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NIDR 1986–1987

In 1986, the National Institute of Dental Research (NIDR) stepped in and organized—at great expense to the U.S. taxpayer—the largest survey of tooth decay ever undertaken in the United States. It examined the teeth of nearly forty thousand children in eighty-four communities. Findings were published in two papers, one by Yiamouyiannis²¹ and the other by Brunelle and Carlos.²²

Yiamouyiannis 1990

When Dr. John Yiamouyiannis (a well-known opponent of fluoridation and author of the book Fluoride: The Aging Factor²³) obtained the raw data from this NIDR study, he found that there was no statistical difference in the DMFTs among children who had lived all their lives in a fluoridated community (F), children who had lived their whole lives in a non-fluoridated community (NF), and children who had lived their lives part of the time in a fluoridated community and part of the time in a non-fluoridated community (PF). In figure 8.1, the three curves for DMFT across the age range from five to seventeen years are plotted for the F, NF, and PF children; the lines are essentially superimposed.

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.

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.

Nicholas Leone and Bartlett-Cameron, 1954

The first formal U.S. health study—the famous Bartlett-Cameron study—did not appear until … four years after the PHS had endorsed fluoridation. This was perhaps the ultimate example of “locking the barn door after the horse escaped” and, to continue our farmyard metaphors, represented a fairly clear case of the fox guarding the chicken coop.

The name most associated with the Bartlett-Cameron study is that of Nicholas Leone, MD, the director of medical research at the NIDR. However, Leone’s name was not on the study when it was first cited by the Committee on Dental Health of the National Research Council’s Food and Nutrition Board.¹⁴ The committee cited the study as follows:

MB Shimkin, FA Arnold, JW Hawkins, HT Dean: Medical aspects of fluorosis: a survey of 114 individuals using water with 8 parts per million fluoride and of 131 individuals using water with 0.4 parts per million fluoride. Am. Assoc. Advancement Sci. 1953 (in press).

However, when the study appeared in the 1954 AAAS symposium report,¹⁵ as well as in a Public Health Report,¹⁶ some of the key authors had changed.

Dean’s and Hawkins’s names had been dropped, and previously unlisted Nicholas Leone appeared as the lead author.

It’s puzzling how the authorship of this crucially important study could have changed within the space of one year. Moreover, Leone seems to have taken on this leading position with practically no background in the matter. From 1951 to 1953 he was working at the National Microbiological Institute. He did not become the chief of medical investigations at the NIDR until March 1, 1953.¹⁷ He really did not have a lot of time to work on this study. The report without his name on it was in press in November 1953, and the report with his name on it appeared in October 1954.

Bartlett-Cameron Study Details

For a study that was destined to become the core of the argument for fluoridation’s safety, the Bartlett-Cameron study was remarkably small and limited. According to Leone et al., the study began in 1943 when a team from the PHS [Public Health Service] examined 116 residents in Bartlett (where the water contained 8 ppm fluoride) and 121 residents in Cameron (where the water contained 0.4 ppm fluoride), both in Texas. The participants were all white and ranged in age from fifteen to sixty-eight. The basic requirement for inclusion in the study was having fifteen years or more of continuous residence prior to 1943.¹⁸

The 1953 investigation—by an entirely different team—involved tracing as many members of the group studied in 1943 as possible. According to Leone et al., 71 percent of the 237 participants still resided in Bartlett or Cameron in 1953. Eight percent of the participants had died, and the forty-seven who had moved were traced; thirty-seven of those were reexamined in 1953, and the other ten were interviewed by telephone or mail and their ten-year medical histories obtained.¹⁹

Each participant received a physical examination, blood and urine tests, and X-rays. Leone et al. tabulated the abnormalities in various characteristics observed in Bartlett and Cameron in 1943 and 1953, including dental fluorosis, arthritic changes, blood pressure, bone changes (density, coarse trabeculation, hypertrophy, spurs, osteoporosis), cataracts or lens opacity, thyroid function, cardiovascular system function, hearing (decreased acuity), tumors or cysts, fractures, urinary tract calculi, and gallstones. Their overall conclusion was that “no significant differences between the findings in the two towns were observed, except for a slightly higher rate of cardiovascular abnormalities in Cameron [0.4 ppm F] and a marked predominance of dental fluorosis in Bartlett [8 ppm F].”²⁰ 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 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
  
  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 Roholm²⁸ and researchers in India^{29, 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 diffi- cult 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

  Modern Surveys of Dental Fluorosis

  In 1997, Heller, Eklund, and Burt reported on the findings of a 1986–1987 survey conducted by the National Institute of Dental Research (NIDR) in the United States.¹³ They revealed that 29.6 percent of children in artificially fluoridated areas (0.7–1.2 ppm) had dental fluorosis on at least two teeth (see table 11.1). In those communities, 22.5 percent of the children had very mild, 5.8 percent had mild, and 3 percent had moderate dental fluorosis.¹⁴ This breakdown by severity level is shown in table 11.2. The figure for all levels combined (29.6 percent) is three times the rate anticipated by Dean, and, of course, not all of the fluorosis was in the very mild category.

  Heller et al. also found that about 21.6 percent of children in non-fluoridated areas (0.3–0.7 ppm) had dental fluorosis, as did about 13.6 percent of children in communities with less than 0.3 ppm.15 Tables 11.1 and 11.2 summarize Heller’s findings.

  Table 11.1 Percentage of children with dental fluorosis (DF) on at least two teeth, as a function of the level of fluoride (F) in the community’s drinking water.
  F (ppm)	% children with DF on at least two teeth
  <0.3	13.5
  0.3 – <0.7	21.7
  0.7 – <1.2	29.9
  >1.2	41.4
  Source: Heller et al.,17 using data from the NIDR survey of U.S. children in 1986–1987.

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  Table 11.2 Percentage of children with different levels of severity of dental fluorosis (based on Dean’s classification) as a function of the level of fluoride (F) in the community’s drinking water.
  F (ppm)	Severity of dental fluorosis (%)
  	very mild	mild	moderate	severe
  <0.3	10.7	2.4	0.4	0.1
  0.3 – <0.7	17.3	3.1	`1.2	0.0
  0.7 – <1.2	22.5	5.8	1.3	0.0
  >1.2	27.2	7.0	5.3	2.0
  Source: Heller et al.,18 using data from the NIDR survey of U.S. children in 1986–1987.

• Both in 1943 and in 1953, “significantly” more abnormalities of the neutrophilic white cells were reported at Bartlett than at The figures given indicated that the differences were in morphology rather than in relative number. Yet for unstated reasons the authors down- played the observation, simply claiming that “when viewed in the light of clinical experience, this finding does not suggest an association with fluoride intake.”27

References

22. Brunelle A, Carlos JP. 1990. “Recent Trends in Dental Caries in U.S. Children and the Effect of Water Fluoridation,” Journal of Dental Research 69:723–27.

23. Yiamouyiannis A. 1993. Fluoride: The Aging Factor, 3rd ed. (Delaware, Ohio: Health Action Press, 1993). Note: First edition published in 1983, and second edition in 1986.

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