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煤矿工人尘肺病的患病率及发病机制

Prevalence and pathogenesis of pneumoconiosis in coal workers.

作者信息

Heppleston A G

机构信息

Institute of Occupational Medicine, Edinburgh, UK.

出版信息

Environ Health Perspect. 1988 Jun;78:159-70. doi: 10.1289/ehp.8878159.

Abstract

Dust dose and composition do not appear to account wholly for changes in the prevalence of coal workers' pneumoconiosis in Europe. In certain coal pits high progression evidently occurred with relatively low dust exposure or vice versa, whereas progression in relation to dust levels might be variable. Exceptionally high quartz concentrations occur in coal mine dust when pneumoconiosis may progress with unusual rapidity. Under such circumstances lesions resembling silicotic nodules may be found, but with the customarily lower levels of quartz the pathological features assume the form characteristic of coal workers. Morphological changes in relation to dust content of human and animal lungs, as well as cellular behavior, have not accounted completely for the epidemiological findings. Considering all the pathological evidence helps explain the pathogenesis of pneumoconiosis and vagaries of progression. The origin of progressive massive fibrosis cannot be explained simply in terms of dust burden or immunological features, and the role of an infective factor cannot be dismissed. Moreover, lipid secretion by alveolar epithelium introduces a new element that could affect the development of simple and complicated pneumoconiosis. In vitro, cytotoxicity appeared to be too variable for predictive purposes, though direct assay of fibrogenicity using the macrophage fibrogenic factor suggested that dust dose was more important than dust composition. Assessing individual susceptibility presents serious obstacles.

摘要

在欧洲,粉尘剂量和成分似乎并不能完全解释煤矿工人尘肺病患病率的变化。在某些煤矿中,明显在相对低的粉尘暴露情况下病情仍有高度进展,反之亦然,而且病情进展与粉尘水平的关系可能存在变数。当煤矿粉尘中石英浓度异常高时,尘肺病可能会异常快速地进展。在这种情况下,可能会发现类似矽结节的病变,但在石英含量通常较低的情况下,病理特征呈现出煤矿工人尘肺病的典型形式。人体和动物肺部的形态学变化与粉尘含量以及细胞行为,尚未完全解释流行病学研究结果。综合所有病理证据有助于解释尘肺病的发病机制和病情进展的异常情况。进行性大块纤维化的起源不能简单地用粉尘负荷或免疫学特征来解释,感染因素的作用也不能被忽视。此外,肺泡上皮细胞的脂质分泌引入了一个可能影响单纯性和复杂性尘肺病发展的新因素。在体外,细胞毒性变化太大,无法用于预测目的,尽管使用巨噬细胞纤维化因子直接测定纤维化能力表明粉尘剂量比粉尘成分更重要。评估个体易感性存在严重障碍。

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