Electronic hookah (waterpipe) vaping reduces vascular endothelial function: the role of nicotine.

Vaping has risen substantially in recent years, particularly among young adults. Electronic (e-) hookahs are a newer category of vaping devices touted as safer tobacco alternatives. Although e-hookah vaping acutely reduces endothelial function, the role of nicotine and the mechanisms by which it may impair endothelial function remain understudied. In a randomized crossover study, we investigated the acute effects of vaping e-hookah, with and without nicotine, as compared with sham on endothelial function assessed by brachial artery flow-mediated dilation (FMD), among 18 overtly healthy young adults. To determine the role of changes in circulating factors in plasma on endothelial cell function, human umbilical vein endothelial cells (HUVECs) were cultured with participants' plasma, and acetylcholine-stimulated nitric oxide (NO) production and basal reactive oxygen species (ROS) bioactivity were assessed. Plasma nicotine was measured before and after the sessions. E-hookah vaping with nicotine, which acutely increased heart rate (HR) by 8 ± 3 beats/min and mean arterial pressure (MAP) by 7 ± 2 mmHg (means ± SE; P < 0.05), decreased endothelial-dependent FMD by 1.57 ± 0.19%Δ (P = 0.001), indicating impairment in endothelial function. Vaping e-hookah without nicotine, which mildly increased hemodynamics (HR, 2 ± 2 beats/min and MAP 1 ± 1 mmHg; P = ns), did not significantly impair endothelial function. No changes were observed after sham vaping. HUVECs cultured with participants' plasma after versus before e-hookah vaping with nicotine, but not without nicotine or sham vaping, exhibited reductions in endothelial cell NO bioavailability and increases in ROS bioactivity (P < 0.05). Plasma nicotine concentrations increased after vaping e-hookah with nicotine (6.7 ± 1.8 ng/mL; P = 0.002), whereas no changes were observed after vaping e-hookah without nicotine or sham (P = ns). Acute e-hookah vaping induces endothelial dysfunction by impairing NO bioavailability associated with increased ROS production, and these effects are attributable to nicotine, not to nonnicotine constituents, present in the flavored e-liquid.NEW & NOTEWORTHY Despite safety claims heavily advertised by the hookah tobacco industry, acute e-hookah vaping induces in vivo endothelial dysfunction by impairing ex vivo NO bioavailability associated with increased ROS production. These effects are attributable to nicotine, not to nonnicotine constituents, present in the flavored e-liquid.

Differential Effects of Electronic Hookah Vaping and Traditional Combustible Hookah Smoking on Oxidation, Inflammation, and Arterial Stiffness.

BACKGROUND: Traditional hookah smoking has grown quickly to become a global tobacco epidemic. More recently, electronic hookahs (e-hookahs)-vaped through traditional water pipes-were introduced as healthier alternatives to combustible hookah. With combustible tobacco smoking, oxidative stress, inflammation, and vascular stiffness are key components in the development and progression of atherosclerosis. The comparable effects of hookah are unknown. RESEARCH QUESTION: What is the differential acute effect of e-hookah vaping vs combustible hookah smoking on oxidation, inflammation, and arterial stiffness? STUDY DESIGN AND METHODS: In a randomized crossover design study, among a cohort of 17 healthy young adult chronic hookah smokers, we investigated the effect of e-hookah vaping and hookah smoking on measures of conduit arterial stiffness, including carotid-femoral pulse wave velocity (PWV), augmentation index-corrected for heart rate before and after a 30-min exposure session. We assessed a panel of circulating biomarkers indicative of inflammation and oxidants and measured plasma nicotine and exhaled carbon monoxide (CO) levels before and after the sessions. RESULTS: e-Hookah vaping tended to lead to a larger acute increase in PWV than hookah smoking (mean ± SE: e-hookah, +0.74 ± 0.12 m/s; combustible hookah, +0.57 ± 0.14 m/s [P < .05 for both]), indicative of large artery stiffening. Compared with baseline, only e-hookah vaping induced an acute increase in augmentation index (e-hookah, +5.58 ± 1.54% [P = .004]; combustible hookah, +2.87 ± 2.12% [P = not significant]). These vascular changes were accompanied by elevation of the proinflammatory biomarkers high-sensitivity C-reactive protein, fibrinogen, and tumor necrosis factor α after vaping (all P < .05). No changes in biomarkers of inflammation and oxidants were observed after smoking. Compared with baseline, exhaled CO levels were higher after smoking than after vaping (+36.81 ± 6.70 parts per million vs -0.38 ± 0.22 parts per million; P < .001), whereas plasma nicotine concentrations were comparable (+6.14 ± 1.03 ng/mL vs +5.24 ± 0.96 ng/mL; P = .478). INTERPRETATION: Although advertised to be "safe," flavored e-hookah vaping exerts injurious effects on the vasculature that are, at least in part, mediated by inflammation. TRIAL REGISTRY: ClinicalTrials.gov; No.: NCT03690427; URL: www.clinicaltrials.gov.

Ascorbic Acid Prevents Vascular Endothelial Dysfunction Induced by Electronic Hookah (Waterpipe) Vaping.

Background Electronic hookah (e-hookah) vaping has increased in popularity among youth, who endorse unsubstantiated claims that flavored aerosol is detoxified as it passes through water. However, e-hookahs deliver nicotine by creating an aerosol of fine and ultrafine particles and other oxidants that may reduce the bioavailability of nitric oxide and impair endothelial function secondary to formation of oxygen-derived free radicals. Methods and Results We examined the acute effects of e-hookah vaping on endothelial function, and the extent to which increased oxidative stress contributes to the vaping-induced vascular impairment. Twenty-six healthy young adult habitual hookah smokers were invited to vape a 30-minute e-hookah session to evaluate the impact on endothelial function measured by brachial artery flow-mediated dilation (FMD). To test for oxidative stress mediation, plasma total antioxidant capacity levels were measured and the effect of e-hookah vaping on FMD was examined before and after intravenous infusion of the antioxidant ascorbic acid (n=11). Plasma nicotine and exhaled carbon monoxide levels were measured before and after the vaping session. Measurements were performed before and after sham-vaping control experiments (n=10). E-hookah vaping, which increased plasma nicotine (+4.93±0.92 ng/mL, P<0.001; mean±SE) with no changes in exhaled carbon monoxide (-0.15±0.17 ppm; P=0.479), increased mean arterial pressure (11±1 mm Hg, P<0.001) and acutely decreased FMD from 5.79±0.58% to 4.39±0.46% (P<0.001). Ascorbic acid infusion, which increased plasma total antioxidant capacity 5-fold, increased FMD at baseline (5.98±0.66% versus 9.46±0.87%, P<0.001), and prevented the acute FMD impairment by e-hookah vaping (9.46±0.87% versus 8.74±0.84%, P=0.002). All parameters were unchanged during sham studies. Conclusions E-hookah vaping has adverse effects on vascular function, likely mediated by oxidative stress, which overtime could accelerate development and progression of cardiovascular disease. Registration URL: https://ClinicalTrials.gov. Unique identifier: NCT03690427.