Abstract

1. Fifty six aluminum smelter workers with 10 to 43 years’ occupational exposure, and who had been previously studied medically, were re-x-rayed. Average urinary fluoride concentrations since 1960 were estimated to range from 2.78 mg/liter preshift and 7.71 mg/liter postshift. 2. Roentgenographic studies in 1960-66 and 1974 failed to reveal any evidence of fluoride associated bony change. 3. Although these workers represent a self-selected group, their magnitude and duration of exposure far outweighs any other group working at present or in the past at this plant. The implication that they have uniformly self-selected as fluoride resistant individuals is improbable. 4. These data indicate that group post-shift ur a long period is not associated with enhanced risk of bony fluorosis. If preshift urinary fluoride concentrations are less than 4 mg/l, the same results appears to apply.

• Related Studies :

  • Occupational skeletal fluorosis

    Conclusion Four cases of skeletal fluorosis are described in individuals who had been working in an aluminum plant for periods up to 12 yens. Two patients exhibited radiological changes indicative of the first stage of the disease and two of the second stage. All patients exhibited backache, pains in arms and

  • An Outbreak of Industrial Fluorosis in Cattle.

    IT may be recalled that in the "Discussion on Fluorosis in Man and Animals" by this Section in February 19411 the occurrence of severe fluorosis in cattle was described on farms in the vicinity of brickworks in Bedfordshire. The purpose of the present communication is to report a similar occurrence

  • Downregulation of miR-4755-5p promotes fluoride-induced osteoblast activation via tageting Cyclin D1.

    Background Endemic fluorosis remains a major public health issue in many countries. Fluoride can cause abnormalities in osteoblast proliferation and activation, leading to skeletal fluorosis. However, its detailed molecular mechanism remains unclear. Based on a previous study, the aim of this study is to explore the role of miRNA in osteoblast

  • Early diagnosis and classification of professional fluorosis

    On the basis of evaluating the clinical course and supplementary method of examination carried out in 132 patients suffering of professional fluorosis and in 200 workers in the premorbid state the author proposes criteria of early diagnosis. Considering Zislin's classification of professional fluorosis, literature data and own findings the author

  • Endemic fluorosis in San Luis Potosi, Mexico. II Identification of risk factors associated with occupational exposure to fluoride.

    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

• Related FAN Content :

  • 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.

  • 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.

  • "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.

  • Fluoride & DISH (Diffuse Idiopathic Skeletal Hyperostosis)

    Among individuals with skeletal fluorosis, the fluoride-induced changes to the spine, and the accompanying symptoms, can bear a close resemblance to DISH (Forestier's Disease). Some authors report that skeletal fluorosis can so closely resemble that DISH that the only way to distinguish the two would be to conduct an invasive bone biopsy. No studies have ever been conducted to determine what role, if any, fluoride plays in the development of DISH.

  • Fluoride & Rheumatoid Arthritis

    The symptoms of skeletal fluorosis can closely resemble rheumatoid arthritis (RA), and thus individuals with fluorosis can "easily be mistaken" as having RA. In addition, clinical research on fluoride-treated osteoporosis patients has found that fluoride exposure can exacerbate pre-existing RA, and recent research shows that the levels of fluoride found in the blood of the general population (19-57 ppb) are sufficient to effect an enzyme (15-lipoxygenase) implicated in the inflammatory process of RA.