Acute Exposure to Electronic and Combustible Cigarette Aerosols: Effects in an Animal Model and in Human Alveolar Cells.
BACKGROUND
Smoking electronic cigarettes (ECIG) is promoted as a safer alternative to smoking combustible cigarettes. This study investigates the effects of ECIG aerosol and cigarette smoke (CS) in an animal model and in human alveolar cell cultures (A549).


METHODS
Mice were divided into Control, ECIG, and CS. Animals were exposed for 6h/d to either lab air, ECIG or CS, for of 3 days. Total particulate matter exposure for the ECIG was set at higher levels compared to CS. Lung injury was determined by: (1) measurement of wet-to-dry ratio; (2) albumin concentration in the bronchoalveolar lavage fluid; (3) transcriptional expression of inflammatory mediators IL-1β, IL-6, TNF-α; (4) oxidative stress; (5) assessment of cell death; and (6) lung histopathology. Human alveolar cell cultures were treated with various concentrations of ECIG and CS aerosol extracts and the effects on cell proliferation were evaluated.


RESULTS
Wet-to-dry ratio was higher in CS when compared to ECIG. Albumin leak in bronchoalveolar lavage fluid was evident in CS but not in ECIG. ECIG exposure was only associated with a significant increase in IL-1β. In contrast, CS exposure resulted in significant increases in IL-1β, IL-6, TNF-α expression, and oxidative stress. TUNEL staining demonstrated significant cell death in CS but not in ECIG. At the cellular level, ECIG and CS extracts reduced cell proliferation, however, CS exhibited effects at lower concentrations.


CONCLUSIONS
Despite higher exposure conditions, ECIG exhibited less toxic effects on lungs of experimental animals and on A549 cell cultures when compared to CS.
Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, American University of Beirut, Beirut, Lebanon;
Ahmad
A
Husari
Department of Mechanical Engineering, American University of Beirut, Beirut, Lebanon; Center for the Study of Tobacco Products, Department of Psychology, Virginia Commonwealth University, Richmond, VA;
Alan
A
Shihadeh
Department of Mechanical Engineering, American University of Beirut, Beirut, Lebanon; Center for the Study of Tobacco Products, Department of Psychology, Virginia Commonwealth University, Richmond, VA;
Soha
S
Talih
Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, American University of Beirut, Beirut, Lebanon;
Yasmine
Y
Hashem
Department of Anatomy, Cell Biology and Physiological Sciences, Faculty of Medicine, American University of Beirut, Beirut, Lebanon; me00@aub.edu.lb zaatari@aub.edu.lb.
Marwan
M
El Sabban
Department of Pathology and Laboratory Medicine, American University of Beirut, Beirut, Lebanon me00@aub.edu.lb zaatari@aub.edu.lb.
Ghazi
G
Zaatari
D000336:Aerosols; D000418:Albumins / Q000032:analysis; D000818:Animals; D001992:Bronchoalveolar Lavage Fluid / Q000737:chemistry; D018929:Cell Culture Techniques; D016923:Cell Death / Q000187:drug effects; D004195:Disease Models, Animal; D066300:Electronic Nicotine Delivery Systems / Q000009:adverse effects*; D006801:Humans; D007249:Inflammation / Q000473:pathology; D008168:Lung / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D008297:Male; D008810:Mice, Inbred C57BL; D009538:Nicotine / Q000494:pharmacology*; D018384:Oxidative Stress; D011650:Pulmonary Alveoli / Q000187:drug effects* / Q000378:metabolism; D012907:Smoking / Q000009:adverse effects* / Q000378:metabolism; D014026:Nicotiana
D000336:Aerosols; D000418:Albumins; D009538:Nicotine