Acute Effects of Electronic Cigarette Inhalation on the Vasculature and the Conducting Airways

Abstract

The use of electronic cigarettes has increased exponentially since its introduction onto the global market in 2006. However, short- and long-term health effects remain largely unknown due to the novelty of this product. The present study examines the acute effects of e-cigarette aerosol inhalation, with and without nicotine, on vascular and pulmonary function in healthy volunteers. Seventeen healthy subjects inhaled electronic cigarette aerosol with and without nicotine on two separate occasions in a double-blinded crossover fashion. Blood pressure, heart rate, and arterial stiffness measured by pulse wave velocity and pulse wave analysis were assessed at baseline, and then at 0 h, 2 h, and 4 h following exposure. Dynamic spirometry and impulse oscillometry were measured following vascular assessments at these time points, as well as at 6 h following exposure. e-Cigarette aerosol with nicotine caused a significant increase in heart rate and arterial stiffness. Furthermore, e-cigarette aerosol-containing nicotine caused a sudden increase in flow resistance as measured by impulse oscillometry, indicating obstruction of the conducting airways. Both aerosols caused an increase in blood pressure. The present study indicates that inhaled e-cigarette aerosol with nicotine has an acute impact on vascular and pulmonary function. Thus, chronic usage may lead to long-term adverse health effects. Further investigation is warranted.Electronic supplementary materialThe online version of this article (10.1007/s12012-019-09516-x) contains supplementary material, which is available to authorized users.

Cardiovascular autonomic effects of electronic cigarette use: a systematic review

“…The vertical dashed line represents no effect, and plots to the right of the vertical dashed line indicate that the effect of ECN is greater than that of EC0. The results of most [8,16,34] but not all [2,9] of these acute vaping studies were consistent with the notion that nicotine-and not the non-nicotine constituents-in the EC aerosol was responsible for the acute sympathomimetic effects of EC vaping. The overall mean differences between the ECN and EC0 studies across all studies was 3.73 mmHg (95% CI 0.59-6.87; p = 0.02) for for SBP, 3.25 mmHg (95% CI 1.21-5.30; p = 0.0018) for DBP and 6.44 bpm (95% CI The forest plot of each study represents the mean differences between TCs and ECs, with the corresponding lower and upper 95% confidence bounds.…”

Electronic cigarettes containing nicotine increase endothelial and platelet derived extracellular vesicles in healthy volunteers

“…E-cigarette usage has been linked to various acute adverse physiological changes in humans. These include increased airway inflammation, increased airway obstruction as well as increased levels of endothelial progenitor cells (indicative of vascular changes) and arterial stiffness (an important independent risk factor for future cardiovascular disease) [7][8][9][10][11].…”

“…Endothelial cell (EC) derived EVs are considered an emerging biomarker for endothelial dysfunction and are pivotal in vascular injury and angiogenesis as well as thrombosis [17]. Increased levels of EC derived EVs are not only associated with endothelial dysfunction, but also increased arterial stiffness as well as a variety of vascular diseases including acute coronary syndrome and severe hypertension with end organ damage [9,17]. Moreover, long term conventional cigarette smoking has been linked to increased levels of EC derived EVs and the elevated levels are indicative of early lung destruction in otherwise healthy cigarette smokers [18].…”

Electronic Cigarettes and Cardiovascular Risk: Caution Waiting for Evidence

“…54 Similarly, acute vaping of propylene glycol/ glycerol aerosol at high wattage with or without nicotine induced significant injury to airway epithelium and impaired pulmonary gas exchange. 55 Electronic cigarettes also induce an ion channel dysfunction in airway epithelial cells, and this was partially explained by the increased acrolein production, thus associating electronic cigarette use with chronic bronchitis onset and progression, as well as chronic obstructive pulmonary disease severity. 56 Additionally, electronic cigarettes induced a greater efflux of inflammatory mediators from chronic obstructive pulmonary disease lung cells, implicating that the use of electronic cigarettes in chronic obstructive pulmonary disease might be associated with a worse clinical picture and exacerbations.…”