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E-cigarettes (e-cigs, also called electronic nicotine delivery systems) were developed as an alternative to tobacco cigarettes and were initially suggested as a tool to help people quit smoking.However, their success as a smoking cessation tool is unclear ( 1 , 2 ).E-cigs heat e-cigarette liquids (e-liquids) and the resultant vapor is inhaled into the lungs.E-liquids typically contain nicotine and flavors in a propylene glycol (PG) and vegetable glycerin (VG) vehicle.Instead of enabling quitting, the inclusion of flavors in e-cigs has actually led to increased smoking, particularly in adolescents where 61.4% of 18 to 24-y olds report using e-cigs without a history of smoking cigarettes ( 2 , 3 ).In this issue of PNAS, Kulle et al. interrogated the impact of e-cigs on alveolar macrophage (AM) movement and function ( 4 ).They used state-of-the-art intravital microscopy (IVM) to image AM movement through lung alveoli in mice, both basally and in response to Pseudomonas aeruginosa infection.E-cig exposure was mediated through a full-body inhalation exposure system such that mice were exposed to e-cig vapor, similar to human exposure.
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Arnett et al. (2024) studied this question.
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