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Chronic exposure to electronic cigarettes results in impaired cardiovascular function in mice.

  • Olfert, I Mark1, 2, 3
  • DeVallance, Evan1
  • Hoskinson, Hannah1
  • Branyan, Kayla W1
  • Clayton, Stuart1
  • Pitzer, Christopher R1
  • Sullivan, D Patrick1
  • Breit, Matthew J1
  • Wu, Zhongxin4
  • Klinkhachorn, Powsiri5
  • Mandler, W Kyle1
  • Erdreich, Brett H6
  • Ducatman, Barbara S7
  • Bryner, Randall W1
  • Dasgupta, Piyali8
  • Chantler, Paul D1, 3
  • 1 Division of Exercise Physiology, School of Medicine, West Virginia University , Morgantown, West Virginia.
  • 2 Department of Physiology, Pharmacology, and Neurosciences, School of Medicine, West Virginia University , Morgantown, West Virginia.
  • 3 Robert C. Byrd Health Science Center, West Virginia Clinical and Translational Sciences Institute , Morgantown, West Virginia.
  • 4 Department of Anatomy and Neurobiology, School of Medicine, West Virginia University , Morgantown, West Virginia.
  • 5 Lane Department of Computer Science and Electrical Engineering, School of Engineering, West Virginia University , Morgantown, West Virginia.
  • 6 Department of Internal Medicine, School of Medicine, West Virginia University , Morgantown, West Virginia.
  • 7 Department of Pathology, School of Medicine, West Virginia University , Morgantown, West Virginia.
  • 8 Department of Pharmacology, Physiology, and Toxicology, School of Medicine, Marshall University, Huntington, West Virginia.
Published Article
Journal of Applied Physiology
American Physiological Society
Publication Date
Mar 01, 2018
DOI: 10.1152/japplphysiol.00713.2017
PMID: 29097631


Proponents for electronic cigarettes (E-cigs) claim that they are a safe alternative to tobacco-based cigarettes; however, little is known about the long-term effects of exposure to E-cig vapor 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 to E-cig vapor, standard (3R4F reference) cigarette smoke, or filtered air ( n = 15/group). Respective whole body exposures consisted of four 1-h-exposure time blocks, separated by 30-min intervals of fresh air breaks, resulting in intermittent daily exposure for a total of 4 h/day, 5 days/wk for 8 mo. Noninvasive ultrasonography was used to assess cardiac function and aortic arterial stiffness (AS), measured as pulse wave velocity, at three times points (before, during, and after chronic exposure). Upon completion of the 8-mo exposure, ex vivo wire tension myography and force transduction were used to measure changes in thoracic aortic tension in response to vasoactive-inducing compounds. AS increased 2.5- and 2.8-fold in E-cig- and 3R4F-exposed mice, respectively, compared with air-exposed control mice ( P < 0.05). The maximal aortic relaxation to methacholine was 24% and 33% lower in E-cig- and 3R4F-exposed mice, respectively, than in 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 mo ( P < 0.05). A similar, although not statistically significant, tendency was also observed with E-cig exposure ( P < 0.10). Histological and respiratory function data support emphysema-associated changes in 3R4F-exposed, but not E-cig-exposed, mice. Chronic exposure to E-cig vapor accelerates AS, significantly impairs aortic endothelial function, and may lead to impaired cardiac function. The clinical implication from this study is that chronic use of E-cigs, even at relatively low exposure levels, induces cardiovascular dysfunction. NEW & NOTEWORTHY Electronic cigarettes (E-cigs) are marketed as safe, but there has been insufficient long-term exposure to humans to justify these claims. This is the first study to report the long-term in vivo vascular consequences of 8 mo of exposure to E-cig vapor in mice (equivalent to ~25 yr of exposure in humans). We report that E-cig exposure increases arterial stiffness and impairs normal vascular reactivity responses, similar to other risk factors, including cigarette smoking, which contribute to the development of cardiovascular disease.

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