Abstract from Nephron 78 (1) 96-103 1998

This study was conducted to test the hypothesis that the margin of safe fluoride exposure is narrowed in rats that are physiologically compromised by renal dysfunction. The study objective was to determine whether increases in fluoride retention and tissue fluoride levels in rats with surgically induced renal insufficiency result in toxic fluoride effects not ordinarily observed in healthy animals. Uremic and sham-operated control rats received 0 µg/ml, 5 (0.26 mmol/l), 15 (0.79), or 50 µg/ml (2.63 mmol/l) of fluoride in their drinking water for 3 or 6 months. Fluoride retention was monitored, and, following euthanasia, tissue fluoride and biochemical markers of tissue function were analyzed. Selected tissues were saved for histology, and bone marrow cells were harvested for determining the frequency of sister chromatid exchange, a marker of genetic damage. In spite of significantly higher levels of fluoride in the tissues of the animals with renal insufficiency, there were no clinically adverse, fluoride-induced, extraskeletal, physiological, biochemical, or genetic effects of chronic exposure to common levels of fluoride in these rats.

Key words: Fluoride metabolism; Fluoride toxicity; Rats; Renal insufficiency.

Reprints: A Dunipace, Oral Health Research Institute, 415 Lansing Street, Indianapolis, IN 46202, USA.

COMMENT

Many studies from the same source have supported the safety of fluoridated water. The authors' position is made clear in the first sentence of their Introduction, which states: "Fluoride is widely used for its beneficial effect in reducing dental caries, . . ." and then states of 1 ppm fluoridated water, citing a 1993 review of the US National Research Council: "under normal conditions it does not cause adverse effects." After reading the full study, I make the following observations:

1) The experiment occupied periods of 3 and 6 months, so is hardly relevant to human populations consuming fluoridated water, as the authors claim.

2) There was a high mortality rate (up to 45%) among the treated groups, clearly a result of the surgery to which the rats were subjected. Although the authors concluded that "there was no association between the level of fluoride exposure and mortality rate", the possibility that the rats more susceptible to surgical trauma might also, had they survived, been more susceptible to non-skeletal effects of fluoride, does not appear to have been considered.

3) The brain tissue of the rats was not examined. Possible neurotoxic effects were not looked for.

It is interesting to compare these authors' findings with those of other studies, e.g. the Brazilian one the abstract of which was published in the last issue of Fluoride ( 31 100-101 May 1998). Over 40 years ago both skeletal and non-skeletal adverse effects on rats fed low levels of sodium fluoride were reported (Ramseyer WF, Smith CAH, McCay CM. Effect of sodium fluoride administration on body changes in old rats. Journal of Gerontology 12 (1) 14-19 1957), but the experiment occupied a longer period of time (520 days) than the Dunipace et al study discussed above.

John Colquhoun

FLUORIDE 31(3) 1998,  pp 151	International Society for Fluoride Research
	Home | Table of Contents | ISFR Board | Subscription Submissions | Announcements | Authors | Subject Index