- Exposure models can predict toxic effects of fluoride consumption in wildlife.
- Exposure models that vary in intensity of field data collection warrant comparison.
- Simple spatial metrics can predict fluoride accumulation in a free-ranging mammal.
- Complex exposure models may not perform better than simple spatial metrics.
Vegetation contaminated by industrial fluoride emissions can cause disease in herbivorous mammals. Spatially explicit exposure models offer a quantitative approach for evaluating and managing the potentially toxic effects of chronic fluoride consumption on wildlife. We monitored eastern grey kangaroos (Macropus giganteus) inhabiting a high-fluoride environment in the buffer zone of an aluminium smelter in southeastern Australia between 2010 and 2013. We measured fluoride levels at 19 pasture sites and determined the foraging range of 37 individual kangaroos. A series of generalised linear models were developed to estimate bone fluoride accumulation as a function of pasture exposure. Model outputs were compared to identify the most appropriate predictive tool for kangaroo bone fluoride accumulation relative to exposure. Accounting for age there was a negative association between bone fluoride concentration and distance of the central emission point from both the mean centre of foraging range and the point of death. The mean foraging range centre was the best predictor, with point of death just as suitable (and simpler), whereas more complex parameters such as monthly and cumulative fluoride exposure were poor predictors of bone fluoride concentration. The more complex dietary fluoride exposure estimates did not improve predictive capability compared with the simple, spatial models. We conclude that in actively managed wildlife populations, simple, locally validated models can provide estimates of bone fluoride accumulation sufficient to support decision-making.
Association between fluoride, magnesium, aluminum and bone quality in renal osteodystrophy
INTRODUCTION: Trace elements are known to influence bone metabolism; however, their effects may be exacerbated in renal failure because dialysis patients are unable to excrete excess elements properly. Our study correlated bone quality in dialysis patients with levels of bone fluoride, magnesium, and aluminum. A number of studies have linked
Fluorine and Fluorosis [June 1944].
Excerpt The first account of mottled enamel in human beings was given in 1902 by Eager of the United States Public Health Service who noticed its frequency among Italian emigrants from Naples. Black and McKay (1916) found it occurring in various parts of the U.S.A. and described it more fully in
Effects of supplementation with conjugated dienes of linoleic acid on fluoride, calcium, and magnesium levels in hard tissues and serum of mice.
With the recognition of their ability to promote weight loss, conjugated dienes of linoleic acid (CLA) have become the main ingredient of certain dietary supplements to counteract obesity. The results of prospective studies, however, indicate there may be long-term side effects that could be of key importance for the safety
Renal osteodystrophy in patients on long-term hemodialysis with fluoridated water
Serum and bone fluoride concentrations of ten patients maintained on long-term hemodialysis with fluoridated water (1 ppm, i.e., 50uM) were correlated with duration of treatment and the occurrence of clinical, radiological, and histological manifestations of bone disease. Two patients had symptomatic renal osteodystrophy when accepted on the program, whereas six
Silencing GSK3ß instead of DKK1 can inhibit osteogenic differentiation caused by co-exposure to fluoride and arsenic.
Highlights Wnt signaling is involved in the osteogenic differentiation caused by co-exposure to F and As. Silencing GSK3ß can inhibit osteogenic differentiation caused by co-exposure to F and As. Silencing DKK1 cannot inhibit osteogenic differentiation caused by co-exposure to F and As. The interaction between F and As of the
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Factors which increase the risk for skeletal fluorosis
The risk for developing skeletal fluorosis, and the course the disease will take, is not solely dependent on the dose of fluoride ingested. Indeed, people exposed to similar doses of fluoride may experience markedly different effects. While the wide range in individual response to fluoride is not yet fully understood, the following are some of the factors that are believed to play a role.
Nutrient Deficiencies Enhance Fluoride Toxicity
It has been known since the 1930s that poor nutrition enhances the toxicity of fluoride. As discussed below, nutrient deficiencies have been specifically linked to increased susceptibility to fluoride-induced tooth damage (dental fluorosis), bone damage (osteomalacia), neurotoxicity (reduced intelligence), and mutagenicity. The nutrients of primary importance appear to be calcium,
Unheeded Warnings: Government Health Authorities Ignore Fluoride Risk for Kidney Patients
Despite the well known fact that individuals with kidney disease are at much higher risk of fluoride toxicity than the general population, there has yet to be any attempt in the United States, or any other country that practices mass-scale water fluoridation to determine the prevalence of fluoride-related effects (e.g.,
Annapolis: Water Fluoridation Linked to Death of Dialysis Patient
EVENING CAPITAL (Annapolis, Maryland) November 29, 1979 Fluoride Linked to Death by Mary Ann Kryzankowicz Staff Writer Fluoride poisoning has been definitely linked to the death of a 65-year-old kidney dialysis patient who became ill during a blood cleaning process Nov 11. State Medical Examiner Dr. (illegible) Guard has ruled that Lawrence Blake, 65, of Arundel
Mayo Clinic: Fluoridation & Bone Disease in Renal Patients
The available evidence suggests that some patients wtih long-term renal failure are being affected by drinking water with as little as 2 ppm fluoride. The finding of adverse effects in patients drinking water with 2 ppm of fluoride suggests that a few similar cases may be found in patients imbibing 1 ppm, especially if large volumes are consumed, or in heavy tea drinkers. The finding of adverse effects in patients drinking water with 2 ppm of fluoride suggests that a few similar cases may be found in patients imbibing 1 ppm, especially if large volumes are consumed, or in heavy tea drinkers and if fluoride is indeed the cause. It would seem prudent, therefore, to monitor the fluoride intake of patients with renal failure living in high fluoride areas.
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