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

Chest. 2022 Jan;161(1):208-218. doi: 10.1016/j.chest.2021.07.027. Epub 2021 Jul 21.

Abstract

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.

Keywords: arterial stiffness; electronic hookah; electronic water pipe; hookah smoking; inflammation; oxidation.

Publication types

  • Randomized Controlled Trial
  • Research Support, N.I.H., Extramural

MeSH terms

  • Adult
  • Antioxidants / metabolism
  • Aryldialkylphosphatase / metabolism
  • C-Reactive Protein / metabolism
  • Carbon Monoxide / metabolism
  • Carboxylic Ester Hydrolases / metabolism
  • Carotid Arteries / physiopathology
  • Carotid-Femoral Pulse Wave Velocity*
  • Cross-Over Studies
  • Electronic Nicotine Delivery Systems
  • Female
  • Femoral Artery / physiopathology
  • Fibrinogen / metabolism
  • Humans
  • Inflammation / metabolism*
  • Male
  • Nicotine / blood
  • Oxidative Stress / physiology*
  • Pulse Wave Analysis
  • Tumor Necrosis Factor-alpha / metabolism
  • Vaping / physiopathology*
  • Vascular Stiffness / physiology*
  • Water Pipe Smoking / physiopathology*

Substances

  • Antioxidants
  • TNF protein, human
  • Tumor Necrosis Factor-alpha
  • Nicotine
  • Carbon Monoxide
  • Fibrinogen
  • C-Reactive Protein
  • Carboxylic Ester Hydrolases
  • arylesterase
  • Aryldialkylphosphatase
  • PON1 protein, human

Associated data

  • ClinicalTrials.gov/NCT03690427