Differential Effects of Electronic Hookah Vaping and Traditional Combustible Hookah Smoking on Oxidation, Inflammation, and Arterial Stiffness
2021; Elsevier BV; Volume: 161; Issue: 1 Linguagem: Inglês
10.1016/j.chest.2021.07.027
ISSN1931-3543
AutoresMary Rezk‐Hanna, Rajat Gupta, Charlie O. Nettle, Daniel Dobrin, Chiao‐Wei Cheng, Angelica Means, Mary-Lynn Brecht, Donald P. Tashkin, Jesús A. Araujo,
Tópico(s)Heart Rate Variability and Autonomic Control
ResumoBackgroundTraditional 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 QuestionWhat is the differential acute effect of e-hookah vaping vs combustible hookah smoking on oxidation, inflammation, and arterial stiffness?Study Design and MethodsIn 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.ResultsE-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 < 0.05 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).InterpretationAlthough advertised to be "safe," flavored e-hookah vaping exerts injurious effects on the vasculature that are, at least in part, mediated by inflammation.Trial RegistryClinicalTrials.gov; No.: NCT03690427; URL: www.clinicaltrials.gov 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 < 0.05 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 Hookah (ie, water-pipe) smoking has grown quickly to become a major global tobacco epidemic.1Maziak W. Taleb Z.B. Bahelah R. et al.The global epidemiology of waterpipe smoking.Tob Control. 2015; 24: i3-i12Crossref PubMed Scopus (281) Google Scholar Contributing to this popularity is the belief that traditional charcoal-heated hookah smoke is detoxified as it passes through the water-filled base, rendering hookah smoking a safer tobacco alternative.2Bhatnagar A. Maziak W. Eissenberg T. et al.Water pipe (hookah) smoking and cardiovascular disease risk: a scientific statement from the American Heart Association.Circulation. 2019; 139: e917-e936Crossref PubMed Scopus (42) Google Scholar In 2014, electronic hookahs (e-hookahs) were introduced as healthier alternatives to hookah smoking.3Dube S.R. Pathak S. Nyman A.L. Eriksen M.P. Electronic cigarette and electronic hookah: a pilot study comparing two vaping products.Prev Med Rep. 2015; 2: 953-958Crossref PubMed Scopus (7) Google Scholar,4Stroup A.M. Branstetter S.A. An introduction to the electronic waterpipe.Addict Behav. 2019; 91: 90-94Crossref PubMed Scopus (4) Google Scholar Data from wave 1 of the Population Assessment of Tobacco and Health Study (2013-2014) show that among adults 18 to 24 years of age, 18.2% reported current hookah smoking.5Kasza K.A. Ambrose B.K. Conway K.P. et al.Tobacco-product use by adults and youths in the United States in 2013 and 2014.N Engl J Med. 2017; 376: 342-353Crossref PubMed Scopus (382) Google Scholar Wave 2 data from the Population Assessment of Tobacco and Health Study (2014-2015) show that 7.7% of youth reported ever e-hookah use.6Rezk-Hanna M, Toyama J, Ikharo E, Brecht ML, Benowitz NL. E-hookah versus e-cigarettes: findings from wave 2 of the PATH Study (2014-2015). Am J Prev Med. https://doi.org/10.1016/j.amepre.2019.05.007.Google Scholar Among adults, 4.6% reported ever e-hookah use, and of these, more than one-quarter (26.8%) reported current use.6Rezk-Hanna M, Toyama J, Ikharo E, Brecht ML, Benowitz NL. E-hookah versus e-cigarettes: findings from wave 2 of the PATH Study (2014-2015). Am J Prev Med. https://doi.org/10.1016/j.amepre.2019.05.007.Google Scholar With traditional hookah, in addition to tobacco combustion products, smokers are exposed to charcoal combustion products from the burning charcoal used to heat the fruit-flavored tobacco product (Fig 1A). These charcoal combustion products include: (1) concentrated carbon-rich nanoparticles, which have a mean aerodynamic diameter that is an order of magnitude smaller than the nanoparticles in cigarette smoke and are postulated to be more potent oxidants to the vasculature7Araujo J.A. Barajas B. Kleinman M. et al.Ambient particulate pollutants in the ultrafine range promote early atherosclerosis and systemic oxidative stress.Circ Res. 2008; 102: 589-596Crossref PubMed Scopus (457) Google Scholar,8Monn C. Kindler P. Meile A. Brandli O. Ultrafine particle emissions from waterpipes.Tob Control. 2007; 16: 390-393Crossref PubMed Scopus (52) Google Scholar; and (2) large amounts of carbon monoxide (CO), a putative vasodilator molecule. E-hookahs are a new category of vaping devices in which e-bowls are combined with and placed on traditional water pipes, allowing the aerosol to pass through a water-filled base before being inhaled (Fig 1B). Because of the absence of combustion, e-hookahs have been marketed as a "safe" alternative to hookah smoking. However, because of the use of the heating element, e-hookahs deliver flavored nicotine by creating an aerosol of nanoparticles and other free radicals that may increase cardiovascular disease risk by activating inflammation and oxidative stress and impairing aortic elastic properties, leading to arterial stiffness. Indeed, substantial evidence suggests that inflammation and oxidative stress are central to the ability of cigarette smoking to cause atherosclerotic vascular disease.9Ambrose J.A. Barua R.S. The pathophysiology of cigarette smoking and cardiovascular disease: an update.J Am Coll Cardiol. 2004; 43: 1731-1737Crossref PubMed Scopus (1409) Google Scholar Large elastic artery stiffness, typically assessed by carotid-femoral pulse wave velocity (PWV) and central BP, is an independent risk factor for cardiovascular disease and all-cause mortality.10Ben-Shlomo Y. Spears M. Boustred C. et al.Aortic pulse wave velocity improves cardiovascular event prediction: an individual participant meta-analysis of prospective observational data from 17,635 subjects.J Am Coll Cardiol. 2014; 63: 636-646Crossref PubMed Scopus (934) Google Scholar,11Vlachopoulos C. Aznaouridis K. Stefanadis C. Prediction of cardiovascular events and all-cause mortality with arterial stiffness: a systematic review and meta-analysis.J Am Coll Cardiol. 2010; 55: 1318-1327Crossref PubMed Scopus (2479) Google Scholar In the community-based Framingham Heart Study, measures of arterial stiffness were associated with the risk of cardiovascular events.12Cooper L.L. Palmisano J.N. Benjamin E.J. et al.Microvascular function contributes to the relation between aortic stiffness and cardiovascular events: the Framingham Heart Study.Circ Cardiovasc Imaging. 2016; 9Crossref Scopus (26) Google Scholar E-cigarette vaping acutely increases arterial stiffness comparable with that of traditional cigarette smoking.13Vlachopoulos C. Ioakeimidis N. Abdelrasoul M. et al.Electronic cigarette smoking increases aortic stiffness and blood pressure in young smokers.J Am Coll Cardiol. 2016; 67: 2802-2803Crossref PubMed Scopus (86) Google Scholar We recently demonstrated that traditional hookah smoking acutely increases arterial stiffness.14Rezk-Hanna M, Doering L, Robbins W, Sarna L, Elashoff RM, Victor RG. Acute effect of hookah smoking on arterial stiffness and wave reflections in adults aged 18 to 34 years of age. Am J Cardiol. https://doi.org/10.1016/j.amjcard.2018.05.033.Google Scholar However, the comparable effect of e-hookah vaping has yet to be investigated. In the present randomized crossover-design study, we investigated the acute differential effect of e-hookah vaping in comparison with traditional charcoal-heated hookah smoking on measures of conduit arterial stiffness, including carotid-femoral PWV, and augmentation index corrected for heart rate and central BP before and after a 30-min hookah smoking or vaping session. We assessed a panel of circulating biomarkers indicative of inflammation (high-sensitivity C-reactive protein [hsCRP], fibrinogen, and tumor necrosis factor α [TNFα]) and lipid peroxidation (paraoxonase-1 [PON-1] activity, arylesterase activity, and high-density lipoprotein [HDL] antioxidant capacity determined by an HDL oxidative index) and measured plasma nicotine and exhaled CO levels before and after the smoking or vaping sessions. The study population included healthy young habitual hookah smokers between 21 and 39 years of age who do not smoke cigarettes and met the following criteria: (1) no evidence of cardiopulmonary disease by history or physical examination; (2) BP < 140/90 mm Hg; (3) BMI of > 18.50 kg/m2 and < 30 kg/m2; (4) resting heart rate of < 100 beats/min; (5) take no prescription medication; (6) not pregnant (confirmed by urine test) or breastfeeding; (7) have smoked hookah at least 12 times in the past 12 months15Robinson J.N. Wang B. Jackson K.J. Donaldson E.A. Ryant C.A. Characteristics of hookah tobacco smoking sessions and correlates of use frequency among US adults: findings from wave 1 of the Population Assessment of Tobacco and Health (PATH) Study.Nicotine Tob Res. 2018; 20: 731-740Crossref PubMed Scopus (25) Google Scholar; (8) have not smoked cigarettes in the past 12 months, smoked fewer than 100 cigarettes in their lifetimes, or both; (9) have not smoked marijuana in the past 12 months and showed negative results on a urine tetrahydrocannabinol screen; and (10) end-expiratory CO of < 10 parts per million before the study (evidence for no recent or current combusted tobacco exposure). All participants agreed to fast for 8 h and abstain from exercise, antioxidants, caffeine, and alcohol for 48 h before the study. Participants were instructed not to smoke or vape e-hookah or any other electronic nicotine device, including e-cigarettes, and to avoid exposure to any secondhand smoke for 72 h before the study. The experimental protocol was approved by the University of California, Los Angeles, Medical Institutional Review Board 3 (Identifier: 18-001559), and informed written consent was obtained from all participants. Using an e-hookah (Starbuzz Wireless E-head) placed on a traditional water pipe, participants were instructed to vape e-hookah fruit-flavored liquid mix containing a 50-50 blend of propylene glycol and vegetable glycerin and 6 mg/mL nicotine (Starbuzz Tobacco, Inc.). Because the e-hookah bowl has various power settings, based on participants' preferences and reported use, the device power was set at 50 W. For hookah smoking sessions, a traditional water pipe was used. Participants were instructed to smoke the most popular brand of maassel cited by hookah smokers and manufactured in the United States16Blank M.D. Cobb C.O. Kilgalen B. et al.Acute effects of waterpipe tobacco smoking: a double-blind, placebo-control study.Drug Alcohol Depend. 2011; 116: 102-109Crossref PubMed Scopus (85) Google Scholar (5%-10% tobacco fermented with molasses, fruit, and glycerin; Starbuzz Tobacco, Inc.) heated with two charcoal briquettes (Coco Nara 100% Natural Coal). To mitigate the impact of carryover effects, sessions were separated by a 7-day washout period. Vaping and smoking topography were standardized in accordance with hookah smoking puffing parameters observed in natural settings.17Shihadeh A. Azar S. Antonios C. Haddad A. Towards a topographical model of narghile water-pipe cafe smoking: a pilot study in a high socioeconomic status neighborhood of Beirut, Lebanon.Pharmacol Biochem Behav. 2004; 79: 75-82Crossref PubMed Scopus (128) Google Scholar,18Maziak W. Rastam S. Ibrahim I. Ward K.D. Shihadeh A. Eissenberg T. CO exposure, puff topography, and subjective effects in waterpipe tobacco smokers.Nicotine Tob Res. 2009; 11: 806-811Crossref PubMed Scopus (125) Google Scholar For the duration of the 30-min inhalation sessions, all participants were cued verbally to inhale a 3-s puff at 20-s intervals, with vapor remaining in the lungs for approximately 3 s of breath-holding after inhalation. Supervision was carried out to prevent superficial vaping or hyperventilation. Experimental sessions took place in a specifically designed smoking room within the University of California, Los Angeles, Clinical and Translational Research Center. All measurements were performed before and immediately after (< 10 min) the sessions. Carotid-femoral PWV was measured by simultaneous waveform capture using both a thigh-specific cuff and carotid artery applanation tonometry (SphygmoCor XCEL; AtCor Medical). Velocity (dsf – dsc (m) / time (s)) was calculated by measuring the time difference between the initial upstroke of the recorded waveforms at each site. The linear distance was measured manually from the suprasternal notch to the top of the thigh cuff at the center line of the leg, at the location of the femoral artery (dsf), and subtracting the distance from the suprasternal notch to the location of the carotid pulse (dsc). The transit time between the carotid and the femoral pulse waves was determined automatically by the SphygmoCor software. The augmentation index and central BP were derived from the contour of the brachial BP waveform. The brachial-artery waveform, calibrated using oscillometric brachial artery BP, was analyzed by the validated brachial-to-aortic SphygmoCor transfer function to generate a central waveform and associated parameters.19Karamanoglu M. O'Rourke M.F. Avolio A.P. Kelly R.P. An analysis of the relationship between central aortic and peripheral upper limb pressure waves in man.Eur Heart J. 1993; 14: 160-167Crossref PubMed Scopus (697) Google Scholar The augmentation index was calculated as the ratio of augmentation pressure (difference between the second and first systolic peaks of the aortic pressure waveform) and pulse pressure expressed as a percentage. Blood samples were obtained from the antecubital vein, drawn into pre-iced heparinized vacutainers, and placed on ice. Three tubes were sent to the University of California, Los Angeles, Clinical Laboratory for inflammatory biomarker analyses, which were performed within 24 h after collection. One tube was centrifuged to separate plasma for antioxidant biomarker analyses, and samples were frozen at –80°C in a cryopreservative solution.20Breton C.V. Yin F. Wang X. Avol E. Gilliland F.D. Araujo J.A. HDL anti-oxidant function associates with LDL level in young adults.Atherosclerosis. 2014; 232: 165-170Abstract Full Text Full Text PDF PubMed Scopus (29) Google Scholar Serum hsCRP levels were analyzed using the immunoturbidimetric method using the Siemens Vista Dimension analyzer, which provides a minimum detection level of < 0.2 mg/L. Quantitative determination of fibrinogen levels were determined by the clotting method (Clauss method). The within-assay coefficient of variation (CV) for fibrinogen is 2.8% to 3.7%, and the interassay CV is 1.2% to 3.0%. TNFα was analyzed using Quantitative Multiplex Bead Assay. Activity was determined by the rate of hydrolysis of phenyl acetate to phenol, as described previously.21Lin Y. Ramanathan G. Zhu Y. et al.Pro-oxidative and proinflammatory effects after traveling from Los Angeles to Beijing: a biomarker-based natural experiment.Circulation. 2019; 140: 1995-2004Crossref PubMed Scopus (20) Google Scholar Briefly, 4 μL plasma was incubated with 3.5 mM phenyl acetate in 9 mM Tris-HCl buffer (pH, 8.0) containing 0.9 mM CaCl2 at RT. The kinetics of phenol formation were determined by recording the absorbance at 270 nm every 15 s for 2 min. The activity was expressed as nanomoles of product formed per minute per milliliter of plasma. We determined the ability of PON-1, associated with HDL, to hydrolyze paraoxon substrate.22Aldridge W.N. Serum esterases. I. Two types of esterase (A and B) hydrolysing p-nitrophenyl acetate, propionate and butyrate, and a method for their determination.Biochem J. 1953; 53: 110-117Crossref PubMed Scopus (474) Google Scholar,23Aldridge W.N. Serum esterases. II. An enzyme hydrolysing diethyl p-nitrophenyl phosphate (E600) and its identity with the A-esterase of mammalian sera.Biochem J. 1953; 53: 117-124Crossref PubMed Scopus (281) Google Scholar The hydrolysis of paraoxon (diethyl-p-nitrophenyl phosphate) to p-nitrophenol by PON-1 was determined by incubating 5 μL of plasma with 1.0 mM paraoxon in 100 mM tris-HCl buffer (pH, 8.5).24Yin F. Lawal A. Ricks J. et al.Diesel exhaust induces systemic lipid peroxidation and development of dysfunctional pro-oxidant and pro-inflammatory high-density lipoprotein.Arterioscler Thromb Vasc Biol. 2013; 33: 1153-1161Crossref PubMed Scopus (99) Google Scholar The kinetics of p-nitrophenol formation was determined by recording absorbance at 405 nm every 15 s for 4 min. The enzyme activity was expressed as micromoles of p-nitrophenol formed per minute for every 1 mL plasma and assayed in triplicates. The intra-assay CV for the assay was 2.60% and the interassay CV was 8.95%. Capacity was determined as the ability of HDL to inhibit LDL-induced oxidation of dihydrodichlorofluorescein into the fluorescent dichlorofluorescein.24Yin F. Lawal A. Ricks J. et al.Diesel exhaust induces systemic lipid peroxidation and development of dysfunctional pro-oxidant and pro-inflammatory high-density lipoprotein.Arterioscler Thromb Vasc Biol. 2013; 33: 1153-1161Crossref PubMed Scopus (99) Google Scholar Capacity was expressed as an HDL oxidative index, determined by the ratio of dichlorofluorescein fluorescence in the presence and absence of HDL and assayed in triplicates. An index of < 1.0 denotes protective antioxidant HDL, whereas an index of > 1.0 indicates pro-oxidant HDL.20Breton C.V. Yin F. Wang X. Avol E. Gilliland F.D. Araujo J.A. HDL anti-oxidant function associates with LDL level in young adults.Atherosclerosis. 2014; 232: 165-170Abstract Full Text Full Text PDF PubMed Scopus (29) Google Scholar The within-assay CV was 6.89%. The interassay CV for four separate measurements over a period of 2 months was 7.30%. Plasma nicotine levels were assayed by gas chromatography with nitrogen-phosphorus detection, using 5-methylnicotine and 1-methyl-5-(2-pyridyl)-pyrrolidin-2-one (ortho-cotinine) as internal standards.25Jacob 3rd, P. Wilson M. Benowitz N.L. Improved gas chromatographic method for the determination of nicotine and cotinine in biologic fluids.J Chromatogr. 1981; 222: 61-70Crossref PubMed Scopus (420) Google Scholar Expired CO measurements were carried out using a CO meter (Micro Smokerlyzer; Bedfont Scientific Ltd.). Paired Student t tests were used to compare continuous variables between sessions before and after exposure. Because of the crossover study design, we used a general linear model approach for repeated measures to examine differences between e-hookah and combustible hookah; the models included two within-subject factors (product type and time point relative to exposure session), and the sequence of type of product exposure was included as a between-group factor. The effect of primary interest was the interaction between the two within-subject factors, product type and time point relative to the exposure session. Effect sizes are for the interaction of product-by-time point relative to exposure in the general linear model repeated-measures analysis and translated from eta-square metric to d-metric.26Lenhard W. Lenhard A. Calculation of effect sizes. 2016. Psychometrica website.https://www.psychometrica.de/effect_size.htmlDate accessed: March 12, 2021Google Scholar Statistical significance was set at .05 and analyses were conducted using SPSS Statistics version 24.0 software (IBM). Sixty-eight potential participants responded to advertisement in local media, colleges, and universities, and 42 were screened for participation. Of these, 17 met study criteria. Twenty-five participants were excluded for the following reasons: positive tetrahydrocannabinol test results on screening (n = 7); history of cigarette or marijuana smoking, or both (n = 11); history of obesity or hypertension (n = 5); and exhaled CO of > 10 parts per million on screening (n = 2). The Consolidated Standards for Reporting Trials diagram is shown in Figure 2. Participant demographics are displayed in Table 1. Our sample mostly comprised college graduates who reported starting to smoke hookah flavored tobacco between 18 and 24 years of age, on average twice weekly for 5.6 ± 0.1 years.Table 1Participant CharacteristicsVariableValueNo.17Sex, female/male5/12Age, y26.0 ± 1.1BMI, kg/m224.8 ± 0.6Race or ethnicity Non-Hispanic White4 Non-Hispanic Black4 Hispanic1 Asian5 Middle Eastern3Education High School2 College14 Graduate school1History of hookah smoking Smoking sessions, no. per wk2 ± 1 Session duration, min120.0 ± 10.3Preferred hookah tobacco/liquid flavor Candy4 Fruit12 Alcohol1 Menthol0Age of hookah smoking onset, y < 172 18-2411 25-324Data are presented as No. or mean ± SEM. Open table in a new tab Data are presented as No. or mean ± SEM. A total of 34 sessions were completed (17 e-hookah vaping and 17 hookah smoking sessions). Within 10 min after the sessions, both products acutely caused a significant increase in heart rate and brachial and central BP (P < .05) (Table 2). With e-hookah vaping sessions, although all participants achieved comparable acute increases in heart rate, BP, and measures of arterial stiffness, four participants reported experiencing throat irritation. Although central pulse pressure did not increase significantly after exposure to either product, e-hookah vaping led to a significant increase in pulse pressure, whereas combustible hookah smoking did not. E-hookah vaping tended to lead to a higher increase in carotid-femoral PWV than combustible hookah smoking (mean ± SE: e-hookah, +0.74 ± 0.12 m/s; combustible hookah, +0.57 ± 0.14 m/s; P < .05 for both). Compared with baseline, only e-hookah vaping induced an acute increase in augmentation index (P = .004). Comparing baseline values of BP and arterial stiffness indexes between the two experimental sessions showed no significant differences.Table 2Hemodynamics, Peripheral and Central BP Changes, Arterial Stiffness Parameters and Smoking Exposure Biomarkers Before and After the Smoking and Vaping SessionsVariableElectronic Hookah VapingCharcoal Hookah SmokingBeforeAfterChange (After – Before)BeforeAfterChange (After – Before)Heart rate, beats/min69 ± 278 ± 3aP < .05.+9 ± 368 ± 277 ± 3aP < .05.+9 ± 2Brachial BP, mm Hg Systolic113 ± 2128 ± 3aP < .05.+15 ± 2110 ± 2119 ± 3aP < .05.+9 ± 2 Diastolic69 ± 278 ± 3aP < .05.+9 ± 266 ± 273 ± 2aP < .05.+7 ± 1 Pulse pressure44 ± 250 ± 2aP < .05.+6 ± 244 ± 246 ± 2+2 ± 2 Mean arterial pressure83 ± 294 ± 2aP < .05.+11 ± 280 ± 288 ± 2aP < .05.+8 ± 1Central BP, mm Hg......+9 ± 298 ± 2106 ± 3aP < .05.+8 ± 2 Systolic101 ± 3110 ± 3aP < .05............. Diastolic69 ± 277 ± 3aP < .05.+8 ± 266 ± 274 ± 3aP < .05.+8 ± 1 Pulse pressure31 ± 134 ± 2+3 ± 131 ± 133 ± 1+2 ± 1 Mean arterial pressure80 ± 288 ± 3aP < .05.+8 ± 277 ± 287 ± 2aP < .05.+10 ± 2Arterial stiffness parameters Augmentation index @ 75, %7.97 ± 2.9713.55 ± 3.24aP < .05.+5.58 ± 1.547.79 ± 2.5410.66 ± 2.98+2.87 ± 2.12 Carotid-femoral PWV, m/sec8.20 ± 0.268.94 ± 0.33aP < .05.+0.74 ± 0.128.15 ± 0.208.71 ± 0.23aP < .05.+0.57 ± 0.1Data are presented as mean ± SEM. PWV = pulse wave velocity.a P < .05. Open table in a new tab Data are presented as mean ± SEM. PWV = pulse wave velocity. In comparison with baseline, the plasma proinflammatory biomarkers hsCRP, fibrinogen, and TNFα significantly increased acutely after e-hookah vaping (from 0.72 ± 0.12 mg/L to 0.76 ± 0.13 mg/L; from 261.41 ± 13.84 mg/dL to 277.47 ± 14.09 mg/dL; from 0.69 ± 0.06 pg/mL to 0.76 ± 0.08 pg/mL, respectively; all P < .05), but not after combustible hookah smoking (from 0.77 ± 0.19 mg/L to 0.77 ± 0.19 mg/L; from 290.82 ± 13.76 mg/dL to 296.59 ± 14.80 mg/dL; from 0.85 ± 0.08 pg/mL to 0.82 ± 0.08 pg/mL, respectively; all P values were not significant) (Fig 3A, 3B ). Although changes from before to after exposure were significantly different between the two types of products for TNFα (P = .005), but not for hsCRP or fibrinogen (both P values were not significant), effect sizes were large for all three measures (d = 1.70, d = 1.09, and d = 1.05, respectively). Antioxidant biomarkers did not change after using either products (Fig 4A, 4B ). Comparing baseline values of both inflammatory and antioxidant biomarkers between the two experimental sessions showed no significant differences (.10 < P < .95).Figure 4A, B, Representative boxplots showing of plasma levels of HOI, arylesterase activity, and paraoxonase-1 antioxidant biomarker activity before and after exposure sessions: e-hookah vaping (A) and combustible hookah smoking (B). The solid horizontal line represents the median, the box represents the 25th to 75th percentiles, and the whiskers represent the 10th and 90th percentiles. HOI = high-density lipoprotein oxidative index.View Large Image Figure ViewerDownload Hi-res image Download (PPT) Exhaled CO levels were significantly higher after combustible hookah smoking than after e-hookah vaping (P < .001) (Fig 5). No difference was found between plasma nicotine concentrations after using either product (P = .478). The increase in flavored hookah tobacco smoking among youth and young adults is global.1Maziak W. Taleb Z.B. Bahelah R. et al.The global epidemiology of waterpipe smoking.Tob Control. 2015; 24: i3-i12Crossref PubMed Scopus (281) Google Scholar,2Bhatnagar A. Maziak W. Eissenberg T. et al.Water pipe (hookah) smoking and cardiovascular disease risk: a scientific statement from the American Heart Association.Circulation. 2019; 139: e917-e936Crossref PubMed Scopus (42) Google Scholar Coinciding with the remarkable increase in electronic nicotine delivery systems (ENDSs), in 2014, the hookah tobacco companies introduced a putatively safe electronic alternative to traditional charcoal-heated hookah smoking, accompanied by unsubstantiated marketing claims that the presence of water "filters out toxins."27Cornacchione J. Wagoner K.G. Wiseman K.D. et al.Adolescent and young adult perceptions of hookah and little cigars/cigarillos: implications for risk messages.J Health Commun. 2016; 21: 818-825Crossref PubMed Scopus (34) Google Scholar,28Griffiths M. Harmon T. Gilly M. Hubble bubble trouble: the need for education about and regulation of hookah smoking.J Public Policy Mark. 2011; 30: 119-132Crossref Scopus (58) Google Scholar In a randomized crossover study among a sample of young healthy adult chronic hookah smokers, we found th
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