- 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
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
Non-Endemic Skeletal Fluorosis: Causes And Associated Secondary Hyperparathyroidism (Case Report and Literature Review).
Highlights Fluorocarbon “huffing” is an under-appreciated cause of skeletal fluorosis (SF) We present a SF case with hyperparathyroidism, osteosclerosis, and osteomalacia SF may go undetected due to variation in symptoms, radiology, and biochemistry Dietary calcium, prior bone health, and skeletal F exposure influence SF features SF is common in
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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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,
Skeletal Fluorosis & Individual Variability
One of the common fallacies in the research on skeletal fluorosis is the notion that there is a uniform level of fluoride that is safe for everyone in the population. These "safety thresholds" have been expressed in terms of (a) bone fluoride content, (b) daily dose, (c) water fluoride level, (d) urinary fluoride level, and (e) blood fluoride level. The central fallacy with each of these alleged safety thresholds, however, is that they ignore the wide range of individual susceptibility in how people respond to toxic substances, including fluoride.
Fluoridation of drinking water and chronic kidney disease: Absence of evidence is not evidence of absence
A fairly substantial body of research indicates that patients with chronic renal insufficiency are at an increased risk of chronic fluoride toxicity. Patients with reduced glomerular filtration rates have a decreased ability to excrete fluoride in the urine. These patients may develop skeletal fluorosis even at 1 ppm fluoride in the drinking water.
Skeletal Fluorosis: The Misdiagnosis Problem
It is a virtual certainty that there are individuals in the general population unknowingly suffering from some form of skeletal fluorosis as a result of a doctor's failure to consider fluoride as a cause of their symptoms. Proof that this is the case can be found in the following case reports of skeletal fluorosis written by doctors in the U.S. and other western countries. As can be seen, a consistent feature of these reports is that fluorosis patients--even those with crippling skeletal fluorosis--are misdiagnosed for years by multiple teams of doctors who routinely fail to consider fluoride as a possible cause of their disease.
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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