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. Our objectives were to investigate the impact of EC aerosols on SARS-CoV-2 infection of human bronchial epithelial cells and identify the causative chemical(s). Fully differentiated human bronchial epithelial tissues (hBET) were exposed at the air liquid interface (ALI) to aerosols produced from JUUL{trade mark, serif} "Virginia Tobacco" and BLU{trade mark, serif} ECs, as well as nicotine, propylene glycol (PG), vegetable glycerin (VG), and benzoic acid, and infection was then evaluated with SARS-CoV-2 pseudoparticles. Pseudoparticle infection of hBET increased with aerosols produced from PG/VG, PG/VG plus nicotine, or BLU{trade mark, serif} ECs; however, JUUL{trade mark, serif} EC aerosols did not increase infection compared to controls. Increased infection in PG/VG alone was due to enhanced endocytosis, while increased infection in PG/VG plus nicotine or in BLU{trade mark, serif} ECs was caused by nicotine-induced elevation of the aerosol's pH, which correlated with increased TMPRSS2 activity. Notably, benzoic acid in JUUL{trade mark, serif} aerosols mitigated the enhanced infection caused by PG/VG or nicotine, offering protection that lasted for at least 48 hours after exposure. In conclusion, the study demonstrates that EC aerosols can impact susceptibility to SARS-CoV-2 infection depending on their specific ingredients. PG/VG alone or PG/VG plus nicotine enhanced infection through different mechanisms, while benzoic acid in JUUL{trade mark, serif} aerosols mitigated the increased infection caused by certain ingredients. These findings highlight the complex relationship between ECs and SARS-CoV-2 susceptibility, emphasizing the importance of considering the specific aerosol ingredients when evaluating the potential effects of ECs on infection risk.