Electronic cigarette aerosol condensate is cytotoxic and increases ACE2 expression in human airway epithelial cells: implications for COVID-19

Background: Tobacco smoking increases ACE2 expression in the lung, enhancing susceptibility to SARS-CoV-2 infection and progression to COVID-19. Electronic cigarettes (e-cig) have the capability to deliver large hits of nicotine, therefore they can also be an avoidable risk factor. Aim: We investigated the cytotoxicity profile of e-cig aerosol condensates and whether e-cig vaping can also elevate ACE2 expression in large and small airway epithelial cells (SAECs). Methods: Bronchial (BEAS-2B) and primary SAECs were exposed to e-cig aerosol condensates produced from PG/VG or watermelon e-liquid (± added nicotine), and cigarette smoke extract (CSE). Cytotoxicity (CCK-8), membrane integrity (LDH), and ACE2 protein expression (IF) and gene expression (qPCR) were measured in BEAS-2Bs and SAECs for both 4 and 24-hours treatments. Results: Nicotine-free condensates (p Conclusions: Our data suggests that vaping is cytotoxic and can increase lung ACE2 expression. Vaping should be avoided, particularly during the COVID-19 pandemic.