A 6-month inhalation study in Apoe-/- mice to investigate cardiovascular and respiratory exposure effects of e-vapor aerosols compared with cigarette smoke
Chronic exposure to cigarette smoke is a risk factor for the development and progression of cardiovascular disease and chronic obstructive pulmonary disease. Considerable attention has been given towards the potential reduced harm of e cigarettes (e cigs). Here, Apoe-/- mice were used to evaluate lung inflammation, atherosclerosis development and the underlying molecular changes upon 6-month exposure to mainstream (MS) cigarette smoke (CS) from a reference cigarette 3R4F or to e cig aerosols generated using capillary aerosol generators from various e liquids (“CARRIER” containing humectants [propylene glycol, glycerin] and water, “BASE” containing humectants, water and 4 % nicotine, and “TEST” containing humectants, water, 4 % nicotine, and flavors). Apoe-/- mice were exposed to CS and the e cig aerosols (“BASE” and “TEST”) at a matched nicotine concentration for 3 hrs/day via whole-body inhalation. The CARRIER exposures were set to match the total particulate matter for “TEST”. Aerosol particle sizes were within the respirable range, from 0.71-0.90 µm for 3R4F MS and 0.74-1.28 µm for e cig aerosols. Pulmonary inflammation and atherosclerotic plaque areas, as well as cholesterol concentrations in serum or lipoprotein fraction, were quantified at months 3 and 6. In contrast to CS, exposure to e cig aerosols resulted in no increase in leukocyte counts, serum cholesterol concentration, aortic plaque formation, and lung matrix metalloproteinase activity compared to fresh air. Furthermore, no such changes were observed between the exposures to CARRIER, BASE, and TEST aerosols. In conclusion, e cig aerosols did not induce disease mechanisms related to atherosclerosis and lung inflammation that were elicited by CS in the Apoe-/- model.