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The Case Against Fluoride Page 14
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Most of the following dubious or incorrect statements were highlighted in the booklet as being representative of the contributors’ views.
Dean: “Fluoridation is a proven effective, cheap and safe method. ” Dean goes on to make the remarkable claim that “the literature about the relation of fluorine to health is now so voluminous that the Kettering Laboratory has developed a complete bibliography of over 8, 500 references. ” Our comment: The reports in this bibliography deal with a whole variety of papers on fluoride stretching back to the nineteenth century. However, very few of them deal with either the safety or effectiveness of water fluoridation per se. Moreover, some of the papers cited underline the dangers posed by fluoride, so to use this bibliography, put together by the industry-funded Kettering Laboratory, as evidence that fluoridation is safe was preposterous. This 8, 500 figure is possibly the origin of the claim sometimes made by proponents that “thousands of publications support fluoridation. ”
Kehoe: “The question of the public safety of fluoridation is non-existent from the viewpoint of medical science. ” Our comment: Here is a precursor for the self-serving statement that there is “no valid debate” on the safety and efficacy of fluoride to which we refer in the introduction and chapter 23.
Leone: “We know without question or doubt, that one part per million fluoride in a water supply is absolutely safe, is beneficial, and is not productive of any undesirable systemic effect in man. ”
Parran: Discussing the “wide” margin of safety between optimal and deleterious levels of fluoride, he states: “Less than 20 pounds of sodium fluoride added to one million gallons of water provides one part per million of fluoride ion. In order to produce the first mild symptoms of toxic fluorosis, more than two tons of sodium fluoride would be required. ” Our comment: To support this patently ludicrous 200-fold margin of safety Parran cites a paper by A. P. Black, head of the department of chemistry, University of Florida. 57 Parran did not mention that members of Black’s family were involved in a company that was selling fluoridation equipment to municipalities and that he might have a conflict of interest in his pronouncements on this subject. 58
Despite this veritable barrage of authority, certainty, and respectability, NYC was not fluoridated until 1965—some nine years after this brochure was issued—and even then not by a process that could well be described as democratic. 59
One notable absentee from the roster of leading fluoridation promoters who contributed to the booklet, displaying such unanimous confidence in the safety of fluoride, was Harold C. Hodge. Yet it was Hodge who probably played the most decisive role in assuring the public and decision makers that fluoridation posed no harm. We return to him after a brief consideration of the influence that Edward L. Bernays had on the fluoridation effort.
The Spin Doctors
If Frank Bull, whose antics we described earlier in the chapter, was a clown of spin, spin’s Machiavelli was surely Edward Bernays, master of the science and art of what he called “engineering consent. ”60 Bernays was undoubtedly one of the most influential propagandists and PR men of the twentieth century. He admitted to Chris Bryson, who interviewed him in 1991 and 1993, that he had played a part in promoting fluoridation, explaining that selling fluoridation was child’s play because of people’s inclination to trust doctors and believe what they were told by them. The full extent of his influence is not clear, but most probably it was pervasive. As Bryson relates, he was certainly in touch with Dr. Leona Baumgartner, health commissioner for New York City, who was steering the fluoridation effort there, and advised her how to approach the media to sow the idea that there was no room for controversy over fluoride and that debate on the issue was inapCAF propriate. Bernays’s suggestion was that it would be like “presenting two sides for anti-Catholicism or anti-Semitism and therefore not in the public interest. ”61
The False Claims of Harold Hodge
We saw in chapter 9 that Cox and Hodge produced an article—at a crucial time—exonerating fluoride of any harm other than dental fluorosis. 62 That article was published in the Journal of the American Dental Association in May 1950, just before the critical U. S. PHS endorsement on June 6, 1950. We note above (“Edward Schlesinger and the Newburgh-Kingston Trial”) Harold Hodge’s intimate involvement in the Newburgh-Kingston trial and also Chris Bryson’s revelations about Hodge’s role as chief toxicologist for the Manhattan Project. We should add that in the years after the PHS endorsement Hodge was the most influential voice on behalf of the safety of the fluoridation program. In government and toxicological circles he was the “guru” as far as toxicology and the safety of fluoridation were concerned.
Readers can get a glimpse of Harold Hodge in action by watching the opening sequence of a video (“Professional Perspectives on Water Fluoridation”) produced by the Fluoride Action Network and accessible on its Web site. 63 In this archived footage we first hear Hodge’s commanding voice saying, “There is no health hazard that justifies postponing fluoridation. ” When Hodge comes into view, we see a handsome man wearing a white lab coat standing in front of a blackboard. When he next appears in this film, he is saying and writing on the blackboard that “fluoridation is safe at 1 ppm. ” His impressive appearance and strong delivery must have inspired both contemporary viewers and his colleagues with confidence. How impressive would he have seemed if they had known what we know now, that Hodge led a team that injected plutonium into the veins of patients without their knowledge?64
But his contemporaries did not know that. What they did know was that Hodge repeated again and again that the science showed that “fluoridation at 1 ppm” was perfectly safe. Between 1950 and 1980 he wrote several influential articles and books or chapters of books in which he continued to exonerate fluoridation of any risks, save that of dental fluorosis. 65–74 These articles, chapters, and books appear authoritative, and his pronouncements on this matter were taken as gospel by fluoridation promoters and government officials alike. Perhaps more than any other single factor, Hodge’s influence allowed the Great Fluoridation Gamble to continue for so many years after 1950. However, many of Hodge’s scientific claims were blatantly false, and he should have known that. We will examine six examples of false claims from Hodge’s publications.
1. There is no extra retention of fluoride by persons with kidney disease. In the 1960s Hodge repeatedly asserted—based on his and Frank Smith’s experiments on humans and animals—that people with kidney disease would not retain more fluoride in their body. Hodge claimed this to be true even for animals and humans with severe kidney disease. In 1963, Hodge stated: “Serious kidney injury or disease does not interfere with fluoride excretion, e. g. in rabbits given near-fatal doses of uranium (a kidney poison), in rats poisoned with fluoride, in elderly patients and in children suffering from kidney disease. ”75
It is difficult to imagine how Hodge and Smith were unable to find increased fluoride retention with kidney disease. Today, it is generally accepted that poor kidney function increases fluoride retention. 76 The fact that Hodge and Smith did not find the effect—in repeated studies—should raise eyebrows about the quality of their research. For more on fluoride and the kidneys, see chapter 19.
2. Fluoridation accidents cannot cause acute poisoning. In 1956, Hodge claimed it was “impossible” for an accident with fluoridation equipment to cause acute fluoride poisoning. He further stated that a major fluoridation malfunction could occur every day for ten years and people would still not suffer “serious toxic consequences. ” He said the following:
Sometimes the question is raised, What would happen if there were a mechanical breakdown at the fluoridation plant and all of one day’s supply of sodium fluoride or sodium silicofluoride were suddenly dumped into the water? If this large weight of fluoride could be dissolved, mixed and distributed within an hour, there would still be a factor of safety sufficient to predict that the water could be drunk for ten years or more without serious toxic consequences. . . it is clearly imposs
ible to produce acute fluoride poisoning by water fluoridation. 77
It is now well known that water fluoridation accidents can, and do, result in acute poisoning—even death. A list of documented poisonings can be accessed from the Fluoride Action Network Web site. 78
3. One hundred ppm is the threshold needed to damage kidneys. Hodge’s 1963 claim that 100 ppm is the lowest concentration of fluoride that can damage kidneys is similarly flawed. 79 He made the claim based, again, on his own animal research, as well as a review of other animal studies. How could he have missed McCay et al. ’s article published in 1957? In that study the authors stated the following:
Microscopic examinations were made on the kidneys from 6 animals which had not received fluoride in the drinking water, on 3 receiving 1 ppm, on 1 receiving 5 ppm, and on 6 receiving 10 ppm. Interstitial nephritis was observed in all the animals examined histologically, and the severity increased in proportion to the level of the sodium fluoride in the drinking water. Renal tubule hypertrophy and hyperplasia were found in those animals receiving sodium fluoride in the water but not in the 6 rats which had not been given sodium fluoride supplementation. 80
How did he overlook the 1955 Siddiqui study on humans in India, which found that people consuming water with fluoride levels between 2. 5 and 12 ppm had a “marked impairment of renal function. The mean figures for the maximum and standard clearance were 26. 24 and 39. 67% of the normal respectively. ”81
Animal research published in the past ten years—including a long-term study by Varner et al. 82 (see chapter 15) and a study by NIH-funded toxicologists Borke and Whitford83 —has indicated that fluoride can damage the kidneys of animals at levels as low as 1 and 10 ppm, depending on the duration of the exposure. 84, 85 According to Borke and Whitford, their study “provides the first evidence that one of the effects of long-term F exposure is a change in expression of the plasma membrane and endoplasmic reticulum Ca++ pumps in the kidney. ”86
4. Fifty ppm fluoride in water is the threshold needed to cause thyroid damage. Hodge claimed that fluoride can damage the thyroid in animals or humans only if the level in water consumed reaches 50 ppm. 87 His purported threshold was questionable at the time he made the claim and is even less tenable now.
As early as 1958, Galletti and Joyet published clinical evidence showing daily doses of just 2 to 10 mg fluoride could reduce the activity of the thyroid in individuals with hyperthyroidism88 (see chapter 16). In 1985, Bachinskii showed that thyroid function in humans could be affected at levels in water as low as 2. 3 ppm, 89 and in 1991 a UNICEF-funded research team in China found that humans with iodine deficiencies may be affected by fluoride levels as low as 0. 9 ppm90 (see chapters 15 and 16).
5. Fluoride-induced bone changes (osteosclerosis) are not observed at urine levels lower than 5 ppm. According to Hodge’s 1963 review paper, bone changes do not occur in fluoride-exposed workers if their urine fluoride levels are below 5 ppm. 91 However, his source for that information is suspect. Hodge and Smith in a 1954 paper tell us that the information was derived from a “personal communication” from Dudley Irwin. 92 What they do not reveal is that Dudley Irwin was the medical director for the Aluminum Company of America (Alcoa), hardly a disinterested source of information on an issue that could cost his company millions of dollars in compensation claims. 93
Worse, in making his claim, Hodge mischaracterizes information from India that had been published in an article in the British Medical Journal in 1955. To understand the mischaracterization, simply compare the following findings from A. H. Siddiqui, the author of the article, with Hodge’s 1963 review of this same article:
• Siddiqui: “The urinary fluoride excretion varied between 1. 2 and 5. 8 ppm”94 [emphasis added].
• Hodge: “Crippling fluorosis has been reported from India and China in patients who apparently had ingested little fluoride. . . Fragmentary data on the urinary fluoride excretion, 13–41 ppm, indicate that the fluoride intake may well have been within the limits known to produce osteosclerosis or crippling fluorosis in Western industry” [emphasis added]. 95
6. Prolonged consumption of 20–80 mg/day is needed to produce crippling skeletal fluorosis. For many years Hodge was cited for the claim that people would have to consume 20–80 mg of fluoride per day to develop crippling skeletal fluorosis (the terminal stage). 96, 97 Even though Hodge himself quietly changed this to 10–20 mg per day in 1979, 98 others continued to cite his higher figure. In 1993 the NRC used the lower figure, 99 and in 1997 the Institute of Medicine also used a lower figure. 100 However, as late as 1986 the U. S. EPA was relying on Hodge’s higher numbers in its determination of the safe drinking water standard for fluoride of 4 ppm101 (see chapter 20). The EPA has continued to use this standard for over twenty years, even though the basis for it had been changed by the very author most frequently cited as its source. The NRC review of March 22, 2006, called upon the EPA to determine a new standard after concluding that 4 ppm was not protective of health. 102 But, as we have pointed out, the EPA has yet to do that. So Hodge’s faulty but confident assertions live on.
To his credit, in his 1963 paper, Hodge does acknowledge the cortical bone defects observed in the Newburgh-Kingston study but conveniently ignored by lead author Schlesinger in 1956 and 1957103, 104 (see the section “Edward Schlesinger and the Newburgh-Kingston Trial” above). Hodge stated, “The higher incidence of cortical defects in the Newburgh children’s long bones, although these changes are considered by the specialist in children’s roentgenology to be ‘normal’ variants (Coffey [the correct spelling is Caffey], 1955), deserves additional study. ”105
Those cortical bone defects certainly did deserve additional study, especially in relation to a possible increase in bone fractures in children in fluoridated areas, but that extra study has not taken place in any fluoridated country in the forty-seven years since Hodge made the suggestion.
The Absence of Study
At the end of the day, this issue is not about studies but about the absence of study. Hodge’s last paragraph in his 1963 paper says it all:
What can be said of the general health of those who drink fluoridated water? A persuasive guarantee of the safety of water fluoridation lies in the fact that over 3 million people in the U. S. A. alone have for their lifetime drunk from naturally fluoridated water supplies containing 1 p. p. m. F or more, and over 7 million from supplies containing 0. 7 p. p. m. F or more. Although a large scale epidemiological study is lacking, physicians and public health experts who live in these areas have not become aware of disorders peculiar to these localities or diseases more frequent, more severe, or different than elsewhere. No ill effect of drinking fluoridated water at 1 p. p. m. is known. 106
Hodge wrote the hymnbook from which all fluoridating public health officials have sung ever since: If there was any problem, we would have seen it by now. However, unless you look, you will not find. There wasn’t much looking before the PHS endorsement in 1950, and there has not been much more since in those countries that fluoridate their water. What studies there are have come largely from countries that do not fluoridate their water but have moderate to high levels of naturally occurring fluoride in their water and, as a result, have areas endemic for fluorosis.
The Gamble Continues
In the United States and other fluoridated countries, the Great Fluoridation Gamble has continued, virtually unaffected by genuine scientific investigation, since the 1950s. While the U. S. and other governments pour millions of dollars into endless studies on teeth, little effort has gone into tracking potential harm from fluoridation in other tissues. In fact, governments spend more time and effort trying to discredit studies done in non-fluoridated countries that have found harm from fluoride than in investigating the matter in their own countries (see chapter 22). Moreover, Waldbott107 and Bryson108 have documented what happens to unsuspecting researchers in the United States when they unwittingly stumble on one of fluoride’s adverse effects. Whole careers have been ruine
d for researchers who found health problems with fluoride and dared publish their findings (see chapter 15).
Summary
The early caution about the possible side effects of fluoridation, shown by dental researchers such as Dean and Ast (see chapter 9), rapidly disappeared once the PHS had endorsed the practice in 1950. After 1950, the emphasis switched from somewhat halfhearted attempts to examine health issues to out-and-out promotion of fluoridation, which has involved downplaying and ignoring health effects. The main players set aside any doubts they may have had and embarked on what they saw as a mission, though in reality it remained a gamble. Doubts and caution were replaced with absolute certainty. The science of investigation was replaced by the politics of promotion. This situation has continued to the present day. As a result, fluoride has become a protected pollutant and fluoridation a protected practice. We examine further examples of the poor science that has protected fluoridation in chapter 22.