Glycerine drives acute lung‐function impairment and airway inflammation after e‐cigarette aerosol exposure in mice

Abstract Electronic cigarettes generate an aerosol by heating an e‐liquid based on propylene glycol (PG) and/or glycerin (VG), with or without nicotine and flavourings. Their acute respiratory effects, particularly with respect to asthma, remain poorly defined. We exposed ovalbumin‐sensitised female BALB/c mice, which were subsequently challenged with ovalbumin (‘asthmatic’) or saline (‘non‐asthmatic’), to one of four e‐cigarette aerosols (PG or VG, each with 0 or 12 mg/mL nicotine) for 30 s. Airway resistance ( R aw ), tissue damping ( G ) and tissue elastance ( H ) were measured once/minute for 60 min using the forced oscillation technique. A second e‐cigarette aerosol was given at the 30‐min mark. Bronchoalveolar lavage (BAL) was taken for assessment of cellular inflammation. Group sizes were 4–9 mice ( n = 53 for lung mechanics and 57 for BAL). All aerosols acutely increased R aw , G and H , and excipient was the dominant determinant. VG produced substantially larger increases than PG across most parameters and exposures ( P < 0.0001, except airway resistance after the first exposure, P = 0.0569), responses approximately doubled after a second exposure, and allergic sensitisation augmented the repeated‐exposure mechanical response. Nicotine was not required for these effects and, where significant, attenuated them. In BAL, granulocytic inflammation was confined to asthmatic mice and was greater with VG than PG. Acute e‐cigarette aerosol exposure is not innocuous; e‐liquid composition, especially the excipient, is a key determinant of acute respiratory effects independent of nicotine.