Association of COVID-19 transmission with high levels of ambient pollutants: Initiation and impact of the inflammatory response on cardiopulmonary disease.

Abstract

Ambient air pollution contributes to 7 million premature deaths annually. Concurrently, the ongoing coronavirus disease 2019 (COVID-19) pandemic, complicated with S-protein mutations and other variants, caused by the novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has resulted in over 2.5 million deaths globally. Chronic air pollution-mediated cardiopulmonary diseases have been associated with an increased incidence of hospitalization and mechanical ventilation following COVID-19 transmission. While the underlying mechanisms responsible for this association remain elusive, air pollutant-induced vascular oxidative stress and inflammatory responses have been implicated in amplifying COVID-19-mediated cytokine release and vascular thrombosis. In addition, prolonged exposure to certain types of particulate matter (PM2.5, d < 2.5 μm) has also been correlated with increased lung epithelial and vascular endothelial expression of the angiotensin-converting enzyme-2 (ACE2) receptors to which the SARS-CoV-2 spike glycoproteins (S) bind for fusion and internalization into host cells. Emerging literature has linked high rates of SARS-CoV-2 infection to regions with elevated levels of PM2.5, suggesting that COVID-19 lockdowns have been implicated in regional reductions in air pollutant-mediated cardiopulmonary effects. Taken together, an increased incidence of SARS-CoV-2-mediated cardiopulmonary diseases seems to overlap with highly polluted regions. To this end, we will review the redox-active components of air pollutants, the pathophysiology of SARS-CoV-2 transmission, and the key oxidative mechanisms and ACE2 overexpression underlying air pollution-exacerbated SARS-CoV-2 transmission.