Endothelial Dysfunction, Inflammation, Oxidative Stress
Conditions
Brief summary
Hookah (water-pipe) tobacco smoking has quickly grown to become a major global tobacco epidemic among youth; with electronic (e-) hookahs more recently increasing in popularity especially among young female adults, who endorse marketing claims that these products are a safer alternative to traditional hookah, but scientific evidence is lacking. The study aims to elucidate the comparative effects of traditional hookah smoking vs. e-hookah vaping on human vascular and endothelial function; and examine the role of inflammation and oxidative stress, as likely mechanisms in hookah-related cardiovascular disease pathogenesis.
Detailed description
Hookah (water-pipe) tobacco smoking is rapidly increasing in popularity worldwide. Contributing to this popularity is the unsubstantiated belief that traditional charcoal-heated hookah smoke is detoxified as it passes through the water-filled basin. More recently, electronic (e-) hookahs-containing flavored e-liquid that is heated electrically but inhaled through traditional water-pipes-are increasing in popularity in the United States among young female adults, who endorse marketing claims that these products are even safer than traditional charcoal-heated hookah products. The objective of this project is to investigate the comparative effects of traditional charcoal-heated hookah smoking versus e-hookah vaping on endothelial and vascular function and their mechanistic role in the development of cardiovascular disease. The investigators will test the hypothesis that: 1) in the absence of burning charcoal briquettes and virtually any carbon monoxide (CO) exposure, e-hookah vaping acutely impairs endothelial function and evokes acute central arterial stiffness, opposite from the endothelial function augmentation observed after traditional charcoal-heated hookah smoking, which is likely mediated by the large CO boost emitted from burning charcoal briquettes used to heat the flavored hookah tobacco; and 2) the processes of oxidative stress and inflammation play a pivotal mechanistic role underlying these vascular changes. Accordingly, in a cross-over study comparing traditional hookah smoking to e-hookah vaping, the investigators will assess endothelial function measured by brachial artery flow-mediated dilation and aortic stiffness by pulse wave velocity and augmentation index in 18 young healthy hookah smokers 21-39 years old, before and after ad lib 30-minute smoking/ vaping exposure sessions. To test for oxidative stress mediation, the investigators will determine if any acute impairment in endothelial function after e-hookah can be prevented by intravenous Vitamin C infusion, a potent anti-oxidant. Inflammatory and oxidant biomarkers, as well as smoking exposure biomarkers will be collected before and after the exposure sessions. The results of this proposal: (a) stand to fill in gaps in our mechanistic understanding of the comparative effect of traditional vs. e-hookah bowl on vascular and endothelial function; and (b) help inform policy decisions by the FDA about regulation of hookah products.
Interventions
OTHERElectronic hookah vaping
Electronic hookah bowl inhalation
OTHERTraditional hookah smoking
Charcoal-heated hookah smoking
Sponsors
National Institutes of Health (NIH)
National Heart, Lung, and Blood Institute (NHLBI)
University of California, Los Angeles
Study design
Allocation
RANDOMIZED
Intervention model
CROSSOVER
Primary purpose
OTHER
Masking
NONE
Intervention model description
Charcoal-heated hookah smoking vs. electronic hookah vaping
Eligibility
Sex/Gender
ALL
Age
21 Years to 39 Years
Healthy volunteers
Yes
Inclusion criteria
* 21-39 years old hookah smokers: smoked hookah \>12x in last 12 months * no history of illicit drugs or marijuana * no evidence of cardiopulmonary disease by history/ physical * no diabetes: fasting blood glucose \<100 mg/dl * BP\<140/90mmHg * resting HR\<100 bpm * BMI\<30kg•m2 * no prescription medication
Exclusion criteria
* exhaled CO\>10 ppm (smoking non-abstinence) * positive pregnancy test * psychiatric illness
Design outcomes
Primary
| Measure | Time frame | Description |
|---|---|---|
| Tumor Necrosis Factor-α (TNFα) Concentrations | Pre- and post- the 30-minute smoking or vaping exposure sessions | Plasma TNFα (inflammatory biomarker) |
| Flow-Mediated Dilation (FMD) | Pre- and post- the 30-minute smoking or vaping exposure sessions | Using ultrasound, FMD of the brachial artery induced by reactive hyperemia, was used to measure endothelium-dependent vasodilator function. Baseline diameter and velocity were recorded for 45 seconds and resumed 30 seconds before cuff deflation and continuously for 2 minutes after deflation to obtain true peak vasodilatory response. |
| Carotid-Femoral Pulse Wave Velocity (Cf-PWV) | Pre- and post- the 30-minute smoking or vaping exposure sessions | Using applanation tonometry, cf-PWV was used to measure central arterial stiffness. |
| HDL Oxidant Index (HOI) | Pre- and post- the 30-minute smoking or vaping exposure sessions | Capacity was determined as the ability of HDL to inhibit LDL-induced oxidation of dihydrodichlorofluorescein into the fluorescent dichlorofluorescein. Capacity was expressed as an HDL oxidative index, determined by the ratio of dichlorofluorescein fluorescence in the presence and absence of HDL. An index of \< 1.0 denotes protective antioxidant HDL, whereas an index of \> 1.0 indicates pro-oxidant HDL. |
| Paraoxonase-1 (PON-1) Activity | Pre- and post- the 30-minute smoking or vaping exposure sessions | PON-1 activity was determined by the ability of PON-1, associated with HDL, to hydrolyze paraoxon substrate. The hydrolysis of paraoxon (diethyl-p-nitrophenyl phosphate) to p-nitrophenol by PON-1 was determined by incubating 5 mL of plasma with 1.0 mM paraoxon in 100 mM tris-HCl buffer (pH, 8.5). Unit of Measure: expressed as micromoles of p-nitrophenol formed per minute for every 1 mL plasma. |
| Arylesterase Activity | Pre- and post- the 30-minute smoking or vaping exposure sessions. | Arylesterase activity (lipid peroxidation biomarker) was determined by the rate of hydrolysis of phenyl acetate to phenol. Briefly, 4 mL 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. Unit of Measure: nanomoles of product formed per minute per milliliter of plasma. |
| High-sensitivity C-reactive Protein (Hs-CRP) Levels | Pre- and post- the 30-minute smoking or vaping exposure sessions | Plasma hs-CRP (inflammatory biomarker) |
Secondary
| Measure | Time frame | Description |
|---|---|---|
| Flow-Mediated Dilation (FMD) | Effect of FMD with e-hookah vaping examined after pretreatment of intravenous infusion of antioxidant ascorbic acid (administered over 60 minutes at 0.5 mL min-1) | Using ultrasound, FMD of the brachial artery, induced by reactive hyperemia, was used to measure endothelium-dependent vasodilator function after intravenous infusion of antioxidant ascorbic acid. Infusion of antioxidant ascorbic acid was done before the e-hookah vaping session. |
| Endothelium-independent Vasodilator Function (Control Test for Endothelium-dependent Vasodilator Function) | Pre- and post- sublingual administration of nitroglycerin (0.15 mg), which was administrated before and after e-hookah vaping. | As a control test for the assessment of endothelium-dependent vasodilator function, using ultrasound the brachial artery, endothelium-independent dilatation was assessed by administering sublingual nitroglycerin. This measure was assessed 10 minutes after FMD testing. Ultrasound images were recorded continuously for a total of 10 minutes |
| Augmentation Index (AI) | Pre- and post- the 30-minute smoking or vaping exposure sessions | AI was used to measure central stiffness. It 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. |
| Interleukin 6 (IL-6) Levels | A change between two points is reported below (e.g., value at post-exposure session minus value at pre-exposure session). | Plasma IL-6 (inflammatory biomarker). |
| Interleukin 10 (IL-10) Levels | A change between two points is reported below (e.g., value at post-exposure session minus value at pre-exposure session). | Serum IL-10 (anti-inflammatory biomarker) |
| Nicotine Levels | Pre- and post- the 30-minute smoking or vaping exposure sessions | Plasma nicotine levels (smoking or vaping exposure biomarker) |
| Carbon Monoxide (CO) Levels | Pre- and post- the 30-minute smoking or vaping exposure sessions | Exhaled CO levels (smoking or vaping exposure biomarker) |
Countries
United States
Participant flow
Recruitment details
Participants were recruited through advertisements posted at Southern California colleges and universities, as well as social media websites, from December 2018 to August 2020.
Participants by arm
| Arm | Count |
|---|---|
| All Study Participants Participants who were randomized to either smoke hookah first followed by vape hookah or vape hookah first followed by smoke hookah. | 19 |
| Total | 19 |
Withdrawals & dropouts
| Period | Reason | FG000 | FG001 |
|---|---|---|---|
| Overall Study | Requested by subject not to complete traditional hookah | 0 | 2 |
Baseline characteristics
| Characteristic | All Study Participants |
|---|---|
| Age, Categorical <=18 years | 0 Participants |
| Age, Categorical >=65 years | 0 Participants |
| Age, Categorical Between 18 and 65 years | 19 Participants |
| Ethnicity (NIH/OMB) Hispanic or Latino | 2 Participants |
| Ethnicity (NIH/OMB) Not Hispanic or Latino | 17 Participants |
| Ethnicity (NIH/OMB) Unknown or Not Reported | 0 Participants |
| Race (NIH/OMB) American Indian or Alaska Native | 0 Participants |
| Race (NIH/OMB) Asian | 6 Participants |
| Race (NIH/OMB) Black or African American | 3 Participants |
| Race (NIH/OMB) More than one race | 0 Participants |
| Race (NIH/OMB) Native Hawaiian or Other Pacific Islander | 0 Participants |
| Race (NIH/OMB) Unknown or Not Reported | 0 Participants |
| Race (NIH/OMB) White | 10 Participants |
| Region of Enrollment United States | 19 Participants |
| Sex: Female, Male Female | 6 Participants |
| Sex: Female, Male Male | 13 Participants |
Adverse events
| Event type | EG000 affected / at risk | EG001 affected / at risk |
|---|---|---|
| deaths Total, all-cause mortality | 0 / 17 | 0 / 19 |
| other Total, other adverse events | 0 / 17 | 0 / 19 |
| serious Total, serious adverse events | 0 / 17 | 0 / 19 |
Outcome results
Primary
Arylesterase Activity
Arylesterase activity (lipid peroxidation biomarker) was determined by the rate of hydrolysis of phenyl acetate to phenol. Briefly, 4 mL 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. Unit of Measure: nanomoles of product formed per minute per milliliter of plasma.
Time frame: Pre- and post- the 30-minute smoking or vaping exposure sessions.
Population: All study participants who completed study visits (unable to obtain data on 1 participant from the e-hookah group and 3 participants from the traditional hookah group).
| Arm | Measure | Group | Value (MEAN) | Dispersion |
|---|---|---|---|---|
| Electronic Hookah | Arylesterase Activity | Arylesterase activity before exposure session | 277.36 units/mL:see Outcome Measure Description | Standard Error 14.26 |
| Electronic Hookah | Arylesterase Activity | Arylesterase activity after exposure session | 295.78 units/mL:see Outcome Measure Description | Standard Error 16.78 |
| Traditional Hookah | Arylesterase Activity | Arylesterase activity before exposure session | 281.38 units/mL:see Outcome Measure Description | Standard Error 19.33 |
| Traditional Hookah | Arylesterase Activity | Arylesterase activity after exposure session | 285.06 units/mL:see Outcome Measure Description | Standard Error 16.78 |
Primary
Carotid-Femoral Pulse Wave Velocity (Cf-PWV)
Using applanation tonometry, cf-PWV was used to measure central arterial stiffness.
Time frame: Pre- and post- the 30-minute smoking or vaping exposure sessions
Population: All study participants who completed study visits (unable to obtain data on 4 participants in the e-hookah group)
| Arm | Measure | Group | Value (MEAN) | Dispersion |
|---|---|---|---|---|
| Electronic Hookah | Carotid-Femoral Pulse Wave Velocity (Cf-PWV) | cf-PWV before exposure session | 8.20 m/sec | Standard Error 0.26 |
| Electronic Hookah | Carotid-Femoral Pulse Wave Velocity (Cf-PWV) | cf-PWV after exposure session | 8.94 m/sec | Standard Error 0.33 |
| Traditional Hookah | Carotid-Femoral Pulse Wave Velocity (Cf-PWV) | cf-PWV before exposure session | 8.15 m/sec | Standard Error 0.2 |
| Traditional Hookah | Carotid-Femoral Pulse Wave Velocity (Cf-PWV) | cf-PWV after exposure session | 8.71 m/sec | Standard Error 0.23 |
Primary
Flow-Mediated Dilation (FMD)
Using ultrasound, FMD of the brachial artery induced by reactive hyperemia, was used to measure endothelium-dependent vasodilator function. Baseline diameter and velocity were recorded for 45 seconds and resumed 30 seconds before cuff deflation and continuously for 2 minutes after deflation to obtain true peak vasodilatory response.
Time frame: Pre- and post- the 30-minute smoking or vaping exposure sessions
Population: All study participants who completed study visits (1 participant had suboptimal ultrasound images from the e-hookah group; and 2 did not have images from the traditional hookah group)
| Arm | Measure | Group | Value (MEAN) | Dispersion |
|---|---|---|---|---|
| Electronic Hookah | Flow-Mediated Dilation (FMD) | FMD after exposure session | 4.79 percentage of arterial diameter | Standard Error 0.58 |
| Electronic Hookah | Flow-Mediated Dilation (FMD) | FMD before exposure session | 6.11 percentage of arterial diameter | Standard Error 0.66 |
| Traditional Hookah | Flow-Mediated Dilation (FMD) | FMD before exposure session | 5.89 percentage of arterial diameter | Standard Error 1.02 |
| Traditional Hookah | Flow-Mediated Dilation (FMD) | FMD after exposure session | 7.31 percentage of arterial diameter | Standard Error 0.82 |
Primary
HDL Oxidant Index (HOI)
Capacity was determined as the ability of HDL to inhibit LDL-induced oxidation of dihydrodichlorofluorescein into the fluorescent dichlorofluorescein. Capacity was expressed as an HDL oxidative index, determined by the ratio of dichlorofluorescein fluorescence in the presence and absence of HDL. An index of \< 1.0 denotes protective antioxidant HDL, whereas an index of \> 1.0 indicates pro-oxidant HDL.
Time frame: Pre- and post- the 30-minute smoking or vaping exposure sessions
Population: All study participants who completed study visits (unable to obtain data on 4 participants in the e-hookah group)
| Arm | Measure | Group | Value (MEAN) | Dispersion |
|---|---|---|---|---|
| Electronic Hookah | HDL Oxidant Index (HOI) | HOI before exposure session | 0.57 index | Standard Error 0.05 |
| Electronic Hookah | HDL Oxidant Index (HOI) | HOI after exposure session | 0.58 index | Standard Error 0.06 |
| Traditional Hookah | HDL Oxidant Index (HOI) | HOI before exposure session | 0.56 index | Standard Error 0.06 |
| Traditional Hookah | HDL Oxidant Index (HOI) | HOI after exposure session | 0.52 index | Standard Error 0.05 |
Primary
High-sensitivity C-reactive Protein (Hs-CRP) Levels
Plasma hs-CRP (inflammatory biomarker)
Time frame: Pre- and post- the 30-minute smoking or vaping exposure sessions
Population: All study participants who completed study visits (unable to obtain data on 2 participants in the traditional hookah group)
| Arm | Measure | Group | Value (MEAN) | Dispersion |
|---|---|---|---|---|
| Electronic Hookah | High-sensitivity C-reactive Protein (Hs-CRP) Levels | hs-CRP before exposure session | 0.72 mg/L | Standard Error 0.12 |
| Electronic Hookah | High-sensitivity C-reactive Protein (Hs-CRP) Levels | hs-CRP after exposure session | 0.76 mg/L | Standard Error 0.13 |
| Traditional Hookah | High-sensitivity C-reactive Protein (Hs-CRP) Levels | hs-CRP before exposure session | 0.77 mg/L | Standard Error 0.19 |
| Traditional Hookah | High-sensitivity C-reactive Protein (Hs-CRP) Levels | hs-CRP after exposure session | 0.77 mg/L | Standard Error 0.19 |
Primary
Paraoxonase-1 (PON-1) Activity
PON-1 activity was determined by the ability of PON-1, associated with HDL, to hydrolyze paraoxon substrate. The hydrolysis of paraoxon (diethyl-p-nitrophenyl phosphate) to p-nitrophenol by PON-1 was determined by incubating 5 mL of plasma with 1.0 mM paraoxon in 100 mM tris-HCl buffer (pH, 8.5). Unit of Measure: expressed as micromoles of p-nitrophenol formed per minute for every 1 mL plasma.
Time frame: Pre- and post- the 30-minute smoking or vaping exposure sessions
Population: All study participants who completed study visits (unable to obtain data on 4 participants in the e-hookah group)
| Arm | Measure | Group | Value (MEAN) | Dispersion |
|---|---|---|---|---|
| Electronic Hookah | Paraoxonase-1 (PON-1) Activity | PON-1 before exposure session | 1071.24 units/mL:see Outcome Measure Description | Standard Error 188.79 |
| Electronic Hookah | Paraoxonase-1 (PON-1) Activity | PON-1 after exposure session | 1151.73 units/mL:see Outcome Measure Description | Standard Error 207.98 |
| Traditional Hookah | Paraoxonase-1 (PON-1) Activity | PON-1 before exposure session | 709.32 units/mL:see Outcome Measure Description | Standard Error 112.43 |
| Traditional Hookah | Paraoxonase-1 (PON-1) Activity | PON-1 after exposure session | 701.29 units/mL:see Outcome Measure Description | Standard Error 110.67 |
Primary
Tumor Necrosis Factor-α (TNFα) Concentrations
Plasma TNFα (inflammatory biomarker)
Time frame: Pre- and post- the 30-minute smoking or vaping exposure sessions
Population: All study participants who completed study visits (unable to obtain data on 1 participant in the e-hookah group)
| Arm | Measure | Group | Value (MEAN) | Dispersion |
|---|---|---|---|---|
| Electronic Hookah | Tumor Necrosis Factor-α (TNFα) Concentrations | TNFα before exposure session | 0.69 pg/mL | Standard Error 0.06 |
| Electronic Hookah | Tumor Necrosis Factor-α (TNFα) Concentrations | TNFα after exposure session | 0.76 pg/mL | Standard Error 0.08 |
| Traditional Hookah | Tumor Necrosis Factor-α (TNFα) Concentrations | TNFα before exposure session | 0.85 pg/mL | Standard Error 0.08 |
| Traditional Hookah | Tumor Necrosis Factor-α (TNFα) Concentrations | TNFα after exposure session | 0.82 pg/mL | Standard Error 0.08 |
Secondary
Augmentation Index (AI)
AI was used to measure central stiffness. It 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.
Time frame: Pre- and post- the 30-minute smoking or vaping exposure sessions
Population: All study participants who completed study visits (unable to obtain data on 4 participants in the e-hookah group and 1 in the traditional hookah group)
| Arm | Measure | Group | Value (MEAN) | Dispersion |
|---|---|---|---|---|
| Electronic Hookah | Augmentation Index (AI) | AI before exposure session | 7.97 percentage of the pulse pressure | Standard Deviation 2.97 |
| Electronic Hookah | Augmentation Index (AI) | AI after exposure session | 13.55 percentage of the pulse pressure | Standard Deviation 3.24 |
| Traditional Hookah | Augmentation Index (AI) | AI before exposure session | 7.79 percentage of the pulse pressure | Standard Deviation 2.54 |
| Traditional Hookah | Augmentation Index (AI) | AI after exposure session | 10.66 percentage of the pulse pressure | Standard Deviation 2.98 |
Secondary
Carbon Monoxide (CO) Levels
Exhaled CO levels (smoking or vaping exposure biomarker)
Time frame: Pre- and post- the 30-minute smoking or vaping exposure sessions
Population: All study participants who completed study visits (unable to obtain data on 1 participant in the e-hookah group; and 1 participant in the traditional hookah group)
| Arm | Measure | Group | Value (MEAN) | Dispersion |
|---|---|---|---|---|
| Electronic Hookah | Carbon Monoxide (CO) Levels | CO before exposure session | 2.58 ppm | Standard Error 0.27 |
| Electronic Hookah | Carbon Monoxide (CO) Levels | CO after exposure session | 2.31 ppm | Standard Error 0.2 |
| Traditional Hookah | Carbon Monoxide (CO) Levels | CO before exposure session | 3.38 ppm | Standard Error 0.49 |
| Traditional Hookah | Carbon Monoxide (CO) Levels | CO after exposure session | 40.19 ppm | Standard Error 6.69 |
Secondary
Endothelium-independent Vasodilator Function (Control Test for Endothelium-dependent Vasodilator Function)
As a control test for the assessment of endothelium-dependent vasodilator function, using ultrasound the brachial artery, endothelium-independent dilatation was assessed by administering sublingual nitroglycerin. This measure was assessed 10 minutes after FMD testing. Ultrasound images were recorded continuously for a total of 10 minutes
Time frame: Pre- and post- sublingual administration of nitroglycerin (0.15 mg), which was administrated before and after e-hookah vaping.
Population: A subset of participants, who completed the e-hookah vaping protocol.
| Arm | Measure | Group | Value (MEAN) | Dispersion |
|---|---|---|---|---|
| Electronic Hookah | Endothelium-independent Vasodilator Function (Control Test for Endothelium-dependent Vasodilator Function) | Dilation before e-hookah vaping | 27.15 percentage of arterial diameter | Standard Error 1.98 |
| Electronic Hookah | Endothelium-independent Vasodilator Function (Control Test for Endothelium-dependent Vasodilator Function) | Dilation after e-hookah vaping | 25.17 percentage of arterial diameter | Standard Error 1.87 |
Secondary
Flow-Mediated Dilation (FMD)
Using ultrasound, FMD of the brachial artery, induced by reactive hyperemia, was used to measure endothelium-dependent vasodilator function after intravenous infusion of antioxidant ascorbic acid. Infusion of antioxidant ascorbic acid was done before the e-hookah vaping session.
Time frame: Effect of FMD with e-hookah vaping examined after pretreatment of intravenous infusion of antioxidant ascorbic acid (administered over 60 minutes at 0.5 mL min-1)
Population: A subset of participants, who completed the e-hookah vaping protocol.
| Arm | Measure | Group | Value (MEAN) | Dispersion |
|---|---|---|---|---|
| Electronic Hookah | Flow-Mediated Dilation (FMD) | FMD before e-hookah vaping | 9.46 percentage of arterial diameter | Standard Error 0.87 |
| Electronic Hookah | Flow-Mediated Dilation (FMD) | FMD after e-hookah vaping | 8.74 percentage of arterial diameter | Standard Error 0.84 |
Secondary
Interleukin 10 (IL-10) Levels
Serum IL-10 (anti-inflammatory biomarker)
Time frame: A change between two points is reported below (e.g., value at post-exposure session minus value at pre-exposure session).
Population: All study participants who completed study visits (unable to obtain data on 5 participants in the e-hookah group)
| Arm | Measure | Value (MEAN) | Dispersion |
|---|---|---|---|
| Electronic Hookah | Interleukin 10 (IL-10) Levels | 0.03 pg/mL | Standard Error 0.03 |
| Traditional Hookah | Interleukin 10 (IL-10) Levels | -0.01 pg/mL | Standard Error 0.01 |
Secondary
Interleukin 6 (IL-6) Levels
Plasma IL-6 (inflammatory biomarker).
Time frame: A change between two points is reported below (e.g., value at post-exposure session minus value at pre-exposure session).
Population: All study participants who completed study visits (unable to obtain data on 5 participants in the e-hookah group)
| Arm | Measure | Value (MEAN) | Dispersion |
|---|---|---|---|
| Electronic Hookah | Interleukin 6 (IL-6) Levels | 0.13 pg/mL | Standard Error 0.08 |
| Traditional Hookah | Interleukin 6 (IL-6) Levels | 0.04 pg/mL | Standard Error 0.06 |
Secondary
Nicotine Levels
Plasma nicotine levels (smoking or vaping exposure biomarker)
Time frame: Pre- and post- the 30-minute smoking or vaping exposure sessions
Population: All study participants who completed study visits (unable to obtain data on 1 participant in the e-hookah group and 1 participant in the traditional hookah group)
| Arm | Measure | Group | Value (MEAN) | Dispersion |
|---|---|---|---|---|
| Electronic Hookah | Nicotine Levels | Plasma nicotine before exposure session | 0.59 ng/mL | Standard Error 0.09 |
| Electronic Hookah | Nicotine Levels | Plasma nicotine after exposure session | 5.83 ng/mL | Standard Error 0.96 |
| Traditional Hookah | Nicotine Levels | Plasma nicotine before exposure session | 0.82 ng/mL | Standard Error 0.24 |
| Traditional Hookah | Nicotine Levels | Plasma nicotine after exposure session | 6.96 ng/mL | Standard Error 1.11 |