Flouride renal toxicity in fetus and neonate.
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A field study of fluoride pollution and of its consequences was made over a period of five years in the vicinity of an alumina reduction plant. This study, based upon the use of a static soda impregnated paper sampler, shows that the results obtained are in good agreement with the atmospheric fluoride concentrations obtained with dynamic samplers, especially when fluoride is present in gaseous form (HF). The results suggest that vertically mounted paper samplers are less sensitive to the collection of particulate fluorides. Collection rate is strongly influenced and increases with speed. If this parameter is known, an accurate estimation of the absolute atmospheric concentration is possible; the values shown by this technique are in good correlation with the value (annual mean) of pasture fluoride content. As a correlation exists between pasture fluoride content and the symptoms shown by cattle, the static filter samplers can predict disease in the case of slow chronic fluorosis. The field study agrees with earlier laboratory experiments and shows the validity of these simple and inexpensive types of exposure methods.
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1. Mandibular fluoride content was recorded in 63 roe deer (33 males, 30 females) between 9 months and 10 years of age, taken from an area in SW Germany not exposed to increased fluoride deposition. 2. Bone fluoride level was positively correlated with age (t-test, P less than or equal to 0.001), the increase in concentration being higher in younger animals and declining in older deer. 3. In the sample studied, no significant sex specific difference in mean mandibular fluoride concentration was found (t-test, P greater than 0.05).
Fluoride renal clearance (CF) was studied in young healthy subjects with standard clearance technique following administration of 3 mg F as a 30-min constant infusion. High urinary flow rates were induced and experiments were performed under both urinary alkaline and acidic conditions. The data showed that a high urinary flow resulted in maximum fluoride clearance. High water diuresis may therefore be an important part in the treatment of acute fluoride intoxication.
Fluoride is an essential trace element. It is incorporated in calcified tissues. At doses lower than 1.5 mg/day, fluoride has a prophylactic action against dental caries by absorption on the enamel surface. At doses ranging from 15 to 25 mg/day, it is used as a therapeutic agent in adults, in the treatment of post-menopausal osteoporosis with vertebral crush fractures. At high doses, fluoride may induce skeletal fluorosis leading in children to pseudorachitism. In children, fluoride supplement has been recommended for several years, as a prophylactic agent against dental caries. It may be given either as dentifrices and toothwash solutions, easy to use and economic but contraindicated in very young children; or as tablets, sure and effective but requiring a daily intake; or as domestic salts supplemented with 250 mg/kg. Fluoride supplement may also be given through drinking water. Fluoride content is limited to 1.5 mg/l but some mineral waters contain high amounts of fluoride and may have a beneficial effect on bone mass. In order to prevent an excessive fluoride intake in children and in adults, different forms of fluoride supplements must not be associated.
The current health care trend is to provide evidence-based recommendations and treatment. Many literature reviews have shown fluoride's effectiveness against caries. The current use of fluoride in the prevention of dental caries is based on community, professional, and individual strategies. Personalized fluoride regimens should include a risk analysis and a review of the patient's current fluoride exposure. The future of fluoride may be found in its slow release and retention in the oral cavity through various modalities. Because of the many uncertainties still associated with fluoride, further research is needed.
Signs of dental discolouration, difficulty in mastication, bony lesions, lameness, debility and mortality in domesticated animals, reared around superphosphate fertiliser plants located approximately 15 km north of Udaipur, Rajasthan prompted us to investigate for the occurrence of fluorosis. Out of 166 animals clinically examined, the prevalence rate was 17.4% (4/23) in calves below 1 year of age, 37.2% (16/43) in cattle between 1 and 3 years, 61.3% (46/75) in cattle above 3 years and 72% (18/25) in buffalo above 1 year. Dental fluorosis was common in buffalo compared to cattle of all the age groups. Fluoride levels in fodder and water, consumed by the animals were much higher than the recommended permissible limit. Mean fluoride concentrations in serum and urine were 1.53 +/- 1.27 and 26.4 +/- 6.17 mg l(-1) in calves below 1 year of age, 0.56 +/- 0.17 and 26.2 +/- 3.86 mg l(-1) in cattle of 1-3 years, 0.49 +/- 1.13 and 27.5 +/- 4.63 mg l(-1) in cattle above 3 years and 0.60 +/- 0.07 and 28.6 +/- 4.73 mg l(-1) in buffalo over 1 year, respectively. The values were significantly (P < 0.01) higher than those of control animals kept over a 15-km distance from the factories. Fluoride concentrations in the environmental sample collected from the affected locality were 534.4 +/- 74.9 mg kg(-1) in fodder, 1.19 +/- 0.29 mg l(-1) in pond water and 0.479 +/- 0.351 mg l(-1) in tube well water. It was concluded that the consumption of fodder and water contaminated by the fumes and dusts emitting from superphosphate fertiliser plants resulted in the development of chronic fluorotic lesions in cattle and buffalo.
The concentration of fluoride was determined in water, forage and urine and serum samples of buffaloes from the Unnao district of India. The water and forage samples contained 2.01 +/- 0.51 and 22.50 +/- 0.82 ppm of fluoride, respectively. The analysis of biosamples collected from the affected animals revealed higher levels of fluoride in serum (0.58 +/- 0.05 ppm) and urine (10.64 +/- 1.23 ppm). Clinical examination identified a 40.34% prevalence rate of clinical lesions suggestive of fluorosis in buffalo of this locality. Dental lesions were present invariably in all affected animals whereas lameness, painful bony exostosis and emaciation were recorded in 28.17%, 8.45% and 76.00% of the animals. Based on the clinical lesions and fluoride content in water, serum and urine, it was concluded that the problem of fluorosis in buffalo is attributable to drinking water containing toxic levels of fluoride.
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BACKGROUND: Osteofluorosis is caused by chronic fluoride intoxication. Fluoride is used in toothpaste for the prevention of dental caries, and dental fluorosis has often been reported among children and attributed to ingestion of fluoride toothpaste. We report a case of chronic fluoride intoxication caused by excess use of toothpaste in an adult. CASE: A 45-year-old woman consulted a rheumatologist for painful swelling of the fingers, phalangeal rather than articular. She also had brown staining on her teeth. Radiography of the hands showed periosteal apposition on the phalanges. Further work-up ruled out tumoral or thyroid causes. Laboratory tests showed elevated fluoride levels in the blood (50.9 micromol/L, normal<1.5 micromol/L) and in the urine (721 micromol/L, normal<46 micromol/L). On questioning, we found only one cause for chronic fluoride intoxication: excess and unusual use of toothpaste. The patient brushed her teeth 18 times a day and swallowed the toothpaste, because she liked the taste. She consumed a tube of toothpaste every 2 days, thereby swallowing 68.5 mg of fluoride every day. Suspecting fluorosis from toothpaste, we asked the patient to use a toothpaste without fluoride. Sixteen weeks later, the pain had ceased, and laboratory tests showed massively reduced but still elevated fluoride levels in the blood (6.9 micromol/L) and urine (92.7 micromol/L). CONCLUSION: In this rare case of fluoride intoxication, misuse of a normally innocuous product caused osteofluorosis.
In order to investigate the molecular mechanism(s) underlying brain dysfunction caused by chronic fluorosis, neuronal nicotinic acetylcholine receptors (nAChRs) in the brain of rats receiving either 30 or 100 ppm fluoride in their drinking water for 7 months were analyzed in the present study employing ligand binding and Western blotting. There was a significant reduction in the number of [3H]epibatidine binding sites in the brain of rats exposed 100 ppm of fluoride, but no alteration after exposed to 30 ppm. On the other hand, the number of [125I]alpha-BTX binding sites was significantly decreased in the brains of rats exposed to both levels of fluoride. Western blotting revealed that the level of the nAChR alpha4 subunit protein in the brains of rats was significantly lowered by exposure to 100 ppm, but not 30 ppm fluoride; whereas the expression of the alpha7 subunit protein was significantly decreased by both levels of exposure. In contrast, there was no significant change in the level of the beta2 subunit protein in the brains of rats administered fluoride. Since nAChRs play major roles in cognitive processes such as learning and memory, the decrease in the number of nAChRs caused by fluoride toxicity may be an important factor in the mechanism of brain dysfunction in the disorder.