Abstract
The west plain region of Jilin province of northeast China is one of the typical endemic fluorosis areas caused by drinking water for many years. Investigations of hydrogeological and ecoenvironmental conditions as well as endemic fluorosis were conducted in 1998. Results show that the ground water, especially, the water in the unconfined aquifer is the main source of drinking water for local residents. The fluoride concentration in groundwater in the unconfined aquifers is higher than that in the confined aquifer in the west plain of Jilin province. The fluoride concentration in the unconfined aquifer can be used to classify the plain into fluoride deficient area, optimum area and excess area, which trend from west to east. High fluoride (>1.0 mg L(-1)) in drinking water resulted in dental and skeletal fluorosis in local residents (children and pregnant women). There exists a positive correlation between fluoride concentration in the drinking water and the morbidities of endemic fluorosis disease (r1 = 0.781, r2 = 0.872). Health risks associated with fluoride concentration in drinking water are assessed. It has been determined that fluoride concentration in excess of 1.0 mg L(-1) exposes residents to high health risks based on risk identification. The study area is classified into five health risk classes as shown in Figure 4. The risk indexes of this area more than 1.0 are accounted for 68% of the total west plain region.
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Bovine fluorosis in Sweden
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
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Further observations on endemic fluoride-induced osteopathies in children
Fluoro-osteopathy has been described in four clildren aged 6 or above, These observations contrast with the concept that skeletal fluorosis cannot develop prior to 10 to 20 years of high fluoride intake. The pathogenesis and the mechanism underlying the causation of this disease is discussed on the basis of the
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Effect of combined therapy with sodium fluoride, vitamin D and calcium in osteoporosis
Fluoride administration in both man and animals has been shown to stimulate new bone formation. However, the bone is poorly mineralized, and osteomalacia and secondary hyperparathyroidism frequently occur. In this study we investigated the effect of variable levels of fluoride and calcium intake, accompanied by vitamin D, on osteoporosis in
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Fluoride-induced chronic renal failure
Renal fluoride toxicity in human beings is difficult to assess in the literature. Although experimental studies and research on methoxyflurane toxicity have shown frank renal damage, observations of renal insufficiency related to chronic fluoride exposure are scarce. We report a case of fluoride intoxication related to potomania of Vichy water,
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[Genetic markers of occupational susceptibility to fluorosis].
To determine markers showing propensity to occupational fluorosis, the authors studied prevalence of ABO, Rh, MN, ABH and Lewis phenotypes, systemic rhesus haplotypes in 229 workers engaged into aluminum production. Propensity to occupational fluorosis was marked by P (+), O (ABO) phenotypes. P (-) phenotype appeared to be a marker
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Fluoride & Osteoarthritis
While the osteoarthritic effects that occurred from fluoride exposure were once considered to be limited to those with skeletal fluorosis, recent research shows that fluoride can cause osteoarthritis in the absence of traditionally defined fluorosis. Conventional methods used for detecting skeletal fluorosis, therefore, will fail to detect the full range of people suffering from fluoride-induced osteoarthritis.
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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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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.
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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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Estimated "Threshold" Doses for Skeletal Fluorosis
For over 40 years health authorities stated that in order to develop crippling skeletal fluorosis, one would need to ingest between 20 and 80 mg of fluoride per day for at least 10 or 20 years. This belief, however, which played an instrumental role in shaping current fluoride policies, is now acknowledged by the National Academy of Sciences (NAS) and other US health authorities to be incorrect.
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