Double trouble: combined cardiovascular effects of particulate matter exposure and coronavirus disease 2019

Abstract

The coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has rapidly grown into a pandemic. According to initial reports, the lungs were thought to be the primary target, but recent case studies have shown its reach can extend to other organs including the heart and blood vessels. The severity of cardiac complications of COVID-19 depends on multiple underlying factors, with air pollutant exposure being one of them, as reported by several recent studies. Airborne particulate matter (PM) attracts heightened attention due to its implication in various diseases, especially respiratory and cardiovascular diseases. Inhaled PM not only carries microorganisms inside the body but also elicits local and systemic inflammatory responses resulting in altering the host's immunity and increasing susceptibility to infection. Previous and recent studies have documented that PM acts as a 'carrier' for the virus and aids in spreading viral infections. This review presents the mechanisms and effects of viral entry and how pollution can potentially modulate pathophysiological processes in the heart. We aimed to concisely summarize studies examining cardiovascular outcomes in COVID-19 patients and postulate on how PM can influence these outcomes. We have also reviewed evidence on the use of renin-angiotensin system inhibitors, namely angiotensin-converting enzyme inhibitors and angiotensin receptor blockers, in patients with COVID-19. The interplay of pollution and SARS-CoV-2 is essential to understanding the effects of accentuated cardiovascular effects of COVID-19 and deserves in-depth experimental investigations.

Keywords: Cardiovascular diseases; Aerosol; Air pollution; Airborne transmission; COVID-19; Particulate matter; SARS-CoV-2.

Figure 1

Host cell entry mechanisms utilized by SARS-CoV-2. ACE2, angiotensin-converting enzyme 2; PM, particulate matter; S protein, spike protein; SARS-CoV-2, severe acute respiratory syndrome coronavirus 2; TMPRSS 2, transmembrane protease serine type 2.

Figure 2

CFR for different comorbid conditions in China. The CFR is calculated by dividing the total number of deaths (n = 1023) from a disease by the number of confirmed cases (n = 44 672). The data were obtained from the Chinese Center for Disease Prevention and Control.

Figure 3

Plausible mechanisms of PM_2.5-induced exacerbated cardiac injury in COVID-19. ACE2, angiotensin-converting enzyme 2; AngII, angiotensin II; Ang1-7, angiotensin 1-7; PM, particulate matter; SARS-CoV-2, severe acute respiratory syndrome coronavirus 2; RAS, renin–angiotensin system.