The effects of e-cigarette (e-cig)
aerosol inhalation by nonsmokers have not been examined to date. The present study was designed to evaluate the acute response to
aerosol inhalation of non-nicotinized e-cigarettes in terms of oxidative stress and indices of endothelial activation in human pulmonary microvascular endothelial cells (HPMVEC). Ten smoking-naïve healthy subjects (mean age ± SD = 28.7 ± 5.5 yr) were subjected to an e-cig challenge, following which their serum was monitored for markers of
inflammation [
C-reactive protein (CRP) and soluble
intercellular adhesion molecule (sICAM)] and
nitric oxide metabolites (NOx). The oxidative stress and
inflammation burden of the circulating serum on the vascular network was also assessed by measuring
reactive oxygen species (ROS) production and induction of
ICAM-1 expression on HPMVEC. Our results show that serum indices of oxidative stress and
inflammation increased significantly (P < 0.05 as compared with baseline), reaching a peak at approximately 1-2 h post-e-cig
aerosol inhalation and returning to baseline levels at 6 h. The circulatory burden of the serum (ICAM-1 and ROS) increased significantly at 2 h and returned to baseline values 6 h post-e-cig challenge. ROS production by HPMVEC was found to occur via activation of the
NADPH oxidase 2 (NOX2) pathways. These findings suggest that even in the absence of
nicotine, acute e-cig
aerosol inhalation leads to a transient increase in oxidative stress and
inflammation. This can adversely affect the vascular endothelial network by promoting oxidative stress and immune cell adhesion. Thus e-cig inhalation has the potential to drive the onset of vascular pathologies.