Does Vaping Increase the Likelihood of SARS-CoV-2 Infection? Paradoxically Yes and No

Abstract

Data on the relationship between electronic cigarettes (ECs) and SARS-CoV-2 infection are limited and contradictory. Evidence indicates that EC aerosols or nicotine increase ACE2, SARS-CoV-2 virus receptors, which increase virus binding and susceptibility. Our objectives were to determine if EC aerosols increased SARS-CoV-2 infection of human bronchial epithelial cells and to identify the causative chemical(s). A 3D organotypic model (EpiAirway) in conjunction with air liquid interface (ALI) exposure was used to test the effects of aerosols produced from JUUL "Virginia Tobacco" and BLU ECs, or individual chemicals (nicotine, propylene glycol, vegetable glycerin (PG/VG), and benzoic acid) on infection using SARS-CoV-2 pseudoparticles. Exposure of EpiAirway to JUUL aerosols increased ACE2, while BLU and lab-made EC aerosols containing nicotine increased ACE2 levels and TMPRSS2 activity, a spike protease that enables viral-cell fusion. Pseudoparticle infection of EpiAirway increased with aerosols produced from PG/VG, PG/VG plus nicotine, or BLU ECs. JUUL EC aerosols did not increase infection above controls. The baseline level of infection in JUUL treated aerosol groups was attributed to benzoic acid, which mitigated the enhanced infection caused by PG/VG or nicotine. The benzoic acid protection from enhanced infection continued at least 48 hours after exposure. TMPRSS2 activity was significantly correlated with e-liquid pH, which in turn was significantly correlated with infection, with lower pH blocking PG/VG and nicotine-induced-enhanced infection. While ACE2 levels increased in EpiAirway tissues exposed to EC aerosols, infection depended on the ingredients of the e-liquids. PG/VG and nicotine enhanced infection, an effect that was mitigated by benzoic acid.