Risk Assessment of Asbestos Workers

为了为石棉相关疾病的早期诊断和有效预防提供基础信息，利用流行病学、细胞遗传学和分子流行病学的最新研究技术，对石棉工人进行了健康风险评估，除了与流行病学研究相关的偏差外，还特别参考了接触粉尘的类型、性别、种族和吸烟。主要研究结果如下：1.青石棉对人PMN产生ROM的机制既涉及细胞表面膜的直接相互作用，又涉及明显的吞噬依赖过程。第一次肺功能测试的结果显示与死亡率和参与随后的复查有关，这表明在肺功能的纵向研究中存在选择效应。3.对不吸烟、无石棉肺的石棉作业女工进行肺功能检查，发现石棉本身对肺体积的减少和DLCO的降低起主要作用。4.对接尘工人的肺功能进行了比较，发现三种粉尘均可引起尘肺X线改变前的肺功能异常。5.描述了NAD(P)H-苯醌氧化还原酶基因多态性的种族分布，并讨论了其对抗肿瘤药物开发和使用的意义。6.一项研究GSTT1和GSTM1基因多态与少数人群肺癌关系的病例对照研究表明，同时存在GSTT1和GSTM1缺失多态的个体患肺癌的风险增加超过相加的风险。7.举例说明了环境分子流行病学在控制空气毒物所致疾病方面的优势和局限性。

To provide basic information for an earlier diagnosis and effective prevention program for asbestos related diseases, using recent progressed research technologies of epidemiology, cyotogenetics, and molecular epidemiology, health risk assessment of asbestos workers wasmperformed with the special reference to type of exposed dust, sex, race, and smoking in addition to bias related to epidemiological studies. The major results obtained were as follows :1. The mechanism of human PMN to generate ROM by crocidolite was shown to involve both to direct cell surface membrane interactions, together with an apparent phagocytic-dependent process.2. Results of the first pulmonary function test were shown to associate with the mortality and participation in a subsequent reexamination, suggesting a selection effects in a longitudinal study of pulmonary function. 3. Pulmonary function of nonsmoking female asbestos workers without asbestosis were examined and found that asbestos-esposure per se predominantly contributes to restircted lung volume and reduced DLco. 4. Pulmonary dysfunction among workers exposed to silica, asbestos, or coalmine dust were compared and all the three dusts was found to cause functional abnormalities that precede radiographic changes of pneumoconiosis. 5. The ethnic distribution of the polymorphism of the NAD (P) H quinone oxidoreductase, was described and its implications for anti-tumour drug development and use were discussed. 6. A case-control study to investigate the association of the GSTT1 and GSTM1 polymorphisms with lung cancer in minority populations suggested that lung cancer risk is increased more than additively for individuals who have both GSTT1 and GSTM1 null polymorphisms. 7. The current strengths and limitations of environmental molecular epidemiology in controlling disease caused by air toxics are illustrated with examples.