The effect of environmental diesel exhaust pollution on SARS-CoV-2 infection: The mechanism of pulmonary ground glass opacity

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.