Summary
Introduction:
This text discusses a study examining the effects of nicotine-containing electronic cigarette (e-cig) vapor on airway mucociliary function in vitro and in vivo. The study uses human bronchial epithelial cells and a large animal model to investigate the impact of e-cig vapor on mucociliary parameters and nicotine delivery.
Key Points:
* E-cig vapor reduced airway surface liquid hydration and increased mucus viscosity of human bronchial epithelial cells in a nicotine-dependent manner.
* acute nicotine exposure increased intracellular calcium levels, an effect primarily dependent on TRPa1 (transient receptor potential ankyrin 1).
* TRPa1 inhibition with a967079 restored nicotine-mediated impairment of mucociliary parameters including mucus transport in vitro.
* Sheep tracheal mucus velocity, an in vivo measure of mucociliary clearance, was also reduced by e-cig vapor.
* Nebulized e-cig liquid containing nicotine also reduced tracheal mucus velocity in a dose-dependent manner and elevated plasma cotinine levels.
* Importantly, nebulized a967079 reversed the effects of e-cig liquid on sheep tracheal mucus velocity.
* The main nicotine effect on mucociliary function is mediated by TRPa1 and not nicotinic acetylcholine receptors.
Main Message:
The study finds that inhalation of e-cig vapor causes airway mucociliary dysfunction in vitro and in vivo. Furthermore, it suggests that the main nicotine effect on mucociliary function is mediated by TRPa1 and not nicotinic acetylcholine receptors. These findings have important implications for the regulation of e-cigarettes and highlight the need for further research into their potential health effects.
Citation
Chung S, Baumlin N, Dennis JS, et al. Electronic Cigarette Vapor with Nicotine Causes airway Mucociliary Dysfunction Preferentially via TRPa1 Receptors. american journal of respiratory and critical care medicine. 2019;200(9):1134-1145. doi:10.1164/rccm.201811-2087OC
