Vainio H, Boffetta P
International Agency for Research on Cancer, Lyon, France.
Scand J Work Environ Health. 1994 Aug;20(4):235-42. doi: 10.5271/sjweh.1402.
The joint effects of exposure to two known lung carcinogens, tobacco smoking and asbestos, are reviewed. The variable pattern of interaction--ranging from supramultiplicative to less than additive--may reflect the fact that both asbestos and smoking are complex carcinogens which can affect more than one stage of lung carcinogenesis. The joint effect of two such agents will depend on the relative magnitude of the effects at each stage. The epidemiologic evidence from studies of insulation workers with high exposures suggests an interaction that approximates the multiplicative model, indicating that each of the two factors has an independent action on the multistage process of carcinogenesis. Very limited information is available on the interaction between these two agents in causing specific histological types of lung cancer. Both tobacco smoke and asbestos fibers can be genotoxic and cytotoxic and cause proliferative lesions in the lungs. Tobacco smoke is known to contain carcinogens that bind to critical genes in DNA (deoxyribonucleic acid) and cause mutations. Asbestos fibers may cause chronic inflammation of the lungs, which releases various cytokines and growth factors, and therefore may provide a possible selective growth advantage for mutated cells.
本文综述了接触两种已知的肺癌致癌物——吸烟和石棉——的联合效应。相互作用的可变模式——从超相乘到小于相加——可能反映了这样一个事实，即石棉和吸烟都是复杂的致癌物，它们可以影响肺癌发生的多个阶段。两种此类致癌物的联合效应将取决于每个阶段效应的相对大小。对高暴露绝缘工人的研究所得的流行病学证据表明，存在一种接近相乘模型的相互作用，这表明这两个因素中的每一个对癌症发生的多阶段过程都有独立作用。关于这两种致癌物在引发特定组织学类型肺癌方面的相互作用，现有信息非常有限。烟草烟雾和石棉纤维都可能具有遗传毒性和细胞毒性，并在肺部引发增殖性病变。已知烟草烟雾中含有与DNA（脱氧核糖核酸）中的关键基因结合并导致突变的致癌物。石棉纤维可能会导致肺部慢性炎症，从而释放各种细胞因子和生长因子，因此可能为突变细胞提供可能的选择性生长优势。
