by Paul Connett
That conclusion contradicted the conclusion from the earlier NRC report (1953) of the same study, which stated, “A greater incidence in the high fluoride group of a certain brittleness and blotching of the fingernails, of hypertrophic changes in the spine and pelvis, and of lenticular opacities of the eye requires further epidemiologic investigation. ”21 Are we seeing here the beginning of the PHS spin placed on negative findings, which has been a hallmark of fluoridation promotion to this day?
The Bartlett-Cameron Study Critiqued
If we forget for the moment that the Bartlett-Cameron study was carried out by an agency that had already declared its support for the policy it was investigating, to a casual observer in 1954 the study must have looked fairly convincing, except for the glaringly obvious fact of having so few people in the study group. However, the study had many other weaknesses, and one of the first to spot them was Dr. Frederick Exner in 1957.
Some of Exner’s criticisms of the report were:
• Both cities had fluoride in their water, Bartlett at 8 ppm and Cameron at 0. 4 ppm. Both were located in Texas, where a lot of water is drunk because of the very hot weather. There, 0. 4 ppm is not a low concentration. (In fact, it is over half the level—0. 7 ppm—recommended by the CDC today for communities in hot climates. ) So it was very unfortunate that the study did not include a genuine control community with little fluoride in its water. Moreover, the 8 ppm figure for Bartlett may not have been accurate. The Texas Health Department listed the value as 6. 6 ppm. 22
• Although all subjects had lived in their respective communities at least fifteen years, only eleven (14. 5 percent) of those studied in Bartlett had been born there, or had lived there during the period of tooth and bone development. Consequently, the statement that 11 or 12 percent of those studied in Bartlett showed evidence of osteosclerosis was misleading; actually, at least 82 percent of those exposed to Bartlett water during the bone-forming period showed evidence of osteosclerosis. 23
• The actual data published were insufficient to allow any independent evaluation. For example, two enzymes important for bone development, called acid phosphatase and alkaline phosphatase, with which fluoride was known to interfere, were tested for “when indicated. ”24 With no information about what the indications were, how many people were so tested, or what was found, the reader was told merely that “when the data are reviewed critically, it is clear that the medical characteristics of the two groups, with the exception of dental fluorosis, do not differ more than would be expected of two comparable towns with or without an excess of fluoride in the water supply. ”25 The trouble with that was that there were no data to review. Instead of recording what was found, the authors simply scored how many people were classified as abnormal in various respects in the two communities. Neither quantitative nor qualitative criteria of normality were given; and there was no possible basis for correlating actual findings with probable fluoride intake or other pertinent factors such as duration of intake or age of exposure. 26
• Both in 1943 and in 1953, “significantly” more abnormalities of the neutrophilic white cells were reported at Bartlett than at Cameron. The figures given indicated that the differences were in morphology rather than in relative number. Yet for unstated reasons the authors downplayed the observation, simply claiming that “when viewed in the light of clinical experience, this finding does not suggest an association with fluoride intake. ”27
To Exner’s criticisms we would add some of our own. Although the authors looked at thyroid function, they did not give any meaningful details of how thyroid function was assessed. As we document in chapter 9, a lot of information about fluoride’s possible interaction with the thyroid was published between the late 1920s and the 1950s. This included animal studies, case studies of doctors treating hyperthyroid patients with sodium fluoride, and cases of fluoride-induced goiter in communities with an adequate iodine intake. So it is most unfortunate that the examiners were not more meticulous in recording their findings on the thyroid.
We also note that the examiners recorded “arthritic change” but did not give any details. There are different forms of arthritis. It would have been more helpful if we had been told how many people complained of backache and aching joints. This reveals an attitude among promoters of fluoridation that has been retained right up to the present time. Promoters have been forced to acknowledge through the work of Kaj Roholm 28 and researchers in India29, 30 that excessive exposure to fluoride can lead to serious bone problems, ultimately leading to crippling skeletal fluorosis, in which the whole backbone is essentially frozen into one curved block. The tendency of promoters for many years has been to take seriously only the latter stages of this problem instead of the earliest manifestations, which are similar to the symptoms of arthritis (see chapter 17). We now know that the first indications of fluoride poisoning of the bone do not show up on X-rays (see chapters 13 and 17), so the emphasis placed on X-rays in the Bartlett-Cameron study, with no discussion of any evidence of pains in the joints and bones, was misplaced. Today, it is well established that there are several distinct stages of skeletal fluorosis, 31 but even in the 1950s researchers should have been aware of more subtle effects on the bones and ligaments than those that showed up on X-ray plates.
When exposing the whole population to a pharmacologically active substance, it is the earliest effects one should be concerned about. The subtle shifts are of critical importance in whole-population exposures; in a very small study like the Bartlett-Cameron study, even the gross effects are difficult to find, let alone more subtle changes. If researchers today suggested that a population of 180 million be exposed to a toxic substance based on studies done on approximately one hundred people, they would be laughed out of court.
An important point was raised by Dr. George Waldbott in The American Fluoridation Experiment when he stated, “Another reason why fluorosis is not recognized is that physicians, like other people, are inclined to accept as normal the things seen frequently. ” Referring to the Bartlett-Cameron study, Waldbott explained, “X-rays were made of Bartlett residents, and read by a competent radiologist at the Scott White Clinic in Texas. He called them all normal. They were then sent to a radiologist in New England. He found abnormal bone density in 11 percent of the people. The findings were normal for Texas, where fluoride waters are common, and quite abnormal in New England, where they are rare. ”32
There are so many weaknesses in this study that one is forced to question the objectivity of the observers. Were they really looking for all indications of harm or were they merely producing a study to vindicate the 1950 PHS decision to go ahead with fluoridation? We know little about the lead author Nicholas Leone’s involvement with fluoridation prior to this report, but we know more about his activities shortly after it was published.
Leone and Industry
Chris Bryson wrote, “In August 1955, during the Martin trial [farmer Paul Martin was suing the Reynolds Metal Company for damage caused to his farm and his family from fluoride emissions], the public servant Leone spoke with a senior attorney for Reynolds, Tobin Lennon, who was also a member of the Fluorine Lawyers Association, directing Lennon to a federal safety study on fluoride that Leone had recently concluded in Texas [the Bartlett-Cameron study]. ” Bryson continues, “As the Martin trial hung in the balance, the government’s Dr. Leone burned up the long distance telephone lines to Oregon answering questions from Reynolds’ attorney. ”33
According to Bryson, Leone was also on friendly terms with Alcoa’s fluoride doctor, Dr. Dudley Irwin, and wrote to Irwin after a meeting, “We are all very enthused about a group presentation at some carefully selected meeting in the near future. . . I hope that you have had the opportunity to give further thought to the type of meeting that would best suit our purpose. ”34
Thus it is not clear whether Nicholas Leone was working in the corporate or the public interest as far as fluoridation’s safety was concerned. For another major player, Dr. Robert Ke
hoe, there is absolutely no doubt in whose interest he was working.
Robert A. Kehoe and the Kettering Laboratory
Kehoe was a key figure in the development of the fluoride story from 1930 onward. As detailed by Bryson, Kehoe came to prominence in the 1920s by successfully “sanitizing” the images of two industrial chemicals developed in the laboratory of Charles Kettering, vice president and director of research at General Motors—the gasoline additive tetraethyl lead (TEL) and the refrigerant gas Freon (Dupont’s trade name for various chlorofluorocarbons that were eventually to become notorious as depleters of the ozone layer). Both of these raised safety concerns at the time, TEL because of its toxicity and Freon because of its lethal decomposition, when heated, into the nerve gas phosgene and the toxic and corrosive gas hydrogen fluoride. Thanks largely to Kehoe’s research, both TEL and Freon enjoyed several decades of profitable existence in automobile fuel tanks and refrigeration units. Kehoe was rewarded in 1930 with the directorship of a new laboratory at the University of Cincinnati, named after Charles Kettering and funded initially by the Ethyl Corporation, DuPont, and the Frigidaire Division of General Motors. The Kettering laboratory under Kehoe became a bastion for industries threatened by numerous lawsuits claiming damage or injury from fluoride and other industrial pollutants. The fluoride-producing industries included aluminum smelting, Freon manufacture, and later the Manhattan Project’s uranium enrichment plants, which exposed workers to high concentrations of fluoride or released large quantities in to the atmosphere. One element in deflecting such lawsuits was to establish in the public mind that fluoride was safe by promoting its addition to the public water supply. 35 In the words of Herbert Needleman, referring to Kehoe’s role in protecting tetraethyl lead, he “was not burdened with a hypertrophied sense of modesty. ”36 His personality enabled him to deal persuasively with lawyers, captains of industry, and senior politicians alike.
Kehoe’s assistant, Edward Largent, devoted much of his time to attempting to disprove the conclusions of Kaj Roholm, whose work implicated fluoride in the production of skeletal deformities (see chapter 9) and provided a basis for compensation claims from workers affected by industrial exposure to fluoride. 37 Whatever it may have admitted in private, the Kettering Laboratory’s public stance was to exonerate fluoride from causing harm in whatever context was under discussion. This was a valuable service to its industrial sponsors and to the Fluorine Lawyers Association (a group of individuals who specialized in defending corporations against fluoride-related litigation).
Although having relatively little overt involvement in the water fluoridation effort, the Kettering Laboratory did publish a PHS-funded booklet in 1963 titled The Role of Fluoride in Public Health: The Soundness of Fluoridation of Communal Water Supplies. A Selected Bibliography. 38 There is no doubt that Kehoe supported water fluoridation or that successful fluoridation campaigns provided a powerful boost to the Kettering Laboratory’s agenda.
Edward Schlesinger and the Newburgh-Kingston Trial
In 1956, the report on the Newburgh-Kingston trial was published. David Ast and others summarized the dental findings39 and Edward Schlesinger, MD, a pediatrician who worked for the New York State Department of Health, was the lead author in the summary of the health findings. 40 It is the latter we examine here. Three very interesting findings pertaining to health emerged, but they were apparent only to those who carefully read the study. First, a greater number of cortical bone defects were found in the fluoridated community compared with the non-fluoridated one. The ratio was about 2:1, and the finding was statistically significant. Second, young girls in the fluoridated community, on average, reached menstruation approximately five months earlier than those in the non-fluoridated community (see chapters 16 and 17). Third, some blood abnormalities were observed. None of these observations were thought to be significant at the time. Schlesinger et al. concluded, “No differences of medical significance could be found between the two groups of children [Newburgh versus Kingston]; thus further evidence was added to that already available on the safety of water fluoridation. ”41
It should also be noted that no studies on adults had been attempted up to that point in the Newburgh trial or any of the other early trials. As far as adults were concerned, the confidence that there would be no long-term effects rested almost entirely on the limited Bartlett-Cameron study discussed above. 42
Edward Schlesinger: A Quick Convert
It is fascinating to see how quickly the lead author of the Newburgh-Kingston trial, Dr. Edward Schlesinger, cast off the mantle of “objective observer” to become an unapologetic promoter of fluoridation. In a presentation given to the annual meeting of the Academy of Pediatrics in October 1956, just six months after publication of the final report of the Newburgh-Kingston study, he produces many examples of the standard rhetoric that have become familiar hallmarks of fluoridation promotion ever since. 43
First, he uses the authority of endorsements. He tells his audience that “the leading medical, dental and related scientific organizations have expressed a belief in the safety of fluoridation of water” and that “water fluoridation is universally accepted among reputable professional groups. ” The opposition, on the other hand, “is based, with rare exceptions, on emotional grounds. ” 44 [all emphasis added]
He argues that the claim “that fluoridation is mass medication” is invalid, since “fluoridation is simply a preventive measure and no different in principle from the legal requirement in some states that all bread and flour sold in these states be enriched to meet established minimal nutritional levels. ”45 He, like promoters who still use that kind of argument today (see chapter 25), fails to note that fluoride is not an essential nutrient like the enrichments added to flour and bread.
As far as the safety of fluoridation is concerned, he uses the typical high-dose versus low-dose claim that “most of the voluminous literature on the toxicology of fluorides is irrelevant to the present discussion because the quantities of fluoride involved are usually the equivalent of drinking water with concentrations at least 100 to 200 times higher than the levels recommended for prevention of dental caries. ”46 No citation is given to support such a blatantly false claim. Schlesinger should have known that researchers in India had found bone problems at levels of fluoride in water much lower than this. For example, Pandit had observed bone problems at levels between 1 and 3 ppm. 47
Schlesinger adds that “the margin of safety for non-dental effects is far greater than any possible increase in intake of fluid for short or long periods of time”48 but fails to reference any margin-of-safety analysis that would support such a claim.
As far as the Newburgh-Kingston trial is concerned, he states that the study “failed to show any non-dental differences that could be ascribed even remotely to the ingestion of fluoridated water” [emphasis added]. 49 He makes no mention of the significant difference in cortical bone defects in boys, the earlier onset of menstruation in young girls, or the blood abnormalities mentioned above. It is one thing to dismiss the relevance or significance of those findings, but to say that there were no differences that were “even remotely” related “to the ingestion of fluoridated water” is a huge stretch.
It is highly likely that Schlesinger inherited this dismissive attitude about fluoridation’s risks from Harold Hodge. Although Hodge’s name does not appear in the list of authors of this final report, he was, according to Bryson, heavily involved in the Newburgh-Kingston study. Reputedly, the officials involved in the Manhattan Project were keen to have low-dose data for fluoride’s impact on humans, for possible use in lawsuits that the nuclear industry might face for fluoride damage to the workers on the production lines or to farms in the localities of their plants. 50
We discuss the important role of Harold Hodge in the promotion of fluoridation in “The False Claims of Harold Hodge” below.
The Push to Fluoridate New York City
The missionary zeal of fluoridation proponents reached it
s full expression in the effort that was deployed to introduce fluoridation in the city of New York. By 1956, thirty million U. S. citizens and ten major cities had fluoridated water. New York would be the jewel in the crown and pave the way for further successes. In 1957 a propaganda campaign was launched with the publication and distribution of a booklet titled Our Children’s Teeth. 51 The sponsor was a body called the Committee to Protect Our Children’s Teeth, Inc. , a group of luminaries that included the celebrated pediatrician and parental guidance guru Benjamin Spock. It was funded by the W. K. Kellog Foundation, famous for both its good works and protecting sugar interests. 52 The booklet included statements from several of fluoridation’s big guns whom we have already met—Dean, Ast, McClure, Schlesinger, Leone, and Kehoe—and some others, including Thomas Parran, a former surgeon general, and Herman E. Hilleboe, the commissioner of health for New York State. The booklet merits attention since it provides a blueprint for the tone, content, and even actual wording of many fluoridation promotion documents that were to follow.
There was a little more reason behind the contributors’ missionary zeal than may be apparent today. For one thing, dental caries were much more prevalent then than now. However, Hilleboe could not be accused of understating the problem in his contribution, describing the “progressive accumulaCAFtion of dental disease” as a “national calamity” that was beyond the muscle of the dental profession to control. 53 In that context, it is understandable that a measure apparently offering some degree of protection was seen by many as a godsend. That said, the booklet is awash with errors, evasions, and half-truths, particularly where it is attempting to sow the idea of fluoridation’s safety. Hilleboe himself set the ball rolling by stating that “no satisfactory explanation has been advanced for the great prevalence of dental decay in our population;”54 he avoided mentioning diet, especially sugar consumption, and microbial activity, although a connection had long been recognized. 55 Hilleboe also adopted the tactic, repeated many times since (see chapter 23), of denigrating opponents, describing them as “food faddists, cultists, chiropractors, and misguided and misinformed people who are ignorant of the scientific facts involved. ”56
