Besaratinia Ahmad, Pfeifer Gerd P
Division of Biology, Beckman Research Institute of the City of Hope National Medical Center, Duarte, CA 91010, USA.
Lancet Oncol. 2008 Jul;9(7):657-66. doi: 10.1016/S1470-2045(08)70172-4.
Since the early 1980s, there has been growing concern about potential health consequences of exposure to second-hand smoke (SHS). Despite SHS being established as a risk factor for lung cancer development, the estimated risk has remained small yet somehow debatable. Human exposure to SHS is complicated because of temporal variabilities in source, composition, and concentration of SHS. The temporality of exposure to SHS is important for human lung carcinogenesis with a latency of many years. To explore the causal effect of SHS in lung carcinogenesis, exposure assessments should estimate chronic exposure to SHS on an individual basis. However, conventional exposure assessment for SHS relies on one-off or short-term measurements of SHS indices. A more reliable approach would be to use biological markers that are specific for SHS exposure and pertinent to lung cancer. This approach requires an understanding of the underlying mechanisms through which SHS could contribute to lung carcinogenesis. This Review is a synopsis of research on SHS and lung cancer, with special focus on hypothetical modes of action of SHS for carcinogenesis, including genotoxic and epigenetic effects.
自20世纪80年代初以来,人们越来越关注接触二手烟(SHS)对健康的潜在影响。尽管二手烟已被确认为肺癌发生的一个风险因素,但估计的风险仍然很小,且在某种程度上存在争议。由于二手烟的来源、成分和浓度存在时间变异性,人类接触二手烟的情况较为复杂。接触二手烟的时间性对潜伏期长达数年的人类肺癌发生过程很重要。为了探究二手烟在肺癌发生中的因果效应,暴露评估应在个体基础上估计对二手烟的长期接触情况。然而,传统的二手烟暴露评估依赖于对二手烟指标的一次性或短期测量。一种更可靠的方法是使用针对二手烟暴露且与肺癌相关的生物标志物。这种方法需要了解二手烟可能导致肺癌发生的潜在机制。本综述是关于二手烟与肺癌研究的概要,特别关注二手烟致癌的假设作用模式,包括遗传毒性和表观遗传效应。