Department of Nanotoxicology and Molecular Epidemiology, Institute of Experimental Medicine of the CAS, Videnska 1083, 142 20, Prague, Czech Republic.
Department of Nanotoxicology and Molecular Epidemiology, Institute of Experimental Medicine of the CAS, Videnska 1083, 142 20, Prague, Czech Republic; Department of Physiology, Faculty of Science, Charles University, Vinicna 7, 128 44, Prague, Czech Republic.
Chemosphere. 2021 Oct;281:130833. doi: 10.1016/j.chemosphere.2021.130833. Epub 2021 May 10.
Road traffic emissions consist of gaseous components, particles of various sizes, and chemical compounds that are bound to them. Exposure to vehicle emissions is implicated in the etiology of inflammatory respiratory disorders. We investigated the inflammation-related markers in human bronchial epithelial cells (BEAS-2B) and a 3D model of the human airways (MucilAir™), after exposure to complete emissions and extractable organic matter (EOM) from particles generated by ordinary gasoline (E5), and a gasoline-ethanol blend (E20; ethanol content 20% v/v). The production of 22 lipid oxidation products (derivatives of linoleic and arachidonic acid, AA) and 45 inflammatory molecules (cytokines, chemokines, growth factors) was assessed after days 1 and 5 of exposure, using LC-MS/MS and a multiplex immunoassay, respectively. The response observed in MucilAir™ exposed to E5 gasoline emissions, characterized by elevated levels of pro-inflammatory AA metabolites (prostaglandins) and inflammatory markers, was the most pronounced. E20 EOM exposure was associated with increased levels of AA metabolites with anti-inflammatory effects in this cell model. The exposure of BEAS-2B cells to complete emissions reduced lipid oxidation, while E20 EOM tended to increase concentrations of AA metabolite and chemokine production; the impacts on other inflammatory markers were limited. In summary, complete E5 emission exposure of MucilAir™ induces the processes associated with the pro-inflammatory response. This observation highlights the potential negative health impacts of ordinary gasoline, while the effects of alternative fuel are relatively weak.
道路交通排放物包括气态成分、各种大小的颗粒以及与之结合的化学物质。接触车辆排放物与炎症性呼吸道疾病的病因有关。我们研究了普通汽油（E5）和汽油-乙醇混合物（E20；乙醇含量 20%v/v）生成的颗粒的完整排放物和可提取有机物（EOM）暴露于人支气管上皮细胞（BEAS-2B）和人气道 3D 模型（MucilAir™）后与炎症相关的标志物。使用 LC-MS/MS 和多重免疫测定法分别在暴露后第 1 天和第 5 天评估了 22 种脂质氧化产物（亚油酸和花生四烯酸的衍生物，AA）和 45 种炎症分子（细胞因子、趋化因子、生长因子）的产生。暴露于 E5 汽油排放物的 MucilAir™观察到的反应最为明显，其特征是促炎 AA 代谢物（前列腺素）和炎症标志物水平升高。在该细胞模型中，E20 EOM 暴露与具有抗炎作用的 AA 代谢物水平升高有关。BEAS-2B 细胞暴露于完整排放物会降低脂质氧化，而 E20 EOM 则倾向于增加 AA 代谢物和趋化因子产生的浓度；对其他炎症标志物的影响有限。总之，MucilAir™ 完整 E5 排放物暴露会引发与促炎反应相关的过程。这一观察结果强调了普通汽油可能对健康造成的负面影响，而替代燃料的影响则相对较弱。
