A Seaton1, J W Cherrie. 1. Department of Environmental and Occupational Medicine, University of Aberdeen Medical School, Scotland.
Abstract
BACKGROUND: Two stonemasons working together in an environment with high concentrations of quartz pursued very different clinical courses; one died of rapidly progressive silicosis and the other developed hilar adenopathy and, later, early massive fibrosis. The exposures to quartz of these two men were investigated to allow comment on the pathogenesis of severe silicosis relative to concentrations of dust. METHODS: Estimates of exposure were based on previously taken personal dust samples, detailed lifetime occupational histories, and semiquantitative exposure modelling. RESULTS: One of the men who died had a 30 year exposure estimated to have averaged < 0.1 mg/m3, leading to hilar node fibrosis and calcification, followed by a five year exposure to about 2 mg/m3 which proved fatal. Estimates of exposure tallied with postmortem measurement of lung burden, suggesting retention of all dust deposited in the lungs over his final period of work. The younger man, working from the start of his apprenticeship alongside the older one, had a six year exposure to about 1.5 mg/m3, which caused hilar node enlargement and subsequent calcification but minimal lung involvement. CONCLUSIONS: Exposures to relatively low concentrations of quartz may be capable of causing hilar node fibrosis, impairing the clearance of any quartz inhaled subsequently. The findings support the concept that destruction of the hilar nodes by silicotic fibrosis, impairing lung clearance, has an important pathogenic role in the development of massive fibrosis, and in men subsequently exposed to very high concentrations of respirable quartz, rapidly progressive silicosis.
BACKGROUND: Two stonemasons working together in an environment with high concentrations of quartz pursued very different clinical courses; one died of rapidly progressive silicosis and the other developed hilar adenopathy and, later, early massive fibrosis. The exposures to quartz of these two men were investigated to allow comment on the pathogenesis of severe silicosis relative to concentrations of dust. METHODS: Estimates of exposure were based on previously taken personal dust samples, detailed lifetime occupational histories, and semiquantitative exposure modelling. RESULTS: One of the men who died had a 30 year exposure estimated to have averaged < 0.1 mg/m3, leading to hilar node fibrosis and calcification, followed by a five year exposure to about 2 mg/m3 which proved fatal. Estimates of exposure tallied with postmortem measurement of lung burden, suggesting retention of all dust deposited in the lungs over his final period of work. The younger man, working from the start of his apprenticeship alongside the older one, had a six year exposure to about 1.5 mg/m3, which caused hilar node enlargement and subsequent calcification but minimal lung involvement. CONCLUSIONS: Exposures to relatively low concentrations of quartz may be capable of causing hilar node fibrosis, impairing the clearance of any quartz inhaled subsequently. The findings support the concept that destruction of the hilar nodes by silicotic fibrosis, impairing lung clearance, has an important pathogenic role in the development of massive fibrosis, and in men subsequently exposed to very high concentrations of respirable quartz, rapidly progressive silicosis.
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