Cases reported "Asbestosis"

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1/4. asbestosis and small cell lung cancer in a clutch refabricator.

    OBJECTIVES: To present a case of asbestosis and small cell lung cancer caused by asbestos in a clutch refabricator. methods: Exposed surfaces of used clutches similar to those refabricated in the worker's workplace were rinsed, and the filtrate analysed by analytical transmission electron microscopy. Tissue samples were also analysed by this technique. RESULTS: Numerous chrysotile fibres of respirable dimensions and sufficient length to form ferruginous bodies (FBs) were detected from rinsed filtrates of the clutch. bronchoalveolar lavage fluid contained many FBs, characteristic of asbestos bodies. Necropsy lung tissue showed grade 4 asbestosis and a small cell carcinoma in the right pulmonary hilum. Tissue analysis by light and analytical electron microscopy showed tissue burdens of coated and uncoated asbestos fibres greatly exceeding reported environmental concentrations (3810 FBs/g dry weight and 2,080,000 structures > or = 0.5 micron/g dry weight respectively). 72% Of the cores were identified as chrysotile. CONCLUSIONS: Clutch refabrication may lead to exposure to asbestos of sufficient magnitude to cause asbestosis and lung cancer.
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2/4. Fatal asbestosis 50 years after brief high intensity exposure in a vermiculite expansion plant.

    The authors report the case of a 65-year-old accountant whose only asbestos exposure was during a summer job 50 years earlier in a california vermiculite expansion plant. Vermiculite is a silicate material that is useful in building and agriculture as a filler and insulating agent. He developed extensive fibrocalcific pleural plaques and end-stage pulmonary fibrosis, with rapidly progressive respiratory failure. Careful occupational and environmental history revealed no other source of asbestos exposure, and the initial clinical diagnosis was idiopathic pulmonary fibrosis; open lung biopsy shortly before his death confirmed asbestosis. Electron microscopic lung fiber burden analysis revealed over 8,000,000 asbestos fibers per gram dry lung, 68% of which were tremolite asbestos. Additional asbestiform fibers of composition not matching any of the standard asbestos varieties were also present at over 5,000,000 fibers per gram dry lung. Comparison analysis of a sample of Libby, montana, vermiculite showed a similar mix of asbestiform fibers including tremolite asbestos. This case analysis raises several concerns: risks of vermiculite induced disease among former workers of the more than 200 expansion plants throughout the united states; health effects of brief but very high-intensity exposures to asbestos; and possible health effects in end-users of consumer products containing vermiculite.
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3/4. idiopathic pulmonary fibrosis in asbestos-exposed workers.

    Diffuse interstitial lung disease in asbestos-exposed workers is presumed to represent asbestosis. Among 176 asbestos-exposed persons for whom lung tissue was available, we found nine with clinical features consistent with asbestosis, but histologic sections failed to demonstrate asbestos bodies, the usual requirement for pathologic diagnosis of asbestosis (Group I). These nine were compared by analytic electron microscopy with nine persons with idiopathic pulmonary fibrosis (Group II), and with nine persons with all the criteria of asbestosis (Group III). The three groups did not differ significantly with respect to lung burden of chrysotile or tremolite and actinolite, but Group III had a lung burden of amosite and crocidolite that was three orders of magnitude greater than in Groups I and II, with no overlap. We conclude that (1) the American Thoracic Society criterion of "a reliable history of exposure" is sometimes difficult to define; (2) asbestos bodies are seen in tissue sections only when exposure has been reasonably high, and given the proper clinical setting, the presence of diffuse fibrosis and asbestos bodies in tissue sections are sensitive and specific criteria for a diagnosis of asbestosis; and (3) the prevalence here of 5.1% nonasbestos-induced interstitial lung disease among asbestos-exposed persons is artefactually high because of atypical case selection. However, because asbestosis is a disappearing disease, such cases will become more frequent. The identification of these other diseases is important because therapy and prognosis may differ from that of asbestosis.
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4/4. Asbestos-related disease associated with exposure to asbestiform tremolite.

    Tremolite is nearly ubiquitous and represents the most common amphibole fiber in the lungs of urbanites. Tremolite asbestos is not mined or used commercially but is a frequent contaminant of chrysotile asbestos, vermiculite, and talc. Therefore, individuals exposed to these materials or to end-products containing these materials may be exposed to tremolite. We have had the opportunity to do asbestos body counts and mineral fiber analysis on pulmonary tissue from five mesothelioma cases and two asbestosis cases with pulmonary tremolite burdens greater than background levels. There were no uncoated amosite or crocidolite fibers detected in any of these cases. Three patients were occupationally exposed to chrysotile asbestos; two patients had environmental exposures (one to vermiculite and one to chrysotile and talc) and one was a household contact of a shipyard worker. The tremolite burdens for the asbestosis cases were one to two orders of magnitude greater than those for the mesothelioma cases. Our study confirms the relationship between tremolite exposure and the development of asbestos-associated diseases. Furthermore, the finding of relatively modest elevations of tremolite content in some of our mesothelioma cases suggests that, at least for some susceptible individuals, moderate exposures to tremolite-contaminated dust can produce malignant pleural mesothelioma.
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