Search:


 
The Emperor Has No Clothes: A Critique of the CDC's Promotion of Fluoridation
 
The Emperor Has No Clothes: A Critique of the CDC's Promotion of Fluoridation

by

Paul Connett, Ph.D.
Professor of Chemistry,
St. Lawrence University,
Canton, NY 13617.

Michael Connett,
Webmaster,
Fluoride Action Network,
http://www.fluoridealert.org

Revised October 3, 2000
Published in Waste Not # 468


Introduction: In 1999 the Centers for Disease Control and Prevention (CDC), an agency of the U.S. Department of Health and Human Services, listed fluoridation as one of the 10 most significant public health advances in the 20th century. The CDC published a review of the fluoridation issue in its publication, Morbidity and Mortality Weekly Report (MMWR), in October 1999. Because CDC's reports and opinions are considered objective and authoritative, and their position on fluoridation is cited in countless editorials and media reports, we felt it was important to present a point-by-point analysis of this report.

Our analysis shows that the CDC report has three fundamental weaknesses.

  • The authors fail to provide any substantial evidence that there is a cause and effect relationship between water fluoridation and the decline of tooth decay in the US and fail to acknowledge that these same declines were occurring in non-fluoridated countries.
  • The authors dismiss health concerns in just three short sentences citing only two out-of-date reviews.
  • The authors fail to acknowledge that the percentage of children impacted by dental fluorosis has dramatically increased since water fluoridation has begun, thus violating its own stated objectives:

    "Adjusted fluoridation is the conscious maintenance of the optimal fluoride concentration in the water supply for reducing dental caries and minimizing the risk of dental fluorosis" (our emphasis) (p iv, 1992 Fluoridation Census).

Their failure to acknowledge the high levels of dental fluorosis and cavalier dismissal of health concerns is disturbing and suggests that the CDC is more interested in the promotion of fluoridation than in presenting a balanced view of this controversial and serious public health issue.

Nothing of the CDC report has been left out of the analysis below. However, to read the full uninterrupted version, you can access it on the web at:
http://www.cdc.gov/epo/mmwr/preview/mmwrhtml/mm4841a1.htm.

In the spirit of open and constructive dialogue, we are sending our critique to the CDC. We will publish any response we receive.


A critique of:

Achievements in Public Health, 1900-1999: Fluoridation of Drinking Water to Prevent Dental Caries. MMWR, 48(41);933-940, October 22, 1999.



CDC 1:

Fluoridation of community drinking water is a major factor responsible for the decline in dental caries (tooth decay) during the second half of the 20th century.

Our response 1:

The reader should keep in mind that this is a thesis, not a statement of fact. Moreover, it is a highly debated thesis and the CDC's paper will stand or fall on how well they martial the data and arguments to support this thesis.

CDC 2:

The history of water fluoridation is a classic example of clinical observation leading to epidemiologic investigation and community-based public health intervention.

Our response 2:

The key point of consideration here concerns the quality (or lack thereof) of the clinical observations and epidemiology (as will be discussed below) which has been used to support water fluoridation.

CDC 3:

Although other fluoride-containing products are available, water fluoridation remains the most equitable and cost-effective method of delivering fluoride to all members of most communities, regardless of age, educational attainment, or income level.

Our response 3:

The statement by the CDC that "fluoridation remains the most equitable and cost effective method" is an opinion that has been rejected by most of the advanced industrialized world (see response 28, below).

The fact that Austria, Belgium, Denmark, Finland, France, Germany, Greece, Italy, Japan, Luxembourg, Netherlands, Norway, and Sweden have all rejected and/or discontinued water fluoridation, puts, we believe, the onus on the CDC to thoroughly explain why fluoridation is more "equitable and cost-effective" than other methods (e.g. widespread use of toothpastes and topical applications) being utilized by these countries. This is particularly important considering the fact that on average there is little difference in DMFTs (Decayed, Missing, and Filled Teeth) between fluoridated and unfluoridated industrialized countries (
see World Health Organization's DMFT data) (Diesendorf 1986, Moore, 1996). However, the CDC provides nothing other than a one sentence sound-bite to back up this comparative assessment.

The CDC claims that fluoridation is the most equitable means of delivering fluoride to the population because it delivers fluoride "to all members" of the community, "regardless of age, educational attainment, or income level." There are however serious problems being glossed over in this argument. First of which is the fact that fluoridated water is not beneficial to infants. The levels of fluoride found in mothers' breast milk (0.01 ppm) are ONE HUNDRED TIMES LOWER than the levels found in fluoridated water (e.g. 0.01 ppm vs 1.0 ppm) (Institute of Medicine, 1997, p 301).

And, as is now generally acknowledged in the dental research community, the fluoride swallowed in the infant and early childhood years DOES NOT, contrary to what was once believed, fortify the developing teeth. As Featherstone stated in the July 2000 issue of the Journal of the American Dental Association, "The fluoride incorporated developmentally - that is, systemically into the normal tooth mineral - is insufficient to have a measurable effect on acid solubility." The CDC needs to explain why it is a sign of fluoridation's effectiveness that fluoride is delivered via the drinking water to this part of the population.

A further point in regards to the so called effectiveness of delivering fluoride to all members of the community, is the fact that according to the ATSDR (Agency for Toxic Substances and Disease Registry):

"Existing data indicate that subsets of the population may be unusually susceptible to the toxic effects of fluoride and its compounds. These populations include the elderly, people with deficiencies of calcium, magnesium, and/or vitamin C, and people with cardiovascular and kidney problems" (ATSDR, 1993, p 112).

One example of those particularly vulnerable to fluoride are the people undergoing dialysis treatments. When the filter of a dialysis system at a Chicago hospital (July 1993) failed to filter out the 1 ppm (part per million) fluoride added to the water, three dialysis patients died and six others suffered from allergic reactions (see http://www.fluoridealert.org/U-of-C.htm). A similar occurrence happened in Annapolis, Maryland, in November 1979, when one dialysis patient died and 8 others suffered from symptoms of fluoride poisoning when the town's fluoridated water got through the dialysis system's filter (see http://www.fluoridealert.org/annapolis.htm). Again, is it a sign of fluoridation's effectiveness that fluoride is delivered to everyone, including people with ailing kidneys?

As stated above, most countries in the developed world have answered no to this question. For example, one of the reasons why Japan rejected fluoridation is because, as its Environment Agency recently stated, the "impacts of fluoridated water on human health depends on each human being so that inappropriate application may cause health problems of vulnerable people" (See our response 28 for more quotes).

Such vulnerable people, it bears pointing out, also include those who have hypersensitivity to fluoride. There is a body of evidence which indicates that there are people who experience a variety of health symptoms when exposed to fluoridated water, and that these symptoms disappear when they drink non-fluoridated water. Both Dr. George Waldbott (1978) and Dr. Hans Moolenburgh (1987) have provided case studies and described double blind studies supporting these claims.

In sum, the fact that fluoridated water delivers fluoride to ALL members of the population is not a virtue but a serious problem. What may appear to be efficient from an engineering point of view, is highly problematic from an ethical and medical perspective.

Dental Caries

CDC 4:

Dental caries is an infectious, communicable, multifactorial disease in which bacteria dissolve the enamel surface of a tooth (1). Unchecked, the bacteria then may penetrate the underlying dentin and progress into the soft pulp tissue. Dental caries can result in loss of tooth structure and discomfort. Untreated caries can lead to incapacitating pain, a bacterial infection that leads to pulpal necrosis, tooth extraction and loss of dental function, and may progress to an acute systemic infection. The major etiologic factors for this disease are specific bacteria in dental plaque (particularly Streptococcus mutans and lactobacilli) on susceptible tooth surfaces and the availability of fermentable carbohydrates.

Our response 4:

The notion of cavities being an "infectious, communicable disease," is misleading. It is true that the bacteria which cause cavities, (e.g. Streptococcus mutans), can be passed from one human to the next (usually from mother to child). However, dental disease is not a disease like cholera, or tubercolosis, in which once someone is "infected" rampant health consequences ensue.

Dental decay occurs via several steps and each step can be mitigated with a number of interventions. For the contracted bacteria to cause the decay they have to be fed a diet of sugary foods. Thereupon the bacteria have to convert the sugary food into acids and then the acids have to attack the minerals in the enamel. Interventions include:

1) Washing teeth after meals to minimize the amount of sugary food left on the teeth.
2) Having a good diet to build up a healthy mineral structure to the enamel.
3) Eating foods which are alkaline, like cheese, which helps to neutralize the acids.
4) Eating foods high in calcium and phosphate to encourage the remineralization process.
5) Using dental products and chewing gum which contain the natural sugar xylitol, which effectively inhibits the functioning of the bacteria (Soderling, 2000; Hujoel, 1999; Makinen, 1996; Trahan, 1996; Scheinin, 1976).

Unlike fluoridation, none of these steps require the draconian measure of forcing medication upon people who don't want or need it through the public water supply.

CDC 5:

At the beginning of the 20th century, extensive dental caries was common in the United States and in most developed countries (2). No effective measures existed for preventing this disease, and the most frequent treatment was tooth extraction. Failure to meet the minimum standard of having six opposing teeth was a leading cause of rejection from military service in both world wars (3,4). Pioneering oral epidemiologists developed an index to measure the prevalence of dental caries using the number of decayed, missing, or filled teeth (DMFT) or decayed, missing, or filled tooth surfaces (DMFS) (5) rather than merely presence of dental caries, in part because nearly all persons in most age groups in the United States had evidence of the disease. Application of the DMFT index in epidemiologic surveys throughout the United States in the 1930s and 1940s allowed quantitative distinctions in dental caries experience among communities--an innovation that proved critical in identifying a preventive agent and evaluating its effects.

Our response 5:

We have no objection to this statement.

History of Water Fluoridation

CDC 6:

Soon after establishing his dental practice in Colorado Springs, Colorado, in 1901, Dr. Frederick S. McKay noted an unusual permanent stain or "mottled enamel" (termed "Colorado brown stain" by area residents) on the teeth of many of his patients (6). After years of personal field investigations, McKay concluded that an agent in the public water supply probably was responsible for mottled enamel. McKay also observed that teeth affected by this condition seemed less susceptible to dental caries (7).

Dr. F. L. Robertson, a dentist in Bauxite, Arkansas, noted the presence of mottled enamel among children after a deep well was dug in 1909 to provide a local water supply. A hypothesis that something in the water was responsible for mottled enamel led local officials to abandon the well in 1927. In 1930, H. V. Churchill, a chemist with Aluminum Company of America, an aluminum manufacturing company that had bauxite mines in the town, used a newly available method of spectrographic analysis that identified high concentrations of fluoride (13.7 parts per million [ppm]) in the water of the abandoned well (8). Fluoride, the ion of the element fluorine, almost universally is found in soil and water but generally in very low concentrations (less than 1.0 ppm). On hearing of the new analytic method, McKay sent water samples to Churchill from areas where mottled enamel was endemic; these samples contained high levels of fluoride (2.0-12.0 ppm).

The identification of a possible etiologic agent for mottled enamel led to the establishment in 1931 of the Dental Hygiene Unit at the National Institute of Health headed by Dr. H. Trendley Dean. Dean's primary responsibility was to investigate the association between fluoride and mottled enamel (see box). Adopting the term "fluorosis" to replace "mottled enamel," Dean conducted extensive observational epidemiologic surveys and by 1942 had documented the prevalence of dental fluorosis for much of the United States (9). Dean developed the ordinally scaled Fluorosis Index to classify this condition. Very mild fluorosis was characterized by small, opaque "paper white" areas affecting less than or equal to 25% of the tooth surface; in mild fluorosis, 26%-50% of the tooth surface was affected. In moderate dental fluorosis, all enamel surfaces were involved and susceptible to frequent brown staining. Severe fluorosis was characterized by pitting of the enamel, widespread brown stains, and a "corroded" appearance (9).


Our response 4:

We would point out here that there are industrial and political aspects to this history which are not discussed here, but yet integral to understanding the full context of these developments. While discussion of this history is beyond the scope of our critique, suffice it to say that in the early and mid 1930's the trend was towards reducing and removing fluoride from public water. In 1939, for instance, the American Water Works Association, proposed that fluoride levels in water not exceed 0.1 parts per million (Babbit, et al; 1939). Such reduction of fluoride levels, however, represented a financial threat to industry, particularly the aluminum industry and later the defense industry, which generated substantial fluoride pollution.

In the same year, 1939, an ALCOA sponsored scientist, Gerald Cox, in light of rat studies showing reduced dental decay from fluoride ingestion, suggested that "The present trend toward complete removal of fluoride from water and food may need some reversal" (Cox, 1939). (When the Public Health Service endorsed fluoridation 12 years later, it was under the jurisdiction of long-time ALCOA lawyer, Oscar R. Ewing.)

Cox's idea of purposefully fluoridating the water supply was criticized by many at the time, including the American Medical and American Dental Associations. The AMA was concerned because, as it stated in 1943,

"Fluorides are general protoplasmic poisons, probably because of their capacity to modify the metabolism of cells by changing the permeability of the cell membrane and by inhibiting certain enzyme systems...The sources of fluorine intoxication are drinking water containing 1 part per million or more of fluorine..." (Editorial, 1943).

The ADA, meanwhile, was concerned because of its view that, "the potentialities for harm far outweigh those for good" (Editorial, 1944).

However, despite the fact that "no new favorable scientific evidence had appeared between 1943 and 1951" (Waldbott, et al; 1978) to allay the AMA's and ADA's concerns about fluoridation, they both endorsed the measure in 1951, following close upon the heels of the endorsement from the Public Health Service.

Lastly, it bears pointing out that it wasn't just the aluminum and defense industries that had some stake in the fluoridation project. Another industry with an interest in it was the Sugar industry. The reason being is that the sugar industry was actively interested at the time in finding a way of reducing cavities without having to reduce sugar consumption. In 1950, a year before the Public Health Service's endorsement of fluoridation, The Sugar Research Foundation (which consisted of 130 corporations involved in the sugar industry), stated that its aim in dental research was:

"to discover effective means of controlling tooth decay by methods other than restricting carbohydrate (sugar) intake" (quoted in Waldbott, 1965).

We raise these points not to suggest that fluoridation had entirely industrial origins, but rather to highlight other historical factors which ought to, but often are not, considered when reviewing the history of fluoridation.

CDC 7:

Dean compared the prevalence of fluorosis with data collected by others on dental caries prevalence among children in 26 states (as measured by DMFT) and noted a strong inverse relation (10). This cross-sectional relation was confirmed in a study of 21 cities in Colorado, Illinois, Indiana, and Ohio (11). Caries among children was lower in cities with more fluoride in their community water supplies; at concentrations greater than 1.0 ppm, this association began to level off. At 1.0 ppm, the prevalence of dental fluorosis was low and mostly very mild.

Our response 7:

A key point that the CDC fails to mention here, is that in many of the places where there was an apparent correlation between high natural fluoride levels in the water and low caries incidence, there were also high levels of calcium and other protective minerals found in the water. Take, for instance, the town of Hereford, Texas, which became known as the "town without a toothache." While proponents focused exclusively on the 2.3 to 3.2 ppm fluoride levels in the water as being the reason for the lack of cavities, Hereford's water also contained generous amounts of calcium and magnesium as well as other minerals (Waldbott, et al; 1978). A study done by the Massachusetts Institute of Technology and published in the New England Journal of Medicine confirmed the fact that the Hereford region had surprisingly high and healthy levels of nutrients (e.g. calcium) in the food produced there (Harris, et al; 1951). Other towns with equally high fluoride levels, but with lower levels of calcium and magnesium had in turn higher cavity levels than Hereford. The town of Colorado Springs, for instance, despite having natural fluoride levels of 2.5 ppm in the water had a higher incidence of caries. One explanation for this difference is that in Colorado Springs "the water is exceptionally soft (low in calcium and magnesium) and does not contain anywhere near the amount of buffering minerals found in the Hereford water (Waldbott, et al. 1978)."

Moreover, the methods Dean used in selecting the 21 cities to study have been criticized by scientists and statisticians. According to Mark Diesendorf in the journal Nature,

"From the viewpoint of modern epidemiology, these early studies were rather primitive. They could be criticized for the virtual absence of quantitative, statistical methods, their nonrandom method of selecting data and the high sensitivity of the results to the way in which the study populations were grouped (Diesendorf, 1986)."

CDC 8:

The hypothesis that dental caries could be prevented by adjusting the fluoride level of community water supplies from negligible levels to 1.0-1.2 ppm was tested in a prospective field study conducted in four pairs of cities (intervention and control) starting in 1945: Grand Rapids and Muskegon, Michigan; Newburgh and Kingston, New York; Evanston and Oak Park, Illinois; and Brantford and Sarnia, Ontario, Canada.

Our response 8:

This was indeed the hypothesis that was tested. However, the notion that adding fluorides to the water, unaccompanied by any calcium and magnesium minerals, would still result in the low cavity rates of towns like Hereford, was highly questionable. It is even more questionable when considering the fact that the fluorides put in the water today are not pharmaceutical grade chemicals but industrial waste products that are accompanied by trace amounts of heavy metals like arsenic and lead. Naturally occurring fluoride, in other words, found with high levels of calcium is a far different story than industrial fluoride (in the form of hexafluorosilicic acid) obtained from the pollution scrubbing devices of the phosphate fertilizer industry (currently used in approximately 90% of the fluoridation programs in the United States).

CDC 9:

After conducting sequential cross-sectional surveys in these communities over 13-15 years, caries was reduced 50%-70% among children in the communities with fluoridated water (12).

Our response 9:

What the CDC neglects to mention here is the controversy surrounding these studies. Independent reviewers of these studies were taken back by what one statistical firm described as "an unfortunate disdain for some of the prerequisites of valid research (De Stefano 1954)." For example, Grand Rapids Michigan, which was the first test community fluoridated in the United States, was designed to be compared with an unfluoridated city (Muskegon, MI) for ten years. However, after just six and a half years, Muskegon was fluoridated and was therefore disbanded as a control city. Interestingly enough, this decision was lost on some in the dental community who as late as 1955 were claiming that Grand Rapids was still being compared to unfluoridated Muskegon (Sutton 1996).

Indeed, this fact was lost on the authors of the study themselves when they wrote the abstract to their work in 1962! In their abstract the authors state that the caries rates from Grand Rapids had been "compared with the caries attack rates in the control group of children in Muskegon, Mich." In the actual paper, however, the authors acknowledge that Muskegon lost its unfluoridated status in 1951 and state that "in subsequent analyses of Grand Rapids data, comparison has been made with...those for Aurora [Michigan]" (See Sutton 1996).

The authors of the Grand Rapids study weren't the only ones to make such a remarkable mistake. In the same year, 1962, the authors (Ast & Fitzgerald) of the Newburgh/Kingston fluoridation trial, referred in their abstract to the Evanston, Illinois, and Grand Rapids, Michigan studies. According to their abstract, "among children 12 to 14 years old... reductions in the DMF rates as compared to the rates in control cities ranged from 48 to 71 per cent." However, in their own paper Ast & Fitzgerald state, "in the Grand Rapids and Evanston studies the control cities were lost before the study was completed, so that the current data have been compared with the base line data." In other words, and as their paper's data goes on to show, these 48 and 71% reductions were not comparisons with the control communities (as they stated), but with the original decay rates (i.e. "base line data") of the test cities before they started fluoridating.

Furthermore, the erratic and arbitrary way in which the sampling of children from these cities was done has raised many an eyebrow. For example, when the Grand Rapids trial began in 1945, children from all 79 schools in Grand Rapids were examined. By 1949, however, examiners observed children from only 25 of these 79 schools. Meanwhile in Muskegon, children from ALL the schools were still being examined. Such problematic changes and inconsistencies in sampling size is further illustrated by the fact that when the Grand Rapids study commenced, the number of 12 to 16 year olds being examined was 7,661, but by the final year of the study, the number of 12 to 16 year olds being studied had dropped to just 1,031 (Sutton 1996).

Along with these arbitrary changes in the study's sampling methods, the study employed multiple examiners to assess the children's teeth. But as has been shown in studies from the American Journal of Public Health (Boyd et al., 1951) as well as the Journal of the American Dental Association (Radusch, 1934), there is a considerable variability between each dentists' assessment of a person's teeth. The study in the Journal of the American Dental Association found, for instance, that when 33 patients were examined by three of eight different dentists, "a deviation of 89% in the number of cavities was recorded (Waldbott 1978)." This being the case, it is significant to note that the examiner variability was NEVER assessed in the Grand Rapids study (Sutton 1996).

When the author Anne-Lise Gotzsche began work on her book The Fluoride Question (1973) she showed the statistics derived from these early fluoridation trials to "scientists working in other and unrelated fields." According to Gotzsche, "I'm afraid, they simply laugh at the 'reshuffling', statistical 'weighting', the sudden disappearance of up to 1000 research subjects (quoted in Sutton 1996)."

Indeed, when a firm of professional statisticians, The Standard Audit and Measurement, Inc., was employed to study the data published from the Grand Rapids trial, they concluded: "the lack of sophistication shown in selecting the sample leads to complete bewilderment as to the precise effects or the extent of the effect of fluoridation (De Stefano 1954)."

Despite these enormous weaknesses, these early studies are cited again and again to support the success of fluoridation. (So much has been made of so little!) As Benjamin Nesin, Director of the New York State Water Laboratories, stated at the time, "It must be emphasized that the fluoridation hypothesis in its entirety rests on a very narrow base of selected experimental information. It is this very base which is vulnerable to scientific criticism. And it is upon this very narrow base that the impressive array of endorsement rests like an inverted pyramid (Nesin 1956)."

Needless to say, Nesin's advice has been ignored by the very institutions, e.g. the CDC, whose endorsement has been largely based on these faulty fluoridation trials.

CDC 10:

The prevalence of dental fluorosis in the intervention communities was comparable with what had been observed in cities where drinking water contained natural fluoride at 1.0 ppm.

Our response 10:

By intervention communities, the CDC here is referring to these early test cities, e.g. Grand Rapids, Evanston, and Newburgh. In this sense, the CDC's comments are quite misleading because the rates of fluorosis prevalence that they are referring to are the rates occurring in the 1950s. The authors are not talking about the levels of fluorosis prevalent TODAY.

In not doing so, they have overlooked the fluoridation experiment's most visible failing. For one of the goals of Dean and other early promoters of fluoridation was to limit the occurrence of dental fluorosis in its mildest form to not more than 10% of the children. However, if we look at the picture today, we will see that the levels of fluorosis have climbed far higher than 10% of the population, reaching as high as 80% in some communities, with some cases of moderate and severe fluorosis now being identified as well. According to the ATSDR (1993),

"There is some evidence that levels of fluorosis have increased due to the multiple, widespread sources of fluoride processed with fluoridated water and dentifrices containing fluoride, in addition to the water of fluoridated communities... the prevalence and severity of fluorosis increased in communities with 0.7 - 1.2 ppm fluoride, with prevalence increasing from about 13% to about 22%... the combined prevalence of the severe and moderate categories went from 0.0% to 0.9%..."

In a more recent survey, Heller et. al (1997), found that 29.9% of the children had dental fluorosis (i.e.approximately 1 in 3) when examining U.S. schoolchildren (15,532) aged 7-17 years who had a history of a single residence in an optimally fluoridated community (0.7 - 12 ppm). This 29.9% figure, however, reflects just those children with at least TWO teeth impacted by dental fluorosis. If we include the children which had signs of dental fluorosis on one tooth, the percentage of children with fluorosis was 66.4%.

This 66% figure is in line with other studies from the US. For example:

  • Williams (1990) found that 81% of a sample (n = 374) of 12-14 year olds in fluoridated Augusta, Georgia had dental fluorosis.
  • Lalumandier (1995) found that 75% of a sample (n = 233) of 5 to 19 year olds had fluorosis in fluoridated Asheville, North Carolina, and
  • Morgan (1998) found that 69% of a sample (n =197) of 7 to 11 year olds in a fluoridated Boston suburb had fluorosis.

Similar high rates of dental fluorosis have recently been reported in the UK. In an article published in the British Dental Journal (Tabari et al, 2000) the authors compared the dental fluorosis levels in a fluoridated and non-fluoridated community. They reported that, "The prevalence of fluorosis was 54% in the fluoridated area and 23% in the fluoride-deficient area when all grades (> 0) of fluorosis were included; percentage prevalence of mild to moderate fluorosis (3) was 3% and 0.5% in the two areas, respectively". The authors conclude that it is a combination of fluoride exposure from the fluoride in the water and from toothpaste which is causing these high rates.

In sum, we are seeing dental fluorosis rates anywhere from 3 to 8 times higher than the rates which the original promoters of fluoridation felt were acceptable (i.e. 30 - 81% versus 10%, the "acceptable" limit). In addition to failing to meet Dean's objective, this large increase in dental fluorosis undermines one of the two objectives of fluoridation as stated by the CDC and DHHS in the "1992 Fluoridation Census,"

"Adjusted fluoridation is the conscious maintenance of the optimal fluoride concentration in the water supply for reducing dental caries and minimizing the risk of dental fluorosis (p iv, our emphasis)."

For the CDC to review the history of fluoridation, and not to discuss its most visible failure, is a serious and fundamental shortcoming in their report.

We will return to the health significance of dental fluorosis later in our critique (see our response 30).

CDC 11:

Epidemiologic investigations of patterns of water consumption and caries experience across different climates and geographic regions in the United States led in 1962 to the development of a recommended optimum range of fluoride concentration of 0.7-1.2 ppm, with the lower concentration recommended for warmer climates (where water consumption was higher) and the higher concentration for colder climates (13).

Our response 11:

In these comments the CDC makes it sound as if the delivery of fluoride is precise and finely tuned to climate conditions. In reality, it is neither precise (since individuals drink different quantities of water and they are exposed to fluoride from many other sources), nor in any coherent way is it finely tuned to climate conditions. For example, according to the "1992 Fluoridation Census," the state of Arkansas (with a very warm climate) is artificially fluoridated at 1.2 parts per million, the same levels used for the state of Alaska (with a very cold climate).

Moreover, in reviewing the CDC's Census, we were shocked to discover that the CDC allows fluoride levels in some school water supplies at over four times the optimal level (levels which excede the EPA's Maximum Contaminant Level of 4 ppm!). For example,

* Indiana: Approximately 56 schools (mostly elementary) fluoridate their drinking water systems at 4.5 ppm. (Source: 1992 Fluoridation Census. The name of each school is identified on pages 271-307). The state of Indiana is listed in the Census as 98.6% fluoridated.

* North Carolina: Approximately 61 schools (mostly elementary) fluoridate their drinking water systems at 4.5 ppm. (Source: 1992 Fluoridation Census. The name of each school is identified on pages 646-668). The state of North Carolina is listed in the Census as 78.5% fluoridated.

* Kentucky: Approximately 64 schools (mostly elementary) fluoridate their drinking water systems at 4.0 ppm. (Source: 1992 Fluoridation Census. The name of each school is identified on pages 366-393). The state of Kentucky is listed in the Census as 100% fluoridated.

* Vermont: As presented in the 1992 Census it appears that 17 schools fluoridate their drinking water systems at 4.9 ppm [if not schools, then they are towns with small populations --see pages 898-902). The state of Vermont is listed in the Census as 57.4% fluoridated.

How can the CDC allow schoolchildren, teachers, and staff to drink water with fluoride levels exceding the EPA's Maximum Contaminant Level?

CDC 12:

The effectiveness of community water fluoridation in preventing dental caries prompted rapid adoption of this public health measure in cities throughout the United States.

Our response 12:

Whether it was the "effectiveness" of water fluoridation or the persuasiveness of the fluoridation advocates of the time which prompted rapid adoption, is open to question. But the simple truth is that the US Public Health Service endorsed the practice of water fluoridation in 1951, BEFORE any single trial (discussed in response 10) had been completed (McClure, 1970).

CDC 13:

As a result, dental caries declined precipitously during the second half of the 20th century.

Our response 13:

"As a result" is, of course, a highly misleading statement as it implies a causal connection between the precipitous decline in dental caries and water fluoridation. This causal connection, however, has not been proved, and remains instead a thesis. In order to make this thesis credible, the CDC has to deal with a large number of studies conducted over the last 20 years which find little or no difference in dental decay between fluoridated and non-fluoridated communities (both in the US and worldwide). These studies include:

a) those which indicate that dental decay was falling in industrialized countries before fluoridation was introduced (Diesendorf, 1986 and Colquhoun, 1997);

b) those which indicate that dental decay has continued to decline even after the presumed benefits of fluoridation would have been maximized (
Diesendorf, 1986, Colquhoun, 1997 and De Liefde, 1998);

c) those which show that when water fluoridation is stopped, tooth decay does not increase but actually in some cases continues to decline (
Seppa, et al, 2000; Kunzel, 1997), and

d) those which indicate that in some instances the level of dental decay actually goes up with the level of fluoride in the water (Steelink, 1990 and Teotia and Teotia, 1994

e) the largest survey ever conducted in the US comparing dental decay in fluoridated and non-fluoridated communities (which found little to no difference) (see CDC 17 and our response).

In short, this presumed "causal connection" relies heavily on one set of poorly conducted trials in the US (e.g. Grand Rapids, Evanston, Newburgh, etc.) -- trials conducted in the context of a "desired outcome" rather than the spirit of open and objective scientific enquiry.

Moreover, had the CDC authors simply stepped outside the shores of the US, their assumption, or conclusion, of "causal connection" would be sorely tested. How is it that the majority of West European countries, which do not fluoridate their water, have experienced the same general decline in cavities (
see World Health Organization statistics) as the fluoridated United States?

The CDC, however, didn't have to go as far as Europe to have their thesis challenged. They could have just gone north to Canada. For according to an article (Gray 1987) in the Journal of the Canadian Dental Association,

"Survey results in British Columbia with only 11 percent of the population using fluoridated water, show lower average DMFT rates than provinces with 40-70 percent of the population drinking fluoridated water."

The author of this article further added that,

"school districts [in British Columbia] reporting the highest caries free rates in the province, were totally unfluoridated."

We think it is beholden on these CDC authors, if they wish to convince us of their thesis, to explain this lack of significant difference in tooth decay rates between fluoridated US and non-fluoridated Europe, as well as between British Columbia and other provinces of Canada. They do not do so.

This, we believe, is a fundamental shortcoming of all fluoridation proponents' arguments -- they do not address the fact that most advanced industrialized countries have experienced the same impressive decline in dental caries over the last half century WITHOUT fluoridating their water.

CDC 14:

For example, the mean DMFT among persons aged 12 years in the United States declined 68%, from 4.0 in 1966-1970 (14) to 1.3 in 1988-1994 (CDC, unpublished data, 1999) (Figure 1).




Our response 14:

We have no reason to doubt this decline in dental caries. However, the key point here is again that the same decline was also happening in unfluoridated European countries during the same period (Diesendorf, 1986). And considering the lack of any significant difference found in dental decay between US fluoridated and non-fluoridated communities in the largest modern study (see response 17), we have no reason to believe that this decline wasn't also occurring in unfluoridated US communities as well.

We further find figure 1 deceptive. If the CDC wanted to graphically make the point that fluoridation has reduced dental decay, it should have produced two graphs comparing the rates of decline in tooth decay between fluoridated and non-fluoridated communities over the same time period. Or, they could have produced a graph that looked at trends in dental decay rates before and after fluoridation. Dr. John Colquhoun, Chief Dental Officer in Auckland New Zealand, did exactly that. He produced a graph (see below) based on New Zealand dental examination records of 5 year olds dating back to the 1930s. When Colquhoun plotted the data from these records on a graph it was quite visibly evident that cavities had begun declining before fluoridation was introduced. In fact, when fluoridation and fluoridated toothpastes were introduced, there was scarcely a kink in this downward slope (see attachment 2). Other graphs produced by Diesendorf (1986), in his seminal paper in the journal Nature, focused on specific communities in Australia, in which he also showed that tooth decay rates continued to decline even after the maximum benefits of fluoridation would have been achieved.

CDC 15:

The American Dental Association, the American Medical Association, the World Health Organization, and other professional and scientific organizations quickly endorsed water fluoridation.

Our response 15:

Indeed, they were all very quick to endorse fluoridation. But we don't view that haste in the same favorable fashion as the CDC does, especially considering the fact that the first endorsement, which triggered these others, was made by the US Public Health Service in 1951, before a single fluoridation trial had been completed.

We also don't necessarily put much faith in the ADA's competency at addressing issues of medical safety and toxicology. For instance, the ADA has promoted the use of mercury amalgams now for over 130 years, despite growing evidence of the hazards of releasing mercury into the mouth. Nor are we impressed with the way the dental community in general has handled new data and evidence regarding the toxicity of these amalgams. The Maryland Dental Health agency, for instance, was recently found guilty in court of violating the Open Meeting's law by instituting what national consumer groups called a "gag order" on state dentists from even discussing the suspected problems of amalgams with patients (CMFR, 2000).

As far as endorsements from other agencies are concerned, more often than not they have been made without any independent research. Instead of surveying the literature themselves, they usually rely on the word of the US Public Health Service at face value (Waldbott, 1978).

CDC 16:

Knowledge about the benefits of water fluoridation led to the development of other modalities for delivery of fluoride, such as toothpastes, gels, mouth rinses, tablets, and drops. Several countries in Europe and Latin America have added fluoride to table salt.

Our response 16:

The CDC raises the important point here that other "modalities for delivery of fluoride" have been developed. It fails, however, to acknowledge that European countries and Japan have either discontinued or rejected fluoridation BECAUSE of the availability of these other modalities! According, for instance, to Finland's Paavo Poteri, the Acting Director of Helsinki Water,

"We do not favor or recommend fluoridation of drinking water. There are better ways of providing the fluoride our teeth need" (Letter, February 7, 2000 -- See photocopy of letter at http://www.fluoridation.com/c-finland.htm).

We find it conspicuous that the CDC fails to acknowledge here the public policy approach taken by these countries. Is it because the CDC is concerned that by acknowledging the fact that these countries have rejected fluoridation, they may be inviting doubt as to whether water fluoridation is really one of the top 10 public health achievements of the 20th century?

Effectiveness of Water Fluoridation

CDC 17:

Early studies reported that caries reduction attributable to fluoridation ranged from 50% to 70%, but by the mid-1980s the mean DMFS scores in the permanent dentition of children who lived in communities with fluoridated water were only 18% lower than among those living in communities without fluoridated water (15).

Our response 17:

Here, to their credit the CDC authors are admitting a very important fact. The study in question was one of the papers (Brunelle and Carlos,1990) which analyzed the data collected by the National Institute of Dental Research (NIDR, now the NIDCR) in the late 1980s. This study, which looked at over 39,000 children from 84 communities, cost the US taxpayers some $3.6 million. When Dr. John Yiamouyiannis used the Freedom of Information Act to access the NIDR data, he found that there was little to no difference in the tooth decay status of fluoridated and non-fluoridated communities (Yiamouyiannis 1990). Also significant is the fact that when Yiamouyiannis selected only those children who had lived their entire life in either a fluoridated or non-fluoridated community, there was still little to no discernible difference in dental decay.

Later, when Brunelle and Carlos (1990) examined a sub-set of this data, they found an 18% difference in DMFS (decayed, missing and filled SURFACES), a more sensitive measure than DMFT, between the two communities. This 18% difference in DMFS, however, represents approximately one half of a tooth surface, a fact which the CDC here fails to mention. Thus, when we later visit the debate (see response 30) over the health effects which may be related to fluoride exposure, it is worth remembering that these health risks, as well as the impositions on those who don't want to drink fluoridated water, are being taken today to secure the possible benefit of one half of a tooth surface!

CDC 18:

A review of studies on the effectiveness of water fluoridation conducted in the United States during 1979-1989 found that caries reduction was 8%-37% among adolescents (mean: 26.5%) (16).

Our response 18:

This is probably true, but these same declines were also occurring in unfluoridated Europe over these same years. Moreover, considering the survey done by the NIDR (see above), and the tooth decay camparisons made between British Columbia and other Canadian provinces (Gray 1987; see response 13), we think there is little reason to doubt that this 8 to 37% decline in adolescent cavities wasn't also occurring in unfluoridated US communities as well.

CDC 19:

Since the early days of community water fluoridation, the prevalence of dental caries has declined in both communities with and communities without fluoridated water in the United States.

Our response 19:

Indeed, and that puts the simplistic notion of a cause and effect relationship between fluoridation and reduction in tooth decay in some doubt. In fact, a very interesting example of these comparable reductions has occurred in Newburgh, NY the second city fluoridated in the US, and its control city, Kingston, NY. To this day, some 55 years after this early trial started, Newburgh has remained fluoridated and Kingston has remained unfluoridated. Today, however, Kingston does not have 40 to 60%, or even 18%, more dental decay than Newburgh, as one would expect after reading fluoridation proponents' literature. On the contrary, there is little significant difference in the DMFTs between the two; actually, Kingston is slightly better (Kumar and Green, 1998).

But not only does Kingston have slightly better caries rates, according to Kumar and Green (1998) it has considerably less incidence of dental fluorosis than does Newburgh (about half as much). Thus, to the above CDC statement, we would add the phrase, "in addition, the prevalence of dental fluorosis is increasing in both fluoridated and non-fluoridated communities but is considerably greater in fluoridated communities."

CDC 20:

This trend has been attributed largely to the diffusion of fluoridated water to areas without fluoridated water through bottling and processing of foods and beverages in areas with fluoridated water and widespread use of fluoride toothpaste (17).

Our response 20:

The question we have here is, how can this "attribution" thesis explain the fact that similar decreases have taken place in non-fluoridated COUNTRIES? In these countries there cannot have been a diffusion effect from processed foods or beverages, since these are not prepared with fluoridated water from elsewhere.

The common response from proponents to this question is that these unfluoridated European countries use fluoridated toothpaste. However, if this is indeed the case, then there is one fundamental question proponents, like the CDC, NEED to answer. If Europe and Japan have achieved the same low levels of dental decay as the United States by using topical fluoride applications like toothpaste, why is it necessary to mandate the fluoridation of water in the United States?

On a further point, we would argue that the decline in dental decay experienced in the industrialized world is a result of other things than just fluoride in toothpaste. Indeed, there are many other factors, we believe, to take into account, such as: higher standard of living (tooth decay is definitely linked to poverty); better dental hygiene (regular brushing, flossing, check-ups etc.); changing diet (significantly more cheese, more fruit and vegetables; more refrigeration to keep the vegetables and fruit fresh); and the presence of preservatives (e.g. benzoates) in processed food which might also (like fluoride) kill the bacteria in the mouth responsible for tooth decay. These suggestions have been made by a number of researchers, including Diesendorf (1986), Colquhoun (1997), De Liefde (1998), and (Bowen, University of Rochester, 2000).

CDC 21:

Fluoride toothpaste is efficacious in preventing dental caries, but its effectiveness depends on frequency of use by persons or their caregivers. In contrast, water fluoridation reaches all residents of communities and generally is not dependent on individual behavior.

Our response 21:

The CDC here is essentially doubting whether society can rely on people to brush their teeth well and regularly. However, if European governments can successfully trust their own people to brush their teeth, we don't see why the United States can not. If the argument, however, is about supplying fluoride to those who can't afford it (as the CDC will later make), we would add that a wiser policy option than fluoridation, is to provide targeted subsidies which provide affordable toothpaste and dental care to the poor.

Moreover, this question of whether to use topical fluoride treatments (e.g. toothpaste) or systemic fluoride treatments (e.g. fluoridated water) becomes further easier to answer, we believe, when one takes into account the fact that leading dental researchers are stating today that fluoride's primary benefits are topical. As Featherstone put it in the July 2000 issue of the Journal of the American Dental Association, "Fluoride, the key agent in battling caries, works primarily via topical mechanisms." Any beneficial effect from fluoride comes from topical application on the tooth; it does not come from swallowing it.

In addition, when considering whether fluoridation is more appropriate than topical applications, one needs to keep in mind that once fluoride is put into the water one cannot control the dose that any individual might get. This is due to the fact that some people (e.g. athletes, diabetics) drink much more water than others, and the fact that people receive varying amounts of fluoride from a whole host of other sources (e.g. food & drink prepared with fluoridated water, fluoridated toothpastes/mouthwashes, fluorides in pesticide residues, and fluorides in pharmaceuticals, etc.).

Not being able to control the dose in the case of a known toxic substance like fluoride is highly serious, especially when the therapeutic dose is is so close to the chronic dose which can damage bones (see our response 30). Worse still, if dental fluorosis is considered a toxic effect, as it should be in our view, then the therapeutic dose for some people actually overlaps with the toxic dose for others.

CDC 22:

Although early studies focused mostly on children, water fluoridation also is effective in preventing dental caries among adults. Fluoridation reduces enamel caries in adults by 20%-40% (16) and prevents caries on the exposed root surfaces of teeth, a condition that particularly affects older adults.

Our response 22:

It is important to point out here that most tooth loss amongst adults is caused by periondantal disease (disease of the gum). According to the ADA's consumer advisor Richard Price, gum disease "is the leading cause of tooth loss among baby boomers and older adults in the United States" (ADA, September, 2000).

The most important factors in predicting gum disease, however, are not lack of water fluoridation but poverty, tobacco use, and deficiencies in calcium. In regards to poverty, a study in the Journal of Periodontology found, according to Reuters Health, that

"individuals with ongoing money troubles were at 70 percent higher risk of periodontal symptoms than financially secure individuals" (cited in ADA Daily News, July 20, 1999).

In regards to calcium intake, the ADA reports of a study where,

"men and women who had calcium intakes of fewer than 500 milligrams, or about half the recommended dietary allowance, were almost twice as likely to have periodontal disease, as measured by attachment loss" (ADA, August 3, 2000).

So, when the CDC refers to fluoridation's beneficial effects on adult's oral health, it is important to keep in mind that fluoridation doesn't do much to prevent, or reverse, the most serious oral health problem affecting adults -- gum disease.

But since the CDC here is referring to fluoridation's effects on dental caries, it is important to also keep in mind that there are plenty of other ways to prevent and minimize caries in adults. Alternatives include: using fluoridated toothpaste; using non-fluoridated toothpaste enriched with calcium-phosphate; maintaining good nutrition and diets; and using topical applications containing the natural sugar xylitol (Hujoel, 1999; Makinen, 1996; Trahan, 1996; Scheinin, 1976).

CDC 23:

Water fluoridation is especially beneficial for communities of low socioeconomic status (18). These communities have a disproportionate burden of dental caries and have less access than higher income communities to dental-care services and other sources of fluoride. Water fluoridation may help reduce such dental health disparities.

Our response 23:

It is true that "communities of low socioeconomic status" have a "disproportionate burden of dental caries" but it does not follow that fluoridation of their water will solve the problem. A more appropriate solution, as stated above, is to finance government programs that better address poverty; that provide better nutrition to the poor; and that provide free dental care.

Moreover, it bears pointing out that the poor are most likely to suffer from poor nutrition (e.g. deficiencies in protein, calcium and vitamin C), which makes them more vulnerable to fluoride's toxic effects (Chinoy, 1994, 2000). Also, as the ATSDR (1993) noted: "Poor nutrition increases the incidence and severity of dental fluorosis... (p 112)."

Biologic Mechanism

CDC 24:

Fluoride's caries-preventive properties initially were attributed to changes in enamel during tooth development because of the association between fluoride and cosmetic changes in enamel and a belief that fluoride incorporated into enamel during tooth development would result in a more acid-resistant mineral. However, laboratory and epidemiologic research suggests that fluoride prevents dental caries predominately after eruption of the tooth into the mouth, and its actions primarily are topical for both adults and children (1). These mechanisms include 1) inhibition of demineralization, 2) enhancement of remineralization, and 3) inhibition of bacterial activity in dental plaque (1).

Our response 24:

The CDC authors have acknowledged a key finding here. For years dentists and health officials and others promoting fluoridation claimed that the benefits were systemic: that you had to swallow the stuff and the earlier the better. That is why doctors prescribed fluoride tablets to pregnant mothers and to babies before their teeth had erupted. Now we know that they were wrong (and if they were wrong on so fundamental a point, one has to wonder what else they could be wrong about). While the CDC cites Featherstone, there have actually been a long line of leading dental researchers who have now concluded that the benefits of fluoride are largely topical, not systemic. These include: Levine (1976); Fejerskov, Thylstrup and Joost (1981); Carlos (1983); Featherstone (1987, 1999, 2000); Margolis and Moreno (1990); Burt (1994); Shellis and Duckworth (1994); and Limeback (1998).

It is unfortunate that the CDC cannot draw the logical deduction from this key finding. Simply put, the benefits are topical, the risks are systemic. If you don't have to swallow the stuff to get the benefits and there are risks from swallowing it, the last thing you should do is put fluoride in the drinking water. Common sense says if you want fluoride, brush your teeth with fluoridated toothpaste and spit it out. If you put it in the water it inevitably gets swallowed and gets flushed through the whole body, running the risk of causing damage, including dental fluorosis, excessive accumulation in the bones and pineal gland and interference with enzymes, hormones and G-proteins in the soft tissues (see our discussion of health concerns in response 30).

CDC 25:

Enamel and dentin are composed of mineral crystals (primarily calcium and phosphate) embedded in an organic protein/lipid matrix. Dental mineral is dissolved readily by acid produced by cariogenic bacteria when they metabolize fermentable carbohydrates. Fluoride present in solution at low levels, which becomes concentrated in dental plaque, can substantially inhibit dissolution of tooth mineral by acid.

Our response 25:

There are other substances besides fluoride which can "inhibit dissolution of tooth mineral by acid." Such substances include the natural sugar xylitol, the efficacy of which has been demonstrated now in numerous peer-reviewed studies (Hujoel, 1999; Makinen, 1996; Trahan, 1996; Scheinin, 1976). Other substances include bases, like baking sodas and alkaline foods (e.g. cheese), which help to neutralize the acid which dissolves the enamel.

CDC 26:

Fluoride enhances remineralization by adsorbing to the tooth surface and attracting calcium ions present in saliva. Fluoride also acts to bring the calcium and phosphate ions together and is included in the chemical reaction that takes place, producing a crystal surface that is much less soluble in acid than the original tooth mineral (1).

Our response 26:

Other things can also enhance remineralization, such as high levels of calcium and phosphate. Indeed, fluoride is by no means essential for the development of healthy teeth. While some could argue that it's beneficial, no one can argue that it's essential. One indication of it's lack of essentiality is the fact that (as discussed in response 3) the level of fluoride in human milk is 100 times lower than the level in "optimally" fluoridated water, e.g., 0.01 vs. 1 ppm.

CDC 27:

Fluoride from topical sources such as fluoridated drinking water is taken up by cariogenic bacteria when they produce acid. Once inside the cells, fluoride interferes with enzyme activity of the bacteria and the control of intracellular pH. This reduces bacterial acid production, which directly reduces the dissolution rate of tooth mineral (19).

Our response 27:

Indeed, not only does fluoride interfere with the bacteria's enzyme activity, it actually kills the bacteria. In other words, fluoride is a bacteriacide. However, there are many other bacteriacides out there, including the preservatives (e.g. benzoates) used in many processed foods (De Liefde, 1998). These bacteriacides, as well as xylitol, may turn out to be just as effective at inhibiting the bacteria, but do so without the side effects of interfering with enzymes elsewhere in the body, including the growing tooth (DenBesten, 1999), the bone (Krook and Minor, 1998), and the pineal gland (Luke, 1998). The reason for this is that many of the preservatives used in processed food are organic substances metabolized in places like the liver. Unlike fluoride they are unlikely to accumulate in the bone or the pineal gland.

The important point is that fluoride's benefit to teeth is partly a toxic effect: killing the bacteria by inhibiting enzymes. Common sense says try to constrain the toxic effect to the surface of the tooth; do not distribute the toxic effect around the body. Fluoridated toothpaste is a more sensible way of delivering this topical toxic effect than drinking water. A key question not addressed by the CDC is: knowing that fluoride inhibits enzymes in the oral bacteria, what enzymes in other parts of our body might fluoride inhibit if swallowed?

Population Served by Water Fluoridation

CDC 28:

By the end of 1992, 10,567 public water systems serving 135 million persons in 8573 U.S. communities had instituted water fluoridation (20). Approximately 70% of all U.S. cities with populations of greater than 100,000 used fluoridated water. In addition, 3784 public water systems serving 10 million persons in 1924 communities had natural fluoride levels greater than or equal to 0.7 ppm. In total, 144 million persons in the United States (56% of the population) were receiving fluoridated water in 1992, including 62% of those served by public water systems. However, approximately 42,000 public water systems and 153 U.S. cities with populations greater than or equal to 50,000 have not instituted fluoridation.

Our response 28:

Proponents of fluoridation often point out that the majority of Americans drink fluoridated water. What they fail to acknowledge is that the vast majority of citizens worldwide, do not. Of the approximate 350 million people in the world who drink artificially fluoridated water, nearly half live in North America. Where other countries have fluoridated they have usually been English speaking (e.g. Australia, Canada, Ireland, New Zealand, and the UK) or subject to American influence. Israel appears to be the latest country to succumb (Gleit, 2000). In other words, fluoridation is a peculiarly Anglo-American phenomenon, born at a time when citizens and officials had a very inflated notion of what chemicals could achieve in society without paying a heavy price down the road. Fluoridation was being launched about the same time that American viewers watched newsreel shots of children being sprayed with DDT at picnics to show how harmless it was and about the same time that advertisements were telling the American people that "19,293 Dentists Advise: Smoke Viceroy Cigarettes."

Many European countries have considered fluoridation, and some have dabbled with it, but most have rejected it, either because they weren't convinced about its safety or they weren't prepared to force it on citizens who didn't want it. Below we have printed a list of some of the countries that do not fluoridate, their populations, and excerpts from some of the statements on fluoridation made by government agencies in these countries. They would certainly not subscribe to the CDC boast that fluoridation is one of the top 10 public health achievements of the Twentieth Century.

Some of the countries that do not fluoridate their water supply:

  • Austria, pop. 8,139,299
  • Belgium pop. 10,182,034
  • Denmark, pop. 5,356,845
  • Finland, pop. 5,158,372
  • France, pop. 58,978,172
  • Germany, pop. 82,087,361
  • Greece, pop. 10,707,135
  • Italy, pop. 56,735,130
  • Japan, pop. 126,182,077
  • Luxembourg pop. 429,080
  • Netherlands pop. 15,807,641
  • Norway pop. 4,438,547
  • Sweden pop. 8,911,296

The following countries fluoridate less than 3% of their water supply:

  • Spain pop. 39,167,744
  • Switzerland pop. 7,275,467

The following statements are from some of these governments concerning fluoridation:

Japan:

"Japanese government and local water suppliers have considered there is no need to supply fluoridated water to ALL users because 1) impacts of fluoridated water on human health depends on each human being so that inappropriate application may cause health problems of vulnerable people, and 2) there is (sic) other ways for the purpose of dental health care, such as direct F-coating on teeth and using fluoridated dental paste and these ways should be applied at one's free will." - Ref: March 8, 2000 letter signed by: Toru Nagayama, Environment Agency, Government of Japan, Tokyo. (Original letter is available at: http://www.fluoridation.com/c-japan.htm).

Belgium:

"This water treatment has never been of use in Belgium and will never be (we hope so) into the future." - Ref: February 28, 2000 letter signed by Chr. Legros, Directeur, Belgaqua Brussels, Belgium. (Original letter available at: http://www.fluoridation.com/c-belgium.htm)

Denmark:

"We are pleased to inform you that according to the Danish Ministry of Environment and Energy, toxic fluorides have never been added to the public water supplies." - Ref: December 22, 1999 letter signed by Klaus Werner Royal Danish Embassy, Washington DC . (Original letter available at: http://www.fluoridation.com/c-denmark.htm)

Norway:

"In Norway we had a rather intense discussion on this subject some 20 years ago, and the conclusion was that drinking water should not be fluoridated." - Ref: March 1, 2000 letter signed by Truls Krogh and Toril Hofshagen, Folkehelsa, Statens institutt for folkeheise (National Institute of Public Health), Oslo, Norway. (Original letter available at: http://www.fluoridation.com/c-norway.htm)

Sweden:

"Drinking water fluoridation is not allowed in Sweden... New scientific documentation or changes in dental health situation that could alter the conclusions of the Commission have not been shown." - Ref: February 28, 2000 letter signed by Gunnar Guzikowski, Chief Government Inspector, Livsmedels Verket, National Food Food Administration, Drinking Water Division, Sweden. (Original letter available at: http://www.fluoridation.com/c-sweden.htm)

Germany:

"In the former Democratic Republic of Germany (DDR) in several districts the drinking water was fluoridated but after the unification of both German states in 1990 fluoridation was stopped. In the Federal Republic of Germany there was in about 1952 a drinking water fluoridation experiment. But it was stopped after one or two years." - Ref: February 11, 2000 letter signed by Dr. K. Ewing (Please see original letter as signature was difficult to read), Geschaftszeichen (Bei allen Antworten bitte angeben), Bonn, Germany. (Original letter available at: http://www.fluoridation.com/c-germany.htm)

Finland:

"We do not favor or recommend fluoridation of drinking water. There are better ways of providing the fluoride our teeth need." - Ref: February 7, 2000 letter signed by Paavo Poteri, Acting Managing Director, Helsinki Water, Finland. (Original letter available at: http://www.fluoridation.com/c-finland.htm)

Austria:

"Toxic fluorides have never been added to the public water supplies in Austria." - Ref: February 17, 2000 letter signed by i.A. Dipl-HTL-Ing M. Eisenhut, Head of Water Department, Osterreichische Yereinigung fur das Gas-und Wasserfach, Schubertring 14, A-1015 Wien, Austria. (Original letter available at: http://www.fluoridation.com/c-austria.htm)

Cost Effectiveness and Cost Savings of Fluoridation

CDC 29:

Water fluoridation costs range from a mean of 31 cents per person per year in U.S. communities of greater than 50,000 persons to a mean of $2.12 per person in communities of less than 10,000 (1988 dollars) (21). Compared with other methods of community-based dental caries prevention, water fluoridation is the most cost effective for most areas of the United States in terms of cost per saved tooth surface (22).

Water fluoridation reduces direct health-care expenditures through primary prevention of dental caries and avoidance of restorative care. Per capita cost savings from 1 year of fluoridation may range from negligible amounts among very small communities with very low incidence of caries to $53 among large communities with a high incidence of disease (CDC, unpublished data, 1999). One economic analysis estimated that prevention of dental caries, largely attributed to fluoridation and fluoride-containing products, saved $39 billion (1990 dollars) in dental-care expenditures in the United States during 1979-1989 (23).


Our response 29:

First of all, if we assume that fluoride provides a benefit to teeth, which cannot be provided by other means (e.g., xylitol) the cost comparison which should be made is between the costs of delivering fluoride through the public water supply and delivering fluoride (or other cavity preventing agents) via toothpaste and other topical applications. A comparison of this sort could be made by comparing the costs accrued by European or Japanese oral health programs with those of the United States (which should include the significant sums the US spends promoting fluoridation). This would seem an essential comparison to make, especially as the CDC states that "compared with other methods of community-based dental caries prevention, water fluoridation is the most cost-effective." Unfortunately, the CDC does not give any indication about what other methods fluoridation was compared to, and what the results of these comparisons were.

Secondly, in calculating the costs of fluoridation, the CDC appears not to have taken into account the costs of treating dental fluorosis, an issue they have clearly avoided in its modern context (see our response 10). This is a particularly important omission considering the fact that the President of the Canadian Association for Dental Research, Dr. Limeback, has stated that in Canada they are spending more money treating dental fluorosis than they would spend treating the very small increase in dental decay that might result if fluoridation were halted. According to Limeback, treating dental fluorosis has now become a multi-billion dollar industry (Limeback, 2000, video). When recognizing this and the fact that upwards of two thirds of children living in fluoridated communities have dental fluorosis, the crudeness of the CDC's cost-benefit equation becomes evident.

Thirdly, and perhaps most significantly, the CDC has not taken into account the large potential costs of increased hip fractures in the elderly which are possibly associated with fluoride exposure (see our response 30). The US spends up to $10 billion a year treating hip fractures, and one in four of elderly patients who experience a hip fracture DIE within a year of their operation and about 50% never return to an independent existence (NPR, 2000). If it is confirmed that fluoridation does contribute towards an increase in hip fracture (along with other health effects), these costs would dwarf the savings calculated by the CDC. Which brings us to the next section, the CDC's discussion of the safety of water fluoridation.

Safety of Water Fluoridation

CDC 30:

Early investigations into the physiologic effects of fluoride in drinking water predated the first community field trials. Since 1950, opponents of water fluoridation have claimed it increased the risk for cancer, Down Syndrome, heart disease, osteoporosis and bone fracture, acquired immunodeficiency syndrome, low intelligence, Alzheimers disease, allergic reactions, and other health conditions (24).

The safety and effectiveness of water fluoridation have been re-evaluated frequently, and no credible evidence supports an association between fluoridation and any of these conditions (25).

Our response 30:

Before going into details, it is amazing to us that a body like the CDC can brush off health concerns in three sentences, based upon two publications (Hodge, 1986 and NRC, 1993), which were 13 and 6 years old at the time that their article was published. Thus, the CDC authors do not consider any of the health concerns reported since 1993. They do not discuss for example, the impact of fluoride on the central nervous system (Mullenix, 1995; Zhao, 1996; Varner, 1998; Guan, 1998; Masters and Coplan, 1999); the pineal gland (Luke, 1998); the thyroid gland (reviewed by Schuld, 1999); G-proteins (reviewed by Strunecka and Patocka, 1999); and the many studies on hip fracture, discussed below.

ENDEMIC FLUOROSIS IN INDIA AND CHINA.

Furthermore, the CDC fails to acknowledge that excess fluoride exposure in countries like India and China with endemic fluorosis has seriously effected millions of people, 65 million in India alone (Susheela, 1998 and Chinoy, 2000). The following is an excerpt from an interview with Dr. Chinoy, an Indian scientist who has studied skeletal fluorosis in India.

Q: Tell us some of the symptoms, some of the visible symptoms of someone suffering fluorosis in India.

A: The main criteria is that if you go to the villages [you] will find that if you request the person who is suffering from fluorosis to pick up something from the floor, he or she will not be able to do it because their bones are very stiff. And [when] they are asked to touch their chin to their chest, that also they can't do, because the neck is very stiff. Then the two hands are supposed to be put at the back of the neck and join the hands. They can't do that. (Chinoy, 2000).

According to the Department of Health and Human Services, the levels of fluoride in the bone which cause "stiffness of joints" and "osteosclerosis of pelvis & vertebral column" is 6,000 to 7,000 parts per million (1991) (for levels of fluoride in Americans' bones today, see discussion below). This condition is known as Clinical Phase 1 Skeletal fluorosis. According to Gordon and Corbin (1992), consuming water at 4 ppm yields an average 6400 ppm bone level fluoride (unfortunately these authors don't say where they got these figures from). Moreover, according to various government reports, we are receiving upwards of 3.5 to 6.6 milligrams a day of fluoride from all total sources (which is 3.5 to 6.6 times greater than the optimal 1 milligram per day dose from fluoridated water, DHHS, 1991; NRCC 1977; NAS 1977). With total fluoride dosage increasing as it is, the margin of safety we have today concerning the levels of fluoride which will or will not damage our bones and joints is precariously small, and a strong reason why we should not be adding more fluoride to our water.

DENTAL FLUOROSIS.

There is no argument (although CDC has avoided the issue) that there has been a large increase in dental fluorosis as a direct and indirect result of water fluoridation (ATSDR, 1993 and Heller, 1997). However, promoters of fluoridation deal with this issue semantically. Dental fluorosis is called a "cosmetic effect" even though it is the first sign of fluoride's toxic effect on the body: it has poisoned enzymes in the growing tooth which facilitate the last step in enamel formation (DenBesten,1999). Instead of dismissing this important finding as a cosmetic effect, the promoters of fluoridation should consider what other enzymes in our body may be inhibited by fluoride when we swallow it (which do not have the same telltale signs as white spots on the tooth).

In regards to fluorosis being a "cosmetic effect", Dr. Geoffrey Smith stated in an article from the New Scientist (1983) that, "To suggest we should ignore such a sign [white spots on the tooth] is as irrational as saying the blue-black line which appears on the gums due to chronic lead poisoning is of no significance because it doesn't cause any pain or discomfort."

HIP FRACTURE

Since 1990, there have been 18 studies (4 unpublished) probing the link between water fluoridation (both natural and artificial) and hip fracture in the elderly. 10 of these found an association, 8 did not. The references for all 18 studies are given at the end of our paper. A number of those which found an association were published in leading medical journals like JAMA and the American Journal of Epidemiology. These reports by themselves refute the CDC's claim that there is "no credible evidence" supporting claims of health effects from fluoridation.

One of the most interesting of the recent papers on hip fracture is one in which the authors (li et al, 1999, unpublished) looked at hip fractures in six Chinese villages with water fluoride concentrations ranging from 0.25 to 7.97 ppm. For subjects exposed to the various fluoride concentrations in the different villages they reported a relative risk ratio for hip fracture for each village compared to the rate for the village with water concentrations in the 1.00 - 1.06 ppm range. These relative risk ratios were: 3.26 for the 4.32 - 7.97 ppm village; 1.75 for the 2.62 - 3.56 ppm village; 2.13 for the 1.45 - 2.19 ppm village; 1.12 for the 0.58 - 0.73 ppm village, and 0.99 for the 0.25 - 0.34 ppm village. These findings are striking. The hip fractures in the village with over 4 ppm fluoride had a threefold increase in hip fracture over the 1 ppm village. Also, the fact that there is almost a linear increase with concentration of fluoride over 1 ppm is suggestive of a cause and effect relationship.

According to the ATSDR's review of the hip fracture studies in 1993,

"The weight of evidence from these experiments suggests that fluoride added to water can increase the risk of hip fracture in both elderly women and men. However, questions remain due to issues such as the lack of information on trends in hip fracture and total individual fluoride consumption. If this effect is confirmed, it would mean that hip fracture in the elderly replaces dental fluorosis in children as the most sensitive endpoint of fluoride exposure." (pp 56-57).

Is the CDC unaware of this statement from the ATSDR?

BONE DAMAGE.

While the evidence of an association between fluoridation and hip fracture in the elderly is mixed, there is no question that fluoride can damage bone, especially at higher doses. Many published studies have shown this, including those by: Roholm (1937); Jolly (1971); Hedlund and Galagher (1989); Riggs (1990); Chlebna-Sokol and Czerwinski (1993); Susheela (1998); and Bely (1998, 2000). What is in question is how close the average person, living in a fluoridated community, will get to fluoride bone levels that cause damage (e.g. brittleness) after a lifetime of exposure.

After more than 50 years of fluoridation, we would have a much clearer understanding of this question today, if only the US Public Health Service had spent less money promoting fluoridation and more on tracking the level of fluoride accumulating in the bones of the American people. Had they done so, we would not be limited by epidemiological studies in which individual fluoride exposures are not known. We would subsequently have a better idea whether higher fluoride levels in bone are associated with higher hip fracture rates. However, despite knowing that 50% of the fluoride we ingest accumulates in our bones, and despite knowing that there has been a significant increase in fluoride exposure since fluoridation began, the CDC and other public health institutions have not done this, and so we have little to no understanding of the levels of fluoride the elderly have in their bones. Therefore, we believe that before the CDC can dismiss hip fracture as a health risk (as it seems eager to do) it should first examine the level of fluoride found in the hip bones of the elderly who have suffered fractures and show that higher levels of fluoride are not found in the fractured bone. Moreover, the CDC should also be seeing how close the levels are getting in the bones of citizens living in fluoridated communities to those which are reported by the DHSS (1991) to be associated with Clinical Phase 1 Skeletal fluorosis (as discussed above).

THE NRC REPORT (1993).

If we now look at the 1993 review by the National Research Council, the most recent report on which the CDC relies for its dismissal of health concerns, we find that it provides a far less thorough analysis of the health concerns of fluoride than the ATSDR toxicological profile discussed below (and which the CDC does not cite). They avoid commenting on the health ramifications of dental fluorosis, saying that it is regulatory matter. Moreover, their dismissal of both the animal (NTP, 1990) and human findings (Hoover, 1991; Cohn, 1992) of increased osteosarcoma in male rats, as well as in young men (10-19 years) in fluoridated areas, is revealing in its casualness to such a serious possibility. There is no notion in their account of how controversial the handling of the NTP animal studies were (i.e. the EPA fired a top toxicologist in the Office of Drinking Water, Dr. William Marcus, after he had concluded from the NTP rat studies that there was "clear evidence of carcinogenicity." The EPA was later found guilty by the Secretary of Labor, Robert Reich, for firing Marcus out of "retaliation" and were ordered to rehire him and provide full back pay and compensation). Moreover, the NRC's readiness to use an unpublished Procter and Gamble study to nullify concern on this matter is disturbing.

Unlike the CDC, however, the authors of the NRC report, despite its limitations, do concede that there are still health questions which have not been resolved, when they state:

"The subcommittee found inconsistencies in the fluoride toxicity data base and gaps in knowledge. Accordingly, it recommends further research in the areas of fluoride intake, dental fluorosis, bone strength and fractures, and carcinogenicity. The subcommittee further recommends that the EPA's interim standard of 4 mg/L (4ppm, PC) should be reviewed when results of new research become available and if necessary, revised accordingly (p 11)."

This need for further research is not acknowledged by the CDC. Nor do they acknowledge the far more extensive recommendations of the ATSDR (an agency of the Department of Health and Human Services) made in their toxicological profile on fluorides, published in the same year as the NRC review (ATSDR, 1993).

THE ATSDR REPORT (1993).

ATSDR identified the following data needs.

* CHRONIC-DURATION EXPOSURE:

- "Epidemiological evidence exists that the incidence and severity of fluorosis has increased in the United States (DHHS 1991; Heifetz et al. 1988). Further examination of the etiology and trends in prevalence may be useful (p 122)."

- "Some data from case studies are available regarding nutritional states that exacerbate fluorosis (Kemp et al. 1931; Pandit et al. 1940). Epidemiological studies addressing the effect of nutrition on the prevalence and severity of dental and skeletal fluorosis may be useful (p 122)."

- "Recent studies indicate that fluoride may increase the rate of hip fractures in elderly men and women (Danielson et al. 1992; Sowers et al. 1991), particularly women with osteoporosis (Riggs et al.1990). Analytical epidemiological studies of the association, if any, between bone fractures and factors such as fluoride intake, fluoride blood levels, diet, and body levels of nutrients such as calcium might be useful (pp 122-123)."

- "Target organs other than bones and teeth for chronic exposure to fluoride for humans are not known. There is some evidence of hepatic and renal effects of fluoride in animals, but minimal information regarding possible effects in humans. Additional studies specifically addressing effects on these systems may be useful, especially since people with renal dysfunction are sensitive to fluoride (p 123)."

* CANCER:

- "The osteosarcoma rate in males living in fluoridated areas has increased markedly in recent years, but thorough statistical analyses concluded that the effect is not due to fluoridation (Hoover et al. 1991). Nonetheless, analytical epidemiology studies to determine the risk factors for osteosarcoma may be useful. Such studies should include analysis of fluoride exposure and bone levels of fluoride. Case-control studies of people with osteosarcoma could be particularly useful. The NTP oral carcinogenicity study for sodium fluoride concluded that there is equivocal evidence that fluoride is a carcinogen in male rats, but not in female rats
or mice of either gender (NTP 1990)... Another rat carcinogenicity study found no evidence that fluoride is a carcinogen [Maurer et al. 1990, an unpublished Procter and Gamble study], but was limited in several different aspects. Additional animal cancer biassays may be useful in addressing this investigation (p 123)."

* GENOTOXICITY:

- "There is a significant database on the genotoxicity of fluoride compounds in several species and several cell types. However, the results from well-characterized systems are much more limited and additional well-designed experiments would be useful in resolving contradictory data (p 123)."

* REPRODUCTIVE TOXICITY:

- "Sixty days of oral exposure to sodium fluoride was observed to cause changes in the seminiferous tubules of CD rat testes and a decreased number of offspring (Araibi et al. 1989)... Additional support for an adverse effect of high fluoride levels on reproduction comes from studies in dogs and birds (Buenter and Hahn 1986; Hoffman et al. 1985; Shellenberg et al. 1990; Van Rensburg and de Vos 1966). Further data concerning reproductive organ pathology following a 90-oral or inhalation study would be useful to clarify the current data on reproductive effects (p 124)."

* DEVELOPMENTAL TOXICITY:

- "... [While] there are no recent studies of conventional design in animals of the developmental effects of oral fluoride... there is a general paucity of data concerning developmental endpoints for fluoride compounds. Further data concerning exposure to fluoride compounds by the oral and inhalation routes for developmental endpoints would be useful (p 124)."

* NEUROTOXICITY:

- "Because fluoride interacts with calcium ions needed for effective neurotransmission, fluoride can affect the nervous system. However, while acute effects on the nervous system have been observed in humans, it is not known whether chronic exposure to hydrogen fluoride or fluoride can cause nervous system effects... Further neurological testing may be warranted to ascertain the conditions involved and the extent to which the nervous system is a target organ for fluoride toxicity (p 125)."

* ABSORPTION, DISTRIBUTION, METABOLISM, AND EXCRETION:

- "Regardless of the route of administration, fluoride is found in the plasma, and accumulates in bones and teeth. Elevated levels are also found in the kidney (Whitford and Taves 1973) and aorta (Smith et al. 1960). Further information concerning distribution would be useful to determine if there are target organs of fluoride exposure in addition to the skeletal, gastrointestinal, and cardiovascular systems. In addition, while it is known that elevated bone fluoride levels decrease with time if the exposure source is removed, more information about the kinetics of this process would be useful (pp 126-7)."

ATSDR's CONCERNS VERSUS CDC CONCERNS.


It is clear to us that there is a very striking difference in the concerns being expressed here by the ATSDR and those above by the CDC. The former appear to be approaching the subject in a cautious and scientific manner, in line with their profiles of other toxic substances, whereas the CDC approaches the matter in a dismissive and cavalier fashion. One cannot escape the conclusions that the CDC seems more interested in protecting the US fluoridation program, than it does in examining the health issue objectively or scientifically.

THE PRECAUTIONARY PRINCIPLE.


As far as human health effects are concerned, we are left with these two vitally important questions: 1) Have not sufficient animal and human studies demonstrated both possible and probable human health effects to put into question a practice which at best saves half a tooth surface? 2) At what point will US regulators recognize it would be more prudent to invoke the Precautionary Principle to resolve these mixed findings, instead of stubbornly pursuing this policy until such time as epidemiological studies convince the most entrenched promoters of fluoridation that we have a problem? Sadly, the latter approach inevitably means by the time the "absolute proof" of harm has been demonstrated, many millions will have been exposed and impacted. We should remember how difficult it was for scientists in the 1970's to prove that very low levels of lead caused sub-clinical effects in young children (Needleman, 1979). It is now generally recognized that the slowness of government to get lead out of gasoline resulted in the unnecessary lowering of the IQ of millions of American children (OTA, 1990).

21st Century Challenges

CDC 31:

Despite the substantial decline in the prevalence and severity of dental caries in the United States during the 20th century, this largely preventable disease is still common. National data indicate that 67% of persons aged 12-17 years (26) and 94% of persons aged greater than or equal to 18 years (27) have experienced caries in their permanent teeth.

Our response 31:

While we agree with this statement, we would add that dental decay is highly concentrated amongst poor, mostly minority groups in society today, (which the recent Surgeon General's report on Oral Health in America helped point out, DHSS, 2000). We would further point out that some of the cities where dental decay is high are ones like Boston, which have been fluoridated for many years (Boston Globe, Nov 11, 1999; Read article at: http://www.fluoridealert.org/f-boston.htm).

CDC 32:

Among the most striking results of water fluoridation is the change in public attitudes and expectations regarding dental health. Tooth loss is no longer considered inevitable, and increasingly adults in the United States are retaining most of their teeth for a lifetime (12). For example, the percentage of persons aged 45-54 years who had lost all their permanent teeth decreased from 20.0% in 1960-1962 (28) to 9.1% in 1988-1994 (CDC, unpublished data, 1999). The oldest post-World War II "baby boomers" will reach age 60 years in the first decade of the 21st century, and more of that birth cohort will have a relatively intact dentition at that age than any generation in history. Thus, more teeth than ever will be at risk for caries among persons aged greater than or equal to 60 years.

Our response 32:

Again these figures are impressive but they have occurred elsewhere in communities and countries which have not been fluoridated. Thus the notion that these changes have been caused largely by water fluoridation are most unlikely.

CDC 33:

In the next century, water fluoridation will continue to help prevent caries among these older persons in the United States.

Our response 33:

This is certainly what these authors at the CDC would like, but if good science and wise public policy prevails, their teeth will be protected by safer and more appropriate means.

CDC 34:

Most persons in the United States support community water fluoridation (29).

Our response 34:

A more accurate statement is that most people in the US are poorly informed about the details of community water fluoridation. We believe that one of the reasons that the the general public is poorly informed on this matter, is because US governmental agencies, like the CDC, have consistently provided them one sided reports which exaggerate the benefits and downplay the many health concerns surrounding fluoridation. Downplaying the risks of fluoridation appears to be the de facto policy of US Public Health institutions. For example, according to Dr. Michael Easley, one of fluoridation's most active propagandists, these institutions should refuse to recognize publicly that any legitimate debate exists. According to Easley (1999), who works closely with the CDC's Oral Health Program,

"A favorite tactic of the fluorophobics is to argue for a debate so that 'the people can decide who is right.' Proponents of fluoride are often trapped into consenting to public debates."

"Debates give the illusion that a scientific controversy exists when no credible people support the fluorophobics' view."

"Like parasites, opponents steal undeserved credibility just by sharing the stage with respected scientists who are there to defend fluoridation"; and,

"Unfortunately, a most flagrant abuse of the public trust occasionally occurs when a physician or a dentist, for whatever personal reason, uses their professional standing in the community to argue against fluoridation, a clear violation of professional ethics, the principles of science and community standards of practice."

In our view, such scorn for scientific dialogue is never warranted. It is indeed a matter of grave concern to us that Easley, who actively supports these unscientific and undemocratic methods, and who fails to support his own arguments scientifically (Connett and Connett, 2000) should be working so closely in his promotion efforts with both local and federal officials, including Thomas Reeves, an engineer in charge of the water fluoridation program at the CDC.

In light of these public institutions' tactic of repeatedly denying any legitimate concerns about fluoridation, is it any wonder that the general public is "accepting" of this practice?

Is it also any wonder that most people are unaware that the "fluoride" added to approximately 90% of the public water drinking systems in the US is a hazardous waste by-product collected in the scrubbing systems of the super-phosphate fertilizer industry? We suspect people would be rather shocked to learn this, and that their opinion on the issue may be influenced accordingly.

So, instead of saying that "most persons in the US support... fluoridation", we believe it would be more accurate to say that most persons in the US are inadequately informed about the issue, (thereby making it difficult for them to make an informed decision when asked randomly by a pollster).

CDC 35:

Although the proportion of the U.S. population drinking fluoridated water increased fairly quickly from 1945 into the 1970s, the rate of increase has been much lower in recent years. This slowing in the expansion of fluoridation is attributable to several factors: 1) the public, some scientists, and policymakers may perceive that dental caries is no longer a public health problem or that fluoridation is no longer necessary or effective; 2) adoption of water fluoridation can require political processes that make institution of this public health measure difficult; 3) opponents of water fluoridation often make unsubstantiated claims about adverse health effects of fluoridation in attempts to influence public opinion (24); and 4) many of the U.S. public water systems that are not fluoridated tend to serve small populations, which increases the per capita cost of fluoridation.

Our response 35:

In regards to making unsubstantiated claims, we'll let the reader judge as to which paper contains more of them: our critique or the CDC's report.

CDC 36:

These barriers present serious challenges to expanding fluoridation in the United States in the 21st century. To overcome the challenges facing this preventive measure, public health professionals at the national, state, and local level will need to enhance their promotion of fluoridation and commit the necessary resources for equipment, personnel, and training.

Reported by Div of Oral Health, National Center for Chronic Disease Prevention and Health Promotion, CDC.


Our response 36:

We disagree. Assuming that rational debate and scientific evidence has any role to play in government decisions, the biggest barrier to expanding fluoridation in the twenty first century will be the same barrier that has existed in Japan and Western Europe, namely that there are too many unanswered questions about its safety, there are better alternatives, and that the Government should not force medication onto people who don't want it.

Our Conclusions:

The CDC's report falls far short of the necessary critical distance on the issue that we should expect from a government institution so integral in protecting the public's health. It reminds us of a quote from an American Medical Association editorial (1963) which stated,

"Being critical may be considered antisocial. But science without criticality is unthinkable, for the only route to scientific objectivity is to question, not to 'accept'."

We believe, and hope the readers will agree, that the CDC in this report accepts too much and questions too little. It accepts the early fluoridation trials on their face value and ignores a body of literature which has raised unrebutted criticisms of them; it accepts the often claimed argument that fluoridation is the primary reason why dental caries have declined in the U.S. without questioning why the same reductions in caries have occurred in other industrialized yet unfluoridated countries. It accepts proponents' claims that there is "no credible evidence" of health risks, and fails to question what the implications are of the last seven years of research indicating fluoride's impairment of the pineal gland, central nervous system, kidneys, and bone quality. It also fails to discuss the dramatic rise in dental fluorosis in both fluoridated and non-fluoridated areas. And lastly, it implicitly accepts that there is no difference between the calcium fluoride found naturally in water and the pollution scrubbing liquid, contaminated hexafluorosilicic acid, used in 90% of US fluoridation programs. Indeed, it doesn't ask one question on the subject!

In sum, the CDC, instead of playing the ever needed role of public watchdog, is playing the institutionally expedient role of zealous promoter. Such expediency in itself represents a serious and profound public health threat. For, if the CDC is not willing to review the health concerns about fluoridation and fluoride exposure, fairly and objectively, who will?


References from the CDC report. Our references follow.

1. Featherstone JD. Prevention and reversal of dental caries: role of low level fluoride. Community Dent Oral Epidemiol 1999;27:31-40.
2. Burt BA. Influences for change in the dental health status of populations: an historical perspective. J Public Health Dent 1978;38:272-88.
3. Britten RH, Perrott GSJ. Summary of physical findings on men drafted in world war. Pub Health Rep 1941;56:41-62.
4. Klein H. Dental status and dental needs of young adult males, rejectable, or acceptable for military service, according to Selective Service dental requirements. Pub Health Rep 1941; 56:1369-87.
5. Klein H, Palmer CE, Knutson JW. Studies on dental caries. Dental status and dental needs of elementary school children. Pub Health Rep 1938;53:751-65.
6. McKay FS, Black GV. An investigation of mottled teeth: an endemic developmental imperfection of the enamel of the teeth, heretofore unknown in the literature of dentistry. Dental Cosmos 1916;58:477-84.
7. McKay FS. Relation of mottled enamel to caries. J Am Dent A 1928;15:1429-37.
8. Churchill HV. Occurrence of fluorides in some waters of the United States. J Ind Eng Chem 1931;23:996-8.
9. Dean HT. The investigation of physiological effects by the epidemiological method. In: Moulton FR, ed. Fluorine and dental health. Washington, DC: American Association for the Advancement of Science 1942:23-31.
10. Dean HT. Endemic fluorosis and its relation to dental caries. Public Health Rep 1938;53:1443-52.
11. Dean HT. On the epidemiology of fluorine and dental caries. In: Gies WJ, ed. Fluorine in dental public health. New York, New York: New York Institute of Clinical Oral Pathology, 1945:19-30.
12. Burt BA, Eklund SA. Dentistry, dental practice, and the community. 5th ed. Philadelphia, Pennsylvania: WB Saunders, 1999.
13. Public Health Service. Public Health Service drinking water standards --revised 1962. Washington, DC: US Department of Health, Education, and Welfare, 1962. PHS publication no. 956.
14. National Center for Health Statistics. Decayed, missing, and filled teeth among youth 12-17 years--United States. Rockville, Maryland: US Department of Health, Education, and Welfare, Public Health Service, Health Resources Administration, 1974. Vital and health statistics, vol 11, no. 144. DHEW publication no. (HRA)75-1626.
15. Brunelle JA, Carlos JP. Recent trends in dental caries in US children and the effect of water fluoridation. J Dent Res 1990;69:723-7.
16. Newbrun E. Effectiveness of water fluoridation. J Public Health Dent 1989;49:279-89.
17. Horowitz HS. The effectiveness of community water fluoridation in the United States. J Public Health Dent 1996;56:253-8.
18. Riley JC, Lennon MA, Ellwood RP. The effect of water fluoridation and social inequalities on dental caries in 5-year-old children. Int J Epidemiol 1999;28:300-5.
19. Shellis RP, Duckworth RM. Studies on the cariostatic mechanisms of fluoride. Int Dent J 1994;44(3 suppl 1):263-73.
20. CDC. Fluoridation census 1992. Atlanta, Georgia: US Department of Health and Human Services, Public Health Service, CDC, National Center for Prevention Services, Division of Oral Health, 1993.
21. Ringelberg ML, Allen SJ, Brown LJ. Cost of fluoridation: 44 Florida communities. J Public Health Dent 1992;52:75-80.
22. Burt BA, ed. Proceedings for the workshop: cost effectiveness of caries prevention in dental public health. J Public Health Dent 1989;49(5, special issue):251-344.
23. Brown LJ, Beazoglou T, Heffley D. Estimated savings in U.S. dental expenditures, 1979-89. Public Health Rep 1994;109:195-203.
24.Hodge HC. Evaluation of some objections to water fluoridation. In: Newbrun E, ed. Fluorides and dental caries. 3rd ed. Springfield, Illinois: Charles C. Thomas, 1986:221-55.
25. National Research Council. Health effects of ingested fluoride. Washington, DC: National Academy Press, 1993.
26. Kaste LM, Selwitz RH, Oldakowski RJ, Brunelle JA, Winn DM, Brown LJ. Coronal caries in the primary and permanent dentition of children and adolescents 1-17 years of age: United States, 1988-1991. J Dent Res 1996;75:631-41.
27. Winn DM, Brunelle JA, Selwitz RH, et al. Coronal and root caries in the dentition of adults in the United States, 1988-1991. J Dent Res 1996;75:642-51.
28. National Center for Health Statistics. Decayed, missing, and filled teeth in adults--United States, 1960-1962. Rockville, Maryland: US Department of Health, Education, and Welfare, Public Health Service, Health Resources Administration, 1973. Vital and health statistics vol 11, no. 23. DHEW publication no.(HRA)74-1278.
29. American Dental Association Survey Center. 1998 consumers' opinions regarding community water fluoridation. Chicago, Illinois: American Dental Association, 1998.


Our References:

In addition to the references for the citations in our commentary above, we have attached references to the 18 papers which examine the relationship between fluoride exposure and hip fracture and the papers by leading dental researchers which conclude that the benefits of fluoride are largely topical not systemic.


REFERENCES FOR OUR RESPONSES.

American Dental Association (2000). Baby Boomers Can Help Prevent Oral Health Problems. ADA News Release. September. http://www.ada.org/newsrel/0009/nr-02.html

American Dental Association (2000). Calcium intake linked to periodontal disease rates. ADA News Daily. August 3. http://www.ada.org/adapco/daily/archives/0008/0803cal.html.ada.org

American Dental Association (1944). Editorial: Effect of Fluorine on Dental Caries. J. Am. Dent. Assoc. 31:1360-1363.

American Medical Association (1943). Editorial: Chronic Fluorine Intoxication. J. Am. Med. Assoc., 123:150.

ATSDR (1993). Toxicological Profile for Fluorides, Hydrogen Fluoride, and Fluorine (F). U.S. Department of Health and Human Service. ATSDR/TP-91/17.

Babbit H.E. & Doland J.J. (1939). Quality of Water Supplies in Water Supply Engineering. 3rd Edition, McGraw Hill, New York.

Bely, M. (1998, 2000) Presentations at both the XXII and XIII world conferences of the International Society for Fluoride Research, Bellingham, Washington and Szczecin, Poland respectively.

Bohatyrrewicz, A (1999). Effects of Fluoride on Mechanical Properties of femoral Bone in Growing Rats. Fluoride, 32 (2), 47-54.

Boyd, J.C., and Wessels N.E. (1951). Epidemiological Studies in Dental Caries. III. The Interpretation of Clinical Data Relating to Caries Advance. J. Am. Public Health, 51: 967-986.

Brunelle, J.A. and Carlos, J.P. (1990). J. Dent. Res 69, (Special edition), 723-727.

Chinoy, N.J. et al (1994) Transient and reversible fluoride toxicity in some soft tissues of female mice. Fluoride, 27, 205-214).

Chinoy, N.J. et al (2000) Presentation at the XXIII International Conference of the International Society for Fluoride Research, Szczecin, Poland, June, 2000.

Chlebna-Sokol, D. and Czerwinski, E. (1993) Bone structure assessment on radiographs of distal radial metaphysis in children with dental fluorosis. Fluoride, 26 (1), 37-44.

Citizens for Mercury Relief (CFMR) (2000). Judge blocks Maryland Dental Board from gagging dentists who discuss risks of mercury fillings. Press Release. August 2, 2000.  

Colquhoun, J. (1987). Child Dental Health Differences in New Zealand. Community Health Studies, XI, 85-90.

Colquhoun, J (1997) "Why I changed my mind on Fluoridation. Perspectives in Biology and Medicine, 41, 1-16. http://www.fluoride-journal.com/98-31-2/312103.htm

Cohn, P.D. (1992). An Epidemiologic Report on Drinking Water and Fluoridation. New Jersey Department of Health, Trenton, NJ.

Connett, P. (2000). Fluoride: A Statement of Concern. Waste Not #59. Waste Not, 82 Judson Street, Canton, NY 13617 on web at http://www.fluoridealert.org/fluoride-statement.htm

Connett, P & Connett, M. (2000). Deconstructing Michael Easley. International Fluoride Information Network. Bulletin #143. http://www.fluoridealert.org/d-easley.htm

Cox, G.J. (1939). Experimental Dental Caries and New Knowledge Regarding Fluorine. J. Am. Water Works Assoc., 31, 1926-1930, 1939.

DHHS (1991). Review of Fluoride: Benefits and Risks, Report of the Ad Hoc Committee on Fluoride of the Committee to Coordinate Environmental Health and Related Programs. Department of Health and Human Services, USA.

De Liefde, B. (1998). The Decline of Caries in New Zealand Over the past 40 Years. New Zealand Dental Journal, 94, 109-113

DenBesten, P (1999). Biological mechanism of dental fluorosis relevant to the use of fluoride supplements. Community Dent. Oral Epidemiol., 27, 41-7.

De Stefano, T.M. (1954) Bull. Hudson County Dent. Soc. 23:20.

Diesendorf, M.(1986). The Mystery of Declining Tooth Decay. Nature, 322, 125-129. http://www.fluoridealert.org/diesendorf.htm

Easley, M. (1999). Community Water Fluoridation in America: The Unprincipled Opposition. http://fluoride.oralhealth.org/papers/adaweb04.pdf

Gleit, H. (2000). Total Fluoridation by Next Year. The Jerusalem Post. May 18, 2000. http://www.fluoridealert.org/f-israel.htm

Gordon, S.L. and Corbin, S.B. (1992). Summary of Workshop on Drinking Water Fluoride Influence on Hip Fracture on Bone Health. Osteoporosis International 2, 109-117.

Gray, A.S. (1987). Fluoridation: Time for a New Base Line? Journal of the Canadian Dental Association. 10: 763-765.

Harris, R.S., and Nizel, A.E. (1951). Caries-Producing Effect on Similar Food Grown in Different Soil Areas. N. Engl. J. Med. 244: 361-362.

Heller KE et al (1997). Dental Caries and Dental Fluorosis at Varying Water Fluoride Concentrations. J of Pub Health Dent, 57;No. 3, 136-143.

Hileman, B. (1988). Fluoridation of water. Questions about health risks and benefits remain after more than 40 years. Chemical and Engineering News. August 1, 1988, 26-42. http://www.fluoridealert.org/hileman.htm

Hileman, B. (1989). New Studies Cast Doubt on Fluoridation Benefits. Chemical and Engineering News, 67 (19) 1-60, May 8, 1989. http://www.fluoridealert.org/NIDR.htm

Hirzy, J.W. (1999). Why the EPA's Headquarters Union of Scientists Opposes Fluoridation. Press release from National Treasury Employees Union, May 1, 1999. http://www.fluoridealert.org/hp-epa.htm

Hujoel, PP, et al. (1999). The optimum time to initiate habitual xylitol gum-chewing for obtaining long-term caries prevention. J Dent Res. Mar; 78(3):797-803.

Jolly, S.S. et al (1971). Human intoxication in Punjab. Fluoride, 4(2) 64-79.

Journal of the American Medical Association. (1963). Editorial. November. Vol. 185.

King, D. (1999). City to launch battle against dental 'crisis.' Boston Globe. November 11, 1999. A01.

Kumar, JV and Green, E.L. (1998). Recommendations for Fluoride Use in Children. NY State Dental Journal, February, 41-48.

Kunzel, W. and T. Fischer (1997). Rise and fall of caries prevalence in German towns with different F concentrations in drinking water. Caries Res 31(3): 166-73.

Lalumandier JA et al (1995). The prevalence and risk factors of fluorosis among patients in a pediatric dental practice. Pediatric Dentistry - 17:1, 19-25.

Limeback, H (2000). "Leading Dental Researcher Speaks Out Against Fluoridation", A videotaped interview available from gg video, 82 Judson Street, Canton, NY 13617. email ggvideo@northnet.org

Luke, J. (1994). Effects of Fluoride on the Physiology of the Pineal Gland (Abstract). Caries Research, 28, 204.

Luke, J (1998) Presentation at the XXII world conference of the International Society for Fluoride Research, Bellingham, Washington Sept, 1998.

Luke, J.(1999). Fluoride, the Pineal Gland and Melatonin: An Interview with and Presentation by Dr Jennifer Luke. Videotape, length 40 minutes. Available from GGVideo, 82 Judson Street, Canton, NY 13617. Tel: 315-379-9544. Fax: 315-379-0448. E-mail: ggvideo@northnet.org

Makinen, KK. (1996). Polyol chewing gums and caries rates in primary dentition: a 24-month cohort study. Caries Res 1996;30(6):408-17.

Marcus, W. (1990). Memorandum from Dr. William Marcus,to Alan B. Hais, Acting Director Criteria & Standards Division ODW, US EPA, DATED MAY 1,1990, and subsequent memos. These can be viewed on the web at http://www.fluoridealert.org/marcus.htm

McClure, F.J. (ed) Water Fluoridation: The Search and the Victory. NIDR, Bethesda, Md, (1970), page 249.

Morgan L et al (1998). Investigation of the possible associations between fluorosis, fluoride exposure, and childhood behavior problems. Pediatric Dentistry - 20:4, 244-252.

Mullenix, P. et al (1995). Neurotoxicity of Sodium Fluoride in Rats. Neurotoxicology and Teratology, 17, 169-177.

Mullenix, P.J. (1999). Statement submitted in connection with an Environmental Assessment for a proposed fluoridation project, May 1999. Full statement available from Phyllis Mullenix, P.O. Box 753, Andover, Ma. 01810-3347.

National Academy of Sciences. (1977). Drinking Water and Health. Safe Drinking Water Committee, National Academy of Sciences, NAS/NRC.

National Public Radio (2000). All Things Considered. September 1, 2000.

National Research Council of Canada (1977). Environmental Fluoride. (NRCC No.16081) Associate Committee On Scientific Criteria For Environmental Quality.

National Toxicology Program [NTP] (1990). Toxicology and Carcinogenesis Studies of Sodium Fluoride in F344/N Rats and B6C3f1 Mice. Technical report Series No. 393. NIH Publ. No 91-2848. National Institute of Environmental Health Sciences, Research Triangle Park, N.C. The results of this study are summarized in the Department of Health and Human Services report (DHHS,1991).

Needleman, H. et al (1979). Deficits in psychologic and classroom performance of children with elevated dentine lead levels. N. Eng. J. Med. 300: 689-695.

Nesin, B.C. (1956) J. Maine Water Util. Assn. 32:33.

O.T.A. (1990). Case Studies: Exposure to Lead, Ch. 10, Neurotoxicity. Office of Technology Assessment, US Congress, Washington, D.C.

Phipps, K. (1995). Fluoride and Bone Health. J. Pub Health Dent. 55(5), 53-56.

Radusch, D.F. (1934). Variability of Diagnosis of Incidence of Dental Caries. J. Am. Dent. Assoc., 28: 1959-1961, 1941.

Reeves, Thomas. (2000). Manufacture of F chemicals. Letter. (June 1, 2000).

Reuters Health (1999). Financial strain may raise gum disease risk. ADA News Daily. July 20. http://www.ada.org/adapco/daily/archives/9907/0720top.html

Riggs, B.L. et al (1990). Effect of Fluoride treatment on the Fracture Rates in Postmenopausal Women with Osteoporosis. N. Eng. J. Med., 322, 802-809.

Scheinin A, et al. (1976). Turku sugar studies. V. Final report on the effect of sucrose, fructose and xylitol diets on the caries incidence in man. Acta Odontol Scand. 34(4):179-216.

Steelink, C. (1982). Letter to Chemical and Engineering News, July 27, pp 2-3.

Schuld, A. (1999). How Do Fluorides Interfere With Thyroid Function. Fluoride Watershed, Journal of the National Pure Water Association, 5, 3-6, NWPA, 12 Dennington Lane, Crigglestone, Wakefield, WF4 3ET, UK, see also Schuld's web site: http://www.bruha.com/fluoride/

Seppa L, Karkkainen S, Hausen H. (2000). Caries in the primary dentition, after discontinuation of water fluoridation, among children receiving comprehensive dental care. Community Dent Oral Epidemiol. Aug;28(4):281-8

Smith, G. (1983). "Fluoridation--are the dangers resolved?" New Scientist. May 5, 1983: 286-287.

Soderling, E., et al. (2000). Influence of maternal xylitol consumption on acquisition of Mutans streptococci by infants. J Dent Res. Mar; 79(3):882-7.

Susheela, A.K. (1993). Prevalence of endemic fluorosis with gastrointestinal manifestations in people living in some North-Indian villages. Fluoride, 26, 97-104.

Susheela, A.K. (1998). Scientific Evidence on Adverse Effects of Fluoride. Presented to Members of Parliament & LORDS, House of Commons, Westminister, London, October 20, 1998.

Sutton, P.R.N. The Greaatest Fraud: Fluoridation. Kurunda Pty. Ltd., Lorne, Australia, 1996. ISBN 0 949491 12 8

Tabari, E.D. et al (2000). Dental fluorosis in permanent incisor teeth in relation to water fluoridation, social deprivation and toothpaste use in infancy. British Dental Journal, 189 (4), 216-220. Read abstract at http://www.fluoridealert.org/BDJ.htm

Trahan L, et al. (1996). Emergence of multiple xylitol-resistant (fructose PTS-) mutants from human isolates of Mutans streptococci during growth on dietary sugars in the presence of xylitol. J Dent Res. Nov;75(11):1892-900.

Teotia, S.P.S. and M,Teotia (1994) Fluoride, 27 (2) 59-66.

University of Rochester (2000). Evidence Suggests Food Preservatives May Help Prevent Cavities. Press Release. April 8.

U.S. Department of Health & Human Services. (U.S. DHHS). 2000. Oral health in America: A Report of the Surgeon General. Rockville, MD: U.S. Department of Health & Human Services. National Institute of Dental and Craniofacial Research, National Institutes of Health.

Waldbott, G.L. (1965). A Struggle with Titans. Carlton Press, New York.

Waldbott, G.L., Burgstahler, A.W. and McKinney, H.L. Fluoridation: The Great Dilemma. Coronado Press, Inc., Lawrence, Kansas, 1978.

Williams JE et al (1990). Community Water Fluoride Levels, Preschool Dietary Patterns, and The Occurrence of Fluoride Enamel Opacities. J of Pub Health Dent; 50:276-81.

Yiamouyiannis, J.A. (1990). Water Fluoridation and Tooth decay: Results from the 1986-87 National Survey of U.S. Schoolchildren. Fluoride, 23, 55-67. http://www.fluoridealert.org/DMFTs.htm


THE 18 STUDIES ON THE POSSIBLE ASSOCIATION OF HIP FRACTURE AND FLUORIDE EXPOSURE.



1. Cauley, J., P. Murphy, et al. (1995). "Effects of fluoridated drinking water on bone mass and fractures: the study of osteoporotic fractures." J Bone Min Res 10(7): 1076-86.

2. a) Cooper, C., C. Wickham, et al. (1991). "Water fluoridation and hip fracture." JAMA 266: 513-514 (letter, a reanalysis of data presented in 1990 paper).

2. b) Cooper, C., C. Wickham, et al. (1990). "Water fluoride concentration and fracture of the proximal femur." J Epidemiol Community Health 44: 17-19.

3. Danielson, C., J. L. Lyon, et al. (1992). "Hip fractures and fluoridation in Utah's elderly population." Jama 268(6): 746-748.

4. Hegmann, K.T. et al (2000) the Effects of Fluoridation on Degenerative Joint Disease (DJD) and Hip Fractures.Abstract #71, of the 33rd Annual Meeting of the Society For Epidemiological research, June 15-17, 2000. Published in a Supplement of Am. J. Epid.

5. Hillier, S., C. Copper, et al. (2000). "Fluoride in drinking water and risk of hip fracture in the UK: a case control study." The Lancet 335: 265-269.

6. Jacobsen, S., J. Goldberg, et al. (1992). "The association between water fluoridation and hip fracture among white women and men aged 65 years and older; a national ecologic study." Annals of Epidemiology 2: 617-626.

7. Jacobsen, S., J. Goldberg, et al. (1990). "Regional variation in the incidence of hip fracture: US white women aged 65 years and olders." J Am Med Assoc 264(4): 500-2.

8. Jacobsen, S.J. et al (1993). Hip Fracture Incidence Before and After the Fluoridation of the Public Water Supply, Rochester, Minnesota. American Journal of Public Health, 83, 743-745.

9. a) Jacqmin-Gadda, H. (1995). "Fluorine concentration in drinking water and fractures in the elderly." JAMA 273: 775-776 (letter).

9 b) Jacqmin-Gadda, H., A. Fourrier, et al. (1998). "Risk factors for fractures in the elderly." Epidemiology 9(4): 417-423. (An elaboration of the 1995 study referred to in the JAMA letter).

10. Karagas,M.R. et al (1996). "Patterns of Fracture among the United States Elderly: Geographic and Fluoride Effects". Ann. Epidemiol. 6 (3), 209-216.

11. Keller, C. (1991) Fluorides in drinking water. Unpublished results. Discussed in Gordon, S.L. and Corbin, S.B,(1992) Summary of Workshop on Drinking Water Fluoride Influence on Hip Fracture on Bone Health. Osteoporosis Int. 2, 109-117.

12. Kurttio, P., N. Gustavsson, et al. (1999). "Exposure to natural fluoride in well water and hip fracture: A cohort analysis in Finland." American Journal of Epidemiology 150(8): 817-824.

13. Lehmann R. et al (1998). Drinking Water Fluoridation: Bone Mineral Density and Hip Fracture Incidence. Bone, 22, 273-278.

14. Li, Y., C. Liang, et al. (1999). "Effect of Long-Term Exposure to Fluoride in Drinking Water on Risks of Bone Fractures." Submitted for publication. Contact details: Dr. Yiming Li, Loma Linda School of Dentistry, Loma Linda, California, Phone 1-909-558-8069, Fax 1-909-558-0328 and e-mail, Yli@sd.llu.edu

15. May, D.S. and Wilson, M.G. Hip fractures in relation to water fluoridation: an ecologic analysis. Unpublished data, discussed in Gordon, S.L. and Corbin S.B.,(1992), Summary of Workshop on Drinking Water Fluoride Inflruenbce on Hip Fracture on Bone Health. Osteoporosis Int. 2, 109-117.

16. Phipps, K. R. (1999). Community water fluoridation, bone mineral density and fractures. R01DE10814-02. HSR/96101800. USA, Oregon Health Sciences University, 611 SW Campus Dr, Portland, OR 97201, IR: (503) 494-8895,. 199309: National Institute of Dental Research (NIDR) - Grant: Noncompeting Continuation (5). To be published in the British Medical Journal.

17. Sowers, M., M. Clark, et al. (1991). "A prospective study of bone mineral content and fracture in communities with differential fluoride exposure." American Journal of Epidemiology 133: 649-660.

18. Suarez-Almazor, M., G. Flowerdew, et al. (1993). "The fluoridation of drinking water and hip fracture hospitalization rates in two Canadian communities." Am J Public Health 83: 689-693.

See also: Riggs, B.L. et al (1990). Effect of Fluoride treatment on the Fracture Rates in Postmenopausal Women with Osteoporosis. N. Eng. J. Med.,
322, 802-809.


REFERENCES ON FLUORIDE'S TOPICAL VS. SYSTEMIC MECHANISM OF ACTION


Burt, B.A. (1994). Letter. Fluoride, 27, 180-181.

Carlos, J.P. (1983). Comments on Fluoride. J.Pedodontics. Winter, 135-136.

CDC (1999). Achievements in Public Health, 1900-1999: Fluoridation of Drinking Water to Prevent Dental Caries. Mortality and Morbidity Weekly Review (MMWR), 48(41);933-940 October 22, 1999.

Featherstone, , J.D.B. (1987) The Mechanism of dental decay. Nutrition Today, May/June, 10.

Featherstone J.D.B. (1999) Prevention and reversal of dental caries: role of low level fluoride. Community Dent Oral Epidemiol. 27:31-40.

Featherstone, J.D.B. (2000). The Science and Practice of Caries Prevention. Journal of the American Dental Association. 131, 887-899.

Fejerskov, O. et al (1981) Rational use of fluorides in caries prevention. Acta. Odontol. Scand., 241-249.

Levine, R.S., (1976). The action of fluoride in caries prevention: a review of current concepts. Brit. Dent. J. 140, 9-14.

Limeback, H. (1999). A re-examination of the pre-eruptive and post-eruptive mechanism of the anti-caries effects of fluoride: is there any caries benefit from swallowing fluoride? Community. Dent. Oral Epidemiol. 27, 62-71.

Limeback, H. (2000) Videotaped Interview. available from GGVideo, 82 Judson Street, Canton, NY 13617. Tel: 315-379-9544. Fax: 315-379-0448. E-mail: ggvideo@northnet.org and www.FluorideAlert.org/limeback-video.htm

Margolis, H.C. and Moreno, E.C. (1990). Physicochemical Perspectives on the Cariostatic Mechanisms of Systemic and Topical Fluorides. J. Dent. Res 69 (Special Issue) 606-613.

Shellis, R.P and Duckworth, R.M.(1994). Studies on the cariostatic mechanisms of fluoride. Int. dent. J. 44, 263-273.

 

 

Fluoride Action Network | 802-338-5577 |info@fluoridealert.org