Proponents for electronic cigarettes(E-cigs) claim they are a safe alternative to smoking tobacco-based cigarettes,however little is known about the long-term effects of E-cig vapor exposure on vascular function.The purpose of this study was to determine the cardiovascular consequences of chronic E-cig exposure. Female mice (C57Bl/6 background strain)were randomly assigned to chronic daily exposure of E-cig vapor, standard cigarette smoke(using 3R4F-reference-cigarette), or filtered-air(N=15/group). Respective whole-body exposures consisted of 4 x 1-hour exposure blocks, separated by 30-minute intervals of fresh air breaks, resulting in intermittent daily exposure for a total of 4h/day, 5days/week for 8-months. Non-invasive ultrasonography was used to assess cardiac function and aortic stiffness (pulse wave velocity)at 3 times points (before, during, after chronic exposure). Upon completion of the 8-month exposure, ex-vivo wire tension myograph and force transduction measured changes in aortic tension in response to vasoactive inducing compounds. Aortic stiffness increased 2.5- and 2.8-times greater in E-cig and conventional tobacco-cigarettes,respectively, compared to filtered-air exposed control mice(p<0.05). The maximal aortic relaxation achieved to methacholine was 24% and 33% lower in E-cig and 3R4F-exposed mice,respectively, compared to controls(p<0.05). No differences were noted in sodium-nitroprusside dilation between the groups. 3R4F exposure altered cardiac function by reducing fractional shortening and ejection fraction after 8-months exposure(p<0.05). A similar tendency, though not statistically significant,was also observed with E-cig exposure(p<0.10). Chronic exposure to E-cig vapor accelerates aortic stiffness,significantly impairs aortic endothelial function,and may lead to impaired cardiac function. The clinical implications from this study are, even at relatively low exposure levels,chronic use of E-cig induces cardiovascular dysfunction.