Saracci R
Int J Cancer. 1977 Sep 15;20(3):323-31. doi: 10.1002/ijc.2910200302.
Three simple models for the asbestos-smoking interaction on human lung cancer production are considered. In the first model the excess incidence of lung cancer independently due to asbestos and to smoking adds together when both agents are present (additive model). In the second the addition of each one of the two agents produces an effect (increase in lung cancer incidence) which is proportional to the effect of the other (multiplicative model). In the third, asbestos can only increase lung cancer incidence in the presence of smoking. As previously found by other investigators, the additive model appears the least plausible in the light of the data from two published epidemiological studies. A discrimination between the other two models is attempted through a detailed analysis of the five published epidemiological studies today available which provide information on occupational asbestos exposure, smoking habits and lung cancer risk. Although the data do not allow a definitive discrimination, the multiplicative model appears to be more plausible, being also consistent with a multi-stage carcinogenic mechanism and with evidence from animal (rat) experiments. It is relevant both for biology and for public health that in this model asbestos and smoking are regarded as independently capable of producing lung cancer in humans and that they act synergistically when exposure to both occurs.
本文考虑了三种关于石棉与吸烟对人类肺癌产生相互作用的简单模型。在第一个模型中,当两种致癌因素同时存在时,石棉和吸烟各自独立导致的肺癌额外发病率会相加(相加模型)。在第二个模型中,两种致癌因素各自的作用(肺癌发病率的增加)与另一种因素的作用成正比(相乘模型)。在第三个模型中,石棉只有在有吸烟的情况下才会增加肺癌发病率。正如其他研究人员之前所发现的,根据两项已发表的流行病学研究数据,相加模型似乎最不合理。通过对目前可获取的五项已发表的流行病学研究进行详细分析,试图区分另外两个模型,这些研究提供了有关职业性石棉暴露、吸烟习惯和肺癌风险的信息。尽管数据无法进行明确区分,但相乘模型似乎更合理,这也与多阶段致癌机制以及动物(大鼠)实验的证据相一致。在这个模型中,石棉和吸烟被认为各自独立地能够在人类中引发肺癌,并且当两者同时暴露时会产生协同作用,这一点对于生物学和公共卫生都具有重要意义。