Abstract
Chronic fluoride intoxication in the form of dental and skeletal fluorosis was surveyed in five villages of the Palamau district, Jharkhand, India. Out of 238 sources of drinking water, mainly from groundwater, the majority had elevated fluoride concentrations capable of causing health risk to the community. In one water source a concentration of 12 mg F/L was observed. Dietary intake of fluoride through food, however, was much less significant compared with drinking water. Among the children, 83% were diagnosed with dental fluorosis, and 47% of adults were afflicted with various stages of skeletal fluorosis. A level of 2.5 mg F/L was found to be a critical threshold for manifestations of crippling skeletal fluorosis. Household defluoridation along with improved nutrition rich in calcium is recommended for amelioration of fluorosis in these villages.
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Spinal cord compression revealing fluorosis
1. Introduction Bone fluorosis due to high fluoride contents in water and soil is endemic in North Africa and India. Neurological complications are rare. They consist of nerve root or spinal cord compression by bony excrescences, which predominate at the cervical spine. We report a new case of spinal cord compression
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Spatial distribution of endemic fluorosis caused by drinking water in a high-fluorine area in Ningxia, China.
Endemic fluorosis is widespread in China, especially in the arid and semi-arid areas of northwest China, where endemic fluorosis caused by consumption of drinking water high in fluorine content is very common. We analyzed data on endemic fluorosis collected in Ningxia, a typical high-fluorine area in the north of China.
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Chronic endemic fluorosis (with bone affections) in the Punjab.
First Page of Study Since the investigation of Black an,d McKay in 1916 into the problem of mottled enamel, and the definite association of this anomaly with the fluorine content of drinking waters by Churchill (1931, 1932), the matter of fluorine intoxication has been studied in detail by different workers in
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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
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High concentration of sodium fluoride in drinking water induce hypertrophy versus atrophy in mouse skeletal muscle via modulation of sarcomeric proteins.
Highlights Short term exposure of mouse to sodium fluoride causes skeletal muscle hypertrophy. Short term exposure causes upregulation of protein synthesis and PI3-AKT pathway. Long term exposure of mouse to sodium fluoride causes muscle atrophy. Long term exposure causes upregulation of Ubiquitin proteasome pathway. Differential protein expression was seen
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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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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.
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