Abstract

Multi-year follow-up of 358 workers of aluminum pot rooms, including 165 individuals suffering from fluorosis, has shown significant changes in the clinical picture of the chronic occupational fluorine intoxication, developed under modern conditions of production, at lower concentrations of fluorine compounds in the air of working area. In this connection, the pathology of the musculoskeletal system plays the dominating role in this clinical picture and has the large variability of combinations of the individual sections destructions of the bone tissue. The main criterion to establish the phase of the disease is still the number and severity of the signs of this destruction. The visceral pathology in contemporary production circumstances is registered with less frequency and loses a number of the previously described clinical manifestations, however, is still of some importance to identify the early signs of the disease and to prevent the fluorosis on time.

• Related Studies :

  • X-ray diagnosis of fluorine-associated arthropathy

    I. Pathological basis and X-ray signs of fluorine-associated arthropathy Long-term uptake of excessive fluorine may cause pathological changes of bone structure and bone periphery; furthermore, animal experiments and epidemiological investigations demonstrate that fluorosis may cause necrosis, degeneration and ulceration of articular cartilage, and also cause necrosis of subchondral bones, leading to

  • [Clinical and imaging study of fluoride-poisoning arthropathy].

    Objective: To probe into the clinical and imaging manifestations and mechanisms of fluorosis-associated arthropathy. Methods: Analyses were conducted on the clinical manifestations, X-rays and magnetic resonance examinations in 18 cases with fluorosis-associated arthropathy. Results: Skeletal fluorosis of different severities was revealed in the 18 cases. Major clinical symptoms were as follows: pain

  • Radiological modifications of the skeletal system among aluminum smelter workers: A 15 year retrospective study

    Previously by the time skeletal fluorosis among aluminum smelter workers due to high fluoride exposure was diagnosed numerous cases of bone fluorosis had already reached stages II and III according to Roholm. Today, as a result of improved working conditions and continuous health care, the picture has changed. This paper

  • Bone and joint pathology in fluoride-exposed workers

    Clinical and radiological investigations were performed for 2,258 aluminum workers exposed to fluoride for an average of 17.6 yr (standard deviation = 7.6). Changes in bone and joints were presented in detail in three groups: (1) exposed up to 5 yr (135 cases), (2) exposed from 6-32 yr (1,463 cases),

  • Clinical and hygienic evaluation of the combined effect of vibration and fluoride in humans

    By L. Ya. Tartatovskaya, G.N. Samokhvalova, A.G. Antropov Medical Science Centre of Prophylactics and Protection of the Health Workers in Industrial Enterprises, Ekaterinburg, Russia. The study of the combined action of vibration and intense noise, muscular loads and cooling has made it possible to assess the probability of the development of vibration

• Related FAN Content :

  • "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 & 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.

  • 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.

  • 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

  • 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.