Crit Rev Toxicol. 2012 Aug;42(7):549-98. doi: 10.3109/10408444.2012.690725. Epub 2012 Jun 2.
A recent review concluded that the evidence from epidemiology studies was indeterminate and that additional studies were required to support the diesel exhaust-lung cancer hypothesis. This updated review includes seven recent studies. Two population-based studies concluded that significant exposure-response (E-R) trends between cumulative diesel exhaust and lung cancer were unlikely to be entirely explained by bias or confounding. Those studies have quality data on life-style risk factors, but do not allow definitive conclusions because of inconsistent E-R trends, qualitative exposure estimates and exposure misclassification (insufficient latency based on job title), and selection bias from low participation rates. Non-definitive results are consistent with the larger body of population studies. An NCI/NIOSH cohort mortality and nested case-control study of non-metal miners have some surrogate-based quantitative diesel exposure estimates (including highest exposure measured as respirable elemental carbon (REC) in the workplace) and smoking histories. The authors concluded that diesel exhaust may cause lung cancer. Nonetheless, the results are non-definitive because the conclusions are based on E-R patterns where high exposures were deleted to achieve significant results, where a posteriori adjustments were made to augment results, and where inappropriate adjustments were made for the "negative confounding" effects of smoking even though current smoking was not associated with diesel exposure and therefore could not be a confounder. Three cohort studies of bus drivers and truck drivers are in effect air pollution studies without estimates of diesel exhaust exposure and so are not sufficient for assessing the lung cancer-diesel exhaust hypothesis. Results from all occupational cohort studies with quantitative estimates of exposure have limitations, including weak and inconsistent E-R associations that could be explained by bias, confounding or chance, exposure misclassification, and often inadequate latency. In sum, the weight of evidence is considered inadequate to confirm the diesel-lung cancer hypothesis.
最近的一篇综述得出结论,流行病学研究的证据尚无定论,需要进一步研究来支持柴油废气与肺癌之间的假设。本更新综述包括 7 项最近的研究。两项基于人群的研究得出结论,认为在累积柴油废气与肺癌之间,显著的暴露-反应(E-R)趋势不太可能完全归因于偏倚或混杂因素。这些研究具有关于生活方式风险因素的高质量数据,但由于不一致的 E-R 趋势、定性暴露估计以及暴露分类错误(基于职称的潜伏期不足)和低参与率的选择偏倚,无法得出明确的结论。非明确的结果与更大的人群研究一致。美国国家癌症研究所/国家职业安全与健康研究所对非金属矿工的一项队列死亡率和嵌套病例对照研究,对一些替代的定量柴油暴露估计值(包括工作场所中最高的可吸入元素碳(REC)暴露)和吸烟史进行了研究。作者得出结论,柴油废气可能导致肺癌。然而,由于这些结论是基于 E-R 模式得出的,其中高暴露被删除以获得显著结果,对结果进行了事后调整,并且对吸烟的“负混杂”效应进行了不适当的调整,即使当前吸烟与柴油暴露无关,因此不可能成为混杂因素,因此结果并不明确。三项公共汽车司机和卡车司机的队列研究实际上是空气污染研究,没有柴油废气暴露的估计值,因此不足以评估肺癌与柴油废气的假说。所有具有定量暴露估计值的职业队列研究的结果都存在局限性,包括 E-R 关联较弱且不一致,这些关联可能归因于偏倚、混杂或偶然因素、暴露分类错误以及潜伏期往往不足。总之,证据的权重被认为不足以证实柴油-肺癌假说。