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Report of the Expert Panel for Water Fluoridation Review - City of Calgary - 1998
A review of the risks-benefits of fluoridation by University of Calgary Professors who were mostly Pro-Fluoride
Editorial Comment by Elke Babiuk: The one redeeming feature in this report below is the dissenting opinion where the author makes an honest attempt to fairly analyze some of the voluminous literature. The scientists and other professionals listed directly below, agree that there are serious problems in the Calgary report. It is also noteworthy to mention that unlike what happened here, in the town of Natick Massachusets, fluoridation review panelists were chosen for their neutrality and objectivity. The scientists there came to an entirely different conclusion as the City of Calgary's panel of Professors. See naticks.htm for the Executive Summary of their report.Click on the individual names directly below for a review of the Majority members' report. The qualifications of these professionals to speak to this issue, or their Curriculum Vitaes, are also available on this site.
- David R. Hill, P.Eng. (Professor Emeritus, University of Calgary) -- I find it hard to believe that "the evidence supporting health concerns" in that section (Minority report) could be considered "weak", as is asserted in the executive summary....
- Dr Phyllis Mullenix, Ph.D (Toxicologist) -- In summary, this report does not appear to be a presentation of the science, but rather a presentation of prejudice against the science. Why does water fluoridation deserve such loyalty?
- Dr William Hirzy, Ph.D, (Environmental Protection Agency scientist) -- It appears to me that the Calgary study group merely adopted the opinions expressed by peer review panels staffed largely by pro-fluoride members and commissioned by an organization (U.S. Public Health Service) whose interest in the subject should have prompted the utmost skepticism by your experts, but seemingly did not.
- Dr Richard Foulkes (B.A., M.D.) -- By its own words, the authors can not rationalize the continuation of fluoridation in Calgary. But recommends, nevertheless, continuation of the process, albeit at a lower concentration.
- Dr. Paul Connett, Ph.D (Chemistry Professor) -- I also find it interesting that when the majority of authors found any evidence of problems associated with the use of fluoride they were very quick to blame sources of fluoride other than the drinking water.
Note by Elke: It is important to note that our Calgary Panel of Professors was NOT (as claimed) appointed by the Standing Committee on Operations and Environment which consists of Council members. Council had NO input. It was appointed by Calgary Regional Health Authority and the City of Calgary Waterworks' department officials, despite our objections that several panel members were known to be staunch fluoridation proponents. Information as to the pre-existing biases of some of the City of Calgary's panelists can be found at calgbias.htm
EXTENDED HYPERLINKS within the document (not yet completed) indicate questionable statements. The links provide proper documentation, corrections, and/or relevant criticisms. See also comments by Elke M. Babiuk, author of calgaryb.htm and Editor of this Web Site
Parts of the Calgary report below are scanned and not yet proof-read so any typos may be mine.
The City's final electronic version starts from Professor Thompson's section to the Appendices
REPORT OF THE EXPERT PANEL FOR WATER FLUORIDATION REVIEW
appointed by Standing Committee on Operations and Environment,
City of Calgary, and Calgary Regional Health Authority - March 1998
Panel members:
Professor David Hanley, University of Calgary, Faculty of Medicine
Professor Hossein Joe Moghadam, University of Calgary, Faculty of Medicine
Professor Miloslav Nosal, University of Calgary, Faculty of Science
Professor Sheldon Roth, University of Calgary, Faculty of Medicine
Professor Dixon Thompson, University of Calgary, Faculty of Environmental Design
Resources: Dr. Read Seidner, Waterworks Division 35, Glenmore Water Treatment Plant, P.O. Box 2100, Calgary, Alberta T2P 2M5 Dr. Richard Musto, Calgary Regional Health Authority
TABLE OF CONTENTS
|
EXECUTIVE SUMMARY ... (i) BACKGROUND AND TERMS OF REFERENCE ... 1 Types of studies and submissions ... 4 The nature of the debate ... 5 Background notes ... 5
WATER FLUORIDATION AND BONE ... 7
EPIDEMIOLOGICAL STUDIES ... 13
TOXICOLOGY OF FLUORIDE ... 20 |
THE NATURAL ENVIRONMENT ... 26 Industrial sources ... 26 Water ... 26 Soils and groundwater .... 27 FLUORIDATION AND DENTAL HEALTH ... 28
SUMMARY ... 41 SUMMARY - MAJORITY OPINION .... 41 RECOMMENDATIONS - MAJORITY OPINION .... 43 BIBLIOGRAPHY ... 44 APPENDICES ... 58 |
EXECUTIVE SUMMARY
City of Calgary, Expert Panel on Water Fluoridation Review, March 1998
The City of Calgary Standing Policy Committee on Operations and Environment and the Calgary Regional Health Authority decided that a review of water fluoridation as a public health policy was needed. A Panel of five experts was appointed. Support was provided by the Waterworks Division and the Calgary Regional Health Authority.
Scientific information was sought through advertisements and was obtained through the efforts of the Panel members. The Terms of Reference for the Panel focussed the work on scientific literature produced since 1989. The Terms of Reference stated that all studies must undergo critical appraisal for design strengths and weaknesses. Results were to be synthesized to form a comprehensive but useable body of evidence.
The Panel held ten meetings between December 3, 1997 and March 18, 1998. Four members reached mutual agreement on the issues, but there were differences with the fifth member which could not be resolved by the deadline for the submission of the Panel's report. Therefore, the report contains a dissenting section. However, the Panel members were very close and the disagreements are largely form, emphasis and level of detail.
Four Panel members agreed that there was not sufficient new scientific evidence upon which to base a recommendation for substantial changes to water fluoridation policy in Calgary. The fifth member concluded that there was evidence supporting health concerns, but that the evidence was weak.
There was a need for further carefully designed studies of total intake of fluoride and health risks of bone fractures and dental fluorosis.
The Panel was unanimous in their support of the reduction of the recommended optimum level of water fluoridation. The Panel majority recommended that the City change from the old level of 1.0 ppm fluoride to 0.7 ppm, which is basically compatible with the recommendation of the other Panel member. That is slightly lower than the new standard recently set by Standards and Guidelines Branch of Alberta Environmental Protection.
ACKNOWLEDGEMENTS
The Panel wishes to thank Dr. Colin Dawes, University of Manitoba and Dr. John Colquhoun,
University of Auckland for taking the time to meet with the panel and to provide supporting
material on the questions about dental biochemistry and dental benefits of water fluoridation. The
technical support provided by Dr. Read Seidner of Waterworks Division and Dr. Richard Musto
of the CRHA was greatly appreciated. The Panel is very grateful for the hard work and late nights put in by Ms. Valerie Matwick in the last minute rush to complete the document.
BACKGROUND AND TERMS OF REFERENCE
At a meeting of the Standing Policy Committee on Operations and Environment in October 1997,
some technical reports on water fluoridation were presented by private citizens. The Committee
then resolved, along with Calgary Regional Health Authority, to have an independent and expert
review of this and other recent information. The ultimate purpose of such a review was to advise
whether water fluoridation is still a desirable public health policy in light of current data or
risk/benefit studies.
Waterworks Division was directed by the Operations and Environment Committee to assume the role of coordinating and organizing an independent and unbiased panel of experts. Waterworks approached various Deans and Department Heads at the University of Calgary for recommendations. The expertise, maturity and independence of university researchers were considered important assets for prospective panel members. An adequate expertise profile to address technical issues of health and safety was sought. An effort was made to exclude mission oriented candidates (either strongly pro-fluoridation or strongly anti-fluoridation).
A copy of the letter of appointment is in the Appendix. List of panel members from the University of Calgary:
Person / Expertise/role
Professor Dixon Thompson, Professor of Environmental Science, Associate Dean Academic, Faculty of Environmental Design
CHAIR, Water pollution and environmental effects, Chemistry
Professor Hossein Joe Moghadam, Professor Emeritus, Departments of Paediatrics and Community Health Sciences, Faculty of Medicine
Community Health, Paediatrics, Epidemiology,
Professor Sheldon Roth, Departments of Pharmacology & Therapeutics and Anaesthesia, Faculty of Medicine, Director Environmental Research Centrer, Pharmacology, Therapeutics, Toxicology
Professor Miloslav Nosal, Department of Mathematics & Statistics, Faculty of Science
Biological and environmental statistics, Health related risk assessment
Professor David Hanley, Head, Division of Endocrinology & Medicine, Department of Medicine, Faculty of Medicine Endocrinology, Bone disorders, Calcium metabolism
Panel resource contacts:
The agencies supporting the Panel appointed two people as resource contacts:
Dr. Read Seidner, Laboratory Superintendent, Waterworks Division
Dr. Richard Musto, Deputy Medical Officer of Health, Calgary Regional Health Authority
The process:
The panel was to report jointly to the Standing Committee on Operations and Environment-City
of Calgary and to the Quality Care Committee-Calgary Regional Health Authority. Ongoing
progress reports to Waterworks Division and Calgary Regional Health Authority were to be
maintained by the chair of the panel.
Work was to commence as soon as possible after the panel was "virtually ratified " on November 20, 1997. The Panel's work was to be completed by a presentation to the Operations and Environment Committee on April 8, 1998. Prior to that a written brief was to be submitted to Waterworks Division and Calgary Regional Health Authority by March 23, 1998.
The focus of effort was to be on literature produced since 1989. In addition to literature which had already been received, submissions were sought through newspaper ads or provided by expert panel members. Verbal presentations would be at the panel's invitation only. If such presentations were required, then an opportunity was provided to parties on both sides of the debate effort to recommend suitable experts. A list of the material received by the Panel is in the Appendix.
Standard scientific criteria for evaluating the relevance of reports and studies was used.
Methodology employed by the Canadian Task Force on the Periodic Health Examination served
as a model. That methodology states that all studies must undergo critical appraisal for design
strengths and weaknesses. Results were to be synthesized to form a comprehensive but useable
body of evidence. The panel developed a suitable process of reviewing and synthesizing the
information in the literature.
The scientific publications and other material reviewed by the Panel appears in the Bibliography. Where appropriate, references to the original source of information, which can be found in the bibliography, appear in the text.
Deadline dates:
- December 12, 1997 Deadline for public submissions
- March 11, 1998 Draft of sections due
- March 13, 1998 First draft completed
- March 16, 1998 Final Draft Completed
- March 23, 1998 Submit written brief to Waterworks and Calgary Regional Health Authority
- April 8, 1998 Presentation to Operations and Environment Committee
The Panel held ten meetings: Dec 3, 1997, Jan 12 and 28, Feb 11, two meetings on Feb 25, March 9, 11, 16, and 18, 1998. Based on the tasks outlined in the Panel's Terms of Reference, the following ground rules were set, as reflected in the minutes of the meetings:
- There would be no outside observers or representatives at the meetings.
- No press interviews were to be granted by Panel members until after the presentation to the Council Committee.
- The Panel's meetings were to be kept confidential.
- The Panel agreed to unity of purpose, but not necessarily unity of opinion; however, the objective was to speak as a Panel.
- Expertise-based sections, to be drafted by Panel members, were to be about 5 pages.
Given the very limited time available to the Panel, the Terms of Reference excluded a detailed examination of pre-1989 scientific articles, although some familiarity with that information was important to set the Panel's work in context and to understand the issues.
The Panel's task was not to search the available literature for information to support one side or the other in the debate. The Panel was not to use an adversarial approach and attempt to weigh the relative merits of arguments put forth by opposing sides. The Panel's task was to examine the scientific literature to see if there was significant credible evidence of increased health risk or environmental risk resulting from fluoridation of Calgary's water supply.
Following the Terms of Reference, in the opinion of the Panel, the fact that questions had been raised about the risks of fluoride was not sufficient to warrant a change in policy. Such questions have been around for decades (Hileman, 1998). Studies using extreme conditions (high concentrations or other unusual circumstances), which showed some adverse health effect, were not relevant to our task. Studies with obvious methodological flaws had to be rejected because they could not provide reliable evidence of risk. The Panel did not place much weight on results which raised questions by showing weak associations but lacked evidence of cause and effect.
Types of Studies and Submissions:
- The Panel received, or found in their searches, six different types of studies and submissions:
- The most weight was given to methodologically sound research reports published in refereed journals (journals in which other experts review articles for suitability for publication). These provide evidence that can be weighed quite heavily in reaching policy decisions.
- The Panel interviewed Dr. Colin Dawes of the Faculty of Dentistry, University of Manitoba and Dr. John Colquhoun of the University of Auckland, New Zealand. The Panel received background material from these dental experts.
- Some studies examined only two variables in a very complex system. These could give indications of where further work is necessary. To provide reliable results there must be an appropriate statistical methodology and careful study design. For example, when comparisons of populations (over time, or in different -locations) study the relationships between water fluoridation and a health benefit or a health problem, results will not be reliable, if other factors which influence the cause and effect relationships are not considered. Those factors would include: all other sources of fluoride (dental products,
- diet, etc.), other dental procedures (topical fluoride, sealants, etc.), medical procedures and other practices affecting the problem (medication, vitamins, exercise and general level of health).
- The Panel also received, or found, a number of scientific reviews or reports by similar panels or agencies in other jurisdictions.
- Another group of studies had serious flaws in methodology (the way the research was carried out), so that the results did not merit consideration. This included studies which were deliberately designed to reach a specific conclusion by the design of the study, by ignoring or eliminating important information, or by reaching conclusions not supported by the research results.
- Other sources of opinions which were received by the Panel, but which could not be given much weight included newspaper and magazine articles, abstracts (not enough detail to assess reliability), letters to the editor, and personal letters.
- Because people on one side of the debate or the other might object, perhaps strenuously, to rejection of some material which they believe supports their position, the Panel stresses that we have applied the same criteria equally to both sides.
The Nature of the Debate
The debate over water fluoridation is very highly polarized. There is little common ground
between those groups prepared to accept fluoridation as a desirable public health measure and
those in opposition. There is apparently little room for mediation and negotiation because of the
absolute nature of the claims about the benefits and the risks of water fluoridation.
Background Notes
- The Panel recognizes that given the gulf that separates the pro-fluoride and anti-fluoride positions, we cannot possibly write a report which will be widely accepted, unless we were prepared to write a report which did not come to any conclusions. There is no way to satisfy the concerns of such diametrically opposed parties.
- Health concerns have been raised (cancer, increased bone fractures, immune system suppression, etc.), which, if true, should lead to a very serious review of the practice of water fluoridation, and a cessation of the practice if they were substantiated.
- Unfortunately, it is much easier to raise the concerns on the basis of preliminary or partial scientific studies or personal opinion, than it is to provide a sound substantiation of those concerns. The fact that concerns have been raised is not, in and of itself, enough to change practices but has led to reports such as this one.
- Questions about the ethics of water fluoridation have been raised with the Panel. Since ethical issues were not in the Terms of Reference they were not addressed.
- Readers should become familiar with units of concentration and dose, to understand the levels of exposure. Parts per million (ppm) and mg/L (milligrams per liter) are equivalent.
- One ppm is 0.0001%, which is equivalent to one minute in 2 years, one cent in $10,000 or one cm in 10 km. Because the impact of a chemical will be influenced by the size of the animal or person exposed, doses are often expressed in terms of the amount of the chemical per unit of body weight (mg/Kg- milligrams per kilogram of body weight).
Membership on the Panel represented five different areas of expertise: Professor David Hanley, a bone specialist; Professor Joe Moghadam, an epidemiologist; Professor Miloslav Nosal, a biostatistician; Professor Sheldon Roth, a toxicologist; and Professor Dixon Thompson, a chemist and environmental scientist. Each Panel member reviewed most, if not all of the scientific literature but focused on the material related to their area of expertise. Each Panel member wrote a short summary of their findings. There will necessarily be some overlap and duplication.
Four of the authors reached mutual agreement on form, emphasis, content and conclusions. However, there were disagreements between those four and the fifth Panel member, which could not be resolved, in spite of more than a week of extra meetings and revisions, which were held in an effort to resolve the differences. Because of the unresolved points of contention between four Panel members and the fifth, his section is included as a dissenting section. However, The Panel is close to agreement.
WATER FLUORIDATION AND BONE
D. Hanley
(a) Biological Effect of Fluoride on Bone
In animal studies with fluoride and in studies of fluoride as a treatment of osteoporosis in humans,
there are several effects which stand out. First, fluoride is incorporated into the mineral crystal of
bone as fluorapatite. As in the case of tooth enamel, fluorapatite seems to be less readily broken
done in the normal process of bone remodelling than is the normal bone crystal, hydroxyapatite. In
high doses in laboratory studies of bone, however, fluoride can actually inhibit normal
mineralization of the protein matrix of bone. These levels can be achieved in experimental studies
of osteoporosis therapy with 4075 mg fluoride per day for several years. Proponents of fluoride
therapy of osteoporosis suggest high levels of calcium intake can offset this potential problem with
fluoride induced defective mineralization of newly formed bone. If fluoride therapy of
osteoporosis stimulates the synthesis of weaker bone, one might find that patients treated with
fluoride might be more prone to fracture. This effect has been documented in clinical trials of very
high dose fluoride therapy of osteoporosis (40- 75 mg/day for four to five years). Reduced
biomechanical strength of bone obtained from fluoride treated patients has been demonstrated in
some studies.
The second action of fluoride on bone, and the one which has caused interest in its use as a treatment of osteoporosis, is its direct stimulation of the cells which synthesize new bone matrix (osteoblasts). This stimulation requires higher extracelluar fluid concentrations than those which would be expected from artificial water fluoridation at 1 mg/L or lower. At these higher doses, fluoride stimulation of the osteoblast and new bone formation appears to bypass the normal bone remodelling cycle. Normally, new bone formation by osteoblasts only occurs in an area of the skeleton after other bone absorbing cells, called osteoclasts, remove a small amount of older bone (resorption). By causing new bone formation without prior activation of bone resorption, high dose fluoride therapy tie. doses of 40-75 mg of sodium fluoride per day, which would be the equivalent of drinking 18-34 litres of Calgary's water per day) causes a dramatic increase in the production of new bone. The problem has been whether this new bone is qualitatively normal.
(b) Studies of Fluoride Therapy of Osteoporosis
The direct stimulation of bone growth by fluoride has made many osteoporosis researchers
interested in this compound as a potential therapy. However, most osteoporosis clinical research
workers regard fluoride as strictly an investigational therapy, because of the equivocal results
from clinical trials with this agent. In osteoporosis studies, fluoride is regarded as having a very
narrow "therapeutic window" for its effect on bone, ie. it has been difficult to demonstrate any
effect below certain dose levels, and above a marginally higher level, toxic effects begin to appear. In the largest
randomized, placebo-controlled clinical trials of fluoride, sponsored by the US National Institutes
of Health in the late 1980's (Riggs et al, 1990; Kleerekoper et al, 1991), there was a dramatic
improvement in bone mass measurements, but no protection against osteoporotic fractures. In fact,
there was a greater incidence of nonvertebral fractures in the fluoride-treated patients in Riggs
study, and Kleerekoper found an increased rate of vertebral fractures. These studies were
criticized on the grounds that the dose of fluoride was too high, such that a deleterious effect on
bone mineralization was occurring. Nevertheless, these were the most thorough randomized,
placebo-controlled trials of fluoride which have been performed, and have relegated fluoride
therapy to a position outside the mainstream of osteoporosis research.
More recently, clinical trials of a lower dose, slow-release formulation of sodium fluoride taken intermittently (12 months on 2 months off) and in combination with calcium citrate supplementation, have shown a significant improvement in bone mass, and a reduction in vertebral fractures (Pak et al, 1994, 1995, and 1996). These studies have been criticized because of the small number of subjects and (in particular) the small number of subjects in the control group. The significance of the fracture prevention has been questioned, but it is clear that the patients had an increase in bone mass with none of the problems which occurred in the Riggs and Kleerekoper studies.
Is the increased bone mass seen in high dose fluoride treatment of osteoporosis normal? Bone biopsy studies accompanying clinical trials of higher dose fluoride therapy of osteoporosis have given varying results. Studies from Europe (Aaron et al, 1991; Boivin et al, 1993; Sogaard et al, .1994) have suggested that the bone obtained from patients receiving long term high dose fluoride therapy is of inferior strength and mineral quality. However, bone biopsy analyses from a study of high dose slow-release fluoride therapy (Antich et al, 1993; Zerkeweh et al, 1996) have suggested that this method of fluoride treatment causes increased amounts of bone that appears to be of normal quality. One explanation for the problems seen in the European bone studies is the wide swings in serum fluoride concentrations which occur when high dose "raw" sodium fluoride or sodium monofluorophosphate is ingested. The rapid absorption of fluoride in these forms gives temporary levels of serum fluoride which are well into a range associated with toxicity. This problem is not seen with the slow-release compound.
(c) Skeletal Fluorosis
When fluoride accumulates in the skeleton to high levels (usually above 5000 parts per million (ppm)in bone ash) a clinical problem of skeletal fluorosis can be documented. At very high levels (usually well above 5000 ppm) of fluoride accumulation, patients may have a crippling osteoarthritis-like syndrome that is attributed to the fluoride stimulation of mineral deposition around the joints and probable multiple micro-fractures in bones adjacent to the joints due to fluoride inhibition of normal mineralization. There is a concern that this level of fluorosis might occur in subjects with a high lifetime intake of fluoride. As we age, our ability to remove fluoride from our body (excretion in the urine) declines, so a theoretical risk in the aged population occurs in areas where water fluoridation is present. Early studies of fluoride content in bone in autopsy specimens from communities with higher levels of water
fluoride than used in Calgary (greater than 1.5 ppm) have shown some individuals had bone levels in the range which has been associated with skeletal fluorosis (over 5000 ppm in bone ash) (Amala et al, 1985). 1 know of no reported cases of skeletal fluorosis that can be related solely to the consumption of artificially fluoridated water at 1 mg/L or less.
A study is currently in progress in Canada, comparing fluoride content of bone from older individuals in communities with (Toronto - 30 years) and without water fluoridation (Montreal). This study has just begun to report its findings from the Toronto area, but has not yet obtained the bone samples from Montreal. We await the results of this project with interest.
(d) Epidemiologic Studies of Fluoridation and Hip Fracture
I have repeated some of the material from Professor Moghadam's report here, in order to add my own interpretations as a bone biologist. Dr. Moghadam reviews them in his section with further
emphasis and analysis of the appropriateness of the epidemiologic methodology.
Since 1989 a number of papers have examined the relationship between the exposure to fluoride in the drinking water in communities and attempted to relate this to the risk of hip fracture. Some have found a weakly positive association. Most have simply examined community health records in areas with higher fluoride content in the water and compared these statistics with communities with low levels of fluoride, with no attempt to look at individual subjects' exposure to fluoride. Virtually none of these studies have assessed the individuals who suffered hip fractures to determine the relationship of the fracture to other known risk factors. For these studies to raise a "red flag" of concern, the studies would have to demonstrate that the relationship between hip fractures and fluoride was still significant after the analysis has controlled for other known risk factors for fracture. Further, they would have to demonstrate that the fractures can be related to a quantity of water ingestion and not to other environmental sources of fluoride, or at least show that fracture rate increases with time of exposure tie. the longer people live in the area, the greater their fluoride intake and the more risk of fracture). None of the studies showing a potential fracture risk with fluoridated water have done all of this. My assessment of several of these studies follows.
In Alberta, a study of individuals aged 45 years or older, who were admitted to hospitals in Calgary and Edmonton with the diagnosis of hip fracture between January 1, 1981 and December 31, 1987 showed no overall statistically significant difference in the age-sex-standardized rates for the two cities (Suarez-Almazor et al, 1993). The hip fracture rate for males over age 65 in Edmonton was only slightly, but significantly, higher than those for Calgary: 4.52 fractures/1000 patient years vs 5.09 fractures/1000 patient years in Edmonton. However, no attempt was made to assess other risk factors for fracture, or differences in osteoporosis prevention and therapy practice in the two cities.
In a study of one fluoridated and two non-fluoridated communities in Utah (Danielson et al, 1992), the investigators examined hip fracture rates during a 7-year period. They found a small but statistically significant increase in the risk of hip fracture in 246 men and women, 65 years of age and older, exposed to artificial fluoridation at 1 PPM (20). Again, the authors did not control for osteoporosis therapy practice in the community, and the only risk factor which was assessed was smoking. In addition, the authors excluded patients who suffered a second hip fracture from the analysis. This excludes a group of patients who are at very high risk for hip fracture, and may have biased the study.
In 1990, Jacobsen and his colleagues reported the geographic distribution of primary hip fracture for women aged 65 years and older at the county level for the entire United States between 1984 and 1987. The age-adjusted rates of hip fractures showed a distinct north to south pattern with higher rates in the south and lower rates in the north. There was a positive association between hip fracture incidence and the percent of 65-year old and older below poverty level and the percent of land in farms. There was also a weak positive association between hip fracture rates and the percent of county residents who received fluoridated water. Again, no assessment of actual fluoride intake or county differences in other well-known risk factors for fracture was possible.
In another study reported by Jacobsen and his colleagues in 1992, hip fracture rates of person 65 years of age and older residing in 129 counties across the United States, considered to be exposed to fluoridated public water supplies were compared with those of the same age group residing in 194 non-fluoridated counties. There was a small positive association between fracture rates and fluoridation. The authors, however, state that confounding factors may be responsible for this observation. For example, boundaries of public water systems rarely coincide with those of counties. Within counties some people use private well water with markedly different fluoride level. One striking finding in this paper was that the incidence of hip fracture was highest in the communities which had been fluoridated for 5 years or less, with no increase in fracture incidence (actually a slight decline) as the duration of fluoridation increased up to 26 years or more. If fluoride has a cumulative deleterious effect on bone, it would be reasonable to expect an increasing fracture rate with increasing duration of water fluoridation.
Jacobsen and his colleagues (1993) examined hip fracture rates in Rochester, Minnesota for the 10-year period before and the 10-year period after the fluoridation of drinking water in 1960. In this time-trend study the authors found no difference in the rate of hip fracture for the two periods.
In 1991, a prospective study of 5 years duration in three demographically similar communities in Iowa was reported by Sowers and her colleagues. Two communities had fluoridated water at 1 mg/liter and one with a fluoride content of 4 mg/liter. Within these communities 827 women, aged from 20 to 80 years, were recruited to participate in the study. Bone mass examinations were conducted at the beginning of the study. Five years later, out of the original sample, 684 women were available for follow-up. Residence in the higher fluoride community was associated with a significantly lower bone mass in all women, an increased rate of radial bone mass loss in pre-menopausal women and significantly more fractures in post-menopausal women. The relative risk of fractures was 2.2 times greater in the high fluoride community compared with low fluoride communities.
From the Pittsburgh centre for the US Study of Osteoporotic Fractures, Cauley et al (1995), reported on an attempt to relate water fluoridation exposure to fracture incidence, in a prospective study of 2076 non-black women of 65 years of age and older who had been recruited to assess predictors of risk of fractures. Bone density was assessed at the spine and hip, and spinal X-rays were taken during the baseline determinations. Vertebral and other fractures were assessed every 4 months. Information on fluoride exposure was limited to community water supplies and was assessed using a residential history questionnaire covering the period from 1950 to 1990. Women exposed to residential fluoridated water for over 20 years had similar spine and hip bone density to women not exposed or women exposed for 20 or fewer years. There was no statistically significant difference of the risk for all fractures in women exposed to fluoridated water for over 20 years and those not exposed. The authors concluded that their results do not support the findings from recent ecological studies which showed an increased risk of hip fracture among individuals exposed to fluoridated public water supplies.
The committee reviewed a number of reports on fluoride effects as well as number of reviews which have analyzed the epidemiologic evidence for a ink between fluoridation and fractures. The vast majority did not support the position that the ecological studies have convincingly demonstrated a causal link between water fluoridation and fractures.
Summary
There have been several well done epidemiologic studies of the incidence of hip fractures or other fractures and their relation to water fluoridation since 1989. Several of these studies have raised the possibility that water fluoridation may be associated with an increase risk of hip fracture, particularly if the level of water fluoridation is above 1 mg/L. The major problem with most of these studies is their inability to assess total fluoride intake in the communities being studied; their inability to assess other environmental sources of fluoride, and their inability to control for other potential causes of hip fracture. An exception would be the study by Cauley and associates (1995). In this small study, there was no association found between actual fluoride exposure in the subjects being studied and the incidence of fractures. However, taken in total, these studies suggest that this issue deserves further attention, with better designed studies.
One study which has found an increased incidence of fractures in a high dose (4 mg/L) water fluoridation area (Sowers et al, 1991) has attempted to address some of the above-outlined weaknesses of these studies by recruiting a cohort of subjects from each of the different fluoridation communities and has continued to follow these subjects for further study. The project has recently been extended to allow a much more detailed analysis, and will attempt to assess actual fluoride intake in these communities. Dr. Sowers informs me that she has just completed the data collection and will begin the analysis later this spring. However, it should be noted that this study compares a centre with fluoridation at 4 mg/L to low fluoride communities which use fluoridation at 1 mg/L. The study may not have relevance to the Calgary situation, where the fluoridation level has never been higher than 1 mg/L.
Conclusion
I am not convinced that there is a clinically verifiable association between water fluoridation at or
below 1.0 mg/L and risk of fractures. Studies are currently in progress in other centres which may
throw more light on this issue, but I do not think the weight of evidence accumulated since 1989 is
enough to change public policy on water fluoridation.
Because of the potential for individuals to have an excessive intake of fluoride from other less readily controlled sources, and the nature of the relationship between fluoride ingestion and dental fluorosis, I would support a recommendation for an overall reduction in the amount of fluoride added to the water to the level of 0.7 mg/L. This level would appear to be adequate to provide dental protection, and would not be likely to be associated with any putative risk to bone health.
The available epidemiologic data would suggest further study is needed with respect to effects of water fluoridation on bone, and the city's public health agencies should be aware of studies that are currently being pursued in this area.
EPIDEMIOLOGICAL STUDIES
H. Moghadam
Definition of Epidemiology
Epidemiology is the study of the causes, distribution and control of diseases in a population. There
are three general types of epidemiological studies employed in the scientific papers which were
reviewed by the Panel: ecological (geographic), temporal or time trend, and case-control.
Ecological (geographic) studies examine the entire population of fluoridated versus non-fluoridated communities to see if a statistically significant relationship can be found between fluoridation of water and possible adverse health effects. They do not question the afflicted individuals with respect to the source of their drinking water (communal water, well water, bottled water), the amount of daily water consumption, other sources of fluoride exposure such as dental products, occupational exposure to fluoride, significant exposure to radiation, familial predisposition to osteoporosis or cancers, migration into and out of fluoridated communities, socioeconomic status, etc. For this reason they do not have a great statistical power. They can provide information about where further studies with greater statistical power are needed.
Another form of reported epidemiological studies is the temporal or time-trend studies which analyses the trends in the occurrence of an adverse health effect over a period of time in the same communities. These studies have a statisticaI power somewhat greater than the ecological studies.
A still greater statistical power is obtained in case-control studies which attempt to assess exposure to the causative agent in both individuals with the disease and those free of it, or follow both the exposed and unexposed individuals to assess the relative occurrence of disease in both groups.
This report reviews briefly the epidemiological studies published since 1989 on possible adverse health effects of the fluoridation of communal water supplies.
Fluoridation of public water supplies has been controversial since its inception in the United States in 1940s. It has been the subject of numerous epidem iological studies during the past several decades. More recently, various health aspects of ingested fluoride have been reviewed by several panels of scientists in the United States, Great Britain, Australia and Canada.
Water fluoridation and cancers
In 1990, the results of studies on "cancer bioassays on sodium fluoride", conducted by the United States' National Toxicology Program (NTP) were published. Male and female rats and mice were given large doses (25-175 mgm/L) of sodium fluoride in their drinking water over a two-year period. These studies demonstrated no carcinogenic effect of fluoride on mice and female rats; but a number of male rats developed osteosarcoma, a very rare cancer of bone. The investigators classified this finding as "equivocal" which is one of five categories in their classification system indicating uncertain findings. One of the investigators did not agree with this classification.
The NTP studies were reviewed by a peer panel of experts who agreed with the conclusions of the majority of the original investigators. The dissent of one of the original investigators, however, prompted the agency to seek additionally an independent review of the NTP study. This review was conducted by other scientists of the United States' Public Health Service and, together with a review of the literature, was published in 1991 (Review of Fluoride, Benefits and Risks). Briefly stated, their conclusion was that water fluoridation was both effective and safe.
Another independent review of the NTP study and the relevant literature was conducted by the National Research Council in the United States in 1993 (Health Effects of Ingested Fluoride). These scientists also concluded that "the weight of evidence from more than 50 epidemiological studies does not support the hypothesis of an association between fluoride exposure and increased risk of cancer in humans".
Still another independent review of the NTP study was conducted in 1991 by Dr. Edward Calabrese, professor of toxicology, School of Public Health, University of Massachusetts at the request of the East Bay Municipal Utility District (water provider for Oakland and Environs, California). Dr. Calabrese, took issue with the word "equivocal" when a statistically significant dose-response was evident in male rats. He went on, however, to state that the toxicological and epidemiological evidence on human health effects of fluoride do not support changes in community fluoridation programs.
In 1990, the scientists at the National Cancer Institute in the United States reported the analysis of 36 years of cancer mortality data. This was an expansion of their earlier analysis reported in 1977. In addition, they analysed 15 years of cancer incidence data from two populatiori-based cancer registries in relation to the fluoridation status of the drinking water supplies in populations. Due to the controversy stemming from the NTP animal studies, osteosarcoma was singled out for detailed analysis. This survey covered 2,300,000 cancer deaths in fluoridated counties across the United States and over 125,000 incidences of cancers in fluoridated and non-fluoridated counties covered by the two population-based cancer registries. It identified no trend in cancer risk which could be ascribed to the consumption of fluoridated drinking water (Hoover, 1990).
In 1992, an international time-trend analysis of bone cancer covering the period 1958 to 1987 was reported by Freni et al. It showed increases in incidence among young men in Canada, the United States and Europe which were not related to fluoridation.
A few smaller epidemiological studies have also been reported during the past several years on the relationship between osteosarcoma and water fluoridation:
In Alberta, rates of osteosarcoma in Edmonton (fluoridated since 1967) were compared with those of Calgary (not fluoridated until 1991) for the period 1970 to 1988 and reported in 1990. No differences were observed (Hurdy et al., 1990).
In New Jersey, in a study of seven counties, reported by Cohn in 1992, a geographic association between osteosarcoma and water fluoridation was found. The author of this study, however, stated that the residence of patients with osteosarcoma was determined at the time of diagnosis. No interviews were conducted and data on residential history, individual's exposure to fluoride or radiation etc. were not available. The author stated that the findings, even when taken with the overall findings currently in the scientific literature, were not sufficient to recommend that fluoridation of communal water supplies be halted.
In a time-trend study, published in 1991, Mahoney et al. analysed the bone cancer rates in New York State. The average age-adjusted incidence rates of osteosarcoma from 1 976 to 1987 in areas supplied with fluoridated water was no different from the rates in the non-fluoridated areas. The data did not support an association between fluoridated drinking water and the occurrence of osteosarcoma.
In another case-control study of childhood osteosarcoma in New York State, published in 1995, the average annual rate of osteosarcoma from 1976 to 1987 was the same for fluoridated and non-fluoridated areas. In this study, information about exposure to fluoride from all sources was obtained through a telephone interview of subjects, their parents or both. The total life-time exposure to fluoride was not significantly associated with the incidence of osteosarcoma (Gelberg et al., 1995).
Another case-control study of osteosarcoma was reported from Wisconsin in 1995. That study did not find a statistically significant association between exposure to fluoride in the drinking water and osteosarcoma (Moss et al., 1995).
Although the majority of these studies suggest no association between fluoride exposure and osteosarcoma, virtually all of the investigators emphasize that with a rare tumor such as osteosarcoma, no epidemiological study can establish a statistically meaningful conclusion.
An ecological study (Tohyama, 1996) was conducted in communities in Okinawa, Japan, some of which had fluoridated water during the American Administration from 1945 to 1 972. The purpose of the study was to investigate the relationship of uterine cancer mortality rates to fluoridation of water in the communities. Multiple correlation analysis of the data indicated an association between fluoride content of the drinking water and the uterine cancer rates. However, like all other ecological studies, this investigation did not take into consideration other confounding factors at the individual level. These include sexual activity, smoking, and the presence of human papilloma virus. Therefore, it cannot be concluded that the association is one of cause and effect.
Water Fluoridation and Hip Fracture
During the past decade a number of epidemiological studies have been conducted on the relationship between the exposure to fluoride in the drinking water and the risk of hip fracture in the elderly population. Many of these studies are ecological (geographic) in nature and have reported conflicting results; some suggesting a weak association between residing in the fluoridated communities and an increased risk of hip fracture, some reporting no association, whilst others finding a negative association. Although some of these studies have used age, sex and race-adjusted rates for comparison (these data are available on hospital discharge records), none of them have studied other individual factors which may have a bearing on the risk of hip fracture. These factors include, the source and amount of the water consumed (communal, well or bottled water), estrogen replacement therapy, calcium and vitamin D intake, caffeine consumption, exercise and activity level, prior history of osteoporosis, occupational and other sources of exposure to fluoride and the duration of residence in the fluoridated communities.
In Alberta, a study of individuals aged 45 years or older, who were admitted to hospitals in Calgary and Edmonton with the diagnosis of hip fracture between January 1, 1981 and December 31, 1987 showed no overall statistically significant difference in the age-sex-standardized rates for the two cities. The rates for males in Calgary were slightly higher than those for Edmonton males (Suarez-Almazor et al., 1993).
In a study reported from Utah in 1992, the investigators examined hip fracture rates in one fluoridated and two non-fluoridated communities during a 7-year period. They found a small but statistically significant increase in the risk of hip fracture in 246 men and women, 65 years of age and older exposed to artificial fluoridation at 1 ppm (Danielson et al, 1993).
In 1990, Jacobsen and his colleagues reported the geographic distribution of primary hip fractures for women aged 85 years and older at the county level for the entire United States between 1984 and 1987. The age-adjusted rates of hip fractures showed a distinct north to south pattern with higher rates in the south and lower rates in the north. There was a positive association between hip fracture incidence and the percent of 65-year olds and older, below poverty level and the percent of land in farms. There was also a weak positive association between hip fracture rates and the percent of county residents who received fluoridated water.
In another study reported by Jacobsen and his colleagues in 1992, hip fracture rates of persons 65 years of age and older residing in 129 counties across the United States, considered to be exposed to fluoridated public water supplies were compared with those of the same age group residing in 194 non-fluoridated counties. There was a small positive association between fracture rates and fluoridation. The authors, however, state that confounding factors may be responsible for this observation. For example, boundaries of public water systems rarely coincide with those of counties. Within counties some people use private well water with markedly different fluoride levels. Finally, there is probably no true "non-exposed" population due to exposure to fluoride in foods and beverages.
In another study, Jacobsen and his colleagues in 1993 examined hip fracture rates in Rochester, Minnesota for the 10-year period before and the 19-year period after the fluoridation of drinking water in 1960. In this time-trend study the authors found no difference in the rate of hip fracture for the two periods.
In a geographic study of a 5% sample of the white US Medicare population, 65 to 89 year olds between 1986 and 1990, fractures of hip, distal forearm, proximal upper arm and ankles were analysed. There were variations of geographic distribution of these fractures which could not be explained by the exposure to fluoride at the group level. Individual exposure to fluoride was not available (Karagas et al, 1996).
In 1991, a prospective study of 5 years duration in three demographically similar communities in Iowa was reported by Sowers and her colleagues. Two communities had fluoridated water at 1 mg/L and one with a fluoride content of 4 mg/L. Within these communities 827 women, aged from 20 to 80 years, were recruited to participate in the study. Bone mass examinations were conducted at the beginning of the study. Five years later, out of the original sample, 684 women were available for follow-up. Residence in the higher fluoride community (4 mg/L) was associated with a significantly lower bone mass in all women, an increased rate of radial bone mass loss in pre-menopausal women and significantly more fractures in post-menopausal women. The relative risk of fractures was 2.2 times greater in the high fluoride community as compared with the low fluoride communities. In this study the effect of calcium content of water was also studied. It had no significant effect on fracture rates.
In a study of osteoporotic fractures at the Pittsburgh Clinic, reported by Cauley and her colleagues in 1995, 2,076 non-black women of 65 years of age and older were recruited. Bone mineral density was assessed at the spinal and hip levels and spinal radiographs were taken during the baseline determinations. Vertebral and other fractures were assessed every 4 months. Information on fluoride exposure was limited to community water supplies and was assessed using a residential history questionnaire covering the period from 1950 to 1990. Women exposed to residential fluoridated water for over 20 years had similar axial and appendicular bone mass to women not exposed or women exposed for 20 or fewer years. There was no statistically significant difference of the risk far all fractures in women exposed to fluoridated water for over 20 years and those not exposed. The authors concluded that their results do not support the findings from recent ecological studies which showed an increased risk of hip fracture among individuals exposed to fluoridated public water supplies.
In conclusion, the above summaries demonstrate that while ecological studies generally find a slightly higher risk of hip fracture among the elderly living in fluoridated communities, this finding is not supported by the case control studies. The latter studies have a stronger statistical power since they examine individuals rather than comparing communities. Epidemiological studies do not provide us with credible scientific evidence to change public policy on water fluoridation.
Dental Fluorosis
Fluorosis is a side effect of excessive fluoride ingested during the process of tooth formation. It cannot occur after the teeth have fully developed. Excessive fluoride leads to improper crystallization of enamel with a less tightly formed crystalline lattice . This can lead to a varying degree of enamel surface porosity. In mild cases it causes various degrees of mottling which are often not visible to untrained eyes. In severe cases it leads to pitting of the enamel surface and enamel fragility. It is known that an intake of even a trace amount of fluoride can lead to a mild fluorosis in some individuals. Since normal human diet always contains small amounts of naturally occurring fluoride, there will always be some dental fluorosis in a population.
In North America the vast majority of dental fluorosis is of very mild to mild types. The moderate and severe types which over the years become discolored as a result of taking up stain from foods, beverages and tobacco smoke are not common.
The prevalence of dental fluorosis has increased during the past several decades in both fluoridated and non-fluoridated communities. In fact this increase has been more marked in some non-fluoridated areas and has been attributed to the inappropriate use of fluoride supplements (drops, tablets, dental products) as well as the consumption of beverages and foods prepared with fluoridated waters (Pendrys et al, 1990).
Pendrys and Stamm (1990) and Lewis and Banting (1994) have reviewed the literature on enamel fluorosis. Both studies concluded that there is a strong association between mild to moderate fluorosis and the use of fluoride supplements in early childhood. Whereas during the past several decades, there has been a 33% increase in the prevalence of enamel fluorosis in the fluoridated communities, the non-fluoridated communities have experienced a 1,000% increase during the same period. Obviously the fluorosis prevalence in the fluoridated communities has also been affected by the inappropriate use of fluoridated dentifrices.
In a more recent publication Pendrys (1995) reported the results of his well-designed retrospective case-control study of middle-school-aged children who grew up in "optimally" fluoridated communities. He calculated that about 25 percent of fluorosis in these communities can be attributed to the inappropriate use of supplements (drops and tablets) and about 71 percent to the inappropriate use of fluoridated dentifrices during the children's first 8 years of life.
It should not come as a surprise that there is a greater prevalence of dental fluorosis in some non-fluoridated communities since fluoride drops and tablets are more frequently used in those communities. When these children use (and swallow) excessive amounts of fluoridated tooth paste and consume beverages and food prepared with fluoridated water, their total fluoride ingestion becomes greater than that of children in the fluoridated communities (Pendrys et al, 1990).
Given the availability and indiscriminate use of fluoridated dental products, it is clear that, at the present time young children can be exposed to excessive amounts of fluoride, which is unnecessary for maintaining their dental health.
TOXICOLOGY OF FLUORIDE
S. Roth
Introduction
This report was prepared from documents made available to the Expert Panel plus other pertinent literature that was obtained from literature searches. The Expert Panel was requested to review the literature on fluoridation that has been published since 1989, and to evaluate whether new scientific literature would affect the current policy of water fluoridation.
This report addresses the toxic or adverse effects of fluoride.
Toxicology is defined as the study of the adverse effects of chemicals on living organisms, and implies that a toxic substance is any agent capable of producing a detrimental response in a biological system. Most known substances have the potential of inducing injury or death if a sufficient amount is present. Paracelsus, a 16th century alchemist, is known for his statement that 'all substances are poisons; there is none that is not a poison. The right dose differentiates a poison and a remedy.'
In section II of the Canadian Environmental Protection Act (CEPA), it is stated that a substance is toxic if it is entering or may enter the environment in a quantity or concentration or under conditions a) having or that may have an immediate or long-term harmful effect on the environment; b) constituting or that may constitute a danger to the environment on which human life depends; or c) constituting or that may constitute a danger in Canada to human life or health. The inorganic fluorides (fluorides derived from inorganic compounds) have been assessed to be entering the environment in quantities or under conditions that may be harmful to the environment (including humans and other biota), and therefore placed on Schedule I of the Act (Canadian Environmental Protection Act, Health Canada, Government of Canada).
Properties and Sources of Fluoride in the Environment
Fluoride is the ionic form of fluorine. It is widely distributed throughout the planet, rarely exists as a free ion in nature, and is bound in minerals and organic compounds. Fluoride combines reversibly with hydrogen to form hydrogen fluoride (HF) which is the major form responsible for the physiological properties such as absorption, distribution and clearance from the body compartments. In aqueous solution, inorganic fluorides dissociate to the monovalent anion (F-) and associated cation. Inorganic fluorides are released into the environment from natural sources (e.g. volcanoes, minerals, marine aerosols), and anthropogenic or man-made sources (e.g., production of aluminum, steel, glass, enamel, brick, ceramics and phosphate fertilizer). The fate of inorganic fluorides in the atmosphere, water, soil and biota is well established. The mean levels of fluoride in air (Canada) range from 0.01 to 1.0 ug/m3. Mean levels near a steel plant were found to be 0.2 ug/m3, and as high as 0.59 ug/m3 near a phosphate fertilizer plant. Since there is considerable fluoride in the earth's crust, all water naturally contains fluorides; sea water contains 0.8 to 1.4 mg/L, and samples of freshwater across Canada range from 0.01 to 11.0 mg/L (mean of 0.05 mg/L). The mean level in Alberta is 0.12 mg/L. In Calgary, average levels in the pretreatment water supply from Bearspaw and Glenmore treatment plants air approximately 0.16 and 0.28 mg/L (City of Calgary Report 02/10/1997).
Dietary Sources of Fluoride
People are exposed to fluoride from a variety of sources, including air, water, soil and food. In addition, intake can occur from fluoridated water, beverages, dietary supplements and dental products. Most foods contain low levels of fluoride (in the range of 0.1 to 2.5 mg/Kg). However, there are many foods which contain higher concentrations, e.g. teas, marine fish, bananas, potatoes, etc. Brewed tea, for example can contain up to 8.6 mg/L fluoride, and it has been reported that decaffeinated teas may contain twice the amount. Certain foods can contain higher fluoride levels if they are processed with fluoride-containing water. One of the current concerns has been fluoride levels in infant foods. It has been reported that fluoride concentrations in 238 commercially available infant foods ranged from 0.01 to 8.38 ug/gm, with the highest in chicken products. Many manufacturers in the USA and Canada have addressed this issue and adjusted the levels accordingly. In comparison, fluoride levels in human milk are low - ranging from 0.007 to 0.011 mg/L. The consumption of bottled water has Increased dramatically in recent years, and some beverages are known to contain high levels of fluoride (from less than 0.1 to 2.74 ppm). Unfortunately many products do not list the levels of fluoride which would be very useful to the consumer. Since people are exposed to fluoride from a variety of sources, total fluoride intake must be considered in assessing toxicity, not only that of fluoridated water. Although total fluoride intake is difficult to calculate, it is necessary to estimate real dose and response. This is because it is the total fluoride intake that is critical, not just the proportion in drinking water.
Kinetics of Fluoride in the Body
Toxicokinetics is the science of how the body handles a substance. It has been termed metabolism in a number of articles on fluoridation. Toxicokinetics considers the exposure, absorption, distribution (and storage), biotransformation (if any) and clearance or excretion in relation to time. The kinetics or metabolism of fluoride has been well reviewed (see Whitford, 1996). Approximately 50 to 90% of ingested fluoride is absorbed from the gastrointestinal tract (GIT), and the time for half maximum absorption is approximately 30 minutes. Peak plasma (blood) levels occur in 30 to 60 minutes. Less absorption occurs from the oral cavity compared to the GIT. The bioavailability of fluoride is generally high, however the rate and amount absorbed are dependent on a number of factors such as pH, presence of other ions, foods, and chemical composition. About 10-25% of the daily intake of fluoride is not absorbed and excreted in the feces. Fluoride absorption is inversely related to dietary calcium; a high calcium level may result in net fluoride secretion into the GIT. Therefore dietary calcium and other factors influencing fluoride uptake, absorption and excretion must be taken into consideration, if studies are to be meaningful.
Fluoride exists in the plasma as two forms - ionic( free) and nonionic (bound). It is the free form that is important in reference to both health benefits and toxic effects and is also the form that is measured with an ion-specific electrode. Plasma (blood) levels are proportional to intake, and can increase slowly over the years. Following fluoride ingestion, the levels in saliva increase corresponding to plasma levels (the normal concentration of fluoride in saliva is about 1 pm, slightly less than plasma). Fluorides are well distributed to most soft tissues, but approximately 50% is associated with calcified tissues (bones and teeth) within 24 hours of ingestion. Nearly 99% of the body burden (total amount of fluoride in the body) is associated with calcified tissues. The major route of removal or elimination of fluoride from the body is via the kidney (urine). Clearance via the kidneys can be influenced by a number of factors, including pH, diet, drugs, age, metabolic and respiratory disorders, altitude, exercise, and of course kidney function. Therefore all these factors have to be considered if studies are to be reliable.
Toxicity of Fluoride
As stated above, all substances have the potential to produce toxic effects if a sufficient amount is ingested and absorbed . Fluoride is no exception to this rule. At sufficient (high) levels, fluoride can produce a number of adverse effects on various target organs in the human body, most of which appear to be concentration-dependent.
Acute poisoning is ingestion of high enough doses that immediate effects are observed. The smaller the amount of substance that causes acute poisoning, the more toxic the material. Chronic effects are due to long term, low levels of exposure and effects are not seen during the beginning of that low level exposure.
There has been considerable information published on the acute toxicity of fluoride in the human body (see Whifford, 1996). Acute toxicity following ingestion of high doses can develop quite rapidly; initial symptoms usually include nausea, gastric distress and vomiting. With larger doses, muscle spasms, tetany and convulsions may develop. Toxicity may progress to include the cardiovascular system resulting in hypotension and arrhythmia. It has been estimated that the lethal dose for humans is 32-64 mg/Kg. This would be 2.25 to 4.5 gm of sodium fluoride for a person of 70 Kg. It would be impossible to drink enough at one time to absorb an acute amount of fluoride from fluoridated drinking water. Of more importance to the issue of water fluoridation is the potential for chronic (low dose) toxicity. The following segments address some of those concerns.
Effects of Fluoride on Target Organs
Effects on the Kidneys: There is no evidence that low levels (up to 8 mg/L in drinking water) of fluoride are associated with kidney dysfunction or increased mortality from a kidney disorder. It is established, however, that persons with renal insufficiency will exhibit decreased clearance of fluoride and thus elevated plasma levels. However, with this medical condition, many adverse affects other than those from fluoride would also have to be dealt with, so changes in fluoridation would not solve the problem.
Immune System:
At concentrations associated with water fluoridation, there is no conclusive evidence that fluoride produces any undesirable effects on the immune system or is related to allergic reactions.
Reproductive System: Although some studies using animal models have demonstrated adverse effects on some reproductive functions, the concentrations of fluoride used in the studies were very high (above 100 mg/L). There is no association between fluoride intake and reproductive outcomes in human subjects.
Cancer (also see previous section)
In 1989, a study conducted by the National Toxicology Program (NTP) of the National Institute of Environmental Health Sciences, showed that sodium fluoride produced osteosarcomas, when administered to rats. This was observed only in male rats and at the highest doses (45 and 79 ppm). There were no osteosarcomas found in female rats or in mice also used in the study. The review of this study by the NTP Review Panel concluded that there was equivocal evidence of carcinogenic activity of sodium fluoride. The use of the term equivocal was questioned. A similar study was commissioned by Proctor and Gamble. An Ad Hoc Subcommittee on Fluoride of the US Public Health Service concluded that both studies failed to establish an association between fluoride and cancer. Another study by the National Cancer Institute did not find a link between the incidence of cancer and water fluoridation, and recent reports by Cook-Mozaffari (1996) and Kantor (1997) also conclude there is no increase in cancer rates in fluoridated and non-fluoridated areas. Hurdy et al (1990) reported a study between Calgary (non-fluoridated) and Edmonton (fluoridated) that failed to reveal any difference of incidence of osteosarcoma. A recent study by Tohyama (1996), found a correlation between fluoride concentration in drinking water and cervical and uterine cancer in 20 municipalities in Japan. The levels of fluoride were apparently 0.02 to 0.37 mg/L, which are close to background levels, whereas other dissolved solids ranged from 106.7 to 485.5 mg/L. There was some control for confounding factors, but the results appeared to be related to other factors which were not studied, rather than fluoride per se. It is important to note that these exposures occurred in an industrial setting.
There is no conclusive evidence that levels of fluoride found in fluoridated water are associated with greater incidence of cancer.
Mutagenicity: Fluoride is not mutagenic (causes mutations in cells) in standard bacterial systems, but has been shown to produce chromosome damage and gene mutations in cultured mammalian cells (Zeigler et al 1993). The same author, however, concluded that the matter is still unresolved since the effects have not been observed in vivo.
Neurotoxicity: The study published by Mullenix et al (1995) has received considerable attention. It demonstrated sex and dose-specific behavioral deficits in rats exposed to fluoride. The doses administered in this study were high (50-60 ppm). The authors justified these doses by the apparent similarity in plasma levels found in humans exposed to high levels. Other studies recently reported behavioral and morphological effects on developing rat brain, but also used high concentrations (60 ppm) in the tests. Although these data do demonstrate that high doses of fluoride may have the potential for adverse effects, there is no evidence for neurotoxicity at levels associated with water fluoridation.
Dental Fluorosis (see also previous section)
Dental fluorosis results from an excess of fluoride in or near enamel, which is being formed, during pre-eruptive development. It is a condition described as a hypomineralization of enamel, characterized by greater surface and subsurface porosity than found in normal enamel. Dental fluorosis is dose-dependent; i.e. exposure to higher levels of fluoride will result in a more severe degree of fluorosis. Dental fluorosis occurs more readily in fluoridated regions compared to non-fluoridated areas. There has been a significant increase of dental or enamel fluorosis during the past years. This has been attributed to an increase in total intake of fluoride.
Very mild fluorosis is change in coloration that is just Visible to the trained eye. Mild fluorosis would not likely be noticed without careful scrutiny. More severe forms cause noticeable staining from foods and beverages.
There is evidence that the prevalence, and to some degree the severity of dental fluorosis, is increasing in both fluoridated and non-fluoridated areas. There are no data that this is occurring in Calgary, however it is of concern and should be addressed. Even low fluoride intake may result in a certain level of fluorosis. This was, in fact, predicted in the earlier work of Dean (1942) who estimated that 10% of the population would exhibit signs of mild fluorosis with water fluoridation at 1.0 ppm. The balance between the health benefits and adverse effects must be evaluated with any treatment. The concentrations of fluoride in drinking water have remained constant, therefore other sources of fluoride may be responsible for an increase in total fluoride intake and associated increase in dental fluorosis. The increase in total fluoride intake has resulted from the use of fluoride supplements and fluoridated products and food. It appears that the primary contributors are fluoridated toothpastes, fluoridated mouth washes, and beverages prepared with fluoridated water. Lewis and Banting (1994) have shown that 60% of the total prevalence of dental fluorosis may be attributed to fluoride sources other than fluoridated water. This has also been documented by others (e.g. Hiller et al 1997, Horowitz 1996, Pendrys and Stamm, 1990, Pendrys, 1995).
Summary
A review of the available literature has not revealed any significant associations between water fluoridation, at the level found in Calgary, and major toxic or adverse reactions. Further research in this field will provide more information on the mechanisms of fluoride toxicity and better estimates of lowest effective concentrations.
THE NATURAL ENVIRONMENT
D. Thompson
Industrial Sources
In Canada, the threats to the natural environment by fluoride are associated with industries using large
amounts in their processes such as production of aluminum, steel and ceramics; mining and processing of
ores high in fluoride minerals, and the phosphate fertilizer industry. Combustion of coal also releases
fluoride (Landis and Yu 1995). In the Priority Substances List Assessment Report on Inorganic
Fluorides, Environment Canada and Health Canada (1993) conclude that where there are large industrial
sources, inorganic fluorides are entering the environment in amounts that pose a threat. In Calgary there
are no active major industrial sources. The only possible industrial source was a phosphate fertilizer plant
which has been shut down for more than a decade. It no longer poses a significant environmental
threat.
Water
Fluoride is one of the natural chemicals found in water. It is routinely measured by Alberta
Environmental Protection. The routine monitoring includes measurements above and below major cities.
Measurements of fluoride in Alberta's rivers are in the range of 0.1 to 0.25 ppm (mg/L). The levels are
well below Alberta Ambient Surface Water Quality Interim Guideline 1.5 ppm (mg/L), Canadian Water
Quality Guideline for Irrigation (1.0 mg/L) and Guidelines for Canadian Drinking Water Quality (Health
and Welfare Canada, 1996). The Panel has been informed that the optimum level for fluoride in drinking
water has recently been lowered from 1.0 ppm to 0.8 ppm by Alberta Environmental Protection (1998).
This is consistent with changes in other jurisdictions. The change reflects the fact that most of the
population receives fluoride from sources other than water.
Fluoride concentrations measured by Alberta Environment (Water Sciences Branch, 1998) at Cochrane (upstream from Calgary) are slightly lower than those at Carseland (downstream from Calgary). It is worth noting that when fluoride concentrations measured downstream from Calgary between 1967 and 1974 are compared to measurements between 1987 and 1991, the difference is very small, in spite of the large population increase. The raw data may show a very small increase (of the order of 0.05 mg/L) between 1991 and 1994 (Standards and Guidelines Branch, 1998). Increases in fluoride concentration downstream from cities cannot be attributed solely to water fluoridation because of the many other sources of fluoride associated with diet and dental practices.
Fluoride is less toxic to aquatic organisms in hard water (water high in carbonate) such as in the Bow River (Environment Canada and Health Canada 1993).
Soils and Groundwater
Concern has been expressed about fluoride from various sources becoming an environmental problem in
soils and groundwater. This could be a concern under two conditions: large industrial sources and acidic
soil conditions. There are no large active sources in Calgary. Further, the soils in this area are basic and
highly buffered, so even if fluoride were to be added to soils, it is unlikely to migrate. Plants take up very
little fluoride from soils unless the soils are very acidic. However, some plants are naturally high in
fluoride, particularly teas (including some herbal teas) and rice and peas (Landis and Yu, 1995).
FLUORIDATION AND DENTAL HEALTH
The Panel's Terms of Reference did not explicitly refer to a review of benefits of fluoride, or lack
thereof, to dental health. However, a review of dental benefits could be included under the reference to
"health and safety measures". We felt obliged to examine the question of benefits, because if no benefits
were obtained from fluoride, then exposure was unnecessary.
No one on the Panel was an expert on tooth biology and biochemistry. We therefore submitted our questions about tooth biology and caries prevention to Dr. Colin Dawes of the Faculty of Dentistry at the University of Manitoba, who was recommended to us by the Faculty of Dentistry at the University of Alberta. To ensure balanced perspectives on the issue, the Panel asked for a recommendation from a group opposed to fluoridation, who recommended that we review the same questions with Dr. John Colquhoun, Professor Emeritus of the University of Auckland, New Zealand.
The Panel met with Dr. Dawes on February 11, 1998. He outlined the basics of enamel physiology, and the proposed biological means by which fluoride might protect enamel and prevent caries. He also provided commentary on some of the epidemiological studies of dental caries and water fluoridation. Dr. Dawes stated that an examination of dental benefits provided by fluoride showed that 0.7 ppm would be the recommended concentration in treated water. He provided the Panel with a short report and supporting documentation.
The Panel held a videoteleconference with Dr. Colquhoun for an hour on the evening of Feb 26, 1998. In Dr. Colquhoun's opinion, fluoridation has no beneficial effect on the incidence of caries, and may even have a detrimental effect. He noted that recommended concentrations of fluoride in treated water had been reduced in New Zealand. He provided the Panel with supporting documentation for his presentation.
The presentations by Dr. Dawes and Dr. Colquhoun were videotaped. The Panel was grateful to Drs. Dawes and Colquhoun for taking the time to assist us.
Dental Health is generally improving. There have been reports since 1989 questioning the impact of water fluoridation on dental health, suggesting that a number of factors, which were not present when water fluoridation was started, have had a greater impact on the decline in the incidence of caries. Most notably, these include better understanding of dental hygiene and use of new techniques in dentistry, changes in diet, other environmental sources of fluoride, and general improvement in the standard of living.
Given the declining incidence of caries in the population, some would suggest that water fluoridation is no longer needed, even if it is beneficial. That is, other sources of fluoride are effective so the argument is about mode of delivery, relative costs and effectiveness. Those favouring water fluoridation say that the low dose of fluoride in water protects those individuals who do not have access to individual fluoride treatment and/or dental care and instruction in dental hygiene. Given the concentrations of fluoride in toothpastes, tablets, and drops, and topical applications, the total amount administered is less uniform and the possibilities of excessive doses increase.
Dr. Colquhoun and Dr. Dawes both discussed the epidemiological evidence that suggested that fluoridation no longer appears to be having significant impact on the declining incidence of caries. Dr. Colquhoun felt that those studies showed that water fluoridation was no longer necessary. Dr. Dawes felt that the studies which showed a continued decline in dental caries in Germany following the cessation of water fluoridation may be explained by a number of other important variables affecting incidence and prevalence of dental caries: the method of defining and reporting caries; the overall changes in dental care including fluoridated dental products; and the increased use of fluoridated salt in Germany. Water fluoridation's effect on dental health may be obscured by other variables.
The Panel agreed that some studies showed that dental health was improving in areas not receiving
fluoridated water or that dental health continued to improve after fluoridation of water supplies was
stopped. However, we believe that to conclude that water fluoridation is ineffective or unnecessary is an
oversimplification. Much more detailed, statistically sound studies of total fluoride intake, dental
practices, etc. must be done to reach such a conclusion with confidence.
BIOSTATISTICAL EVIDENCE OF EFFECTS OF FLUORIDE ON HUMAN HEALTH
(Dissenting Opinion), M. Nosal
1. Introduction
In this report I will review the most important recent findings related to the effect of fluoride on
bones and incidence of dental caries. For the sake of required brevity I will omit here other
considerations, covered elsewhere. Fluoride is available to the human body from many sources
such as food, drinking water, prepared drinks, dental care products and treatments, environmental
exposure etc. It is the total fluoride intake which is critical. However to factor out the
contribution of each source is very complex and thus an apportionment of the risk due to water
fluoridation alone is extremely difficult.
2. Human fluoride intake and its apportionment
Total fluoride intake in humans varies considerably with age, weight, geographical area,
nutritional status etc. and an exhaustive analysis is therefore very difficult. There are several
reports which published estimation of the total intake and its apportionment due to various
sources. I will provide these findings for later use in fluoride risk assessment. All calculations are
related to a standard 70 kg adult consuming fluoridated drinking water at about 1 ppm, equal to 1
milligram of fluoride per litre of water.
Canadian Environmental Protection Act, Inorganic Fluorides Assessment Report, Table 3, gives the total fluoride intake as 3.28 - 4.07 mg/day with fluoride from drinking water being 1.00 - 1.56 mg/day. These figures seem to be slightly low compared to data reported elsewhere.
Dietary Reference Intakes, National Academy of Sciences, Table 8-2, at the bottom, reports an average daily fluoride intake from prepared foods served to adult hospital patients (excluding drinks) as 1.8 mg/day. Additional 2 l/day of drinking water recommended by nutritionists at 1 ppm fluoride yields 2 mg/day of fluoride.
Burgess in his Fluoride Ingestion from Dental Products estimates the total fluoride ingestion from various dental care products at .43 mg/day (dentifrice + rinse + topical gel). Thus the total fluoride ingestion is approximately 4.43 mg/day (depending on age), with 2 mg/day from the drinking water. These figures are very close to the fluoride ingestion data reported in the above paragraph.
Public Health Service, U.S. Department of Health and Human Services, in the report Review of Fluoride, Benefits and Risks, gives the total amount of ingested fluoride as 2.21 - 9.24 mg/day with fluoride from the drinking water being .84 - 4.48 mg/day. Even though the range of the ingested fluoride is rather wide, it is generally comparable to the ranges reported above.
The above given ranges have to be adjusted upwards for subpopulations such as tea drinkers, marine fish eaters, heavy labourers working in increased temperature environments, athletes and many others. It should be noted, that in all these reports the apportionment of fluoride from the fluoridated drinking water is not negligible. It can be estimated to be ranging approximately within 30 - 45% of the total daily fluoride intake by adults.
Historically, the fluoride intake in Canada used to be much lower. The Health Canada report titled Investigation of Inorganic Fluoride and its Effect on the Occurrence of Dental Caries and Dental Fluorosis in Canada estimates (see Table 1) that during 1940's (before the fluoridation of water was introduced) the total fluoride intake from food was about 1.05 mg/day. Other reports give a baseline fluoride intake during 1940's as .45 - .55 mg/day which is consistent with the Health Canada report.
3. Bone biomechanical quality and fractures.
3.1 Effect of water fluoridation on bone fractures
Following studies are epidemiological and some of them are using ecological methodology by
addressing entire groups rather than individual subjects. Such studies have often limited ability to
reach unequivocal conclusions because they are unable to address fully all important variables,
covariates, factors and their relationships and their findings might be only circumstantial.
Nevertheless such studies may provide statistically significant information about relations between
factors and associations of variables of interest.
Cauley (1995): Authors studied 2076 non-black women, all aged over 65 years, and incidence of osteoporotic fractures. The variable was the number of years of exposure to fluoridated water. They compared the relative risk (RR) of various types of fractures between fluoride treated and non-fluoride women. All the comparisons turned out as statistically non-significant. The mean number of years of fluoride exposure was too low at 12.7 years to be able to demonstrate any significant effect. Furthermore, the confidence intervals for RR were incredibly wide (e.g. 0.10 - 1.89) demonstrating a poor statistical quality of the data which resulted in the fact that the findings were statistically non-conclusive.
Danielson (1992): The authors tested the effect of 1 ppm fluoridated water on the incidence of hip fractures in the elderly population in Utah. The incidence of femoral neck fractures in patients 65 years of age or older was compared in three communities in Utah: one with and two without water fluoridated to 1 ppm. Authors excluded from the study spurious cases. The relative risk of hip fracture in the fluoridated area was 1.27 (95% confidence interval 1.08-1.46) for women and 1.41 (1.00-1.81) for men. This significant increase in the risk of hip fracture in both men and women exposed to artificial fluoridation at 1 ppm suggests that low level of fluoride may increase the risk of hip fracture in the elderly. The authors examined a population with a different life-style (Latter-Day Saints church) which has lower exposure to various risk factors for osteoporosis, such as smoking and alcohol. Thus the relative contribution of fluoride to hip fracture may have been more evident than in other studies, which dealt with a more heterogenous populations.
Jacobsen (90/92): In order to assess the association between water fluoridation and hip fractures, authors identified 129 counties across US considered to be exposed to public water fluoridation and 194 counties without exposure. Data from Health Care Financing Administration and Veterans Affairs were used to calculate the incidence of hip fractures among white persons aged 65 years of more. There was a statistically significant weak positive association between fracture rates and fluoridation. The corresponding 95% confidence interval for the relative risk for men was very narrow at 1.13 - 1.22 pointing to the statistically significantly increased risk of hip fracture in fluoridated areas compared to nonfluoridated areas.
Jacqmin-Gada (1995): Authors report results of a population study of the relationship between concentration of fluorine and calcium in drinking water and risk of hip fractures or fracture at any site. The study investigated 3777 subjects aged 65 years or older living at home in 75 parishes of southwest France. The mean time the individuals remained in the same parish was 41 years. Fluorine and calcium concentration in water was measured from each parish. Five covariates were investigated: age, sex, Quetelet index (weight/height squared), smoking status and sport activity. Authors performed multiple logistic regression for data explanation. The risk of hip fracture was significantly higher when water fluorine concentration was higher than 0.11 mg/litre (p=.04). Thus adjusting for major risk factors, this study suggests a possible deleterious effect of fluorine in drinking water on the risk of hip fractures, even for moderate concentrations of fluorine.
Sowers (1986): Bone mass of women in three rural communities with different mineral water content was studied. Mean fluoride and calcium were 4 ppm and 16 ppm respectively for the first community, 1 ppm / 375 ppm for the second and 1 ppm / 65 ppm for the third. Bone mass was measured by photon absorption and women were interviewed about fracture history, dietary intake and other important covariates. Authors observed no protective effect with high fluoride intake. Women in high fluoride area reported significantly increased incidence of fractures. This is a very important study because individual subjects were evaluated for various specific variables which have a possible effect on hip fractures.
Sowers (1991): This is a follow-up of the previous study by Sowers (1986). In 1989 there were 684 women still living in same communities as earlier. Residence in the higher fluoride community was associated with a significantly lower radial bone mass in pre-menopausal and post-menopausal women and significantly higher incidence of fractures among post-menopausal women. The corresponding 5-year relative risk for women in high fluoride community, compared with the control community, was significantly high at 2.2. Estimates of risk were adjusted for age and body size.
Suarez-Almazor (1993): The purpose of this study was to compare hip fracture hospitalization rates between Edmonton and Calgary. Edmonton had fluoridated water since 1967 and Calgary, which at the time of the study (1981-1987) did not have fluoridated water. Case subjects were individuals aged 45 years or older. The hip fracture rates were adjusted for age and sex. No statistically significant difference was found for the entire population or for women only. However the hip fracture rate for men 65 years and older in Edmonton was 5.09 while for Calgary the rate was 4.47. This increased hip fracture incidence is statistically significant and represents an increase of almost 14%.
Whitford (1996 page 138) as well as the National Research Council report on Health Effects of Ingested Fluoride (page 59) state: "Most estimates indicate that crippling skeletal fluorosis occurs when 10 - 20 mg of fluoride have been ingested on a daily basis for at least 10 years".
3.2 Effect of therapeutic dose fluoride
There are many clinical trials reporting the effect of high dose fluoride intake administered for
therapeutic purposes in osteoporosis control. These results are not entirely relevant for our
consideration of the effect of moderate to low fluoride intake from fluoridated drinking water.
Disparity between the total non-therapeutic fluoride intake from all sources (3 - 9 mg of
fluoride/day) and therapeutics dose (40 - 75 mg of NaF/day corresponding to 17.67 - 33.14 mg of
fluoride/day) is quite large and hence the actual effect can be expected to be quite different.
However a long term (20-60 years) of low dose exposure (3 - 9 mg/day) may, in a cumulative
sense, have rather similar effect as shorter (1-6 years) but higher dose exposure (18 - 33 mg/day).
These studies demonstrate the corresponding process how fluoride intake may affect bone.
Fratzl (1994): Bone biopsies were taken from three patients with postmenopausal osteoporotic bone before and after fluoride therapy (60 mg NaF/day for 1-2 years) as well as from three normal controls. An increasing amount of new bone is laid down on the surface of preexisting bone. Its mineral structure is identical to that of heavy fluorosis and is characterized by the presence of additional large crystals, presumably located outside of the collagen fibrils. These large crystals, which were not present in the controls and before the fluoride treatment, contribute to increase the mineral density without significantly improving the biomechanical properties of the bone. As soon as significant amounts of fluoride are present, bone turnover leads to the replacement of old normal bone by new pathological bone. Decreasing biomechanical properties of the bone may even lead to deterioration in the overall mechanical stability of the skeleton.
Hedlund (1989): The authors compared the incidence of hip fractures of four groups of osteoporotic women. 22 treated with placebo, 17 with fluoride and calcium, 18 with fluoride and calcitrol, and 21 with calcitrol alone. Slow release sodium fluoride, 50 mg/day, for 12 months was used as fluoride treatment. The difference in fracture rates for fluoride treatment versus nonfluoridated treatment is highly significant (p=.006). Moreover, the six hip fractures occurring in patients receiving fluoride treatment for 72 patient-years of treatment is 10 times higher than would be expected in normal women.
Riggs (1990): To assess the effect of fluoride treatment on the fracture rate in osteoporosis, the authors concluded 4-year clinical trial with 202 postmenopausal women with osteoporosis who were randomly assigned to receive sodium fluoride (75 mg/day) or placebo. In total 66 in the fluoride group and 69 in the placebo group concluded the trial. The number of non-vertebral fractures was significantly higher in the treatment group than in the placebo group (72 versus 24).
Riggs (1994): Authors present observations on osteoporotic 50 women receiving 50 mg/day of NaF or placebo for up to 6 years. Multivariate statistical analysis revealed a very complex pattern in which vertebral fracture rate was influenced by several variables. There was a two fold statistically significant increase in hip fracture occurrence in a randomized controlled study when the women were administered a relatively low dose of only 50 mg of sodium fluoride per day.
Sogaard (1994): In order to evaluate the effect of sodium fluoride (40-60 mg/day) on bone mechanical competence, iliac crest biopsies were taken before and after one year of treatment in 12 osteoporotic patients, and before and after five years of treatment in 14 patients. Bone fluoride content increased after both treatments. A significant reduction of 45% was found in trabecular bone strength after 5 years treatment and 58% reduction was found in trabecular bone quality. The results of this study indicate that long term administration of NaF may be detrimental to bone quality.
4. Decrease in caries
There are many studies investigating the effect of water fluoridation on the incidence of dental
caries. Most of these studies investigate incidence rates of decayed (D), missing (M) and filled (F)
teeth (DMFT) in various age cohorts and their relation to fluoridated water. The conclusions are
rather varied, depending on the propriety of the dental and biostatistical methodology used and
also on the quality of the available data.
Report of the Second Alberta Dental Health Survey, 1985, compared incidence of DMFT rates between various regions of Alberta. Of particular interest is the comparison between Calgary, which did not have fluoridated drinking water at that time and Edmonton, which provided fluoridated water since 1967. The report concentrated on the cohorts of 13 years old children. Edmonton Board of Health Annual Report for 1985 reported for these Edmonton children mean DMFT rate as 2.80. The corresponding DMFT rate for the Calgary cohort was 2.995 DMFT. This difference is not statistically significant. How can it be explained that Edmonton with fluoridated drinking water did not have statistically lower incidence of DMFT than Calgary with nonfluoridated water? The authors stated that all children in Calgary in 1985 were rated as "fluoridated" due to exposure to fluoride from other sources (toothpaste, dental treatments etc.) even though fluoride was not added to the water.
Heller (1997): The purpose of this study was to investigate the relationship between caries experience and dental fluorosis at different fluoride concentrations in drinking water. The impact of other fluoride products was also assessed. The use of fluoride tablets, drops, professional fluoride treatments and school fluoride rinses were ascertained from caregiver questionnaires. The sharpest declines in DMFS were associated with increase in water fluoridation between 0 and 7 ppm. F, with little additional decline between .7 and 1.2 ppm. Fluorosis prevalence was 13.5%, 21.7%, 29.9% and 41.4% for children who consumed <.3 ppm, .3 to .7 ppm, .7 to 1.2 ppm and over 1.2 ppm fluoridated water. The author states that a suitable trade between caries and fluorosis appears to be around .7 ppm F. Data from this study suggest that a reconsideration of the policies concerning most appropriate water fluoridation might be appropriate.
Hildebolt (1989): The objective was to determine how the prevalence of caries vary between regions of Missouri. In the total sample, there were no significant difference between those children drinking optimally fluoridated water and those drinking suboptimally fluoridated water.
Ismail (1993): An epidemiological assessment of differences in caries prevalence between children in Truro (<.1 ppm fluoride in water) and Kentville (1.1 ppm fluoride), Nova Scotia was completed. Among other findings, the percentage of all caries free children in non-fluoridated area (26.8%) is higher (even though not significantly) than the fluoridated area (23%). The percentage of very high caries (5 or more) is lower in the fluoridated area (10.3% versus 22%). However the overall mean number of all caries in the fluoridated area (3.5) does not significantly differ from the mean number of all caries in the non-fluoridated area (4.2) and the difference is only .7 caries.
Kunzel (1997): The authors investigate the rise and fall of caries prevalence (DMFT) and its relation to changing F concentration of drinking water and other health related factors based on findings of more 286,000 subjects of either sex. Water fluoridation at 1 ppm was implemented in Chemnitz (formerly East Germany) in 1959 and was operated till unification of Germany in 1990. A comparison is made with Plauen, city with F poor (.2 ppm) water. In 1959 the mean caries incidence in two cities was quite comparable at about 4. Since 1959 till 1971 Chemnitz water was fluoridated at .9 ppm and caries incidence significantly decreased to about 2 despite an increase in sugar consumption from 27 to 35 kg per capita/year. Over the same period, the caries incidence in Plauen (receiving F poor water) increased to about 5.
There were no caries-preventive facilities or oral hygiene program in either city during this period and number of topical dental F applications was very low. Water fluoridation was introduced in Plauen in 1972 and caries incidence started decreasing till about 3 in 1990. Due to technical difficulties in Chemnitz water fluoridation was interrupted in 1971 for a longer period of time and the caries incidence again rose to about 3 in 1990. After 1990 water fluoridation was terminated in both cities due to new laws after reunification of Germany and both cities received only F poor water. However the caries incidence continued to decrease in both cities to the lowest level ever at 2 in 1995. This is explained by completely different conditions for management of caries: F-enriched domestic salt was offered since 1992 and reached 15% of the market in 1995. The sugar consumption decreased from 42 kg to 35 kg in 1993 due to nutritional education. The use of fluoridated toothpaste increased from 18% to 88% after 1992. The dental care system was entirely restructured in this period and its efficiency greatly increased. The authors conclude that the relation between F concentration in drinking water and the caries level valid from 1959 to mid 1980's is no longer true. The main differences between 1959 - 1971 period and after 1990 period are broader F availability (mainly toothpaste) and increased awareness of oral hygiene. An argument that changes in diagnostical criteria may partially explain the decline may have some merit but the decline was evident even before the new diagnostic criteria were introduced in 1993.
Johnston (1986): Dental caries prevalence in Ontario health units from 1951 to 1956 and data from 1972 to 1984 for children aged 5, 7, 9, 11 and 13 years are analyzed to determine the rate of decline in caries over those years. The provincial average rate decline over the last two decades was 50% and there is no evidence that this is lessening. Decline in tooth decay cannot be fully explained by water fluoridation.
Newburn (1989): The efficacy of communal water fluoridation in reducing dental caries has been reviewed based on surveys conducted in the last decade in fluoridated and nonfluoridated communities in the US, Australia, New Zealand, Britain, Canada and Ireland. The efficacy is greatest for the deciduous dentition and decreases as the age increases. Effectiveness of water F has decreased as the benefits of other forms of F have spread to communities lacking optimal water F. Splieth (1996): Water fluoridation in East Germany was introduced in 1959 and continued until 1990 unification of Germany. Despite the discontinuation of water fluoridation, caries incidence is decreasing. Extensive use of F toothpaste after 1990 in East Germany led to caries reduction even though water fluoridation discontinued. Also the use of dental sealants and dental prevention programs were expanded.
5. Conclusions
There are older studies documenting a beneficial effect of water fluoridation on decreasing the
incidence of dental caries. Most of these studies are based on data from 1950's to 1970's when
general conditions of nutrition knowledge and availability as well general level of dental care and
fluoride availability from other sources than drinking water (such as food and dental care
products) were significantly lower than today. Recent studies however indicate that with the
improvement in nutrition and availability of better dental care as well as with increased availability
of fluoride from other sources, the relative importance of beneficial effect of water fluoridation
has decreased.
The significant decrease in the incidence of dental caries over the past 20 years cannot be explained only as a consequence of water fluoridation. It was estimated that total fluoride intake in 1940's was about .5 - 1 mg/day. However, this is clearly not true any more: the total fluoride intake from various sources is estimated to be almost 10 times higher (3-9 mg/day). There are many other very important factors such as improved knowledge and availability of high quality nutrition, improved oral hygiene and care and mainly very pervasive fluoride availability in food (bottled water, salts, grains, tea, marine fish etc.) and in the form of dental products (toothpaste, rinses, gels and paints etc.) which now contribute to statistically
significant caries decline even in areas with nonfluoridated water. Many studies provide evidence that today water fluoridation is not the main reason of caries decline and such practice should be reconsidered. The 1985 Alberta Dental Health Survey provides data documenting that caries rate among 13 year old children in Edmonton (water fluoridated since 1967) and Calgary (water not fluoridated) was not statistically different. Another study by Kunzel demonstrates that during 1960 to mid 1980's, the increase or decrease in the incidence of dental caries in Germany was very closely associated with levels of fluoride in the water. However, after 1990 the fluoridation was terminated everywhere in Germany, yet caries incidence keeps declining to its lowest levels ever.
Some authors argue that specific cohorts of the general population, particularly those with lower socioeconomic status, may benefit from continued water fluoridation. However, these studies show either the effect on deciduous (first) teeth only but not on permanent teeth which are most important for human health or the difference is very small and equal to about .1 - .7 surface of a tooth. Other studies emphasize that cohorts with lower socioeconomic status are deprived of high quality nutrition and as a consequence are exposed to increased health risks from fluoride exposure. Furthermore, the lack of knowledge about importance of oral care and availability of proper dental care has a very significant effect in this regard.
The inference that "crippling skeletal fluorosis occurs when 10 - 20 mg of fluoride have been ingested on a daily basis for at least 10 years" (Whitford (1996 page 138); the National Research Council report on Health Effects of Ingested Fluoride (page 59)) is generally accepted in the scientific literature. The actual range of total ingested fluoride (as reported in section 2 above) in cases of 1 ppm fluoridated water is 3 - 9 mg/day. Compared to the above range given by Whitford, the documented total fluoride intake represents a potential risk of mild to moderate skeletal fluorosis in adult populations drinking water fluoridated at 1 ppm over long periods of time. Similarly increased risks are present for population cohorts with increased fluoride ingestion such as heavy tea drinkers, consumers of marine fish or for cohorts with impaired fluoride metabolism such as renal dysfunctions.
There is also evidence that an exposure to drinking water containing fluoride at 1 ppm over a long period of time may be associated with a statistically significant increase in the hip fracture incidence and corresponding relative risk. Possibility of a such effect on bone is further documented by studies using high doses of fluoride over a shorter period of time for therapeutic treatment. Of special interest is the study by Suarez-Almazor, which shows that the hip fracture rate for men 65 years and older in Edmonton (fluoridated water) was significantly higher than in Calgary before the introduction of water fluoridation.
Heller concluded that a suitable trade-off between a potential caries decrease and fluorosis increase appears to be around .7 ppm F and that there is not much improvement in caries decrease for fluoridation over .7 ppm. However, fluoridation over .7 ppm sharply increases prevalence of fluorosis.
Toxicological Profile for Fluorides (1993) issued by the Agency for Toxic Substances and Disease Registry unequivocally states that there are populations which are unusually susceptible to the toxic effects of fluoride. These populations include the elderly, people with deficiency of calcium, magnesium, and/or vtamin C, and people with cardiovascular and kidney problems. Because the fluoride is excreted through the kidneys, people with renal insufficiency would have impaired renal clearance of fluoride. Poor nutrition increases the incidence and severity of dental fluorosis and skeletal fluorosis.
Summarizing the above facts I can conclude that recently published literature provides biostatistical evidence of possible statistically significant association between fluoride intake from drinking water and increased hip fracture rates as well as skeletal fluorosis incidence. This association cannot be construed as clear cut deterministic cause - effect relationship and much more research will be needed to clarify very complex relationship between fluoride intake and human health.
However prudence dictates that potential risks cannot be disregarded either. Unfortunately there is no actual data available at this time to critically assess the effect of water fluoridation on general health in Calgary.
Recommendations
- It is recommended that water fluoridation in Calgary should not continue at its present concentration of 1 ppm. Should it continue at all, then the fluoride concentration in drinking water should decrease to at most .5 - .7 ppm.
- It may be more appropriate to provide required dental benefits using other means such as oral care and nutritional education and increased availability of dental care for lower socioeconomic strata of the society.
- Calgary Regional Health Authority should collect detailed data on dental health in Calgary region which should be analyzed for temporal trends, its relation to general health and wellness and other important factors allowing to clarify the problems raised by this report.
SUMMARY
The Panel is in unanimous agreement on the need to relate health and safety questions to total
fluoride intake, not just to one source such as drinking water. We were also in unanimous
agreement that the optimum concentration of fluoride in treated water should be reduced, because
the total fluoride intake is now higher than it was when the optimum level was set at 1.0 ppm.
SUMMARY - MAJORITY OPINION
The Panel has found no new scientific evidence on the health and safety effects of fluoridation of
Calgary's water which would support a substantial change to current policy. This conclusion was
reached by applying the review criteria, which were established in the Terms of Reference, to the
materials submitted to the Panel and to the information obtained during the work of the Panel
members.
The Panel agrees that there are documented health benefits, in the control of tooth decay, from the fluoridation of water. Water fluoridation is a safe and inexpensive mechanism to improve the health of Calgarians, especially the 25% with lowest incomes, who can least afford alternatives. The Panel also notes that some other means of providing protection from tooth decay are more likely to lead to inadvertent ingestion of high fluoride doses, particularly when young children swallow toothpaste containing high concentrations of fluoride. The relative health benefits are now less than they were forty years ago, because of other sources of fluoride in the diet, better oral hygiene and better dental procedures, as well as a general improvements in overall health. However, these other improvements have not reduced the benefits of water fluoridation to the point where it is no longer needed.
Dental fluorosis occurs when total fluoride ingested is too high during the formation of enamel on children's teeth. Because the total intake of fluoride from all sources is increasing, more fluorosis is being observed although much of it is of the mild forms, which are only apparent to the trained eye or upon very close inspection. The Panel recommends that health authorities pay more attention to identifying uncontrolled sources of fluoride, especially intake due to children swallowing high fluoride toothpaste. Reducing uncontrolled sources of fluoride would be a more effective means of reducing dental fluorosis than eliminating fluoridation of water.
The scientific literature on fluoride and bone fractures, especially hip fractures in the elderly, did not provide evidence that would lead to substantial changes in water fluoridation policy. Questions about exercise and activity, calcium and vitamin D intake, overall health status, other sources of fluoride, use of other medication, and general standards of osteoporosis medical practice in the studied communities have to be addressed before the results of the inconclusive epidemiological studies can be confirmed.
From the perspective of epidemiology and toxicology, the available scientific literature has not substantiated the claims that water fluoridation was a factor in other adverse health effects. The results found in the literature have not eliminated the need for further research. Carefully designed studies, which take into account total fluoride intake and all other relevant factors, are required. There is no need for or value in further studies which attempt to relate water fluoridation per se to adverse health effects.
Although there is considerable literature on the effects of fluoride, many of these studies were related to high dose toxicity or to the effects of high therapeutic doses. Studies at these high levels were not considered relevant by the Panel.
The scientific literature has not revealed significant health concerns about fluoride at currently estimated levels of intake. However, there are legitimate health concerns about higher levels of total intake, which are not generally associated with fluoridated water but are due to other sources which increase the total intake above safe levels.
Fluoride is a natural component of soils and water. In the Calgary region, there are no large active industrial sources. Such industrial sources have produced environmental problems in other parts of Canada. Because of the carbonate base for our soils and the hard water in our surface and ground water, environmental concerns are lower relative to areas with soft water and acid soils.
The Panel is pleased to note that Alberta Environmental Protection has recommended that the optimum level of fluoride in treated water has been reduced from 1.0 mg/L (1 ppm) to 0.8 mg/L (0.8 ppm). A similar reduction has been made in other jurisdictions and reflects the recognition that total fluoride intake has increased since the standard was first established.
The fact that these issues have been articulated for more than 50 years, and have received a good deal of study, suggests that if there are cause and effect relationships between water fluoridation and adverse health effects, they are small and very complex. Otherwise, more substantial results would have been achieved by the studies undertaken to date. Although there are recommendations for further research, the results of which would have made this Panel's work easier, the absence of that work did not substantially affect the Panel's conclusions.
RECOMMENDATIONS - MAJORITY OPINION
The Panel recommends that the City of Calgary reduce the concentration of fluoride in treated
water to 0.7 ppm. (This is basically compatible with the similar recommendation in the dissenting
section.)
With respect to fluorosis, the Panel recommends that health authorities provide more advice on control of total intake in young children, especially from dental products.
The Panel recommends that carefully designed studies of the possible adverse health effects of
total fluoride intake, which consider other relevant factors (diet, health status, vitamin and mineral
intake, other medication, etc.), be undertaken. The Panel recommends that health authorities
undertake careful studies of total fluoride intake, with particular emphasis on identifying
significant possible sources high in fluoride, and effective means of reducing exposures.
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Reports:
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- Edmonton Board of Health, Annual Report, 1985
- Environment Canada, Priority Substances List Canadian Environmental Protection Act, (CEPA), 1993.
- Environment Canada & Health Canada, Inorganic Fluorides, Canadian Environmental Protection Act, 1993.
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- Health and Welfare Canada, Guidelines for Canadian Drinking Water Quality, Sixth Edition, 1996.
- Health Unit Association of Alberta, Report of the Second Alberta Dental Health Survey, 1985, 1987.
- Hoover, R.N. et al. 1990: Fluoridation of drinking water and subsequent cancer incidence and mortality. National Cancer Institute.
- Institute of Medicine, Dietary Reference Intakes, Calcium, Phosphorus, Magnesium, Vitamin D, and Fluoride, National Academy of Sciences, 1997.
- Kelman, A.M. Fluoridation - the Israel experience.
- National Cancer Institute, Fluoridation of drinking water and subsequent cancer incidence and mortality, 1990.
- National Health and Medical Research Council, Effectiveness of Water Fluoridation, Australian Government Publishing Services, Canberra, 1991.
- National Institutes of Health, Toxicology and Carcinogenesis Studies of Sodium Fluoride in Rats and Mice, US Department of Health and Human Services, Public Health Service, 1990.
- National Research Council, Health Effects of Ingested Fluoride, National Academy Press, Washington, 1993.
- National Toxicology Program, Toxicology and Carcinogenecity Studies of Sodium Fluoride in F 344/N Rats and B 6C3F Mice. Technical Report Series No. 393, 1990.
- New Jersey Department of Health, An Epidemiologic Report on Drinking Water and Fluoridation, prepared by B. Siegel for Environmental Health Service, November 1992.
- Standards and Guidelines Branch, Fluoride, Alberta Environmental Protection, Environmental Assessment Division, August 1996, edited February, 1997.
- US Department of Health and Human Services, Toxicological Profile for Fluoride, Hydrogen Fluoride, and Fluoride, PB93-182566, Agency for Toxic Substances and Disease Registry, 1993.
- Water Sciences Branch, Long term trend analyses of dissolved fluoride. Alberta Environmental Protection, Natural Resources Service, 1998.
- Working Group on Fluorides, Fluoride Ingestion from Dental Products, prepared by R.C. Burgess, 1993.
- World Health Organization, Fluorides and Oral Health: Report of a WHO Expert Committee on Oral Health
Status and Fluoride Use, WHO Technical Report Series 846, Geneva, 1994.
Videotapes:
- Dr. Colquhoun's Presentation, February 25, 1998, Length: 1:16:30.
- Dr. Dawes' Presentation, February 11, 1998, Length: 1:45:00.
- "Don't swallow your toothpaste" with Drs. Paul Connet & Phyllis Mullenix. 2 parts, June 19, 1997. Cannel 4 -UK, Fulcrum/Daylight Health Alert.
TERMS OF REFERENCE - EXPERT PANEL FOR WATER FLUORIDATION REVIEW
BACKGROUND
At a recent meeting of the Standing Policy Committee on Operations and Environment some technical
reports on water fluoridation were presented by private citizens. The Committee then resolved, along with
Calgary Regional Health Authority, to have an independent and expert review of this and other recent
information. The ultimate purpose of such a review is to advise whether water fluoridation is still a
desirable public health policy in light of current data or risk/benefit studies. The Committee would then be
assisted in its deliberation and subsequent reporting to City Council over the advisability of a 1998
plebiscite on the continuation of fluoridation of Calgary's drinking water supply.
Waterworks Division is involved in the fluoridation issue only as a purveyor, giving sole attention to the proper operation, monitoring and compliance of the fluoridation process. Thus, it has been directed by the Operations and Environment Committee to assume the role of coordinating and organizing an independent and unbiased panel of experts. Waterworks approached various maturity and independence of university researchers were considered important assets for prospective panel members. an adequate expertise profile to address technical issues of health and safety was sought. An effort was made to exclude mission oriented candidates (either strongly pro-fluoridation or strongly anti-fluoridation).
LIST OF PANEL MEMBERS (PERSON, EXPERTISE/ROLE
- Professor Dixon Thompson, CHAIRMAN, Water pollution and environmental effects, Chemistry, University of Calgary, Faculty of Environmental Design
- Professor Hossein Joe Moghadam, Community Health, Pediatrics, Epidemiology, University of Calgary, Faculty of Medicine
- Professor Sheldon Roth, Toxicology, Pharmacology, Therapeutics, University of Calgary, Faculty of Medicine
- Professor Miloslav Nosal, Biological and environmental statistics, Health related risk assessment, University of Calgary, Faculty of Science
- Professor David Hanley, Endocrinology, University of Calgary, Faculty of Medicine, Bone disorders, Calcium metabolism
PANEL RESOURCE CONTACTS:
Dr. Read Seidner, Laboratory Superintendent, Waterworks Division
Dr. Richard Musto, Deputy Medical Officer of Health, Calgary Regional Health Authority
PANEL FUNCTIONALITY
1. The panel will report jointly to the Standing Committee on Operations and Environment-City of Calgary and to
the Quality Care Committee-Calgary Regional Health Authority. Ongoing progress reports to Waterworks
Division and Calgary Regional Health Authority is to be maintained by the panel chairman.
2. Work is to commence as soon as possible and completed by a presentation to Operations and Environment Committee. Prior to that a written brief is to be submitted to Waterworks Division and Calgary Regional Health Authority. The panel chairman is responsible to verbally present the panel's findings to the Standing Committee on Operations and Environment.
3. The focus of effort will be on literature produced since 1989. Literature additional to already received submissions will be sought through newspaper ads or may be provided by expert panel members. Verbal presentations at the panel's invitation only may be sought. If such are sought, then effort will be made to include equal opportunity from both sides.
4. Standard scientific criteria as to evaluating the pertinence of reports and studies will be employed. Methodology employed by the Canadian Task Force on the Periodic Health Examination will serve as a model. The panel will decide its own process of dividing up submitted literature.
5. All costs will be split equally by Calgary Regional Health Authority and Waterworks Division. Secretarial and library search assistance will be provided to the panel. The panel is to assess additional resources needed once all submissions are received.
DEADLINE DATES
Deadline for public submissions - December 12,
Submit written brief to Waterworks and Calgary Regional Health Authority - March 23,
Presentation to Operations and Environment Committee - April
SUMMARY OF MATERIAL RECEIVED FOR FLUORIDE REVIEW PANEL: March 9, 1998
-
LETTERS TO THE CITY
- Lancaster, letter to Mayor, September 5, 1997
- Schatz, letter to Jones, September 8, 1997
- Connett, letter to Jones, September 8, 1997
- Mullenix, letter to Jones, September 9,1997
- Foulkes, letter to Jones, September 9, 1997
- Schatz, cover letter to Waterworks, November 25, 1997
- Friesen, cover letter to Seidner, November 28, 1997
- Foulkes, letter to Waterworks attn. Seidner, December 8, 1997
- Stoeckle, cover letter to Waterworks, December 10, 1997
- HANS Health Action Network Society (1984), letter to Mayor and Council, December 10, 1997
- Olson, note to Waterworks with copy to Hawkesworth, undated
- Mansfield, e-mail to Seidner, December 11, 1997
- Health Action Network Society (Alberta), letter to Mayor and Council, December 11, 1997
- Health Action Network Society (Alberta), cover letter to Seidner, December 12, 1997
- Cholette, letter to Seidner, December 12, 1997
- Friesen, letter to Seidner, December 12, 1997
- Lord, letter to Vennard and response, January 27, 1998
- Dawes, response to panel questions, January 29, 1998
- Health Action Network, letter to Seidner and panelists, February 9, 1998
- Health Action Network, letter to Seidner and panelists, February 10, 1998
- Colquhoun, response to panel questions, February 13, 1998
- Carsted, letter to Bronconnier, February 25,1998
- Calgarians for Choice (Val Fitch), letter to Mayor and City Council, February 25
- Health Action Network, letter to Seidner. March 3. 1998
- STATEMENTS, MAGAZINE ARTICLES & LETTERS
- Babiuk, Scientists take stand against fluoridation, blue cover summary, September 10, 1997
- Burgstahler, Summary statement on water fluoridation, September 9, 1997
- Babiuk, Another fluoridation plebiscite? Strong health advisory? Or, stop it now?, September 1997
- Babiuk, DMFT statistics (Calgary and Edmonton) and errata, November 25, 1997
- Susheela, Fluorosis control cell, September 24, 1996
- Hirzy, National association of federal employees, July 2, 1997
- Diesendorf, Submission to the City of Calgary's panel on fluoridation, November 23, 1997
- Schatz, Low-level fluoridation and low-level radiation: two case histories of misconduct in science,
- 1996
- Lee, Summary of the Calabrese report to East Bay Municipal Utility District, 1991
- webpage, Why thinking people oppose fluoridation, 1997
- webpage, America: over-dosed on fluoride, 1997
- webpage (Hitchcock) Fluoride, 1996, submitted by Stockle
- Sibbison, USA: More about fluoride, letter in Lancet, 1990
- Friesen, Health of the Calgary Region 1997,
- Is fluoride good for you?, summer 1992
- Connett, The fluoridation of drinking water: a house of cards waiting to fall. Part 1: The Science,
- 1996
- Foulkes, Celebration or shame? Fifty years of fluoridation (1945-1995), 1995
- Babiuk, Against fluoridation, undated
- Chinniah (AEP), Status of Canadian fluoride regulation, October 23, 1997.
- Flaherty, letter, 1979.
-
RESUMES
- Schatz
- Mullenix
- Connett
- Foulkes
- Richardson
- Dawes
- Colquhoun
Background briefs on Connett, Mullenix, Schatz, Foulkes, Hirzy and Burgstahler
-
GOVERNMENT PUBLICATIONS
- Priority substances list assessment report: Inorganic fluorides, 72 pp., CEPA, 1993
- Preparing the second priority substances list: response to stakeholders' comments, 17 pp., CEPA, 1994
- Review of fluoride benefits and risks, 134 pp. + append., USPHS, 1991
- The effectiveness of water fluoridation, 193 pp., Australia Government Public Service, 1991
- Public Health Service report on fluoride benefits and risks, USPHS, 1991
- Guidelines for Canadian Drinking Water Quality, excerpts from 6he ed., Health Canada, 1996
- Fluorides and oral health, WHO, 1994
-
REPORTS TO GOVERNMENTS & AUTHORITIES
- Cohn, An epidemiological report on drinking water and fluoridation,New Jersey Department of
- Health
, 1992
- Calabrese, Evaluation of the national toxicology program (NTP) cancer bioassay on sodium fluoride, East Bay
- Municipal Utility District, 1991
- Mancuso, Should Natick fluoridate?, Town of Natick, Maine, 1997
- Lewis, Investigation of inorganic fluoride and its effect on the occurrence of dental caries and dental fluorosis in Canada, 1993 (draft only)
-
PUBLISHED REVIEWS & REPORTS
- Schatz, The importance of paradoxical effects of fluoride with respect to fluoridation and the toxicology of fluoride, 1964
- Diesendorf, New evidence on fluoridation, 1997
- Dietary reference intakes, VIII, fluoride, in press
- Fejerskov, The nature and mechanisms of dental fluorosis in man, 1990
- Whitford, The physiological and toxicological characteristics of fluoride, 1990
- Cantor, Drinking water and cancer, 1997
- Challacombe, Does fluoride harm the immune function?, 1996
- Cook-Mozaffari, Cancer and fluoridation, 1996
- Hargreaves, Water fluoridation and fluoride supplementation: considerations for the future, 1990
- Hinman, The US experience with fluoridation, 1996
- Horowitz, The future of water fluoridation and other systemic fluorides, 1990
- Horowitz, The effectiveness of community water fluoridation in the United States, 1996
- Kelman, Fluoridation-the Israel experience, undated
- Lewis, Water fluoridation: current effectiveness and dental fluorosis, 1994
- Loh, Thirty-eight years of water fluoridation-the Singapore scenario, 1996
- Newbrun, Effectiveness of water fluoridation, 1989 (see also letter to editor by Colquhoun)
- Newbrun, Current regulations and recommendations concerning water fluoridation, fluoride supplements and topical fluoride agents, 1992
- Newbrun, The fluoridation war: a scientific dispute or a religious argument?, 1996
- Pendrys, Risk of fluorosis in a fluoridated population, 1995
- Raheb, Water fluoridation, bone density and hip fractures: a review of recent literature, 1995
- Riordan, Dental caries and fluoride exposure in western Australia, 1991
- Ripa, A Half-century of community water fluoridation in the United States: review and commentary, 1993
- Spencer, Water fluoridation in Australia, 1996
- Stockwell, Dental caries experience in schoolchildren in fluoridated and non-fluoridated communities in western Australia, 1990
- National Research Council, Health effects of ingested fluoride, 1993
- Hrudey, Drinking water fluoridation and osteocarcoma, 1990
- Hileman, Fluoridation of Water, 1988
- Foulkes, review of Investigation of inogranic fluoride and its effects on the occurrence of dental carries and dental fluorosis in Canada-final report, (1995)
- Colquohoun, Why I changed my mind about water fluoridation, 1997
-
PUBLISHED RESEARCH JOURNAL ARTICLES
- Diesendort, New evidence on fluoridation, 1997
- Mullenix, Neurotoxicity of sodium fluoride in rats, 1995
- Schatz, Increased death rates in Chile associated with artificial fluoridation of drinking water with implications for other countries, 1976
- Colquhoun, Child dental health differences in New Zealand, 1987
- Colquhoun, Influence of social class and fluoridation on child dental health, 1985
- Colquhoun, Flawed foundation: a re-examination of the scientific basis for a dental benefit from fluoridation, 1990
- Dieseldorf, The mystery of declining tooth decay, 1986
- Freni, Exposure to high fluoride concentrations in drinking water is associated with decreased birth rates, 1994
- Johnston, The decline of dental caries in Ontario school children, 1986
- Danielson, Hip fractures and fluoridation in Utah's elderly population, 1992
- Jacobsen, The association between water fluoridation and hip fracture among white women and men aged 65 years and older, 1991
- Jacobsen, Regional variation in the incidence of hip fracture, 1990
- Sowers, A prospective study of bone mineral content and fracture in communities with differential fluoride exposure, 1990
- Aardema, Sodium fluoride-induced chromosome aberrations in different stages of the cell cycle: a proposed mechanism, 1989
- Smith, Is fluoridation a fraud? 1988
- Jones, Sodium fluoride promotes morphological transformation of Syrian hamster embryo cells, 1988
- Tsutsui, Sodium fluoride-induced morphological and neoplastic transformations, chromosome aberrations, sister chromatid exchanges, and unscheduled DNA syntheses in cultured Syrian hamster embryo cells, 1984.
- Brown, The effect of fluoride consumption and social class on dental caries in 8-year-old children, 1990
- Hillier, Water fluoridation and osteoporotic fracture, 1996
- Murray, Efficacy of preventative agents for dental caries, 1993
- Pendrays, Relationship of total fluoride intake to beneficial effects and enamel fluorosis, 1989
- Suarez-Almazor, The fluoridation of drinking water and hip fracture hospitalization rates in two Canadian communities, 1993
- Cauley, Effects of fluoridated drinking water on bone mass and fractures: the study of osteoporotic fractures, 1995.
- Arnold, The effect of water fluoridation on the bone mineral density of young women, 1997.
- Dawes, Kinetics of fluoride in the oral fluids, 1990
- Heller, Denatal caries and dental fluorosis at varying water fluoride concentrations, 1997
- Kunzel, Rise and fall of caries pervalence in German towns with different F concentrations in drinking water, 1997
- Tohyama, Relationship between fluoride concentration in drinking water and mortality rate from uterine cancer in Okinawa Prefectury, Japan, (1996)
- Murray, Fluorice therapy for osteoporosis, (1996)
- Herbison/Dieseldorf/Webb/Jackman/Durham, Letters and replies in ANZJPH, (1997-98)
- Colquhoun, Influence of social class and fluoridation on child dental health, (1985)
- Alhava, The effect of drinking water fluoridation on the fluoride content, strength and mineral density of human bone, (1980)
- Arnala, Effects of fluoride on bone in Finland, (1985)
- Tarja, Effect of drinking water fluoridation on the fluoride content of human bone in and around Kuopio,
- Central Finland. An analytical study
, (1976) - Sogaard, Marked decrease in trabecular bone quality after five years of sodium fluoride therapy, (1994)
- Turner, Fluoride treatment increased serum IGF-1, bone turnover and bone mass, but not bone strength, in rabbits, (1997)
- Turner, High fluoride intakes cause osteomalacia and diminished bone strength in tats with renal deficiency, (1996)
- Frantzl, Abnormal bone mineralization after fluoride treatment in osteoporosis: a small angle x-ray scattering study, (1994)
- Papadimitropoulos, Current and projected rates of hip fractures in Canada, (1997)
- Chrischilles, Costs and health effects of osteoporotic fractures, (1994)
- TEXTBOOK MATERIAL
- Green, Dental public health
Rozier, Dental public health
Kimmelman, Fluoride: is there a limit?, 1995
- Lewis, Periodic health examinations, 1995 update: prevention of dental caries, 1995
- Landis, Fluoride chapter in Introduction to environmental toxicology-impacts of chemicals upon ecological systems Whitford, The metabolism and toxicity of fluoride, 1996
-
CONFERENCE PRESENTATIONS & DISCUSSIONS
- Hill, Fluoride: risks and benefits? Disinformation in the service of big industry, 1992
- Marcus, Memorandum on fluoride conference to review the NTP draft fluoride report,1990
- Pollick, The effect of fluoride concentrations of water supplies on caries experience in California children attending preschools and grades K-3, 1997
- Stephen, Rational use of fluorides in prevention and therapy, 1990
- Whitford, Metabolism of fluoride
-
OTHER MATERIAL
- Babiuk, Crest toothpaste label
- Babiuk, photo of mottled teeth
- Babiuk, home page address for background material
- Friesen, fluoridation bibliography, 4 pp., November 27 1997
- Babiuk, abstracts of fluoride studies, 10 pp., December 7, 1997
- Babiuk, abstracts of fluoride studies, 12 pp., December 10, 1997
- Babiuk, abstracts of fluoride studies, 16 pp., December 12, 1997
- Babiuk, fluoride bibliography, 5 pp., December 12, 1997
- Babiuk, photocopies of table of contents of Fluoride
- Babiuk, loan of 1990 to 1997 issues of Fluoride
- Stoeckle, 6 abstracts
- Friesen, list of contacts on fluoridation
- Friesen, fluoridation bibliography, 2 pp. December 12, 1997
- Babiuk, videocassettes (5) Don't swallow your toothpaste, British TV, 1997
- Alberta Environmental Protection, 1995 Surface water quality data tabulation
CHRA, handout on toothpaste.
- Table of fluoridation status in B.C. communities
- Summary of Natick fluoridation study committee
- Summary of letters to Calgary Herald editor
- Calgary Waterworks, Finished water fluoride analysis daily results for 1997
- City of Calgary, Sewage effluent fluoride levels, 24 hourly sampling in 1998 and 3 samplings in 1995
- Clippings from Kamloops
- Medline abstracts 1998 to 1993
- Babiuk, e-mail forward of Precautionary Principle
- Calgary Waterworks, H2SiF6 analyses
- Calgary Waterworks, Finished water analysis summary
- Calgary Waterworks, Calcium and magnesium analysis summary for 1997
- Yu, Goals and objectives of ISFR
- Chinniah (AEP), Supporting documentation for fluoride standard
- Whitfield, Anabolic treatments for osteoporosis (abstract), (1997)
- Dawes, interview (videocassette)
- Colquhoun, interview (videocassette)
- Colquhoun, dental statistics form
- Medical Council of Canada Newsletter, Fluoride,: good for your bones?