Roadside proximity and exposure to mixed vehicular emissions (MVE) have been linked to adverse pulmonary and vascular outcomes. However, because of the complex nature of the contribution of particulate matter (PM) versus gases, it is difficult to decipher the precise causative factors regarding PM and the copollutant gaseous fraction. To this end, C57BL/6 and apolipoprotein E knockout mice (ApoE^−/−) were exposed to either filtered air (FA), fine particulate (FP), FP+gases (FP+G), ultrafine particulate (UFP), or UFP+gases (UFP+G). Two different timeframes were employed: 1-day (acute) or 30-day (subchronic) exposures. Examined biological endpoints included aortic vasoreactivity, aortic lesion quantification, and aortic mRNA expression. Impairments in vasorelaxation were observed following acute exposure to FP+G in C57BL/6 animals and FP, UFP, and UFP+G in ApoE^−/− animals. These effects were completely abrogated or markedly reduced following subchronic exposure. Aortic lesion quantification in ApoE^−/− animals indicated a significant increase in atheroma size in the UFP-, FP-, and FP+G-exposed groups. Additionally, ApoE^−/− mice demonstrated a significant fold increase in TNFα expression following FP+G exposure and ET-1 following UFP exposure. Interestingly, C57BL/6 aortic gene expression varied widely across exposure groups. TNFα decreased significantly following FP exposure and CCL-5 decreased in the UFP-, FP-, and FP+G-exposed groups. Conversely, ET-1, CCL-2, and CXCL-1 were all significantly upregulated in the FP+G group. These findings suggest that gas–particle interactions may play a role in vascular toxicity, but the contribution of surface area is not clear.

中文翻译：

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车辆颗粒物（PM）特性影响吸入后的血管结局。

路边的接近性和混合车辆排放物（MVE）的暴露与不良的肺和血管结局有关。但是，由于颗粒物（PM）对气体的贡献具有复杂的性质，因此很难解释有关PM和共污染物气态组分的精确原因。为此，C57BL / 6和载脂蛋白E基因敲除小鼠（ApoE ^-/-）暴露于过滤空气（FA），细颗粒（FP），FP +气体（FP + G），超细颗粒（UFP）或UFP +气体（UFP + G）中。使用两种不同的时间范围：1天（急性）或30天（亚慢性）暴露。检查的生物学终点包括主动脉血管反应性，主动脉病变定量和主动脉mRNA表达。在C57BL / 6动物和FP，UFP和ApoE ^-/-动物的FP，UFP和UFP + G急性暴露于FP + G后，观察到血管舒张受损。在亚慢性暴露后，这些作用被完全消除或明显减轻。ApoE ^-/-动物的主动脉病变定量表明，暴露于UFP-，FP-和FP + G组的动脉粥样硬化大小显着增加。此外，ApoE ^-/-FP + G暴露和UFP暴露后，ET-1小鼠的TNFα表达明显增加。有趣的是，C57BL / 6主动脉基因表达在不同暴露组之间差异很大。在暴露于FPP，FP-和FP + G的组中，FP暴露后TNFα显着降低，而CCL-5降低。相反，FP + G组的ET-1，CCL-2和CXCL-1均显着上调。这些发现表明，气体与颗粒之间的相互作用可能在血管毒性中起作用，但表面积的贡献尚不清楚。