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Chronic Inhalation of Electronic (E)-Cigarette Vapor Increases Susceptibility to Acute Lung Injury
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A3568 - Chronic Inhalation of Electronic (E)-Cigarette Vapor Increases Susceptibility to Acute Lung Injury
Author Block: A. Moshensky1, M. Hepokoski1, C. M. Bojanowski1, N. Nguyen1, L. E. Crotty Alexander2; 1University of California, San Diego, San Diego, CA, United States, 2Medicine, UCSD and VASDHS, San Diego, CA, United States.
Alexander Moshensky
Mark Hepokoski, MD
Christine M. Bojanowski, MD
Nicholas Nguyen
Laura E. Crotty Alexander, MD
Introduction: Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are life-threatening conditions which frequently require mechanical ventilation. The annual incidence is 190,000, with a strikingly high mortality rate of 30-40%. Electronic (e)-cigarette use is consistently increasing amongst all ages, sexes, and races. There is a growing “vape” culture that has given rise to new e-cigarette devices, vaping techniques, flavors, and popularity. Prior studies in our lab have shown that non-flavored, nicotine-containing vapor generated from e-cigarettes causes inflammation of airways and deleteriously affects the function of innate immune cells. In humans, multiple cases of ALI and ARDS in the setting of e-cigarette use have been seen. Thus, we hypothesized that chronic inhalation of e-cigarette vapor would increase susceptibility to ALI.
Methods: Female 6-8 week-old C57BL/6j mice were exposed to e-cigarette vapor (Kanger mod and tank via SciReq inExpose system; 70% propylene glycol, 30% glycerin, and 12mg/mL nicotine) for 60 minutes per day, five days a week, for one month. Half of the e-cigarette mice were exposed for 20 minutes three times daily to more accurately mimic human e-cigarette use patterns. The other half of the e-cigarette mice were exposed for 60 minutes once daily. Air controls underwent the same restraining procedures, but were exposed to room air only. After the final e-cigarette vapor exposure, to induce ALI, mice were mechanically ventilated (SciReq FlexiVent) with a high tidal volume (20cc/kg) and PEEP of 2.5, for three hours. Lung mechanic scans were done every hour and prior to the end of ALI induction. Mice underwent bronchoalveolar lavage (BAL), blood and lung tissue collection.
Results: Decreased lung compliance was found in e-cigarette mice compared to Air controls. E-cigarette mice also had higher total protein in the bronchoalveolar lavage (BAL).
Conclusions: Chronic inhalation of non-flavored, nicotine containing, e-cigarette vapor alters the inflammatory profile of the lung under homeostatic conditions, such that e-cigarette exposed lungs have increased ALI when an acute insult such as mechanical ventilation is applied. Thus, e-cigarette users may be at higher risk of ALI compared to non-vapers.
Author Block: A. Moshensky1, M. Hepokoski1, C. M. Bojanowski1, N. Nguyen1, L. E. Crotty Alexander2; 1University of California, San Diego, San Diego, CA, United States, 2Medicine, UCSD and VASDHS, San Diego, CA, United States.
Alexander Moshensky
Mark Hepokoski, MD
Christine M. Bojanowski, MD
Nicholas Nguyen
Laura E. Crotty Alexander, MD
Introduction: Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are life-threatening conditions which frequently require mechanical ventilation. The annual incidence is 190,000, with a strikingly high mortality rate of 30-40%. Electronic (e)-cigarette use is consistently increasing amongst all ages, sexes, and races. There is a growing “vape” culture that has given rise to new e-cigarette devices, vaping techniques, flavors, and popularity. Prior studies in our lab have shown that non-flavored, nicotine-containing vapor generated from e-cigarettes causes inflammation of airways and deleteriously affects the function of innate immune cells. In humans, multiple cases of ALI and ARDS in the setting of e-cigarette use have been seen. Thus, we hypothesized that chronic inhalation of e-cigarette vapor would increase susceptibility to ALI.
Methods: Female 6-8 week-old C57BL/6j mice were exposed to e-cigarette vapor (Kanger mod and tank via SciReq inExpose system; 70% propylene glycol, 30% glycerin, and 12mg/mL nicotine) for 60 minutes per day, five days a week, for one month. Half of the e-cigarette mice were exposed for 20 minutes three times daily to more accurately mimic human e-cigarette use patterns. The other half of the e-cigarette mice were exposed for 60 minutes once daily. Air controls underwent the same restraining procedures, but were exposed to room air only. After the final e-cigarette vapor exposure, to induce ALI, mice were mechanically ventilated (SciReq FlexiVent) with a high tidal volume (20cc/kg) and PEEP of 2.5, for three hours. Lung mechanic scans were done every hour and prior to the end of ALI induction. Mice underwent bronchoalveolar lavage (BAL), blood and lung tissue collection.
Results: Decreased lung compliance was found in e-cigarette mice compared to Air controls. E-cigarette mice also had higher total protein in the bronchoalveolar lavage (BAL).
Conclusions: Chronic inhalation of non-flavored, nicotine containing, e-cigarette vapor alters the inflammatory profile of the lung under homeostatic conditions, such that e-cigarette exposed lungs have increased ALI when an acute insult such as mechanical ventilation is applied. Thus, e-cigarette users may be at higher risk of ALI compared to non-vapers.
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