Adlkofer F
Stiftung VERUM, Munich, Germany.
Int Arch Occup Environ Health. 2001 May;74(4):231-41. doi: 10.1007/s004200000221.
Even from the scientific literature it is difficult to conclude whether the increased risk of lung cancer due to exposure to environmental tobacco smoke (ETS), as reported in many epidemiological studies, is based on sound data from reliable studies, or rather on passionate assertions derived from unsound investigations. To shed some light on this matter the differences between cigarette mainstream smoke (MS)--inhaled by the smoker- and ETS--inhaled by everyone exposed-, the concentration of ETS under real life conditions, the internal dose of toxic compounds due to ETS exposure, and the risk of lung cancer as found in epidemiological studies are discussed.
MS and ETS differ considerably in their physical, chemical and toxicological characteristics because of the different conditions under which they are generated, the dilution in air, and the degree of ageing. Based on toxicological data, a very low internal dose of potentially genotoxic compounds can be measured in people after ETS exposure. The epidemiological data suggest a slightly increased risk of lung cancer in non-smokers chronically exposed to ETS. However, it is equally well known, that none of these studies is free from bias and confounding effects.
The average intake of toxic and genotoxic compounds due to ETS exposure is that low that it is difficult, if not impossible, to explain the increased risk of lung cancer as found in epidemiological studies. The uncertainty is further increased because the validity of epidemiological studies on passive smoking is limited severely by numerous bias and confounding factors which cannot be controlled for reliability. The question of whether or not ETS exposure is high enough to induce and/or promote the carcinogenic effects observed in epidemiological studies thus remains open, and the assumption of an increased risk of lung cancer due to ETS exposure is, at present, more a matter of opinion than of firm scientific evidence.
即便从科学文献中也难以断定，诸多流行病学研究报告的因接触环境烟草烟雾（ETS）而增加的肺癌风险，是基于可靠研究的可靠数据，还是源于不合理调查得出的主观论断。为阐明这一问题，本文讨论了吸烟者吸入的香烟主流烟雾（MS）与所有接触者吸入的ETS之间的差异、现实生活条件下ETS的浓度、ETS暴露导致的有毒化合物体内剂量，以及流行病学研究中发现的肺癌风险。
由于生成条件、空气稀释和老化程度不同，MS和ETS在物理、化学和毒理学特性上有很大差异。根据毒理学数据，ETS暴露后人体中可检测到极低剂量的潜在基因毒性化合物。流行病学数据表明，长期接触ETS的非吸烟者患肺癌的风险略有增加。然而，同样众所周知的是，这些研究都存在偏差和混杂效应。
ETS暴露导致的有毒和基因毒性化合物的平均摄入量很低，难以（即便并非不可能）解释流行病学研究中发现的肺癌风险增加。不确定性进一步加大，因为关于被动吸烟的流行病学研究的有效性受到众多偏差和混杂因素的严重限制，这些因素无法确保可靠性。因此，ETS暴露是否足以引发和/或促进流行病学研究中观察到的致癌效应这一问题仍然悬而未决，目前，因ETS暴露而增加肺癌风险的假设更多是一种观点，而非确凿的科学证据。
