by Paul Connett
Brunelle and Carlos 1990
Subsequently, Brunelle and Carlos, who worked for the NIDR, published their own analysis of the data. 24 However, they increased the sensitivity of the study by analyzing tooth decay using DMFS (decayed, missing, and filled permanent surfaces) as a measure of decay. All teeth except the cutting teeth have five surfaces per tooth, so this increased the sensitivity by a factor of nearly five over a measure of DMFT (decayed, missing, and filled permanent teeth). Even so, they found very little difference in tooth decay in the permanent teeth of children who had lived all their lives in a fluoridated community compared to those who had always lived in a non-fluoridated community.
In the abstract of their article, the authors reported the average difference in tooth decay for five- to seventeen-year-olds as 18 percent. However, table 6 in their paper shows that this reported saving amounts to an average of just six-tenths of a single tooth surface, and that is out of approximately one hundred tooth surfaces in a child’s mouth. Nor did the authors subject this to any analysis to see if the result was statistically significant. What we may be looking at here are the arithmetical vagaries of comparing two small numbers. Reporting that small difference as a percentage can be very misleading. For an unsuspecting citizen or official, an 18 percent difference in tooth decay sounds a lot better than the saving of 0. 6 of one tooth surface. Even so, 18 percent is a lot less than the figure of 60 percent that was being used by promoters of fluoridation at that time.
Figure 8. 1. Yiamouyiannis’s plot of DMFT for children living all their lives in a fluoridated community (F), children living all their lives in a non-fluoridated community (NF), and children living part of their lives in both (PF). 25
Even if we take the best figure in table 6 of their paper, an absolute saving of 1. 58 surfaces for seventeen-year-olds (8. 59 DMFS in non-fluoridated and 7. 01 DMFS in fluoridated), this represents only an absolute saving of approximately 1. 2 percent of the 128 tooth surfaces in the seventeen-year-old’s mouth (1. 58 / 128 × 100).
Despite that very unimpressive saving in tooth decay, this is what the authors stated in their abstract: “The results suggest that water fluoridation has played a dominant role in the decline in caries and must continue to be a major prevention methodology. ”26
For most people, an average saving (averaged for five- to seventeen-year-olds) of just 0. 6 of one tooth surface, or even 1. 58 tooth surfaces for seventeen-year-olds, would hardly seem to justify the time, money, and angst involved in imposing this practice on reluctant individuals and communities. Nor would it justify taking any of the health risks outlined in chapters 11–19.
It is not unusual for dental researchers who report either meager or no savings to claim in the abstract of their paper that the results support water fluoridation (e. g. , Spencer, Slade, and Davies27 ). Cynics might suggest that this is the price that has to be paid to ensure future funding for their dental research from pro-fluoridation sources. Whatever the truth of that, the claim has often proved effective for those decision makers who read only the abstract and not the details in the results section.
Spencer, Slade, and Davies 1996
Subsequently, a large survey conducted in two states in Australia found an even smaller difference in tooth decay in the permanent teeth than did the NIDR authors. Spencer et al. 28 found an average difference in tooth decay in the permanent teeth—again measured as DMFS—between children who had lived all their lives in fluoridated versus non-fluoridated communities of between 0. 12 and 0. 3 tooth surfaces per child. This is one-fifth to one-half of the meager finding of 0. 6 DMFS found by Brunelle and Carlos. 29 Even if these differences are real, they represent a very small fraction of the tooth surfaces in a child’s mouth. The figure of 0. 3 of one tooth surface out of 128 tooth surfaces represents an absolute saving of just 0. 23 percent.
de Liefde 1998
In 1998, Dr. Betty de Liefde, in a survey of tooth decay in New Zealand, confirmed what John Colquhoun had been saying for nearly twenty years. She found very little difference in permanent-tooth decay between fluoridated and non-fluoridated communities. She described the difference as “clinically meaningless. ”30
Locker 1999
In a report prepared for the Ontario Ministry of Health and Long-Term Care, Dr. David Locker of the University of Toronto reported, “The magnitude of [fluoridation’s] effect is not large in absolute terms, is often not statistically significant, and may not be of clinical significance. ”31
Two years later Locker coauthored an article on the science and ethics of fluoridation with Howard Cohen, in which they state the following:
Over the past 25 years there has been a marked reduction in rates of dental caries among children, such that the benefits of water fluoridation are no longer so clear. Although current studies indicate that water fluoridation continues to be beneficial, recent reviews have shown that the quality of the evidence provided by these studies is poor. . . In addition, studies that are more methodologically sound indicate that differences in rates of dental decay between optimally fluoridated and non fluoridated child populations are small in absolute terms. . . Canadian studies of fluoridated and nonfluoridated communities provide little systematic evidence regarding the benefits to children of water fluoridation. 32
Cohen and Locker concluded,
Ethically, it cannot be argued that past benefits, by themselves, justify continuing the practice of fluoridation. This position presumes the constancy of the environment in which policy decisions are made. Questions of public health policy are relative, not absolute, and different stages of human progress not only will have, but ought to have, different needs and different means of meeting those needs. Standards regarding the optimal level of fluoride in the water supply were developed on the basis of epidemiological data collected more than 50 years ago. There is a need for new guidelines for water fluoridation that are based on sound, up-to-date science and sound ethics. In this context, we would argue that sound ethics presupposes sound science. 33
Armfield and Spencer 2004
In 2004, Armfield and Spencer published a study of tooth decay in ten thousand children in South Australia. 34 While they found a small difference in the primary teeth, they found no statistically significant difference in tooth decay in the permanent teeth between those children who had drunk tank water (rainwater) or bottled water all their lives and those who drank fluoridated water.
Despite the fact that these authors clearly stated in their abstract, “The effect of consumption of nonpublic water on permanent caries experience was not significant, ” Spencer has responded angrily when opponents of fluoridation, including Mark Diesendorf, have reported their finding, claiming that their work is being misrepresented. 35, 36 Armfield and Spencer have also publicly advocated the fluoridation of bottled water in Australia.
Komárek et al. 2005
In a study published in the January 2005 issue of the journal Biostatistics, a European research team of scientists from Belgium and Finland sought to answer the question of whether fluoride intake at a young age has a protective effect on caries in permanent teeth. 37 For their response, they utilized data from the Signal Tandmobiel trial, 38 which, according to Komárek et al. , “is possibly the largest longitudinal study executed with such great detail on dental aspects. ”39
In their analysis (a “Bayesian survival analysis”), the authors used dental fluorosis as the measure of the children’s fluoride ingestion. The authors explained why they did that as follows: “Unfortunately, fluoride-intake in children cannot be measured accurately. Indeed, fluoride-intake can come from: (1) fluoride supplements (systemic), (2) accidental ingestion of toothpaste or (3) tap water. Further, the intake from these sources can be recorded only crudely. Therefore, it was decided to measure fluoride-intake by the degree of fluorosis on some reference teeth. ”40
The authors also took into account something that most dental studies ignore: a possible fluoride-induced delay in tooth eruption. Again,
the authors explained their reasoning: “Since the emergence of permanent teeth might be delayed by fluoride-intake, evaluating the impact of fluoride-intake should take into account the time at risk for caries. Hence, in our analysis, the response will be the time between emergence and the onset of caries development. ”41
Whereas in an earlier analysis (Vanobbergen et al. 42 ) the authors found a positive effect of fluoride on primary teeth, in this analysis by Komárek et al. the authors failed to find a significant effect on three of the four groupings of permanent teeth they analyzed. They reported, “Our analysis shows no convincing effect of fluoride-intake on caries development. . . This agrees with current guidelines for the use of fluoride in caries prevention, where only the topical application (e. g. fluoride in toothpaste) is considered to be essential. ”43
Pizzo et al. 2007
In 2007, a team of Italian researchers from the University of Palermo concluded the following from their review of the literature: “It is now accepted that systemic fluoride plays a limited role in caries prevention. Several epidemiological studies conducted in fluoridated and non-fluoridated communities clearly indicate that CWF [community water fluoridation] may be unnecessary for caries prevention, particularly in the industrialized countries where the caries level has become low. ”44
Waren et al. 2009.
The study by Warren et al. , otherwise referred to as the “Iowa Study, ” is the only study that has examined tooth decay in children as a function of individual exposure to fluoride. All the other studies discussed above have been population studies, with only the Komárek study giving any indication of individual exposure to fluoride. The authors of the Iowa study found no relationship between caries experience and individual fluoride intakes at various ages during childhood. Caries rates at ages five and nine were similar for all levels of fluoride intake. The authors state that “the benefits of fluoride are mostly topical” and that their “findings suggest that achieving a caries-free status may have relatively little to do with fluoride intake” [emphasis in the original]. The authors’ main conclusion: “Given the overlap among caries/fluorosis groups in mean fluoride intake and extreme variability in individual fluoride intakes, firmly recommending an ‘optimal’ fluoride intake is problematic. ”45
Dental Crises
There have been numerous press reports over the last few years of dental crises in U. S. cities that have been fluoridated for over twenty years. The fact that these crises are occurring in low-income areas again demonstrates that there is a far greater (inverse) relationship between tooth decay and family income levels than between tooth decay and water fluoride levels (see chapter 6). It also demonstrates that the tooth decay associated with low family income levels is not being eliminated by fluoridation programs.
The following excerpt from the Cincinnati Enquirer is fairly typical of many other press reports. Cincinnati has been fluoridated since 1979.
City and regional medical officials say tooth decay is the city’s No. 1 unmet health-care need. “We cannot meet the demand, ” says Dr. Larry Hill, Cincinnati Health Department dental director. “It’s absolutely heartbreaking and a travesty. We have kids in this community with severe untreated dental infections. We have kids with self-esteem problems, and we have kids in severe pain and we have no place to send them in Cincinnati. People would be shocked to learn how bad the problem has become. ”46
Similar reports have appeared in the papers of other fluoridated cities, including the Boston Globe, 47 New Haven Register, 48 Pittsburgh Tribune-Review, 49 Washington Post, 50 Lexington Herald-Leader, 51 and Fosters Daily Democrat (Connecticut). 52
In addition to these newspaper reports, formal studies have also found high levels of tooth decay in communities that have been fluoridated for several decades. For example, Burt et al. reported in a 2006 study of tooth decay in Detroit that “83 percent of low income African-American adults, 14-years-old and over, had severe tooth decay and. . . almost all of five-year-olds have cavities and most of them go unfilled. ”53
In his book Savage Inequalities: Children in America’s Schools, Jonathan Kozol writes, “As in New York City’s poorest neighborhoods, dental problems also plague the children here [in East St. Louis]. . . Bleeding gums, impacted teeth and rotting teeth are routine matters for the children I have interviewed in the South Bronx. . . I have seen children in New York with teeth that look like brownish, broken sticks. I have also seen teen-agers who were missing half their teeth. ”54 The book was published in 1991; New York City’s water has been fluoridated since 1965, and East St. Louis has received fluoridated water since 1968.
Almost all U. S. states produce regular oral health reports. The majority of these indicate high levels of tooth decay in low-income families, even in states with a high percentage of the water fluoridated. 55 Clearly, fluoridation is not addressing the impacts of income disparities as far as tooth decay is concerned.
Summary
Several studies and reviews published since the 1980s have confirmed that any protective effect of fluoridation is extremely small, amounting on average to only a fraction of a tooth surface for the permanent teeth and not much more for the baby teeth. Several modern studies have shown that if fluoridation is stopped, decay rates do not increase. The dental crises reported in cities across the United States and elsewhere that have long been fluoridated show that fluoridation is insufficient to combat dental caries, especially in children from low-income families.
PART THREE
The Great
Fluoridation Gamble
In chapter 9, we examine the events that led up to the U. S. Public Health Service (PHS) endorsement of fluoridation in 1950 from a dental perspective, a health perspective, and an industrial perspective. We address two key questions:
1. How much of fluoride’s dangers were known to the PHS in 1950?
2. What other pressures were acting on the PHS in the years leading up to this crucial event?
In chapter 10, we continue with the history of what we call the Great Fluoridation Gamble from 1950 to the present.
•
9 •
The Great Fluoridation Gamble, 1930–1950
Coauthored by Peter Meiers
In this chapter we look at the historical events leading up to the decision by the U. S. Public Health Service (PHS) to endorse fluoridation in 1950. Several texts have been most helpful in writing this chapter. In The Fight for Fluoridation, Donald McNeil gives an intriguing view of the history of the period from the dental and pro-fluoridation perspective. 1 Ruth Roy Harris gives a slightly less slanted view of that history in her book Dental Science in a New Age: A History of the National Institute of Dental Research. 2 In their book The American Fluoridation Experiment, published in 1957, the same year as McNeil’s book, Exner and Waldbott give us the view of scientists who were opposed to fluoridation and were highly critical of the evidence offered for both its safety and effectiveness. 3 Finally, Chris Bryson’s The Fluoride Deception, published in 2004, with a revised paperback edition published in 2006, discusses the industrial interests that either were directly involved in the early promotion of fluoridation or were beneficiaries of it. 4
The Great Fluoridation Gamble Defined
As far back as the 1930s, two facts were well established. First, adding fluoride to the water would increase the number of children with dental fluorosis (see chapter 11), and, second, fluoride caused this condition by some systemic (internal) mechanism. What was not known was whether other developing tissues in the child’s body would be affected by a mechanism similar to that which was damaging the growing tooth cells. Dental fluorosis is obvious. It is visible to the naked eye, and, as such, it cannot be denied. On the other hand, systemic effects on other tissues would not be so obvious or easy to detect without careful study.
“The Great Fluoridation Gamble” was founded on the blind trust that drinking water containing 1 ppm fluoride could damage growing tooth cells without harming any other tissues
in a child’s developing body and without causing any injury to adults after a lifetime of exposure.
A key question overhanging this discussion is the following: Did the U. S. Public Health Service in 1950 have enough information about the safety of ingesting fluoride at levels of 1 ppm in the water to confidently recommend that communities across the United States fluoridate their water? In this chapter we examine the evidence of harm that was available to decision makers prior to the approval of fluoridation, including the research they ignored.
This period essentially begins in 1931 with the discovery that fluoride causes mottling of tooth enamel (dental fluorosis)5–7 and ends with the U. S. PHS endorsement in 1950. The PHS endorsement was crucial: Not only did it trigger further endorsements from most American dental, medical, and public health associations, but it was also the starting point for the massive support that the governments of the United States and a few other countries have given to fluoridation ever since.
Enthusiasm vs. Caution
Once it had been assumed (with only a modicum of scientific evidence; see chapter 7) that fluoride might reduce tooth decay, we see a battle developing between those who were enthusiastic to get water fluoridation launched, such as Gerald Cox, 8 and those who were cautious about (1) the acceptability of increasing the incidence of dental fluorosis and (2) the possibility that other conditions might be triggered by ingesting fluoride. We examine the evidence for the latter and how eventually doubts about safety were submerged.
