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 attracts heightened attention due to its implication in various diseases, especially respiratory and cardiovascular diseases. Inhaled particulate matter not only carries microorganisms inside the body but also elicits local and systemic inflammatory responses resulting in altering host’s immunity and increasing susceptibility to infection. Previous as well as recent studies have documented that particulate matter 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 (CV) outcomes in COVID-19 patients and postulate on how particulate matter can influence these outcomes. We have also reviewed evidence on the use of rennin-angiotensin system (RAS) inhibitors, namely, ACE 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.

Positive association between outdoor air pollution and the incidence and severity of COVID-19. A review of the recent scientific evidences

“…Regarding the potential influence of these air pollutants on the transmission of SARS-CoV-2, the scientific evidence is much more limited, among other reasons since it has been much less investigated. However, it has been reported, for example, that PM could aggravate neurological symptoms of SARS-CoV-2 ( Borisova and Komisarenko, 2020 ), as well as respiratory and cardiovascular effects of COVID-19 ( Espejo et al, 2020 ; Tanwar et al, 2021 ). Air pollution could also mean a possible dangerous synergy with COVID-19 for semen quality and male fertility ( Montano et al, 2021a , b ).…”

Vehicle emissions-exposure alters expression of systemic and tissue-specific components of the renin-angiotensin system and promotes outcomes associated with cardiovascular disease and obesity in wild-type C57BL/6 male mice

“…While more recent interest in air pollution and RAS signaling has emerged because of the reported association between air pollution exposure and COVID-19 (SARS-CoV-2) susceptibility in the lungs [ 40 , 41 ], and associated cardiovascular effects [ 42 , 43 ]; there are still significant gaps in knowledge related to how air pollution alters systemic and adipose tissue-specific RAS signaling and how this may promote CVD and metabolic syndrome or obesity. Understanding key mechanistic pathways by which traffic-generated air pollution exposure can promote inflammatory comorbid disease states such as CVD, metabolic syndrome, and obesity is necessary for preventative and therapeutic targets, and also environmental regulatory outcomes.…”

Air pollution and cardiovascular disease: Can the Australian bushfires and global COVID‐19 pandemic of 2020 convince us to change our ways?

“…[ 92 ] Recent reports also suggest that SARS‐CoV‐2 can absorb onto the surface of PM creating PM‐SARS‐CoV‐2 particles. [ 97 ] The creation of particle‐virus hybrids may conceivably facilitate entry of the virus deep into the alveoli or facilitate translocation directly into the circulatory system, thus increasing viral load. As both PM and SARS‐CoV‐2 are known to induce systemic inflammatory responses, their combined effects may elicit the so‐called “cytokine storm” characteristic of COVID‐19.…”