Introduction E-cigarette (EC) and vaping use continue to remain popular amongst teenage and young adult populations, despite several reports of vaping associated lung injury. One of the first compounds that EC aerosols comes into contact within the lungs during a deep inhalation is pulmonary surfactant. Impairment of surfactant’s critical surface tension reducing activity can contribute to lung dysfunction. Currently, information on how EC aerosols impacts pulmonary surfactant remains limited. We hypothesized that exposure to EC aerosol impairs the surface tension reducing ability of surfactant. Methods Bovine Lipid Extract Surfactant (BLES) was used as a model surfactant in a direct exposure syringe system. BLES (2ml) was placed in a syringe (30ml) attached to an EC. The generated aerosol was drawn into the syringe and then expelled, repeated 30 times. Biophysical analysis after exposure was completed using a constrained drop surfactometer (CDS). Results Minimum surface tensions increased significantly after exposure to the EC aerosol across 20 compression/expansion cycles. Mixing of non-aerosolized e-liquid did not result in significant changes. Variation in device used, addition of nicotine, or temperature of the aerosol had no additional effect. Two e-liquid flavours, menthol and red wedding, had further detrimental effects, resulting in significantly higher surface tension than the vehicle exposed BLES. Menthol exposed BLES has the highest minimum surface tensions across all 20 compression/expansion cycles. Alteration of surfactant properties through interaction with the produced aerosol was observed with a basic e-liquid vehicle, however additional compounds produced by added flavourings appeared to be able to increase inhibition. Conclusion EC aerosols alter surfactant function through increases in minimum surface tension. This impairment may contribute to lung dysfunction and susceptibility to further injury.

E-cigarette (EC) and vaping use continue to remain popular amongst teenage and young adult populations, despite several reports of vaping associated lung injury. This popularity is due in part to the vast variety of appealing flavours and nicotine concentrations easily accessible on the market. One of the first compounds that EC vapour comes into contact within the lungs during a deep inhalation is pulmonary surfactant. This lipid protein mixture lines the alveoli, reducing surface tension and preventing alveolar collapse. Impairment of surfactant’s critical surface tension reducing activity can contribute to lung dysfunction. Currently, information on how EC vapour impacts pulmonary surfactant remains limited. We hypothesized that exposure to EC vapour impairs the surface tension reducing ability of surfactant. BLES was used as a model surfactant in a direct exposure syringe system. BLES (2ml) was placed in a syringe (30ml) attached to an EC. Vapour was drawn into the syringe and then expelled, repeated 30 times. Biophysical analysis after exposure was completed using a constrained drop surfactometer (CDS). Minimum surface tensions increased after exposure to vapour. Variation in device used, addition of nicotine, or temperature of the vapour had no additional effect. Two e-liquid flavours, menthol and red wedding, had further detrimental effects, resulting in higher surface tension than the vehicle exposed BLES. Alteration of surfactant properties through interaction with vapour was observed with a basic e-liquid vehicle, however additional compounds produced by added flavourings appeared to be able to increase inhibition, however the exact mechanism remains unclear. In conclusion, EC vapour alters surfactant function through increases in minimum surface tension. This impairment can contribute to lung dysfunction and susceptibility to further injury.

Introduction: The use of e-cigarettes (ECs) remains a popular habit for young populations, in part due to the variety of appealing flavours available. However, EC use has been associated with acute lung injury via unknown mechanisms. During a deep inhalation, one of the first compounds the EC aerosol comes into contact within the lungs is pulmonary surfactant. This complex mixture of lipids and surfactant associated proteins lines the alveolar surface and reduces surface tension to near zero values upon exhalation. Surfactant dysfunction, associated with serum protein leak and oxidative stress, contributes to lung injury. We hypothesized that exposure to EC aerosol impairs pulmonary surfactant function, and thereby increases its susceptibility to protein inhibition or oxidative stress. Methods: Bovine lipid extract surfactant (BLES) was used as a model exogenous surfactant. 2ml of BLES (2mg/ml) was placed in a syringe (30ml) attached to an EC, drawing in and expelling the aerosol 30 times. Vehicle e-liquid (VG:PG 50:50) as well as e-liquid containing flavouring additives and nicotine were utilized. Two models of injury were used, the first being addition of serum containing plasma proteins and the second oxidization by hypochlorous acid following aerosol exposure. Surface tension reduction of all samples after exposure was performed using a constrained drop surfactometer (CDS), where samples underwent 20 dynamic compression and expansion cycles. Results: Minimum surfaces tensions were significantly higher after exposure to EC aerosol across 20 compression/expansion cycles. Menthol and red wedding flavoured aerosol exposure resulted in significantly increased minimum surface tensions compared to unflavoured vehicle e-liquid, although nicotine had no additional effects beyond that of the vehicle e-liquid. The addition of plasma containing serum proteins significantly increased minimum surface tensions in aerosol exposed samples compared to those unexposed to serum and air controls. Oxidized surfactant had higher minimum surface tensions compared to control, however EC aerosol exposure had no additional effect on the inhibition of the surfactant’s function. Conclusion: EC aerosols alter surfactant function through increases in minimum surface tension. Variability in the severity of inhibition exists between flavouring additives, however the base common across all e-liquids is able to effectively inhibit surfactant. This inhibition is amplified in the presence of serum proteins. From these results we conclude that vaping impairs the pulmonary surfactant system and increases susceptibility to damage by secondary insults. Lawson Health Research Institute, NSERC This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.