Traffic-derived particulate matter and angiotensin-converting enzyme 2 expression in human airway epithelial cells

Abstract

Take home messageCulture of airway epithelial cells with traffic-derived particulate matter less than 10 microns in aerodynamic diameter (PM 10 ) upregulates the expression of angiotensinconverting enzyme 2 -the receptor used by SARS-CoV-2 to infect host cells. Abstract BackgroundThe mechanism for the association between traffic-derived particulate matter less than 10 microns (PM10) and cases of COVID-19 disease reported in epidemiological studies is unknown. To infect cells, the spike protein of SARS-CoV-2 interacts with angiotensin-converting enzyme 2 (ACE2) on host airway cells. Increased ACE2 expression in lower airway cells in active smokers, suggests a potential mechanism whereby PM10 increases vulnerability to COVID-19 disease. ObjectiveTo assess the effect of traffic-derived PM 10 on human airway epithelial cell ACE2 expression in vitro. MethodsPM 10 was collected from Marylebone Road (London) using a kerbside impactor.A549 and human primary nasal epithelial cells were cultured with PM10 for 2 h, and ACE2 expression (median fluorescent intensity; MFI) assessed by flow cytometry.We included cigarette smoke extract as a putative positive control. Data were analysed by either Mann-Whitney test, or Kruskal-Wallis with multiple comparisons test.

Air pollution and COVID-19 mortality in the United States: Strengths and limitations of an ecological regression analysis

“…Although an ecological regression analysis cannot provide insight into the mechanisms underlying the relationship between PM 2.5 exposure and COVID-19 mortality, studies are starting to shed light on the potential biological mechanisms that may explain the relationship between air pollution and viral infection outcomes (16). For example, it has been hypothesized that chronic exposure to PM 2.5 causes alveolar angiotensin-converting enzyme 2 (ACE-2) receptor overexpression and impairs host defenses (17). This could cause a more severe form These overlap with the confounder sets used in much of the previous literature on air pollution and health (25,26) Difficult to formalize the notion of "epidemic stage," which may be an important confounder…”

The Secretive Liaison of Particulate Matter and SARS-CoV-2. A Hypothesis and Theory Investigation

“…The increase of cytokines involved in systemic inflammation, following the exposure to PM, has been related to the increase of the risk and severity for cardiovascular disease in humans (Pope et al, 2016;Miyashita et al, 2020), and it has been confirmed in animal models, where a PM-related mechanism involving the renin-angiotensin-bradykinin system has been postulated (Aztatzi-Aguilar et al, 2015;Lin et al, 2018;Sharma et al, 2019).…”

“…This geographical stretch includes regions and areas characterized by high levels of air pollution. Therefore, it was speculated that environmental pollution had played a key role in the spread of the COVID-19 disease, and even debated whether the atmospheric airborne (PM) may act as a carrier of the virus SARS-CoV-2 (Contini and Costabile, 2020;Conticini et al, 2020;Miyashita et al, 2020). Using Italian data (until 21st March 2020) and comparing lethality in Lombardy and Emilia-Romagna with the rest of Italy, Conticini et al (2020) have speculated that chronic exposure to air pollution can increase the susceptibility for respiratory disease, and might render an individual more susceptible to SARS-CoV-2 and other respiratory infections, when compared to residents in areas with lower pollution.…”

Significant Unresolved Questions and Opportunities for Bioengineering in Understanding and Treating COVID-19 Disease Progression

“… 253 , 279 Traffic related PM has also been shown to increase ACE2 expression in both pulmonary and nasal epithelial cells in vitro. 159 Independent of COVID-19, exposure to PM is heavily correlated to cardiovascular disease. 222 , 233 PM exposure causes barrier dysfunction and elevated IL-6 production in HUVEC cultures 55 as well as the formation of intracellular reactive oxygen species (ROS) and eventual cellular senescence, even at relatively low levels.…”