by Paul Connett
EPA Pesticide Division
However bad the science used by the EPA’s Office of Water in its derivation of the MCLG of 4 ppm, it pales compared to the outrageous manipulations the EPA’s Office of Pesticides applied to the same MCLG in deriving a so-called safe reference dose (RfD) for infants. In three successive risk assessments, 62–64 the EPA Office of Pesticides derived three different RfDs for infants: 0. 114 mg/kg/day, 0. 57 mg/kg/day, and 1. 14 mg/kg/day. The final one, 1. 14 mg/kg/ day, is ten times higher than the RfD for adults. 65 That is indeed a remarkable conclusion.
Here we examine the three different methods used by the EPA Office of Pesticides to derive these three different RfDs for infants. It is important to note that the second and third derivations came as a consequence of interventions by the Fluoride Action Network (FAN), the Environmental Working Group (EWG), and Beyond Pesticides (BP). Ironically, even though the EPA arrived at three different RfDs for infants the starting point for their calculations was the same in each case: the EPA Office of Drinking Water’s 1986 derivation of the MCLG (4 ppm). If readers are puzzled as to how the EPA in good conscience could derive three different end points beginning with the same starting point, so are we!
This is how the EPA Pesticide division says it did this.
In the first health risk assessment, it assumed that the RfD for children was the same as adults: 0. 114 mg/kg/day. The latter is obtained by dividing the so-called “safe dose” for adults used in the 1986 derivation of the MCLG (8 mg/day) by an adult’s bodyweight of 70 kg. 8 mg/day divided by 70 kg = 0. 114 mg/kg/day.
In the second health risk assessment (after FAN intervened and had shown that some children are already exceeding this dosage of 0. 114 mg/kg/day) the EPA used a different approach in order to derive a different RfD for infants. For this the EPA used a back-calculation from the notion that if 4 ppm fluoride in water would be safe for everyone, then it would also be safe for a 7-kg infant. Assuming such an infant consumed one liter of water per day, the EPA estimated that it was safe for a 7-kg child to ingest dose of 4 mg/day (i. e. one liter of water at 4 ppm contains 4 mg of fluoride). Dividing 4 mg/day by an infant’s bodyweight of 7 kg would yield a RfD of 0. 57 mg/kg/day. This is now five times the RfD for an adult.
In the third health risk assessment, after FAN, EWG, and BP had intervened again, the EPA assumed that if 8 mg/day was safe for a 70-kg adult it was also safe for a 7-kg infant. Such an assumption flies in the face of basic toxicology and common sense. It is akin to saying that if 1000 mg/day of aspirin is safe for an adult it is also safe for an infant. This is patently absurd. However, it allowed the EPA to derive a third RfD for infants even higher than the previous ones. If one divides 8 mg/day of fluoride by the bodyweight of an infant (7 kg) one arrives at an RfD for infants of 1. 14 mg/kg/day, which is now ten times the RfD for an adult!
All this was done, we believe, in an effort to set very high tolerance levels for fluoride residues left by the use of Dow AgroSciences’ sulfuryl fluoride fumigant on food in warehouses and processing plants. Protecting Dow’s interests was apparently more important than protecting the health of babies or infants. FAN, EWG, and BP continue to appeal the EPA’s approval of the new fluoride tolerance limits for sulfuryl fluoride use based on these highly dubious calcuations. Because of the long time that the EPA has taken in responding to several appeals on this matter, it is expected that the issue will end up in court.
As a consequence of these scientifically unjustifiable manipulations of the reference dose for infants, the EPA’s permitted tolerances (i. e. , of fluoride residues left after sulfuryl fluoride treatment) have risen from the previous level of 7 ppm (used for cryolite applications on fruit and vegetables) to levels on over six hundred foods (and many more if we include processed foods) that range from a low of 5 ppm for dried raisins to a high of 125 ppm for wheat flour. 66 Since wheat flour is used in everything from cakes to pizza dough, these tolerances will greatly increase the total dose of fluoride that the average American gets from all sources combined. In this last application for increased tolerances the EPA permitted Dow to have a tolerance (i. e. , residue) of 900 ppm fluoride on powdered eggs. Not surprisingly this tolerance appears to have been withdrawn because as FAN pointed out even a modest consumption of eggs at this level could make someone acutely ill.
Summary
Proponents tend to use phrases like “high doses” and “not relevant to water fluoridation at 1 ppm” to dismiss concerns about harm caused by fluoride in areas endemic for fluorosis, arguing that the relatively high doses in these studies make the results irrelevant for exposures at 1 ppm concentration. They seldom discuss the concept of margin of safety, which is absolutely essential to determine a safe dose sufficient to protect everyone in society from a substance known to cause harm. When government agencies have been forced to address the margin-of-safety issue for fluoride’s adverse health effects, they have invariably used safety factors that cannot be defended scientifically. In addition, they have often violated the very procedures they used in permitting or regulating other chemicals or pollutants. The worst example of an unacceptable manipulation of science in this respect has come from the EPA’s Office of Pesticides in the help it has given Dow AgroScience in its efforts to use sulfuryl fluoride as a fumigant on food in warehouses and processing plants. Just as fluoride has been dubbed the “protected pollutant, ” we can now add that water fluoridation is the “protected practice” and sulfuryl fluoride is the “protected fumigant. ”
All of this represents very poor science. We return in chapter 22 to other examples of the dubious calculations that have characterized the promotion of fluoridation for over sixty years.
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The Precautionary Principle
The precautionary principle (PP) has come into play, particularly in Europe, because it has been found that in the time it takes to get definitive, scientific proof that a chemical or practice has caused harm, the health of some people has been damaged irreversibly. This was the case with lead, benzene, asbestos, and smoking. The PP acknowledges this problem and posits the notion that when there is reasonable doubt about safety, we should err on the side of caution and not insist on absolute evidence of harm before eliminating or rejecting a substance or practice.
Joel Tickner and Melissa Coffin state the PP clearly: “If there is uncertainty, yet credible scientific evidence or concern of threats to health, precautionary measures should be taken. In other words, preventive action should be taken on early warnings even though the nature and magnitude of the risk are not fully understood. ”1
For more on the PP, readers may wish to consult the book Protecting Public Health and the Environment: Implementing the Precautionary Principle. 2
Applying the Precautionary Principle
Use of the PP is not without its critics, especially from those who fear that blanket use of the principle could block any form of industrial or economic development. 3–5 Clearly, unless the PP is to stymie progress, it should not be applied in a cavalier fashion; certain criteria should be met before it is invoked. We offer the following criteria to be considered in the case of water fluoridation:
1. Is the risk of harm plausible? YES. There is no adequate margin of safety for known detrimental health effects at moderate to high doses sufficient to protect everyone consuming fluoridated water and fluoride from other sources (see chapter 20).
2. Is the evidence of harm supported by a number of peer-reviewed, published studies? YES. Many such studies are reviewed in the 2006 NRC report6 (see chapters 14–19).
3. Is the potential harm serious? YES. Arthritis affects about 46 million Americans. Hip fractures are very serious for the elderly and can lead to a permanent loss of independence and even to an early death (see chapter 17). Hypothyroidism brings with it a litany of problems, including lethargy, depression, and obesity (see chapter 16). Lowering IQ in children has serious consequences both for individuals, by robbing them of their full poten
tial, and for society, by reducing the number of highly intelligent people and increasing the number of mentally handicapped (see chapter 15). Even the one adverse effect that is not denied by proponents—dental fluorosis—can lead to a loss of self-esteem, especially in teenagers (see chapter 11).
4. Are the effects reversible? MANY ARE NOT. A change in the intellectual development of a child in his early years cannot be erased. Fluoride steadily accumulates in the bone over a lifetime of exposure. If the source of fluoride is removed, the fluoride will gradually leave the bone, but the estimated half-life is very long, up to twenty years (see chapter 12). Treatment is possible for a fractured hip bone, but it can be difficult for the patient to make a full recovery.
5. Is the public being fully informed of the potential health risks? NO. The very opposite is occurring. Spokespersons for local, state, and federal health agencies deny any health risks at all.
6. Does the proposed intervention achieve the desired benefit? QUESTIONABLE. As we saw in chapters 6–8, the evidence that swallowing fluoride actually reduces decay in the permanent teeth is weak.
7. How significant are the consequences if the practice is halted? NOT VERY. At least four modern studies conducted in Finland, East Germany, Cuba, and British Columbia found that in communities that stopped fluoridation, tooth decay rates did not go up (see chapter 2).
8. Are there alternatives? YES. The vast majority of European countries do not fluoridate their water, and yet, according to World Health Organization figures, their children’s teeth are as good if not better than children’s teeth in fluoridating countries.
In summary, all these sensible criteria for applying the PP to the implementation of fluoridation are easily met.
The Precautionary Principle and Fluoridation
In the March 2006 issue of the Journal of Evidence-Based Dental Practice, Tickner and Coffin examined the water fluoridation controversy in the context of the PP. According to those authors, the PP has become a core guiding principle of environmental health regulations in Europe. They noted, “The need for precaution arises because the costs of inaction in the face of uncertainty can be high, and paid at the expense of sound public health. ”7
They wrote that when determining whether the PP should be applied to fluoridation, one should consider the following questions:
• Whether there are other ways of delivering fluoride besides the water supply
• Whether fluoride needs to be swallowed to prevent tooth decay
• Whether tooth decay has dropped at the same rate in countries with and without water fluoridation
• Whether people are now receiving fluoride from many other sources besides the water supply
• Whether studies indicate fluoride’s potential to cause a range of adverse systemic health effects
• Whether, since fluoridation affects so many people, “one might accept a lower level of proof before taking preventive actions”8
While the authors never state their personal opinion on water fluoridation, their analysis confirms our view that the practice is incompatible with the PP.
Summary
In advance of any application of the precautionary principle, it is important to lay out and make transparent the important criteria that first need to be satisfied. We, as well as specialists in the field, have done this, and it is clear that the practice of water fluoridation is a violation of the precautionary principle on all the criteria presented.
PART SIX
The Promoters and the
Techniques of Promotion
In chapter 22, we summarize the evidence, much of it covered in earlier chapters, that fluoridation has been propagated for over sixty years using poor science. In chapter 23, we examine some of the promoters’ strategies and tactics that have kept this outdated policy alive for so many years. In chapter 24, we critique some of the self-serving reviews commissioned or conducted by pro-fluoridation government agencies. In chapter 25, we identify and respond to the “chestnuts” used to promote fluoridation, along with less frivolous arguments. In chapter 26, we venture into the very tricky area of trying to understand what motivates the proponents of fluoridation.
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Weak and Inadequate Science
We saw in chapters 6–8 that evidence for the notion that swallowing fluoride (as opposed to applying it topically) reduces tooth decay is very weak. The exaggerated claims of fluoridation’s benefits have been supported by very dubious science, but the matter does not stop there; poor science has characterized the whole promotion and defense of the fluoridation program over its long history. Some of this we discussed in chapters 9 and 10, where we saw how little science existed on the safety of fluoridation before the U. S. Public Health Service (PHS) endorsed it in 1950, a decision that was a key step in the Great Fluoridation Gamble. That gamble was based on the belief that somehow ingested fluoride could damage the growing tooth (causing dental fluorosis) without damaging any other tissue in the body, even the delicate tissues of a newborn baby.
After the PHS endorsed fluoridation in 1950, other professional bodies swiftly followed with their own endorsements. Promoters have used those endorsements as a substitute for well-conducted science ever since. In the following paragraphs we discuss several other examples of the poor science, evasions of science, and poor administration used to promote and defend fluoridation.
The Food and Drug Administration has not been involved.
Today, before a new drug can be approved by the Food and Drug Administration (FDA) for clinical use, it must be rigorously tested for efficacy in randomized clinical trials (RCT). Such trials have been recognized for many years as being the only scientifically reliable way to determine whether a drug actually works. No such requirement existed when fluoridation was introduced in the 1940s and the methodology of testing was haphazard and superficial by modern standards (see chapter 7). Even the conditions and criteria that were put in place for the early fluoridation trials were not always adhered to. Even if those trials had been meticulously conducted, it would have been impossible to exclude a range of possible confounding variables.
In the light of such shortcomings, it is astonishing that, sixty years later, the efficacy of ingested fluoride in preventing dental caries has never been tested in an RCT. Nor, as we saw in chapter 2, has the FDA taken any active interest in fluoride, possibly the most extensively taken drug in history.
Another thing the FDA requires when drugs are approved is tracking reports of their possible side effects. Had the FDA been involved at any stage, it would have had to tabulate the many accounts of individuals complaining of fairly common symptoms (e. g. , tiredness not relieved by sleep, headaches, rashes, and gastrointestinal problems) that were easily reversed when the source of fluoride was removed (see chapter 13). Had the FDA tracked these complaints, at some point it might have felt obliged to review the issue scientifically. Remarkably, no health agency in the United States or any of the other fluoridated countries has pursued this.
Fluoride exposure is poorly monitored.
There has never been a comprehensive analysis of the fluoride levels in the bones, blood, or urine of citizens in the United States or other fluoridated countries. Based on the sparse data that have become available, however, it is increasingly evident that some people, particularly people with kidney disease, are accumulating fluoride levels in their bones that have been associated with harm to both animals and humans (chapter 18).
In 1991, a panel of the Australian National Health and Medical Research Council (NHMRC) recommended that measurements of fluoride levels in bone be collected. In its recommendation, the panel wrote, “If skeletal fluorosis is occurring at all in Australians, it is likely to be slight, and it will most likely occur in those who drink large amounts of water, or whose renal function is impaired. Studies of bone fluoride collected at autopsy in selected individuals could provide needed reassurance that the current policy is not resulting in hazardous level
s of accumulation in bone. ”1 In the nineteen years since that recommendation was made, no Australian health authority has sought such reassurance.
Measuring fluoride in urine is a much easier task than measuring fluoride in bone, and yet even that simple procedure to gauge exposure, and overexposure, is not performed on a routine basis in fluoridated countries. When measurements have been made by independent researchers, such as Dr. Peter Mansfield in the UK, the results have been disturbing. 2 Mansfield has found that some urine levels are very high in the UK, perhaps because the British drink a lot of tea, but no one is checking urine fluoride levels in other fluoridating countries, and some of those (e. g. , Australia, Ireland, and New Zealand) also have heavy tea drinkers. Someone needs to find out what the total exposure of fluoride is in those countries from all sources (including tea), and the simplest and quickest way to do that would be to measure the fluoride levels in urine.
Few basic health studies have been done in fluoridated communities.
One of the most shocking aspects of the promotion of fluoridation is the failure of the DHHS and health authorities promoting fluoridation in other countries to study, in a comprehensive fashion, the health of individuals and communities that have been exposed to fluoridated water, whether for relatively short periods or over a lifetime.
In chapter 5, we quote Trevor Sheldon’s comment from a letter to the House of Lords about there being “a dearth of reliable evidence with which to inform policy”3 and the surprise of Dr. John Doull (2006 NRC panel chair) at how “we have much less information [on health issues] than we should, considering how long this [fluoridation] has been going on. ”4 Note that these comments from independent observers were made fifty-one and fifty-eight years, respectively, after the DHHS endorsed fluoridation.
