Differential responses to e-cig generated aerosols from humectants and different forms of nicotine in epithelial cells from nonsmokers and smokers

In the United States, millions of adults use electronic cigarettes (e-cigs), and a majority of these users are former or current cigarette smokers. It is unclear, whether prior smoking status affects biological responses induced by e-cigs. In this study, differentiated human nasal epithelial cells (...

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Bibliographic Details
Published in:American journal of physiology. Lung cellular and molecular physiology 2021-06, Vol.320 (6), p.L1064-L1073
Main Authors: Escobar, Yael-Natalie H, Morrison, Cameron B, Chen, Yuzhi, Hickman, Elise, Love, Charlotte A, Rebuli, Meghan E, Surratt, Jason D, Ehre, Camille, Jaspers, Ilona
Format: Article
Language:English
Subjects:
Aerosols
Biological effects
Cell differentiation
Cigarette smoke
Cigarette smoking
Cytokines
Electronic cigarettes
Electronic Nicotine Delivery Systems
Epithelial cells
Epithelial Cells - drug effects
Epithelium
Exposure
Glycerol
Glycerol - pharmacology
Humans
Hygroscopic Agents - pharmacology
Inflammation
Lung - drug effects
Mucin
Nicotine
Nicotine - pharmacology
Non-Smokers
Propylene
Propylene glycol
Propylene Glycol - pharmacology
Salts
Smokers
Smoking
Tobacco smoke
Vaping - adverse effects
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Summary:In the United States, millions of adults use electronic cigarettes (e-cigs), and a majority of these users are former or current cigarette smokers. It is unclear, whether prior smoking status affects biological responses induced by e-cigs. In this study, differentiated human nasal epithelial cells (hNECs) from nonsmokers and smokers at air-liquid interface were acutely exposed to the e-cig generated aerosols of humectants, propylene glycol (PG), and glycerol (GLY). Mucin levels were examined in the apical washes, and cytokine levels were assessed in the basolateral supernatants 24 h postexposure. The aerosol from the GLY exposure increased mucin 5, subtype AC (MUC5AC) levels in the apical wash of hNECs from nonsmokers, but not smokers. However, the aerosol from GLY induced pro-inflammatory responses in hNECs from smokers. We also exposed hNECs from nonsmokers and smokers to e-cig generated aerosol from PG:GLY with freebase nicotine or nicotine salt. The PG:GLY with freebase nicotine exposure increased MUC5AC and mucin 5, subtype B (MUC5B) levels in hNECs from nonsmokers, but the nicotine salt exposure did not. The PG:GLY with nicotine salt exposure increased pro-inflammatory cytokines in hNECs from smokers, which was not seen with the freebase nicotine exposure. Taken together, these data indicate that the e-cig generated aerosols from the humectants, mostly GLY, and the type of nicotine used cause differential effects in airway epithelial cells from nonsmokers and smokers. As e-cig use is increasing, it is important to understand that the biological effects of e-cig use are likely dependent on prior cigarette smoke exposure.
ISSN:1040-0605
1522-1504
DOI:10.1152/AJPLUNG.00525.2020