Hemmingsen Jette Gjerke, Møller Peter, Jantzen Kim, Jönsson Bo A G, Albin Maria, Wierzbicka Aneta, Gudmundsson Anders, Loft Steffen, Rissler Jenny
Section of Environmental Health, Department of Public Health, Faculty of Health and Medical Sciences, University of Copenhagen, Øster Farimagsgade 5A, DK-1014 Copenhagen, Denmark.
Division of Occupational and Environmental Medicine, Lund University, SE-22185 Lund, Sweden.
Mutat Res. 2015 May;775:66-71. doi: 10.1016/j.mrfmmm.2015.03.009. Epub 2015 Mar 28.
Particulate air pollution increases risk of cancer and cardiopulmonary disease, partly through oxidative stress. Traffic-related noise increases risk of cardiovascular disease and may cause oxidative stress. In this controlled random sequence study, 18 healthy subjects were exposed for 3h to diesel exhaust (DE) at 276 μg/m(3) from a passenger car or filtered air, with co-exposure to traffic noise at 48 or 75 dB(A). Gene expression markers of inflammation, (interleukin-8 and tumor necrosis factor), oxidative stress (heme oxygenase (decycling-1)) and DNA repair (8-oxoguanine DNA glycosylase (OGG1)) were unaltered in peripheral blood mononuclear cells (PBMCs). No significant differences in DNA damage levels, measured by the comet assay, were observed after DE exposure, whereas exposure to high noise levels was associated with significantly increased levels of hOGG1-sensitive sites in PBMCs. Urinary levels of 8-oxo-7,8-dihydro-2'-deoxyguanosine were unaltered. In auxiliary ex vivo experiments whole blood was incubated with particles from the exposure chamber for 3h without effects on DNA damage in PBMCs or intracellular reactive oxygen species production and expression of CD11b and CD62L adhesion molecules in leukocyte subtypes.
3-h exposure to DE caused no genotoxicity, oxidative stress or inflammation in PBMCs, whereas exposure to noise might cause oxidatively damaged DNA.
空气中的微粒污染会增加患癌症和心肺疾病的风险，部分原因是通过氧化应激。与交通相关的噪音会增加患心血管疾病的风险，并可能导致氧化应激。在这项对照随机序列研究中，18名健康受试者分别暴露于来自乘用车的浓度为276μg/m³的柴油废气（DE）或过滤空气中3小时，同时暴露于48或75dB(A)的交通噪音中。炎症（白细胞介素-8和肿瘤坏死因子）、氧化应激（血红素加氧酶（去环化-1））和DNA修复（8-氧代鸟嘌呤DNA糖基化酶（OGG1））的基因表达标志物在外周血单核细胞（PBMC）中未发生改变。通过彗星试验测量的DNA损伤水平在暴露于DE后未观察到显著差异，而暴露于高噪音水平与PBMC中hOGG1敏感位点水平的显著增加有关。尿中8-氧代-7,8-二氢-2'-脱氧鸟苷的水平未发生改变。在辅助的体外实验中，全血与暴露室中的颗粒一起孵育3小时，对PBMC中的DNA损伤、细胞内活性氧的产生以及白细胞亚型中CD11b和CD62L粘附分子的表达均无影响。
暴露于DE 3小时未在PBMC中引起遗传毒性、氧化应激或炎症，而暴露于噪音可能会导致DNA氧化损伤。
