The Case Against Fluoride Read online

  In the history of the rhetorical support given to fluoridation we see several transitions:

  • Fluoride is bad for teeth becomes fluoride is good for teeth (at low levels).

  • Fluoride is bad for bones becomes fluoride is good for bones (at low levels).

  • Fluoride is a toxic substance becomes fluoride is a nutrient.

  These transitions, all made in the interest of promoting fluoridation, presage similar transitions we examine in later chapters.

  A Short Chronology

  The chronology of events leading up to the crucial year of 1950 can take on very different complexions depending on one’s perspective, whether it be dental, medical, or industrial. We have tried to distinguish these various perspectives by providing a chronology using three different typefaces. We show the dental events in normal type, the medical in bold, and the industrial in italics.

  1800s–1950s—From the late nineteenth century on, there are many lawsuits pertaining to emissions near phosphate fertilizer plants and aluminum and other metal smelters. From about 1930, the cause of harm is suspected to be fluoride. 9

  1902–1931—Mottling of tooth enamel is observed and studied.

  1916—Classic study on dental mottling is conducted by Black and McKay. 10

  1920s–1950s—Doctors are using sodium fluoride to lower thyroid activity in patients with hyperthyroidism.

  1928—McKay observes that tooth decay appears to be less prevalent in communities with dental mottling. 11

  1930—While studying industrial fluoride pollution in Europe, Cristiani suggests that fluoride makes bones more brittle and reports marked lesions in the thyroids of guinea pigs dying from chronic fluorine intoxication. 12, 13

  1931—Three separate research teams identify fluoride in drinking water as the cause of dental mottling, which is renamed dental fluorosis. 14–16

  1931—Alcoa scientists privately confirm dental fluorosis cases near Alcoa’s aluminum smelter in Massena, New York, where the fluoride levels in drinking water are very low. 17

  1932—H. Trendley Dean of the U. S. PHS begins his studies on the incidence of dental fluorosis in the United States and also classifies its various levels of severity. Dean publishes his first paper on dental fluorosis in 1933. 18

  1932—Moeller and Gudjonsson report damage to bone caused by fluoride in Denmark. 19

  1933—DeEds (U. S. Department of Agriculture) reviews fluoride’s toxicity. 20

  1933—Frank McClure publishes “A Review of Fluorine and Its Physiological Effects. ”21

  1937—Roholm publishes his famous treatise Fluorine Intoxication. He bases his massive work on studies of animals and workers from the cryolite industry. 22

  1937—Shortt et al. publish the first study on skeletal fluorosis in India. 23

  1938—Dean reviews Roholm’s study. 24

  1939—Steyn first reports an association between high fluoride levels and goiter in South Africa. 25

  1939—Gerald Cox, an industry-financed researcher, first recommends fluoridation of the water. 26

  1940—Greenwood publishes a review, “Fluoride Intoxication. ”27

  1940—Pandit et al. discover skeletal fluorosis cases at levels as low as 1–3 ppm F in drinking water and find that poor nutrition exacerbates the problem. 28

  1942—Dean et al. publish their famous two-part, twenty-one-city study claiming to demonstrate an inverse relationship between levels of fluoride in the water and tooth decay. Dean’s hypothesis: 1 ppm fluoride lowers tooth decay without causing dental fluorosis in its mildest form in more than 10 percent of children. 29, 30

  1944—McClure claims that boys and young adult men exposed to fluoride up to 5. 2 ppm in water show no increased bone fractures, no difference in height or weight, and no indication of renal injury. 31, 32

  1945—McClure claims that all fluoride ingested up to 4–5 mg per day is excreted in the urine, that none is retained in the bones, and that only higher levels of fluoride ingestion would lead to accumulation in bones. 33

  1945—Ten- to fifteen-year trials of artificial fluoridation begin.

  1948—In Donora, Pennsylvania, during a three-day air inversion, pollution from local factories in a valley kills over twenty people and makes many others sick. Scientific evidence points to fluoride as the culprit, but the U. S. Public Health Service denies this. 34

  1949—The Sugar Research Foundation (representing 130 sugar interests) declares that it needs to find a way to reduce dental caries without reducing sugar consumption. 35 It funds researchers at universities, most notably Dr. Frederick Stare at Harvard, to investigate fluoridation, as well as sugar’s role in nutrition (see chapter 26).

  1950—Cox and Hodge publish an article stating, “There is no other known toxic effect of drinking water containing 1 ppm fluorine than the ‘very mild’ mottling of the teeth. ”36

  1950—The U. S. Public Health Service endorses fluoridation. The American Dental Association and other professional organizations quickly follow suit.

  The Events in More Detail

  We now review this history with the object of examining how much the promoters knew or suspected about fluoride’s other health effects in addition to dental fluorosis (see chapter 11 for more about dental fluorosis).

  1931: Dental Research Begins at PHS

  The history of dental research within the U. S. Public Health Service started in 1931, when one dental officer, Henry Trendley Dean, DDS, was detailed to the Division of Pathology and Bacteriology with the (preliminary) assignment of investigating the occurrence of dental fluorosis throughout the United States. 37 The condition had just been ascribed to fluoride by several groups of researchers. 38–40

  It was to be expected that mottling and staining of the teeth would not be the only toxic effect of fluoride, though this was apparently the only one within the scope of dentistry. After the examination, in February 1932, of a group of children in Minonk, Illinois (where naturally occurring fluoride in the public water system was 2. 8 ppm), Dean wrote in his report to the surgeon general:

  Following the Minonk examination, a new phase of this question seems ripe for further study. Is mottled enamel merely an oral manifestation of a general toxicity, or something similar? The hair of some of these mottled enamel cases is unusually coarse, almost like horse hair. Finger nails are apparently not normal. Two of the three local physicians state that there is apparently an unusually large amount of skin disorders among those using the city water supply. Future surveys will attempt to obtain this additional dermatological data in order to determine whether it correlates with the mottled enamel. 41

  There was no follow-up, however.

  Texas Observations Begin

  According to Dean, in 1934 a pediatrician (Lemmon) from Amarillo, Texas, reported “defective development of the long bones in babies whose diet includes water with fluorides in toxic amount. . . Some of these babies have more tendency to bowing of the legs, even in the face of constant anti-rachitic therapy, thus supporting the theory that the toxic fluorides interfere with bone and dental metabolism. ”42

  In 1936, Dean made two references to the possibility that fluoride might damage the skeleton. In one paper, after discussing the period when children were vulnerable to fluoride’s damage to the enamel, he cited Boissevain and Drea (1933)43 and stated, “There is some indication that the skeletal system might likewise be affected; if this is true, it would be necessary to extend the time range [of the study] to include adults. ”44 Dean also acknowledged that fluoride might make bones more fragile. He gave the following citation to Cristiani’s work: “Cristiani working with guinea pigs found that the fragility of the bones was increased about 20 per cent in the fluorized animals. ”45, 46

  In 1936, even though the PHS felt a need to conduct a “chronic disease survey” in several Texas cities, no mention of bone was made in a memo Dean sent to the assistant surgeon general. 47

  Fluoride’s Toxic Effects

  A number of studies a
nd reviews of fluoride’s toxic effects were published between 1930 and 1940. These included reviews by Floyd DeEds (1933, 1936), 48, 49 Frank McClure (1933), 50 and D. A. Greenwood (1940). 51 DeEds worked for the U. S. Department of Agriculture, which appeared to be far more concerned about the ramifications of fluoride pollution than the U. S. Public Health Service. In addition to DeEds’s work, reports appeared on fluoride’s impact on non-dental tissues, including studies on the bone. 52–56 In 1939, George Abbott published a short communication describing fluoride’s impact on blood structure. 57 Several animal studies were published in Europe, as well as by Phillips et al. in the United States, on fluoride’s possible interaction with the thyroid and parathyroid glands. 58–67 There were also numerous reports from around the world that doctors were using fluorides to lower thyroid function in patients with hyperthyroidism. 68–73

  In 1939, Steyn published the first in a series of studies from South Africa in which he reported the incidence of goiter, an enlargement of the thyroid gland that leads to a gross swelling of the neck and is normally associated with a deficiency of iodine. However, Steyn found goiter occurring in areas that were not deficient in iodine but had high levels of fluoride in the water. 74–76 In 1940, Wilson and DeEds reported dental fluorosis in rats as a result of a synergistic action of fluoride and thyroid hormones. 77

  Dean’s Review of Roholm

  In a very short review of Roholm’s treatise in 1938, Dean was highly respectful but drew no major conclusions about any risks that might be anticipated from people drinking fluoridated water, based on either the osteosclerosis (bone hardening) observed in cryolite workers or the osteomalacia-like disease (bone-softening disease) observed in animals grazing near certain factories in Europe. In his final remarks he merely indicated that the doses that caused skeletal fluorosis appeared to be higher than those that caused dental fluorosis. 78 So it is clear that Dean, as early as 1938, was well aware of serious side effects of fluoride, even though he may have contented himself with the idea that they were occurring at higher doses than those causing dental fluorosis in the communities he was studying.

  Hodges et al. 1941

  Inspired by reports by Roholm and others, and considering that fluoride contamination of food was increasing in this period, Paul C. Hodges and colleagues at the University of Chicago examined people in Kempton, Illinois, where the water contained 1. 2–3 ppm fluoride, and Bureau, Illinois, where the water contained 2. 5 ppm fluoride. They found no radiologically demonstrable sclerosis of the skeleton but suggested that they continue the search for skeletal sclerosis in American communities where the fluoride content of drinking water exceeded 3 ppm. 79 Hodges should not be confused with Harold Hodge, who was to play a very important role in the promotion and defense of the safety of fluoridation (see “Cox and Hodge 1950” below).

  In April 1944, during a meeting of the Technical Advisory Committee for the Newburgh (New York) Fluoridation Study, Dean questioned the validity of the results of the Illinois study because there was no statement as to how long the corresponding water supplies had been in use. There could have been several changes in the water supplies for the study areas, he said, and, further, “we really do not know what the exposure was previous to 20 years ago. ” Dean was of the opinion “that it was necessary to begin with a water supply of a specified number of years of continuous use, such as 30, 40 or 50 years, without any physical changes in the communal water supply involving the installment of new wells or the abandonment of old ones. ”80

  Editorial in JAMA (1943)

  On September 18, 1943, an editorial, “Chronic Fluorine Intoxication, ” appeared in the Journal of the American Medical Association. It stated, “Fluorides are general protoplasmic poisons, probably because of their capacity to modify the metabolism of cells by changing the permeability of the cell membrane and by inhibiting certain enzyme systems. ”

  Most important, the editorial reviewed or referenced some of the key studies on fluoride’s effect on bone and drew special attention to the finding of Pandit et al. , 81 who showed that fluoride’s impacts on bone are made worse by a poor diet, particularly when it is low in vitamin C. Among the symptoms of chronic intoxication by fluoride listed by JAMA were “loss of weight, impairment of growth in young persons, loss of appetite, anemia and cachexia [wasting and weakness]. ”82

  Texas Communities

  At the April 1944 meeting of the Technical Advisory Committee for the Newburgh Fluoridation Study, Dean gave details of still unpublished recent findings from examinations made by the PHS in 1943 at Bartlett and Cameron, Texas, and Britton, South Dakota. Bartlett had 8 ppm fluoride in its water supply; Cameron, 0. 4 ppm; and Britton, about 7 ppm. Dean explained to the committee the following:

  At 8. 0 ppm F some bony changes were found although they did not result in functional impairment. These changes start in the lumbar region and the pelvis. Increased density was found in 13 of the 111 persons with over 20 years’ exposure that were found by house to house enumeration in a population of 1700 to 1800. No changes were found in the controls who were using a water supply with 0. 4 ppm F. In those persons who had osteosclerosis hemoglobin values averaged 2 grams less per person than in those with no evidence of osteosclerosis. It appeared that if fluorine affects the hemoglobin it does so indirectly by producing accretional bony changes which encroach on the bone marrow cavity rather than by direct toxic effect of the hemoglobin producing system.

  No evidence of impaired hearing was reported.

  There were indications of increased incidence of cataract among those 50 years of age or older in the fluoride areas. . .

  Another change was noted in the nails. From 10–20 percent of the younger individuals examined had a rather unusual type of nail structure, the most characteristic aspect being transverse white blotches often completely across the nail, usually symmetrical, and on all the nails, there very frequently being from three to five of these per nail. The incidence of these finally decreased with age, the oldest patient being 57. In the control area with 139 high school students examined, none showed transverse striations. 83

  The 1943 U. S. PHS findings referred to above had not been published. Parts appeared in the famous Bartlett-Cameron study reports that came out in 1954, 1955, and 1957, 84–87 but none of those findings were published before the PHS endorsed fluoridation in 1950.

  Dean’s report of these early Bartlett-Cameron findings at the April 1944 meeting nearly ended the Newburgh fluoridation “demonstration” even before it was begun, as Dean “could not agree that the proposed program could be considered a perfectly safe procedure from a public health point of view. ”88 There is a hint, however, that he was raising these concerns to delay the beginning of the Newburgh-Kingston study so that “his” study in Grand Rapids would be the first fluoridation trial. This idea was articulated many years later by David Bernard Ast, dental director of the New York State Health Department, who alluded to Dean’s behavior at that 1944 meeting as follows: “Territorial prerogative has always existed and continues to exist not only in the animal kingdom, but in the areas of scientific research as well. It is the kind of hide-and-seek play which frequently goes on among research people who have an overriding urge to be on record as the first to discover or the first to publish. ”89

  Despite Dean’s apparent opposition, members of the Newburgh Fluoridation Study group argued in support of the Newburgh-Kingston experiment. Minutes of this meeting indicate that Edward Rogers, assistant commissioner of the Medical Administration, said:

  The proposed demonstration has had much publicity. The cities of Newburgh and Kingston are ready to give enthusiastic cooperation. The setup and authorizations are complete but to date no fluorine has been added. The project can be dropped with no more serious result than embarrassment to the Department. However, committees are getting ready to do this sort of thing and it is much better that it be done under controlled conditions. Cumulative effects, if any, will not appear for a number of years. If D
r. Dean’s studies produce evidence that the cumulative effects may be serious the demonstration can be discontinued. In the past the efficacy of new public health procedures has been difficult to measure because control periods were not set up clearly enough. With the exception of cataract the untoward effects presented here by Dr. Dean can be offset against the advantages which it is hoped will be obtained. 90

  Dr. Rogers also pointed out that further studies might not supply the data necessary to show whether or not there might be any untoward effects. 91

  Others at the meeting concurred that the trial should go ahead. No one mentioned the fact that this ten-year trial would not be giving any information on lifelong exposure to fluoride. 92 The meeting was chaired by Harold Hodge, the chief toxicologist of the Manhattan Project.

  Editorial in JADA (1944)

  Clearly, some of the information about fluoride’s side effects was reaching the editors of the Journal of the American Dental Association (JADA). In a 1944 editorial describing the history of research on dental fluorosis and indicating that fluoride might lower dental caries rates, the editors stated:

  While these data [studies on the fluoride–caries relationship] are certainly speculatively attractive as leading to possible mass treatment of caries, our knowledge of the subject certainly does not warrant the introduction of fluorine in community water supplies generally.