Introduction: Smoking is a major cause of cardiovascular morbidity and mortality worldwide. Hookah (ie, waterpipe) smoking is a centuries-old revived yet understudied global epidemic of tobacco use. Because of the traditional set-up of a hookah-pipe, in addition to inhaling tobacco-combustion products, smokers are also exposed to large amounts of charcoal combustion products from the burning charcoal briquettes used to heat the hookah flavored tobacco. Despite being heavily advertised and actively glamorized in the mass media as a healthier tobacco alternative, the toxicological constituents of hookah smoke—including nicotine, carbon monoxide, particulates, oxidants, heavy metals, phenols and flavorants—indicate the potential to cause adverse cardiovascular events.Methods: Herein, we review evidence on hookah smoke toxicological constituents, cardiovascular effects and potential mechanisms by which hookah smoke aerosol could cause cardiovascular disease.Results: The evidence reviewed here indicates that contrary to the widespread popular belief that hookah is a healthier tobacco alternative, the constituents of hookah smoke aerosol contains similar chemicals compared to cigarette smoke, many of which are known to be harmful to cardiovascular health and mediated by similar pathophysiologic processes. Because the burning charcoal briquettes are a unique source of toxicant emissions specific to hookah smoking, some constituents differ in their quantities from cigarettes with some of their cardiovascular effects unknown.Conclusions: To date, much more is known about the constituents and their toxicology than about the effects of hookah smoking on human cardiovascular health. Further research on long-term consequences of hookah use is needed.Implications: This review provides an overview on the potential impact of hookah smoking on cardiovascular health. Readers will gain an insight into evidence on its toxicological constituents, human health effects, and pathophysiological mechanisms by which hookah smoking might cause cardiovascular disease. The review also highlights current research gaps regarding the cardiovascular consequences of hookah smoking, specifically the long-term consequences in the United States and Europe among flavored-hookah tobacco users.

Background: Hookah smoking is marketed to youth as a harmless alternative to cigarettes. Although cigarette smoking acutely impairs endothelial function, the effect of smoking fruit-flavored hookah tobacco is unknown. Because charcoal traditionally is used to heat the hookah tobacco in the waterpipe, hookah smoke delivers tobacco toxicants and nicotine plus charcoal combustion products: not only carbon-rich nanoparticles, oxidants that may destroy nitric oxide and impair endothelial function, but also large amounts of carbon monoxide (CO), a putative vasodilator molecule. Methods: To test the acute effect of hookah smoking on endothelial function, in young adult hookah smokers (n=30, age 26±1 years, mean±SE), we measured plasma nicotine, exhaled CO, and brachial artery flow-mediated dilation (FMD) before and after charcoal-heated hookah smoking. To remove the effect of charcoal combustion, the same measurements were performed when the same flavored hookah tobacco product was heated electrically (n=20). As a positive internal control, we studied age-matched cigarette smokers (n=15) who smoked 1 cigarette. To isolate the effect of the CO boost on FMD, hookah smokers (n=8) inhaled a 0.1% CO gas mixture to approximate their CO boost achieved with charcoal-heated hookah smoking. Results: Nicotine levels increased similarly with all types of smoking, whereas exhaled CO increased 9- to 10-fold more after charcoal-heated hookah than after either electrically heated hookah or cigarette smoking. FMD did not decrease after smoking charcoal-heated hookah but instead increased by +43±7% ( P <0.001). In contrast, FMD decreased by –27±4% ( P <0.001) after smoking electrically heated hookah, comparable to the decrease after cigarette smoking. FMD increased markedly by 138±71% ( P <0.001) after breathing CO gas, 2.8 times more than the increase induced in the same subjects after smoking charcoal-heated hookah ( P <0.001), despite comparable increases in exhaled CO (24±1 versus 28±3 ppm, hookah versus CO). Conclusions: Smoking hookah tobacco, similar to cigarette tobacco, acutely impairs endothelial function. With traditional charcoal-heated hookah smoking, the acute endothelial dysfunction is masked by high levels of carbon monoxide, a potent vasodilator molecule generated by charcoal combustion. With respect to large-artery endothelial function, smoking hookah is not harmless. Clinical Trial Registration: URL: https://www.clinicaltrials.gov . Unique identifiers: NCT 03616002 and NCT 03067701.

Hookah (water pipe) smoking is a major new understudied epidemic affecting youth. Because burning charcoal is used to heat the tobacco product, hookah smoke delivers not only nicotine but also large amounts of charcoal combustion products, including carbon-rich nanoparticles that constitute putative coronary vasoconstrictor stimuli and carbon monoxide, a known coronary vasodilator. We used myocardial contrast echocardiography perfusion imaging with intravenous lipid shelled microbubbles in young adult hookah smokers to determine the net effect of smoking hookah on myocardial blood flow. In 9 hookah smokers (age 27 ± 5 years, mean ± SD), we measured myocardial blood flow velocity (β), myocardial blood volume (A), myocardial blood flow (A × β) as well as myocardial oxygen consumption (MVO2) before and immediately after 30 minutes of ad lib hookah smoking. Myocardial blood flow did not decrease with hookah smoking but rather increased acutely (88 ± 10 to 120 ± 19 a.u./s, mean ± SE, p = 0.02), matching a mild increase in MVO2 (6.5 ± 0.3 to 7.6 ± 0.4 ml·minute(-1), p <0.001). This was manifested primarily by increased myocardial blood flow velocity (0.7 ± 0.1 to 0.9 ± 0.1 second(-1), p = 0.01) with unchanged myocardial blood volume (133 ± 7 to 137 ± 7 a.u., p = ns), the same pattern of coronary microvascular response seen with a low-dose β-adrenergic agonist. Indeed, with hookah, the increased MVO2 was accompanied by decreased heart rate variability, an indirect index of adrenergic overactivity, and eliminated by β-adrenergic blockade (i.v. propranolol). In conclusion, nanoparticle-enriched hookah smoke either is not an acute coronary vasoconstrictor stimulus or its vasoconstrictor effect is too weak to overcome the physiologic dilation of coronary microvessels matching mild cardiac β-adrenergic stimulation.

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. What is the differential acute effect of e-hookah vaping vs combustible hookah smoking on oxidation, inflammation, and arterial stiffness? 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. 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). Although advertised to be "safe," flavored e-hookah vaping exerts injurious effects on the vasculature that are, at least in part, mediated by inflammation. ClinicalTrials.gov; No.: NCT03690427; URL: www.clinicaltrials.gov.