1998, pp 166-169
| FLUORIDE 31(3) 1998, pp 166-169 |
International Society for Fluoride Research | Table of Contents |
|
In our article 'New Evidence on Fluoridation' we referred to recently published comprehensive data which indicate an association between fluoridation and damage to bone (hip fracture, skeletal fluorosis and possibly osteosarcoma).1 We pointed out the limitations of some other studies which reported no such association. We then drew attention to other relevant studies which support a causal explanation for the association.
We reject the charge levelled at us in the June issue by Herbison, and by Webb and Donald, that we cited only studies which support our view.2,3 That charge is more fairly directed at the extensive pro-fluoridation literature. For example, Webb and Donald in their submission supporting fluoridation of Brisbane's water supply, excluded any mention, in either their text or their reference list, of the fact that fluoride accumulates in bones and reaches levels consistent with widely recognised adverse effects - an important aspect of causality which we note they also omit in their attempt to criticize our article.4 They likewise excluded all studies reporting harm from fluoride published in Fluoride, journal of the International Society for Fluoride Research. They also did not cite a single original paper reporting skeletal fluorosis in areas naturally fluoridated at concentrations between 0.7 and 2.5 parts per million. A 1990 review by one of us (MD)5 examined nine such papers from five countries.6-14 That information is very relevant to the issue of causality.
Our lengthy reference list could not possibly include all published studies, but cited representative ones, which is the usual convention. We also did not cite a recent paper reporting a positive correlation between fluoridation and hip fractures, which supported our assessment.15
Our critics seem to hold a naive belief that conclusions can be based on the quantity, rather than the quality, of published papers on controversial issues. They list studies that, in their view, counterbalance the comprehensive data on which we based our conclusion that fluoridation should be discontinued. Such publications do not nullify the compelling evidence of harm represented by the comprehensive data we reviewed. In any case, even if the evidence is conflicting, so that conclusions remain in dispute, the precautionary principle is itself grounds for discontinuing the mass uncontrolled fluoride dosing of entire populations.
We wonder why our critics do not apply the same stringent requirements for proof of causality that they seem to apply to evidence of harm from fluoride to the many flawed studies claiming a fluoride dental benefit. At the Brisbane Lord Mayor's Taskforce on Fluoridation, Professor Donald was asked that question and replied that he had not examined the fluoridation studies because he had never been asked to. We wonder how many other professors at medical schools continue to advocate fluoridation without examining the evidence for it.
An examination of the quality of some of the studies our critics cite to support their case is revealing. They include two studies, which their authors claim suggest that fluoride may be protective against the rare bone cancer, osteosarcoma (which we pointed out has increased among young males aged 9 to 19 years in fluoridated areas of America, but not in unfluoridated areas).16,17 One of these studies, from the dental literature, was based on only two cases, of unstated age and sex, who spent more than a third of their life or childhood in a fluoridated area, and seven cases, also of unstated age and sex, who spent less than a third of their life or childhood in a fluoridated area.16 In the other study, which appeared to suggest a protective effect from fluoride, the study design was based on an assumption that osteosarcoma victims would require (if ingested fluoride was the cause) higher fluoride exposure than those without the disease.17 The possibility that such victims might be more susceptible to equal or smaller fluoride exposures was not considered. A critical review of that report was not cited by our critics.18
Other studies they cited do not, on close examination, support their claim of no fluoride/osteosarcoma link.19-21 For example, Hrudey et al. admitted that their data from small populations 'do not allow any definitive conclusions about the role of fluoridation as a risk factor for osteosarcoma in humans'.19 The claim of Mahoney et al., of no difference in bone cancer incidence between fluoridated and unfluoridated areas of New York State, can be disputed on the grounds that the authors failed to consider male rates separately.20 The Moss et al. study did not calculate the water fluoride-osteosarcoma association for 10- to 19-year-old males, the age- sex group for which the association has been reported.21 It combined both sexes for its two age groupings (under and over 45 years) and combined all ages for its female and male calculations.
Two studies that they described as 'ecological' were claimed by Webb and Donald to show no osteosarcoma-fluoride association.22,23 The first, a letter to editor by Cook-Mozaffari et al., simply expressed the same opinion of our critics, and presented no new evidence.22 The other does not deal with osteosarcoma at all, but reported instead that water fluoride reduces human male fertility.23
Another study, claimed by Herbison to counteract our observations on a possible fluoride/osteosarcoma link, is a very good study by an eminent researcher and his associates, but is irrelevant to this discussion because it deals with male and female adult workers exposed to fluoride, not with young males growing up in fluoridated areas.24
Other studies discounting an association between fluoride and hip fracture (for example, that of Jacobsen et al. 199325) are of doubtful value because, as we pointed out in our article (citing a review26), many are of small samples or the women were not exposed to fluoride before menopause. The same applies to the more recent Cauley et al. study: of the 41 hip fracture cases aged 65 or over, only four had lived more than 10 years in a fluoridated area.27 The study by Suarez-Almazor et al. compared one fluoridated and one unfluoridated Canadian city.28 It is true that this study did not find more hip fractures in women in the fluoridated area, as other studies have done. However, it did find significantly more hip fractures in men in the fluoridated city. The authors of another recent study cited by our critics (Karagas et al.), stated: 'Our findings with respect to water fluoridation have important limitations, however'.29 These limitations included: 'Fluoride exposure was assessed at the time of fracture and thus does not necessarily reflect exposure during what may have been a more relevant time period (for example, during peak bone formation)'.
The recent Finnish study which our critics cited reported no differences in the prevalence of female fractures in its fluoridated and nonfluoridated groups, and slightly higher (1 to 2.6 per cent) bone mineral density in women exposed to fluoride for more than 25 years.30 However, the fluoride-exposed women were younger, more physically active, and more likely to use hormone replacement therapy.
Our other critics, Pat Jackman of the Dental Association and Gillian Durham of the New Zealand Ministry of Health, objected to our views even being published, but added nothing of substance to the debate.31,32 However, we thank our critics for contributing and hope the debate continues in a scholarly manner.
Mark Diesendorf
Institute for Sustainable Futures
University of Technology, Sydney
John Colquhoun
Honorary Research Fellow, School of Education
University of Auckland
Bruce Spittle
Department of Psychological Medicine
University of Otago Medical School, Dunedin
References
| FLUORIDE 31(3) 1998, pp 166-169 |
International Society for Fluoride Research |  |
|
Home |
Table of Contents |
ISFR Board |
Subscription Submissions | Announcements | Authors | Subject Index |