Exposure to air pollution exerts direct effects on respiratory organs; however, molecular alterations underlying air pollution-induced pulmonary injury remain unclear. In this study, we investigated the effect of air pollution on the lung tissues of Sprague-Dawley rats with whole-body exposure to traffic-related PM1 (particulate matter < 1 μm in aerodynamic diameter) pollutants and compared it with that in rats exposed to high-efficiency particulate air–filtered gaseous pollutants and clean air controls for 3 and 6 months. Lung function and histological examinations were performed along with quantitative proteomics analysis and functional validation. Rats in the 6-month PM1-exposed group exhibited a significant decline in lung function, as determined by decreased FEF25–75% and FEV20/FVC; however, histological analysis revealed earlier lung damage, as evidenced by increased congestion and macrophage infiltration in 3-month PM1-exposed rat lungs. The lung tissue proteomics analysis identified 2673 proteins that highlighted the differential dysregulation of proteins involved in oxidative stress, cellular metabolism, calcium signalling, inflammatory responses, and actin dynamics under exposures to PM1 and gaseous pollutants. The presence of PM1 specifically enhanced oxidative stress and inflammatory reactions under subchronic exposure to traffic-related PM1 and suppressed glucose metabolism and actin cytoskeleton signalling. These factors might lead to repair failure and thus to lung function decline after chronic exposure to traffic-related PM1. A detailed pathogenic mechanism was proposed to depict temporal and dynamic molecular regulations associated with PM1- and gaseous pollutants-induced lung injury. This study explored several potential molecular features associated with early lung damage in response to traffic-related air pollution, which might be used to screen individuals more susceptible to air pollution.

中文翻译：

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长期暴露于交通相关颗粒物和气态污染物与大鼠肺损伤的不同分子机制有关

暴露于空气污染会对呼吸器官产生直接影响；然而，空气污染引起的肺损伤的分子改变仍不清楚。在本研究中，我们调查了空气污染对全身暴露于交通相关 PM1（空气动力学直径小于 1 μm 的颗粒物）污染物的 Sprague-Dawley 大鼠肺组织的影响，并将其与暴露于高效微粒空气过滤气态污染物和清洁空气控制 3 和 6 个月。肺功能和组织学检查与定量蛋白质组学分析和功能验证一起进行。6 个月 PM1 暴露组的大鼠肺功能显着下降，如 FEF25–75% 和 FEV20/FVC 下降所确定；然而，组织学分析揭示了早期的肺损伤，这可以通过 3 个月暴露于 PM1 的大鼠肺中的充血和巨噬细胞浸润增加来证明。肺组织蛋白质组学分析确定了 2673 种蛋白质，这些蛋白质突出了在暴露于 PM1 和气态污染物的情况下，参与氧化应激、细胞代谢、钙信号、炎症反应和肌动蛋白动力学的蛋白质的差异失调。PM1 的存在在亚慢性暴露于交通相关 PM1 下特异性增强氧化应激和炎症反应，并抑制葡萄糖代谢和肌动蛋白细胞骨架信号传导。这些因素可能导致修复失败，从而导致长期接触交通相关 PM1.5 后肺功能下降。提出了详细的致病机制来描述与 PM1 和气体污染物引起的肺损伤相关的时间和动态分子调节。本研究探讨了与交通相关空气污染引起的早期肺损伤相关的几个潜在分子特征，这些特征可能用于筛查更容易受到空气污染影响的个体。