Electronic Cigarette Aerosol Is Cytotoxic and Increases ACE2 Expression on Human Airway Epithelial Cells: Implications for SARS-CoV-2 (COVID-19)

Tobacco smoking has emerged as a risk factor for increasing the susceptibility to infection from severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) via increased expression of angiotensin-converting enzyme-2 (ACE2) in lung, linked disease 2019 (COVID-19) development. Given modifiable nature electronic cigarettes and delivery high concentrations nicotine, we investigate whether cigarette vaping potential increase SARS-CoV-2 infection. We exposed BEAS-2B cells (bronchial epithelium transformed with Ad12-SV40 2B) primary small airway epithelial (SAECs) aerosol condensates produced propylene glycol/vegetable glycerin or commercially bought e-liquid (±added nicotine) smoke extract if exposure, like smoke, increases ACE2 lung cells. In cells, cytotoxicity (CCK-8), membrane integrity (LDH), protein (immunofluorescence) were measured both 4- 24 h treatments 4 SAECs; gene was using quantitative polymerase chain reaction (qPCR) treatment Nicotine-free higher nicotine-containing cytotoxic Higher LDH release reduced seen treated condensates. observably all compared cell controls, particularly exposures. significantly locally condensate nicotine concentration controls. Our study suggests that alone can result an expression. Vaping are avoidable factors COVID-19, which, avoided, could help reduce number COVID-19 cases severity disease. This is first utilize condensates, novel developed our laboratory, investigating human