The Case Against Fluoride

by Paul Connett

  Douglass’s Methodology

  The methodology described by Douglass et al. could not test the central thesis of Bassin’s work, because the biometric of exposure those authors used—bone fluoride levels found at the time of diagnosis or autopsy—could not ascertain exposure during the years of age (six to eight) so critical to Bassin’s thesis. 75, 76 Fluoride accumulates over time, so a level at, say, age twenty gives no indication of the level of exposure at six, seven, or eight years of age.

  Moreover, the controls used in the promised Douglass-Hoover study are other bone cancers. The choice of that control makes the assumption that none of those bone cancers are caused by fluoride. The study would be invalidated if fluoride were associated with any of those cancers, like Ewing’s sarcoma, which is not impossible. 77

  Despite the non-appearance of the promised Douglass-Hoover study, and the limitations in the methodology they have used to refute Bassin’s work, the Douglass-Joshipura letter is being used by fluoridation proponents in several countries as if it were the final word on the issue. To use the promise of an unpublished study to negate Bassin’s published conclusions is extraordinary. Clearly, a double standard is operating here. The same proponents who are now using the promise contained in the Douglass-Joshipura letter of 2006 to negate Bassin’s findings previously used the fact that her thesis was unpublished to deflect attention from her work.

  This is how the Australian National Health and Medical Research Council (NHMRC) used the Douglass-Joshipura letter in the systematic review it published in 2007:

  The attention of the reader is drawn to a Letter to the Editor that appeared in the same issue of Cancer Causes and Controls by co-investigators on the larger Harvard study (Douglass &Joshipura, 2006). The authors point out that they had not been able to replicate the findings of Bassin and colleagues in the larger study that included prospective cases from the same 11 hospitals. Furthermore, the bone samples that were taken in the broader study corroborate a lack of association between the fluoride content in drinking water and osteosarcoma in the new cases. As Bassin and colleagues acknowledged, the shortcomings of their study mean that their results should be interpreted with caution pending publication of the larger study results. 78

  A local health authority pushing for fluoridation in Southampton, UK, used the Douglass-Joshipura letter in its public consultation brochure in 2008. The authors do not make it clear that the reference (13) they cite is not a study or a “comprehensive review” but a letter promising a study:

  Since 2006, fluoridation opponents have pointed to a study in the United States of America (12) [the Bassin study] that appears to suggest a possible increase in osteosarcoma (bone cancer) rates in young males—but not females—living in fluoridated areas. However, this was part of a larger study (13) [the Douglass letter] looking at many more osteosarcoma cases over a longer period of time and including an examination of bone samples. This more detailed and comprehensive review had found no link between water fluoride levels and osteosarcoma. The researchers therefore advised caution in selectively interpreting the results of the smaller study in isolation. 79

  This is how Dr. Peter Cooney, the chief dental officer of Canada, described the Bassin study and the Douglass-Joshipura letter in a presentation he gave in Dryden, Ontario, on April 1, 2008: “You are going to hear about osteosarcoma. . . some of the studies that did show that there may have been a concern in young males with osteosarcoma have been—in the bigger studies—completely discounted. ”80

  California Proposition 65

  Proposition 65 is the name given to the California Safe Drinking Water and Toxic Enforcement Act of 1986. This act requires the governor of California, at least once a year, to publish a list of chemicals known to the state to cause cancer or reproductive toxicity and to inform citizens about exposures to these chemicals. In March 2009 the California Office of Environmental Health Hazard Assessment (OEHHA) solicited public comments on thirty-eight chemicals selected for prioritization for evaluation by the state’s Carcinogen Identification Committee. “Fluoride and its salts” were included, and in October the state announced that that was one of five chemicals selected for consideration. 81

  Very extensive comments were sent into the OEHHA by a number of individuals and organizations, including Paul Connett and Chris Neurath of the Fluoride Action Network;82 the Environmental Working Group;83 and Kathleen Thiessen, PhD, an NRC panel member. 84 There is a wealth of additional material in these submissions for those who want more details than we can provide in this chapter.

  It is interesting to note on the Web site of the California Dental Association (CDA) that the organization received $200, 000 from the ADA to help stop the state’s investigation of the carcinogenicity of fluoride. The CDA states that “ADA granted CDA $200, 000 to assist in our effort to prevent the placement of ‘fluoride and its salts’ on the List of Chemicals Known to the State to Cause Cancer or Reproductive Toxicity that is produced by the State of California, Environmental Protection Agency, Office of Environmental Health Hazard Assessment (OEHHA). ”85

  Here we see yet another example of how the ADA seems more determined to protect the fluoridation program than to protect the health of the American people, even on an issue that is life threatening. We look at more examples of the tactics and strategies used by proponents of fluoridation in chapter 23.

  On October 15, 2009, a sixty-day comment period began on the five chemicals (including fluoride and its salts), out of thirty-eight originally nominated. This comment period ended on December 15, 2009. 86 To our knowledge, as of July 2010, the carcinogenicity of fluoride is still being considered by the California OEHHA.

  Summary

  The possibility that fluoridation may be associated with an increase in osteosarcoma in boys and young men was raised as long ago as 1955. The matter was raised again, in 1977, by one of the authors of an NAS panel, which recommended that osteosarcoma rates be examined in young men less than thirty years of age in fluoridated areas. Nothing was done about this suggestion until an NTP study in 1990 reported a dose-related association between osteosarcoma in male rats that were fed fluoride. In 1991 the NCI reported that there was such an association in young males but not females in the U. S. population but discounted it on the grounds that it appeared unrelated to the duration of exposure. From 1991 to 2001 reports on this possible association have been mixed. In 1992, in a study of fluoridated communities in New Jersey, Cohn reported an association; other studies have not. In 2001, using a different approach, Elise Bassin found that young boys exposed to fluoridated water in their sixth, seventh, and eighth years had a five- to sevenfold greater risk of contracting osteosarcoma by the age of twenty.

  Bassin’s thesis research sponsor, Chester Douglass, failed to warn the public, his peers, the NRC, or his funders about this issue for four years. Bassin’s thesis did not appear in public until 2005, and her data were not published until 2006. When they were published, the same journal published a letter from Douglass in the same issue claiming that his larger study would refute Bassin’s findings. That study was promised for the summer of 2006, but after four years it has not appeared. This same study had been mentioned even earlier in 2002 by Douglass at a meeting organized by the BFS in London. A possible reason that Douglass’s paper has not appeared is that his methodology is seriously flawed: It cannot test the central finding of Bassin’s thesis.

  Meanwhile, promoters of fluoridation are using that promise of a study as a way of dispelling concern over the possibility that drinking fluoridated water may contribute to boys and young men contracting a disease that is frequently fatal. All parties agree that it is highly plausible from a biological perspective that fluoride could cause bone cancer. Fluoride reaches its highest concentration in bone and the pineal gland. Fluoride is known to increase bone turnover, and it is also established that fluoride can interfere with the genetic machinery of the cell in a variety of ways. Mutations (genetic mistakes) are most likely to occur during
rapid bone turnover. Rapid bone turnover occurs during the mid-childhood growth spurt that corresponds to the window of vulnerability discussed by Cohn and identified by Bassin.

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  19 •

  Fluoride and the Kidneys,

  and Other Health Issues

  Two issues pertain to fluoride and the kidneys. The first is the possibility that fluoride can damage the kidneys, especially at high levels. The second is the fact that someone with poor kidney function has a limited ability to clear fluoride from the body, which would make that person more vulnerable to fluoride’s other toxic effects.

  Fluoride Damage to the Kidney

  With the exception of the pineal gland, the kidney accumulates more fluoride than all other soft tissues in the body. 1–3 It is well known that high doses of fluoride can damage the kidney after short periods of exposure—for example, to an anesthetic that contains fluorinated hydrocarbons such as methoxyfluorane, which are metabolized to free fluoride ion. 4–8

  There is also evidence that low doses of fluoride, taken over longer periods of time, can damage the kidney. For example, both Varner et al. 9 and McKay, Ramseyer, and Smith10 found kidney damage in rats drinking water with just 1 ppm of fluoride. Manocha, Warner, and Olkowski11 found kidney damage in monkeys drinking water with 5 ppm fluoride; while Borke and Whitford found significant biochemical damage to the kidney in rats drinking water with 10 ppm fluoride. In the latter study, the average blood fluoride levels of the rats with kidney damage was 38 ppb—a concentration commonly exceeded in people living in 1 ppm areas. Borke and Whitford state:

  Our 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. In summary, we provided rats with fluoride in their drinking water, which produced graded, plasma fluoride concentrations that occur in humans. Our studies showed that chronic high fluoride ingestion decreases the rate of Ca++ transport across renal tubule endoplasmic reticulum and plasma membranes, and reduced the amount of ER and PM Ca++ pump protein present in the kidney membranes. We conclude that chronic high fluoride ingestion may decrease the expression, increase the breakdown, or increase the rate of turnover of plasma membrane and endoplasmic reticulum Ca++ pump proteins and possibly other enzymes as well. The observed decreases in the rate of Ca++ transport and associated decreases in plasma membrane and endoplasmic reticulum Ca++ pump expression could affect in vivo Ca++ homeostasis. 12

  Complementing this animal research, many studies have found kidney disease to be a common feature of human skeletal fluorosis. 13–22

  Also, and perhaps most significant, a human study by Liu et al. in China has found a dose-dependent relationship between fluoride ingestion and kidney damage in children. 23 The study found evidence of kidney damage among children drinking water with as little as 2. 6 ppm fluoride.

  Consequences of Poor Kidney Function

  Of huge concern is the impact of drinking fluoridated water on people with impaired kidney function. It is well known that in a healthy person approximately 50 percent of ingested fluoride is excreted. However, when someone has impaired kidney function, far less fluoride is excreted, leading to higher accumulations of fluoride, especially in the bones. 24 It has been reported that individuals with impaired kidney function have developed skeletal fluorosis drinking water at levels as low as 1. 7 ppm. 25

  2006 NRC Report

  The NRC report said the following about fluoride and the kidney:

  Human kidneys. . . concentrate fluoride as much as 50-fold from plasma to urine. Portions of the renal system may therefore be at higher risk of fluoride toxicity than most soft tissues. . . Early water fluoridation studies did not carefully assess changes in renal function. . . 26

  On the basis of studies carried out on people living in regions where there is endemic fluorosis, ingestion of fluoride at 12 mg per day would increase the risk for some people to develop adverse renal effects. 27

  The NRC made these recommendations for future research on fluoride and the kidneys:

  Future studies should be directed toward determining whether kidney stone formation is the most sensitive end point on which to base the MCLG. . . 28

  The effect of low doses of fluoride on kidney and liver enzyme functions in humans needs to be carefully documented in communities exposed to different concentrations of fluoride in drinking water. 29

  Kidney and Other Stones

  Little investigation has taken place on the possible involvement of fluoride in the formation of kidney stones or, once stones have formed, on the possible accumulation of fluoride in or on them. Similar considerations may apply to other tissues (gallbladder, brain) where calcified deposits may occur. We agree with the NRC panel members that more research is needed on what might be a very important concern.

  Other Health Issues

  The 2006 NRC panel reviewed a number of other health issues, including potential fluoride interactions with the gastrointestinal, hepatic, immune, and reproductive systems. 30 Effects on the gastrointestinal system are discussed in chapter 13. Most of the concerns about the immune system are largely speculative; once again the scarcity of literature on this reflects a lack of interest by governments that promote fluoridation. The same can be said about reproductive effects; despite an extensive literature indicating that, at high levels of exposure, effects of fluoride on the reproductive system have been observed in a wide range of animals and reptiles, very few human studies on the subject have been published or even undertaken. In chapter 22 we refer to the unscientific way that the ADA dismissed a significant study on this subject by Freni. 31 For a wide-ranging review of fluoride effects on the reproductive system, see Long et al. (2009). 32

  Effects on the Cardiovascular System

  There is little evidence of attention to the possibility of effects of fluoride on the cardiovascular system. The 2006 NRC report mentions cardiovascular effects only with respect to thyroid function. However, two recent studies of sixty-three adults with “endemic fluorosis” and forty-five healthy controls found that fluorotic individuals had decreased elasticity of the aorta and dysfunctions of the left ventricle. 33, 34 The papers include references to other studies on fluoride and the cardiovascular system.

  Summary

  Most of the possible impacts of fluoride on tissues such as the kidneys and the reproductive, hepatic, and immune systems suffer from a lack of serious study in fluoridated countries. Since the kidneys concentrate fluoride to a greater extent than any other soft tissue except the pineal gland, they may be particularly at risk. Also, if the kidneys are not functioning well to begin with, less fluoride is excreted, and more lodges in the skeleton. Moreover, because kidneys become less efficient with age, the elderly are at greater risk. The issue of a possible relationship between fluoride and kidney stones (and stones in other tissues) is potentially important but has not been explored.

  Studies on the other systems mentioned do not leave much room for complacency. Some people ridicule opponents of fluoridation for the long list of health effects sometimes claimed for the simple fluoride ion. It is easy to score cheap points here, but the fact is that, as we indicated in chapter 12, fluoride has a high biological activity that is very general in nature—for example, it inhibits many enzymes, it interacts with calcium ions (either directly or indirectly), and in the presence of a trace amount of aluminum, it interferes with hormonal messaging systems. Since enzymes and hormones are essential to all physiological processes, such activities are likely to produce a wide variety of effects.

  PART FIVE

  Margin of Safety and the

  Precautionary Principle

  In part 5 we address the kind of information that a thoughtful decision maker might wish to consider before endorsing or halting fluoridation.

  In chapter 20, we discuss what is meant by a margin of safety. It is not disputed that, at moderate to high doses, fluoride can cause serious health pro
blems and other adverse effects. The crucial question is whether there is a sufficient margin of safety between the doses that cause those effects and the doses experienced in fluoridated communities. We explain why this margin of safety has to be sufficiently large to protect everyone, including the most vulnerable, not just the average person. Moreover, it has to be large enough to protect the whole population over a lifetime of exposure.

  In chapter 21, we discuss the precautionary principle. Application of this principle allows decision makers a way of resolving public health and environmental issues when the evidence of harm is mixed and has not reached the level of absolute certainty.

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  20 •

  Margin of Safety

  Proponents of fluoridation in Australia, 1 Canada, 2 the UK, 3, 4 and the U. S. 5, 6 have all dismissed the 2006 National Research Council report7 as being irrelevant to water fluoridation, claiming that it applies only to “high” exposure to fluoride. However, none of these promoters or agencies has explained what is meant by the word “high” or attempted to quantify the term in any meaningful way. To do this requires a consideration of the margin of safety.

  The concept of margin of safety is normally used by toxicologists, pharmacologists, and regulatory officials when establishing so-called safe levels of a known toxic substance to which the public may be exposed. Such a margin of safety (or safety factor) is set to ensure protection for everyone from an identified or anticipated harmful effect. This margin of safety has to take into account the full range of sensitivities to a toxic substance that can be anticipated in any human population (intraspecies variation). In the case of fluoride, an extra safety factor will be needed when setting a safe level for fluoride in water (either natural or added) to take into account the full range of exposure for a population drinking uncontrolled amounts of water and getting fluoride from other sources as well.