Vaping versus Smoking: A Quest for Long-term impact in a mouse model

Abstract Background Most smokers consider that electronic cigarettes are safer than tobacco and are marketed as safe products. Nevertheless, recent reports show the exposure to high levels of electronic cigarette vapors (ECV) activates lung cells and triggers lung inflammation and structural alterations after chronic exposure. In order to assess the potential harmful effect of moderate exposure to ECV, we investigated in mice, its effect on lung and systemic inflammation and on lung structure and function. Methods To reproduce closely the situation frequently encountered in human, we exposed mice during 1h/day during 3 or 6 months with two levels of electronic cigarette power in comparison with mice exposed to cigarette smoke (CS). Lung and systemic inflammation was evaluated by measuring cell recruitment and activation as well as cytokine concentrations. Lung transcriptome, respiratory function and body weight were also measured. Results Our data revealed that chronic exposure to moderate levels of ECV increased specifically lung inflammation including NK cells and T lymphocyte recruitment and the production of CXCL1 and CXCL2 chemokines as well as IL-22 after 3 months, these effects being different from the profile induced by CS. Surprisingly, there is no strong overlap between the impact of the 3 types of emissions on lung transcriptome. Modulation of pro-inflammatory pathways are limited to mice exposed to e-cig set to low power. In contrast, alteration of respiratory function is observed in high-power ECV-exposed mice but not at low power, with a different profile than in CS-exposed mice. Conclusion Subchronic (or mid-term) exposure to ECV might alter the respiratory function independently of the inflammatory response and in a different manner than CS.