Abstract
Fluorotic lesions were studied in cows and calves on farms belonging to 2 agricultural companies. From company HP 3 calves, 4 heifers and 2 cows were examined and from the other (B), 12 bull-calves. The material consisted of a carcass from 1 dead calf and skull, metacarpus and kidneys from slaughtered animals. The F content of feed and water samples was determined. In HP material extensive enamel defects and strong wear were found in the deciduous incisors. Fluorotic lesions in calves were not described previously. One calf had osteoporosis. In the rest of the material osteosclerosis and subperiosteal bone apposition and tubular atrophy in the kidneys were seen. Kidney lesions were not observed previously in bovine fluorosis. Dark furrows and enamel defects appeared in the teeth of the heifers and the cows. In the skeleton osteosclerosis and subperiosteal bone apposition were found. Microscopically the skeleton showed signs of repair. The F content of the skeleton varied between 135 and 300 ppm in the ash. In water samples 1.5-4.0 ppm of F were found. The mineral supply used contained 300-500 ppm of F. The fluorosis in these animals was caused by a combination of the F of the water and the mineral supplement. Considering the microscopic picture and the low skeletal F level, the lesions in the bull-calves of company B were interpreted as fluorosis in a process of repair. The ingested fluorine in these animals was reduced during the fattening period.
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[Genetic factors predisposing to occupational fluorosis].
Having analyzed a total amount of all systems, the authors specified the most important genetic markers predisposing to chronic flour intoxication: the patients demonstrated higher frequency of ACP1*A and PGM1*1-alleles, phenotypes of acid phosphatase AA, of phosphoglucomutase 1+1+ and 2+2+, of dry cerumen consistence--d. The results could help to improve
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[Bone fluorosis without occupational exposure in chronic renal insufficiency].
Report on a 70-year-old male with bone fluorosis which was ascertained radiologically, by section and fluor analysis in the bone ash. With empty professional anamnesis as cause was found the presence of a chronic renal insufficiency with simultaneously increased fluor content of drinking water. The decreased renal excretion of fluoride
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Matrix metallopeptidase-2 gene rs2287074 polymorphism is associated with brick tea skeletal fluorosis in Tibetans and Kazaks, China.
Brick tea skeletal fluorosis is still a public health issue in the north-western area of China. However its pathogenesis remains unknown. Our previous study reveals that the severity of skeletal fluorosis in Tibetans is more serious than that in Kazaks, although they have similar fluoride exposure, suggesting the onset of
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Exposure to fluoride in smelter workers in a primary aluminum industry in India
BACKGROUND: Fluoride is used increasingly in a variety of industries in India. Emission of fluoride dust and fumes from the smelters of primary aluminum producing industries is dissipated in the work environment and poses occupational health hazards. OBJECTIVE: To study the prevalence of health complaints and its association with fluoride level
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High levels of fluoride in groundwater from Northern parts of Indo-Gangetic plains reveals detrimental fluorosis health risks.
Highlights This study provides an overview of fluoride distribution and health risks in the fluoride endemic region of Northern Indo-Gangetic Plain. Groundwater fluorides concentration exceeded the safe drinking water limit in 98% of sampling locations. Health hazard index (HQFluoride) exceeded the unitary value in all the individual groups signifying that
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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.
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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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Fluoridation, Dialysis & Osteomalacia
In the 1960s and 1970s, doctors discovered that patients receiving kidney dialysis were accumulating very high levels of fluoride in their bones and blood, and that this exposure was associated with severe forms of osteomalacia, a bone-softening disease that leads to weak bones and often excruciating bone pain. Based on
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Kidney Patients Are at Increased Risk of Fluoride Poisoning
It is well established that individuals with kidney disease are susceptible to suffering bone damage and other ill effects from low levels of fluoride exposure. Kidney patients are at elevated risk because when kidneys are damaged they are unable to efficiently excrete fluoride from the body. As a result, kidney patients
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"Pre-Skeletal" Fluorosis
As demonstrated by the studies below, skeletal fluorosis may produce adverse symptoms, including arthritic pains, clinical osteoarthritis, gastrointestinal disturbances, and bone fragility, before the classic bone change of fluorosis (i.e., osteosclerosis in the spine and pelvis) is detectable by x-ray. Relying on x-rays, therefore, to diagnosis skeletal fluorosis will invariably fail to protect those individuals who are suffering from the pre-skeletal phase of the disease. Moreover, some individuals with clinical skeletal fluorosis will not develop an increase in bone density, let alone osteosclerosis, of the spine. Thus, relying on unusual increases in spinal bone density will under-detect the rate of skeletal fluoride poisoning in a population.
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