlier death if the painting solution + contains 1 ppm fluoride (as sodium fluoride) in ad-dition to the hydrocarbon + [Wagner 1981]. Beryllium compounds are carcinogenic, but exposure of animals + to be-ryllium fluoride enhances the growth of lung tumors induced by the + beryllium [Schepers 1961]. Fluoride and fluorophosphate promote tumor growth + induced in vitro by benzo(a)pyrene and many other compounds [Jones et al. + 1988]. In this assay the promoter effect came to a halt as soon as the + fluoride was omitted from the culture medium. Thus the early experiments of Taylor [1952, 1954, + 1965] are fully supported by more recent evidence.

According to a WHO + scientific group "the occurrence of tumors earlier than in the controls, + without increased incidence" is among the types of responses "used + to classify chemicals as carcinogens" [WHO 1969].

Enhancing effects are + also apparent from some life table data published in the National Toxicology + Program carcinogenicity test of sodium fluoride [NTP 1990]. This test had + been requested by the U.S. Congress during hearings in 1977. Back then, NCI + representative Kraybill [1977] presented a list of publications which, he + al-leged, had already shown that sodium fluoride has no carcinogenic + activity. However, not a single one of the publications on his list had + anything to do with fluoride and cancer. Anyway, the start of the + carcinogenicity test requested by Congress was announced four years later + [Whitmire 1981]. After another four years, a first result was declared + inadequate because the low fluoride semisynthetic diet "was deficient in + several vitamins and minerals" [NTP 1985]. Another two-year study was + scheduled to begin in October 1985. The report, released in 1990, focused on + the occurrence of a rare form of cancer, osteosarcoma, in several of the male + (but not the fe-male) dosed rats used in the study [NTP 1990]. This evidence + of carcinogenicity was downgraded to be "equivocal".

Nevertheless, a few + epidemiological studies addressed a possible influence of water fluoridation + on the incidence of osteosarcoma in humans. It occurs in less than one in + 100,000 people or about 0.1 percent of all reported can-cers, and therefore + it would be hard to detect small increases in risk (on the order of five to + ten percent) [USPHS 1991]. Examinations in a very limited number of + afflicted people led to conflicting results. The study designs (e.g. + exclusion of people formerly exposed to some radiation) reveal that still the + search for a per se carcinogenic effect of fluoride was in the foreground. + There seems to be agreement that osteosarcoma incidence in the U. S. + increased in people below age 30 with some decrease at later age. A + contribution by water fluoridation could not be ascertained by these limited + studies, but obvious difficulties in classification of exposure to + fluoridated drinking water and examination of exposure from other sources + need to be more carefully addressed in more thorough future investigations. + The York team + apparently was not aware of these shortcomings.

In summary, the York review fits well in a history of + attempts to downgrade possible risks associated with expo-sure to fluoride. + Selection of data, inconsistent use of exclusion criteria, disregard of experimental + studies which could have offered a clue to proper evaluation of + epidemiological investigations render the York review useless. Either the York team was not + really interested (to say the least), aimed at supporting proponents´ views, + or was hopelessly lost in its task.
+

References:

American Dental + Association (1952): "Washington + News Letter", J. Am. Dent. Assoc. 44: 461

Cohn P.D. (1992): "A + brief report on the association of drinking water fluoridation and the + incidence of osteosarcoma among young males"; New Jersey Department of + Health, Nov. 8

Doll R., Kinlen L. + (1977): "Fluoridation of water and cancer mortality in the U.S.A."; + The Lancet I (June 18):1300

Dophuoc H., Bompart G., + Bourbon P. (1981): "Effects of hydrogen fluoride on benzo(a)pyrene and + dimethylnitrosamine metabolism in rats"; Naturwiss. 68: 621

Dophuoc H., Bompart G., + Bourbon P., Bouteille L. (1983): "Action du fluorure sur le métabolisme + hépatique de la diméthyl-nitrosamine et du benzo(a)pyrène chez le rat"; + Toxicol. Eur. Res. 5: 31

Fredrickson D.S. (1976): + Letter to Hon. J. J. Delaney, Feb. 6, 1976; reproduced in: The National + Cancer Program, Part II: Fluoridation of Public Drinking Water , + Hearings before a subcommittee of the committee on government operations, + House of Representatives, 95th Congress, 1st session, Sept. 21 and Oct. 12, + 1977; Washington, p. 356

Graham J.R., Burk D., + Morin P. (1987): "A current restatement and continuing reappraisal + concerning demographic variables in American time-trend studies on water fluoridation + and human cancer"; Proc. Pennsylv. Acad. Sci. 61:138

Irving C.C. (1966): + "Enzymatic deacetylation of N-Hydroxy-2-Acetylaminofluorene by liver + microsomes"; Cancer Res. 26:1390

Jones C.A., + Callaham M.F., Huberman E. (1988): "Sodium fluoride promotes + morphological transformation of Syrian Ham-ster Embryo cells"; + Carcinogenesis 9:2279

Kinlen L. (1974): + "Cancer incidence in relation to fluoride level in water supplies"; + Commun. Health 6:69

Kinlen L. (1975): + "Cancer incidence in relation to fluoride level in water supplies"; + Brit. Dent. J. 138:221

Kinlen L., Doll R. + (1977): "Cancer and Fluoride"; The Lancet II, 1039

Kraybill H. (1977): + "The National Cancer Program, Part II: Fluoridation of Public Drinking + Water, Hearings before a sub-committee of the committee on government + operations, House of Representatives, 95th Congress, 1st session, Sept. 21 + and Oct. 12, 1977; Washington , Government Printing Office, p. 239

Lasne C., Lu Y.P., + Chouroulinkov L.(1988):"Transforming activities of sodium fluoride in + cultured Syrian Hamster Embryo and BALB/3T3 cells"; Cell Biol. Toxicol. + 4:311

Mahoney M.C., Nasca P.C., + Burnett W.S., Melius J.M. (1991): "Bone cancer incidence rates in New York State: Time trends and fluoridated + drinking water"; Am. J. Publ. Health 81:475

McDonagh M., Whiting P., + Bradley M., Cooper J., Sutton A., Chestnutt I., Misso K., Wilson P., Treasure + E., Kleijnen J. (2000): "A systematic review of public water + fluoridation", NHS Centre for Reviews and Dissemination, University of + York

Meiers P. (1984): + "Zur Toxizität von Fluorverbindungen mit besonderer Berücksichtigung der + Onkogenese"; Verlag für Medizin, Heidelberg

Meiers P. (1986): + "Experimente ueber Fluoridwirkungen im Krebsgeschehen", + Erfahrungsheilkunde No. 6:424-432

NTP (1985): "Statement + to accompany preliminary data tables from the NTP two-year sodium fluoride + study performed Dec. 1981 to Dec. 1983 – prepared July 29, 1985"

NTP (1990): + "Toxicology and carcinogenesis studies of sodium fluoride (CAS No. + 7681-49-4) in F344/N rats and B6C3F1 mice (Drinking Water Studies)", + National Toxicology Program, Technical Report Series 393, U.S. Department of + Health and Human Services

Oldham P.D., Newell D.J. (1977): + "Fluoridation of Water Supplies and Cancer – A Possible + Association?"; Appl. Statist. 26:125 +

Oldham P.D., Newell D.J. + (1979): "Letter to the editors"; Appl. Statist. 28: 184

Perkins C.E. (1952): + "The truth about water fluoridation"; published by the Fluoridation + Educational Society, Washington + D.C., pp. 32-33

Schepers G.W.H. (1961): + "Neoplasia experimentally induced by beryllium compounds"; Progr. + Exp. Tumor Res. 2:203

Schlesinger E.R., Overton + D.E., Riverhead L.I., Chase H.C., Cantwell K.T. (1956): + "Newburgh-Kingston caries-fluorine study. XIII. Pediatric findings after + ten years"; J. Am. Dent. Assoc. 52:296

Schuld A. (2000): + "UK Review", http://www.bruha.com/fluoride/html/uk_review.html + (Oct. 2000)

Smith A. H. (1980): + "An examination of the relationship between fluoridation of water and + cancer mortality in 20 large US + cities"; New Zealand Med. J. 91:413

Swanberg H. (1953): + "Fluoridation of water and its relation to cancer", Mississippi Valley + Medical Journal 75:125

Tannenbaum A., + Silverstone H. (1949): "Effect of low environmental temperature, + dinitrophenol, or sodium fluoride on the formation of tumors in mice", + Cancer Res. 9:403

Taylor A. (1952): + Testimony, Feb. 19, "Chemicals in Food and Cosmetics", Hearings + before the House Select Committee to investigate the use of chemicals in + foods and cosmetics, House of Representatives, 82nd Congress, 2nd session, + pursuant to H. Res. 74 and H. Res. 447, Part 3, U. S. Government Printing + Office

Taylor A. (1954): + "Sodium fluoride in the drinking water of mice", Dental Digest + 60:170

Taylor A., Taylor N.C. + (1965): "Effect of sodium fluoride on tumor growth", Proc. Soc. + Exp. Biol. Med. 119:252

Tsutsui T., Suzuki N., + Ohmori M.(1984): "Sodium fluoride-induced morphological and neoplastic + transformation, chromo-some aberrations, sister chromatid exchanges, and + unscheduled DNA synthesis in cultured Syrian Hamster Embryo cells"; + Cancer Res. 44:938

USPHS (1991): + "Review of fluoride. Benefits and Risks. Report of the ad hoc + subcommittee on fluoride of the Committee to coordinate environmental health + and related programs", Department of Health and Human Services, U. S. + Public Health Service; (Study of Hoover et al. (NCI) in Appendix F)

Wagner H. J. (1981): + "Der Einfluß von Fluorid, Licht und 3,4-Benzpyren auf die Tumorinduktion + bei NMRI-Mäusen"; Inau-gural Dissertation, Erlangen-Nürnberg

Whitmire C.E. (1981) : + "Carcinogenesis bioassay of sodium fluoride"; Tox-Tips 56:56-19

WHO (1969) : + "Principles for the testing and evaluation of drugs for carcinogenicity. + Report of a WHO Scientific Group", World Health Organization, Technical + Report Series, No. 426, Geneva, + p. 19

Yiamouyiannis J., Burk D. + (1975): "Cancer from our drinking water?", Congressional Record, + Proceedings and debates of the 94th Congress, 1st session

Yiamouyiannis J. (1977): + "The National Cancer Program, Part II: Fluoridation of Public Drinking + Water", Hearings before a subcommittee of the committee on government + operations, House of Representatives, 95th Congress, 1st session, Sept. 21 + and Oct. 12, 1977; Washington, Government Printing Office

Yiamouyiannis J., Burk D. + (1977): "Fluoridation and cancer. Age dependence of cancer mortality + related to artificial fluori-dation"; Fluoride 10:101

Ziegelbecker R. (1987): + "Zur Frage eines Zusammenhangs zwischen Trinkwasserfluoridierung, Krebs + und Leberzirrhose"; gwf – Wasser – Abwasser 128: 111

Reprinted with permission of the + author, Peter Meiers.

Andrew Saul is the author of the books FIRE + YOUR DOCTOR! How to be Independently Healthy (reader reviews at + http://www.doctoryourself.com/review.html + ) and DOCTOR YOURSELF: Natural Healing that Works. (reviewed at http://www.doctoryourself.com/saulbooks.html + )

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