by Paul Connett
Sodium fluoride is a highly toxic substance, and while its application in safe concentrations, and under strict control by competent personnel, may prove to be useful therapeutically, under other circumstances it may be definitely harmful.
To be effective, fluoride must be ingested into the system during the years of tooth development, and we do not yet know enough about the chemistry involved to anticipate what other conditions may be produced in the structure of the bone and other tissues of the body generally.
We do know that the use of drinking water containing as little as 1. 2 to 3. 0 parts per million fluorine will cause such developmental disturbances in bones as osteosclerosis, spondylosis and osteoporosis, as well as goiter, and we cannot afford to run the risk of producing such serious disturbances in applying what is at present a doubtful procedure intended to prevent development of dental disfigurements among children.
With regard to the safety margin in the fluoride content of drinking water, the reported amount of fluorine in the water cannot be taken as the criterion for the amount taken in the system, as in an intensely hot climate much larger quantities of water would be imbibed and hence a much larger quantity of fluorine would be taken into the body. Another feature of the complex problem that demands consideration, in attempting to take advantage of the therapeutic value of fluorine, is the quantity absorbed by the system at various age periods of life. . .
Because of our anxiety to find some therapeutic procedure that will promote mass prevention of caries, the seeming potentialities of fluoride appear speculatively attractive, but, in the light of our present knowledge of the chemistry of the subject, the potentialities for harm outweigh those for good. 93
These comments were made just a few months before the first trials of fluoridation were to begin.
A few weeks after the JADA editorial, on October 30, 1944, David Ast acknowledged in a paper he gave at the meeting of the New York Institute of Clinical Oral Pathology that there were unresolved health questions about the addition of fluoride to the public water system when he asked, “Are there any cumulative effects—beneficial or otherwise, on tissues and organs other than the teeth—of long continued ingestion of such small concentrations as 1. 0 part per million of fluorine in water? Again, there is much presumptive evidence that there are no such effects: but, until that is demonstrated, the procedure outlined in this paper must be regarded as an investigation. ”94
Reassuring the New York Health Commissioner
A letter from Dean’s boss, Rolla E. Dyer, director of the National Institutes of Health, reached the desk of New York State’s health commissioner, Edward S. Godfrey, in November 1944. 95 In an attempt to downplay the unpublished Bartlett-Cameron findings, this letter referred to some “selective service” data acquired in the meantime by biochemist Frank James McClure (see the following section), who claimed an equilibrium between the fluoride content of water and fluoride excretion in the urine. Furthermore, in Colorado Springs, where the water supply contains about 2. 5 ppm fluoride naturally, three of five physicians interviewed by Dean were of the opinion that there was nothing unusual in respect to the prevalence of cataracts. Evidently, Dyer’s letter did not wholly clarify some of the issues raised earlier.
McClure’s 1944 and 1945 Papers
In 1944, Frank McClure published a paper on the relation of fluoride levels in water to the height, weight, and bone-fracture experience of 1, 458 high school boys and 2, 529 young men taking a physical examination during army recruitment. He concluded that “there was no relation of fracture experience to fluoride exposure. The average height and body weight of all the boys compared favorably with other height-weight data and accepted standards. The height-weight data were not related to fluoride exposure. ”96
In 1955, Dr. Fred Exner, in a report prepared for the City of New York, pointed out several problems with the McClure and Kinser study:
The data for about one-fourth of the subjects were copied from army records which had nothing to do with either bone fragility or fluorides. The other subjects were asked by McClure where they lived and how many broken bones they had had. That was the examination. . . In some cases he measured the height and weight himself. In other cases, they measured each other. . . He took urine samples which he pooled. . . Two of the fluoride localities had only 0. 2 ppm of fluoride in the water; while one of the non-fluoride places had 1. 8 ppm. . . McClure, in his introduction, observes that sometimes fluorine makes bones fragile, and sometimes it makes them stronger. This would invalidate his statistical study in advance. 97 [emphasis added]
In 1945, on the basis of a study of five young men aged nineteen to twenty-four, Frank McClure published an article stating that all the fluoride ingested, up to 4–5 mg per day, was excreted in the urine; none was retained in the bones. Only higher levels of fluoride ingestion, he claimed, would lead to accumulation in bones. 98
A subsequent study by Patricia Wallace-Durbin in 1954 using radioactively labeled fluoride showed that this was not correct (at least not in rats), 99 and today most scientists accept that approximately 50 percent of ingested fluoride is excreted in the urine and most of the rest is stored in the bone. 100 However, at the time, McClure’s erroneous finding was very influential in diminishing concerns about fluoride’s impact on bone.
Exner explained why he spent so much time critiquing McClure’s work: “There are quite reliable reports, over a period of more than 40 years and from all over the world, of serious cumulative, chronic fluoride poisoning, especially of the teeth and skeletal structures. All these are lightly brushed aside on the basis of McClure’s work, as having no applicability where there is only one part per million of fluoride in the water. ”101
The AAAS Conference 1944
The American Association for the Advancement of Science (AAAS) held its first conference on fluoride in Dallas in December 1941. Its second conference, at which McClure presented a summary of his 1944 article, was held in Cleveland in September 1944. The proceedings, titled Dental Caries and Fluorine, were published in 1946, 102 which allowed McClure to update his paper to include his 1945 findings. 103 Most of the other papers concerned only dental effects, but several statements indicated that some of the other authors were aware that not everything was known about the long-term health effects of fluoridation. Thus the timing of the conference (1944) and the publication (1946) is interesting because one came before the fluoridation trials began and the other came after.
In the foreword, for example, Kitchin and Moulton opined that the belief that fluoride might reduce tooth decay “does not imply that the cities and villages in this country should precipitately begin to introduce fluoride into water supplies. Science is too cautious and thorough-going for such actions. But the evidence is now sufficient to raise high hopes for the future. ”104
H. Trendley Dean, while noting that “the question of low fluoridation of the domestic water supply for the control of caries appears sound, ” provided a note of caution when he said, “Much investigative work, however, is necessary before a recommendation can be given for its general application. . . specifically planned, epidemiological studies should clearly demonstrate the safety of low fluoridation as it might relate to other aspects of the community’s general health. ”105
Robert Weaver, in discussing studies conducted in the British Isles and India, stated, “In Somerset, Dagmar Wilson (1941) examined a number of children in two areas where the incidence of goiter was high, and found that about 15 percent of the children had some degree of dental fluorosis. She considers that fluorine may be one factor, though possibly only of subsidiary importance, in the causation of endemic goiter. ” This should have been another warning signal to look for changes in thyroid function in the upcoming fluoridation trials. 106, 107
Weaver also discussed Marshall Day’s studies of fluorosis in India. 108 In Kasur, a village in the Punjab with nine water supplies, of which one had a fluoride level of less than 1 ppm, five had levels between 1 and 2 p
pm, and three contained 2. 2, 4. 2, and 6. 2 ppm, respectively, Day reported that 96 percent of 203 children had dental fluorosis, according to Weaver. 109 Summing up Day’s work, Weaver says he found that “the children of Kasur showed no signs of fluorosis other than the characteristic dental condition and, though rheumatoid and other arthritic conditions have been observed in old people in the endemic area, there was no convincing evidence that these conditions had anything to do with fluorosis. ”110 This not only should have been a warning signal to look for early signs of arthritic symptoms in naturally fluoridated areas, but also should have drawn further attention to the problems of looking only at children, not at adults, in the upcoming fluoridation trials.
Preliminary Report from Newburgh-Kingston Study
The Newburgh-Kingston fluoridation experiment started in 1945 and was closely tracked, as mentioned previously, by Harold Hodge of the Manhattan Project. 111 A preliminary report, presented on October 25, 1949, before the Dental Health Section of the American Public Health Association, “failed to disclose any significant deviation in any of the factors studied. ”112 However, only children—no adults—were examined in Newburgh and Kingston. The preliminary report was not published until June 1950—that is, after the Public Health Service had endorsed fluoridation. In the meantime, according to McNeil, certain fluoridation “zealots, ” especially in Wisconsin, where the state dental director, Frank Bull, was leading the charge, were making huge efforts to install fluoridation in as many cities in that state as possible. 113
Cox and Hodge 1950
Before we examine the important research paper published by Cox and Hodge in 1950, 114 let us remind ourselves who Cox and Hodge were. Gerald Judy Cox was a researcher at the Mellon Institute whose research in the 1930s was funded by the Aluminum Company of America (Alcoa). According to Bryson, it was Alcoa’s director of research who suggested to Cox that fluoride might make strong teeth. 115 Cox soon reported that fluoride gave rats cavity-resistant teeth and in 1939 made the first public proposal to add fluoride to public water supplies. Shortly after there were rumblings at the American Water Works Association that the safe level of fluoride in water should be lowered to 0. 1 ppm to protect against dental fluorosis, Cox wrote, “The present trend toward complete removal of fluorine from water and food may need some reversal. ”116
Harold Carpenter Hodge, from the University of Rochester, was the chief toxicologist for the U. S. Army’s Manhattan Project. In her book The Plutonium Files, Eileen Welsome documents that during that project Hodge supervised experiments in which unsuspecting hospital patients were injected with uranium and plutonium. 117 After the war Hodge chaired the National Research Council’s Committee on Toxicology and became the leading scientific promoter of water fluoridation in the United States. 118 We return to Hodge’s important role in promoting fluoridation in chapter 10.
In an article titled “The Toxicity of Fluorides in Relation to Their Use in Dentistry, ” which appeared in the April 1950 issue of The Journal of the American Dental Association, Cox and Hodge reviewed some of the literature on fluoride’s health effects and in their eight-point summary concluded the following: “3. Chronic, crippling fluorosis will never appear as a result of dental uses of fluorides. . . 6. There is no other known toxic effect of drinking water containing 1 ppm fluorine than the ‘very mild’ mottling of the teeth. ”119
In order to dismiss concerns about fluoride’s effects on bone, Cox and Hodge relied entirely on the studies of McClure discussed previously. 120 To dismiss the possibility that fluoride might interfere with thyroid function, they cited only one study, by Evans and Phillips. 121 Cox and Hodge wrote, “Evans and Phillips reviewed the evidence of fluorides as influencing the course of hyperthyroidism. They analyzed thyroids of forty thyroidectomy cases for fluorine and iodine and compared the findings with the basal metabolic rates. They concluded: ‘The data obtained gave no definite evidence that fluorine in any way played a part in human hyperthyroidism by its action on the thyroid gland. ’”122
There are several problems with Cox and Hodge using this single citation to dismiss concerns about this important issue:
1. The article by Evans and Phillips they referenced was actually an article by Evans, Phillips, and Hart that appeared in the Journal of Dairy Science and was titled “Fluoride Storage in Cattle Bones, ” which seems a long way from the subject matter quoted by Cox and Hodge. In addition, the quote cited by Cox and Hodge does not appear in that article. Cox and Hodge probably meant to reference another article by Evans and Phillips titled “The Fluorine Content of the Thyroid Gland in Cases of Hyperthyroidism, ”123 which does contain the quote.
2. While citing this single paper coauthored by Phillips, Cox and Hodge ignored the series of experiments that this same author and his coworkers performed with a number of animals (e. g. , rats and chicks), in which fluoride did show interactions with the thyroid. 124–127
3. They failed to mention other animal studies indicating fluoride’s interaction with the thyroid and parathyroid glands. 128–133
4. They ignored all the clinical evidence provided by doctors in Argentina and Germany who were using fluorides to lower thyroid function in patients with hyperthyroidism, cited previously in this chapter. 134–139
5. They ignored Steyn’s work in South Africa, in which he reported cases of goiter occurring in areas that were not deficient in iodine but had high levels of fluoride in the water. 140, 141
6. They ignored the evidence from U. S. Department of Agriculture scientists Wilson and DeEds, who reported dental fluorosis in rats as a result of the synergistic action of fluoride and thyroid hormones. 142
Cox and Hodge thus used one paper from McClure to dismiss all concerns about fluoride in bone and one paper from Evans et al. (with the wrong citation) to dismiss all concerns about fluoride and the thyroid.
As far as the agenda of those promoting fluoridation was concerned, this Cox and Hodge article came at a propitious time—about a month before the PHS endorsed fluoridation.
A Key Year in the History of Fluoridation
As far as the dental-medical perspective was concerned, 1950 was the key year in the history of water fluoridation in the United States. We will step back and summarize the forces at play. At that time there was a clash between two groups. On the one hand, now that the fluoridation trials were under way and the early results looked promising, dentists and dental researchers had moved from the hope that ingesting fluoride would reduce tooth decay with minimal side effects to a wild enthusiasm for a simple way of fighting tooth decay with no downside. On the other hand, a few skeptics were concerned that the rush to fluoridate was premature and that not enough was known about its long-term impacts on other tissues.
On the side of the skeptics was a considerable amount of scientific literature, particularly from Europe and from the U. S. Department of Agriculture, that fluoride posed problems to the bone and the thyroid. Some skeptics had gone as far as to write editorials on the matter in the journals of both the AMA143 and the ADA. 144
Those who argued that fluoridation was safe—safe enough to warrant fluoridating any community in the United States—countered the health concerns with just five studies:
1. McClure’s 1944 study claiming no increased bone fractures, or changes in weight or height, in young boys and army recruits from areas with fluoridation levels as high as 5. 2 ppm145
2. McClure’s 1945 study claiming that no fluoride below an input of 5 mg a day accumulated in the bone146
3. A short review of health concerns in an article by Cox and Hodge147
4. Dean’s report on the unpublished 1943 findings from the ongoing studies in Bartlett (8 ppm) and Cameron (0. 4 ppm), Texas148
5. Preliminary unpublished findings from the Newburgh, New York, trial, which had been in progress for only a few years (those preliminary findings did not appear in print149 until after the PHS endorsement)
On that basis, without any of the trials completed, the f
luoridation enthusiasts won the day and the U. S. Public Health Service endorsed fluoridation in 1950. 150
Donald McNeil’s account of these events would lead the reader to believe that this was merely a battle between cautious and overzealous dental researchers. 151 Three other things occurred, however, that may have helped put pressure on the PHS to endorse fluoridation.
The Donora Accident
In October 1948, in Donora, Pennsylvania, an air inversion in the valley trapped the air pollution from a steel works and a zinc smelter for three days, killing at least twenty people and making hundreds of others sick. The most likely culprit, from a scientific point of view, was fluoride, but a report from the PHS denied it. This raises a serious question: Why would the PHS rush to aid the U. S. steel industry on this matter? A full answer to this question can be obtained by reading Chris Bryson’s thoroughly documented book The Fluoride Deception. 152
Suffice it to say here that this incident must have caused great fear among the industries producing fluoride emissions. First of all, fluoride emissions were produced in large quantities by many industries in the United States, especially the metal industries. Second, with post–World War II expansion those emissions were expected to rise considerably. Third, they left a unique telltale biomarker in children (dental fluorosis) that was visible to the naked eye. By this time it was known that children living near aluminum smelters were showing signs of dental fluorosis even when there was little or no naturally occurring fluoride in their water supply. 153 Fourth, the Donora incident made it clear that this pollutant could kill people. There could no longer be any question that, in addition to lawsuits from farmers complaining of damage to their crops and cattle (relatively small settlements), there would be complaints from people that their health—and even their lives—had been compromised by fluoride emissions downwind of those plants. That could have led to far more costly settlements. Then there was the even more costly threat that workers in the plants themselves (particularly workers in the aluminum smelter pot rooms) might sue for damages to their health.
