Claxton Larry D, Woodall George M
Environmental Carcinogenesis Division, National Health and Environmental Effects Research Laboratory, Office of Research and Development, US Environmental Protection Agency, Research Triangle Park, NC 27711, USA.
Mutat Res. 2007 Nov-Dec;636(1-3):36-94. doi: 10.1016/j.mrrev.2007.01.001. Epub 2007 Mar 18.
Although ambient air was first shown to be carcinogenic in 1947 and mutagenic in 1975, no overarching review of the subsequent literature has been produced. Recently, Claxton et al. [L.D. Claxton, P.P. Matthews, S.H. Warren, The genotoxicity of ambient outdoor air, a review: Salmonella mutagenicity, Mutat. Res./Rev. Mutat. Res. 567 (2004) 347-399] reviewed the literature on the mutagenicity of urban air in the Salmonella mutagenicity assay. Here, we review the literature on the mutagenicity of urban air in other test systems and review the carcinogenicity of urban air in experimental systems. Urban air was carcinogenic in most of the reports involving rodents. Studies ascribed carcinogenic activity primarily to PAHs, nitroarenes, and other aromatic compounds. Atmospheric conditions, along with the levels and types of pollutants, contributed to the variations in carcinogenic and mutagenic activity of air from different metropolitan areas. The majority of the mutagenesis literature was in the Salmonella assay (50%), with plant systems accounting for most of the rest (31%). The present data give little support to the use of plant systems to compare air mutagenicity among multiple sites or studies. Studies in mice have shown that particulate air pollution causes germ-cell mutations. Air sheds contain similar types and classes of mutagens; however, the levels of these compounds vary considerably among air sheds. Combustion emissions were associated with much of the mutagenicity and carcinogenicity of urban air. Most studies focused on the particulate fraction; thus, additional work is needed on the volatile and semi-volatile fractions, metals, and atmospheric transformation. Smaller particles have greater percentages of extractable organic material and are more mutagenic than larger particles. Although hundreds of genotoxic compounds have been identified in ambient air, only a few (<25) are routinely monitored, emphasizing the value of coupling bioassay with chemistry in the monitoring of air for carcinogenic and mutagenic activities and compounds.
尽管环境空气在1947年首次被证明具有致癌性，1975年被证明具有致突变性，但后续文献尚未进行全面综述。最近，克拉克斯顿等人[L.D.克拉克斯顿、P.P.马修斯、S.H.沃伦，《室外环境空气的遗传毒性综述：沙门氏菌致突变性》，《突变研究/突变研究评论》567 (2004) 347 - 399]综述了沙门氏菌致突变性试验中城市空气致突变性的文献。在此，我们综述了其他测试系统中城市空气致突变性的文献，并综述了实验系统中城市空气的致癌性。在大多数涉及啮齿动物的报告中，城市空气具有致癌性。研究将致癌活性主要归因于多环芳烃、硝基芳烃和其他芳香族化合物。大气条件以及污染物的水平和类型，导致了不同大都市地区空气致癌和致突变活性的差异。大多数诱变文献采用沙门氏菌试验（50%），其余大部分采用植物系统（31%）。目前的数据几乎无法支持使用植物系统来比较多个地点或研究之间的空气致突变性。对小鼠的研究表明，颗粒物空气污染会导致生殖细胞突变。空气流域含有相似类型和类别的诱变剂；然而，这些化合物的水平在不同空气流域之间差异很大。燃烧排放与城市空气的大部分致突变性和致癌性有关。大多数研究集中在颗粒物部分；因此，需要对挥发性和半挥发性部分、金属以及大气转化进行更多研究。较小颗粒中可提取有机物质的百分比更高，并且比大颗粒更具致突变性。尽管在环境空气中已鉴定出数百种遗传毒性化合物，但常规监测的只有少数几种（<25种），这凸显了在监测空气致癌和致突变活性及化合物时将生物测定与化学分析相结合的价值。
