Exposure to nicotine-free and flavor-free e-cigarette vapors modifies the pulmonary response to tobacco cigarette smoke in female mice

Ariane Lechasseur, Carol-Ann Huppé, Maude Talbot, Joanie Routhier, Sophie Aubin, Marie-Josée Beaulieu, Caroline Duchaine, David Marsolais, Mathieu C Morissette
2020 American Journal of Physiology - Lung cellular and Molecular Physiology  
Background. Most of electronic cigarette (e-cigarette) users are also smoking tobacco cigarettes. Due to the relative novelty of this habit, very little is known on the impact of vaping on pulmonary health, even less on the potential interactions of dual e-cigarette and tobacco cigarette use. Methods. Therefore, we used well-established mouse models to investigate the impact of dual exposure to e-cigarette vapors and tobacco cigarette smoke on lung homeostasis. Groups of female BALB/c mice were
more » ... exposed to room air, tobacco smoke only, nicotine-free flavor-free e-cigarette vapors only or both tobacco smoke and e-cigarette vapors. Moreover, since tobacco smoke and electronic cigarette vapors both affect circadian processes in the lungs, groups of mice were euthanized at two different time points during the day. Results. We found that dual-exposed mice had altered lung circadian gene expression compared to mice exposed to tobacco smoke alone. Dual-exposed mice also had different frequencies of dendritic cells, macrophages and neutrophils in the lung tissue compared mice exposed to tobacco smoke alone, an observation also valid for B-lymphocytes and CD4+ and CD8+ T lymphocytes. Exposure to e-cigarette vapors also impacted the levels of immunoglobulins in the bronchoalveolar lavage and serum. Finally, e-cigarette and dual exposures increased airway resistance compared to mice exposed to room air or tobacco smoke alone, respectively. Discussion. Taken together, these data suggest that e-cigarette vapors, even without nicotine or flavors, could affect how the lungs react to tobacco cigarette smoke exposure in dual users, potentially altering the pathological course triggered by smoking.
doi:10.1152/ajplung.00037.2020 pmid:32845704 fatcat:pv4xof3wbbb2jhc4ynvtr4gh4q