Abstract
SUMMARY: The city of San Luis Potosi (SLP), Mexico, is located in an area where drinking water contains excessive quantities of natural fluoride. Also in this city is located a small industry that produces hydrofluoric acid. In order to investigate both routes of exposure to fluoride (industrial air and drinking water), we conducted a pilot study in workers of this industry. The study involved 60 male workers, divided into two groups according to their work area: the production and the office groups. Although the exposure to fluoride by the water ingestion pathway was similar for both groups, the occupational-exposure to fluoride was 12 times higher in the production area. Workers in this area had higher levels of fluoride in urine than workers in the office area. This difference was observed in the preshift and the postshift samples. A multivariate regression analysis showed that the workplace explained 33% of the fluoride content of the urinary samples, whereas tap water ingestion explained only 8%. The higher air fluoride levels in the production area could explain the high number of workers who present a pre-clinical phase of skeletal fluorosis. Although our results illustrate the exposure to fluoride of workers in the production area by two pathways, water and workplace air, it would be advisable to explore in more detail the participation of other path-ways of exposure, like diet and soft drinks.
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Reversibility of skeletal fluorosis.
At two x ray examinations in 1957 and 1967, 17 cases of skeletal fluorosis were identified among long term cryolite workers in Copenhagen. In 1982 four of these patients were alive, eight to 15 years after exposure had ended. Radiographs were obtained, and the urinary fluoride excretion was measured. A
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Impact of Community Defluoridation on a Village Endemic for Hydric Fluorosis in Rural Karnataka, India.
Introduction: Excessive intake of fluorides can lead to the development of fluorosis, a serious public health issue in India. The objective of this study was to assess the impact of community defluoridation in preventing fluorosis in Kaiwara village. Methodology: This community interventional trial was conducted in Kaiwara
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FRZB1 rs2242070 polymorphisms is associated with brick tea type skeletal fluorosis in Kazakhs, but not in Tibetans, China.
Skeletal fluorosis is a metabolic bone and joint disease caused by excessive accumulation of fluoride in the bones. Compared with Kazakhs, Tibetans are more likely to develop moderate and severe brick tea type skeletal fluorosis, although they have similar fluoride exposure. Single nucleotide polymorphisms (SNPs) in frizzled-related protein (FRZB) have
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Skeletal fluorosis from brewed tea
BACKGROUND: High fluoride ion (F(-)) levels are found in many surface and well waters. Drinking F(-)-contaminated water typically explains endemic skeletal fluorosis (SF). In some regions of Asia, however, poor quality "brick tea" also causes this disorder. The plant source of brick, black, green, orange pekoe, and oolong tea, Camellia
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Effects of water improvement and defluoridation on fluorosis-endemic areas in China: A meta-analysis.
Highlights The first analysis of the effect of improving water quality and reducing fluoride in China over 40 years. Analysis of the effect of water improvement and fluoride reduction in different provinces of China. We analyzed the effect of water improvement on dental fluorosis, skeletal fluorosis, and fluoride content
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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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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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Exposure Pathways Linked to Skeletal Fluorosis
Excessive fluoride exposure from any source -- and from all sources combined -- can cause skeletal fluorosis. Some exposure pathways , however, have been specifically identified as placing individuals at risk of skeletal fluorosis. These exposure pathways include: Fluoridated Water for Kidney Patients Excessive Tea Consumption High-Fluoride Well Water Industrial Fluoride Exposure Fluorinated Pharmaceuticals (Voriconazole
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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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