UC Riverside

In the United States, the recent surge of electronic cigarette (e-cig) use has raised questions concerning the safety of these devices. This study seeks to assess the pro-inflammatory and cellular stress effects of the vaped humectants propylene glycol (PG) and glycerol (GLY) on airway epithelial cells (16HBE cells and differentiated human bronchial epithelial cells) with a newly developed aerosol exposure system. This system allows for chemical characterization of e-cig generated aerosol particles as well as in vitro exposures of 16HBE cells at an air-liquid interface to vaped PG and GLY aerosol. Our data demonstrate that the process of vaping results in the formation of PG- and GLY-derived oligomers in the aerosol particles. Our in vitro data demonstrate an increase in pro-inflammatory cytokines IL-6 and IL-8 levels in response to vaped PG and GLY exposures. Vaped GLY also causes an increase in cellular stress signals HMOX1, NQO1, and carbonylated proteins when the e-cig device is operated at high wattages. Additionally, we find that the exposure of vaped PG causes elevated IL-6 expression, while the exposure of vaped GLY increases HMOX1 expression in human bronchial epithelial cells when the device is operated at high wattages. These findings suggest that vaporizing PG and GLY results in the formation of novel compounds and the exposure of vaped PG and GLY are detrimental to airway cells. Since PG and/or GLY is universally contained in all e-cig liquids, we conclude that these components alone can cause harm to the airway epithelium.