Diesel exhaust particles (DEP) are the major components of atmospheric particulate matter (PM) and chronic exposure is recognized to enhance respiratory system complications. Although the spread of SARS-CoV-2 was found to be associated with the PMs, the mechanism by which exposure to DEP increases the risk of SARS-CoV-2 infection is still under discussion. However, diesel fine PM (dPM) elevate the probability of SARS-CoV-2 infection, as it coincides with the increase in the number of ACE2 receptors. Expression of ACE2 and its colocalized activator, transmembrane protease serine 2 (TMPRSS2) facilitate the entry of SARS-CoV-2 into the alveolar epithelial cells exposed to dPM. Thus, the coexistence of PM and SARS-CoV-2 in the environment augments inflammation and exacerbates lung damage. Increased TGF-β1 expression due to DEP accompanies the proliferation of the extracellular matrix. In this case, “multifocal ground-glass opacity” (GGO) in a CT scan is an indication of a cytokine storm and severe pneumonia in COVID-19.

柴油机尾气颗粒 (DEP) 是大气颗粒物 (PM) 的主要成分，长期暴露会增加呼吸系统并发症。尽管发现 SARS-CoV-2 的传播与 PM 相关，但暴露于 DEP 会增加 SARS-CoV-2 感染风险的机制仍在讨论中。然而，柴油细颗粒物 (dPM) 会增加 SARS-CoV-2 感染的可能性，因为它与 ACE2 受体数量的增加相吻合。ACE2 及其共定位激活剂跨膜蛋白酶丝氨酸 2 (TMPRSS2) 的表达促进 SARS-CoV-2 进入暴露于 dPM 的肺泡上皮细胞。因此，环境中 PM 和 SARS-CoV-2 的共存会加剧炎症并加剧肺损伤。DEP 引起的 TGF-β1 表达增加伴随着细胞外基质的增殖。在这种情况下，CT 扫描中的“多灶毛玻璃混浊”(GGO) 表明 COVID-19 中存在细胞因子风暴和严重肺炎。