Our study confirms the results of previous studies that water pipe users absorb nicotine resulting in plasma nicotine levels similar to those observed in cigarette smokers. Plasma nicotine concentrations rose over the course of the smoking session, peaking on average at about 45 minutes. Based on the measured nicotine content of the tobacco preparation, the maximum available dose, 32 mg, was equivalent to the nicotine content of tobacco of 2–3 cigarettes [15
]. On average, the waterpipe smokers took in a systemic dose of 2.5 mg, equivalent to the dose from smoking 2–3 cigarettes. Waterpipe only smokers took in an average of 1.8 mg, while the mixed users took in an average of 5.4 mg. The latter is comparable to smoking 3–5 cigarettes. Overall the systemic bioavailability of nicotine (that is, the fraction of nicotine contained in the tobacco that is systemically absorbed) was about 8% from waterpipe tobacco, which is similar to bioavailability from cigarettes.
As reported in previous studies,[9
] waterpipe smokers absorbed substantially more CO than cigarette smokers, presumably due to its generation by the burning charcoal placed on top of the tobacco product. The expired CO boost after hookah smoking averaged 38 ppm compared to about 17 ppm typically observed in cigarette smokers [17
] Long-term CO exposure elevates the total red blood cells (RBC) mass in smokers as a result of oxygen carrying capacity and availability reductions (i.e., hypoxemia.) The increased RBC mass significantly increases blood viscosity and contributes to a hypercoagulable state in smokers [18
]. Exposure to CO in obstructive coronary artery disease results in an increase in the number and complexity of ventricular arrhythmias during exercise that produced 6% increase in the carboxyhemoglobin [19
]. Consequently, the high level of exposure to CO in waterpipe smokers poses a potential health risk, especially for people with cardiovascular or pulmonary diseases.
Unique to this study is the report of increased urinary levels of tobacco-specific nitrosamines (TSNA) and polycyclic aromatic hydrocarbons (PAHs) following waterpipe smoking. TSNA and PAHs are major classes of carcinogens present in tobacco smoke and are believed to be causative agents for lung cancer and other cancers [20
]. 4-(Methylnitrosamino)-1-(3-pyridyl)-1- butanol (NNAL), a metabolite of the potent lung-selective carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1- butanone (NNK) is frequently used as a biomarker for the TSNA class of carcinogens. We found that urine NNAL concentrations increased significantly following waterpipe smoking, and then declined slowly, consistent with its long half-life of 10 – 18 days [21
] (). The peak urine NNAL concentrations, on the order of 5–20 pg/mL (~0.02 to ~0.10 pmol/mg creatinine), were much lower than typically found in cigarette smokers, which are generally in the range of 50 to 3000 pg/mL [22
]. This is presumably due to the long half-life of NNAL [21
], which results in accumulation over time and therefore higher concentrations in habitual smokers, in contrast to the lower concentrations in our subjects who were not habitual smokers and smoked only once during the study day. Recently, Schubert et al
reported 24 hour urinary excretion of NNAL following one waterpipe smoking session, but excretion was not different from what was found in a group of non-smokers[7
]. Presumably, this was due to relatively high secondhand smoke exposure in their subjects compared to our subjects, whose baseline urine NNAL concentrations averaged 1.2 pg/mL (0.014 pmol/mg creatinine). Assuming 2 L of urine is excreted in 24 hr, the concentration of NNAL in the 24 hr urine of non-smokers was about 10 pg/mL in the Schubert study.
PAHs are products of incomplete combustion of organic materials, including tobacco, and some, such as benzo[a]pyrene, are potent carcinogens. Since the potent PAH carcinogens are usually present in low amounts and are extensively metabolized, making their measurement difficult, metabolites of more abundant PAHs, such as naphthalene, fluorene, phenanthrene, and particularly pyrene are generally used as biomarkers for PAH exposure [23
]. We measured urine concentrations of the PAH metabolites 2-naphthol, 2-hydroxyfluorene, hydroxyphenanthrenes, and 1-hydroxypyrene. Excretion of all metabolites increased following water pipe smoking, increasing 50 to 100% above baseline, indicating that water pipe smoking is a significant source of exposure to this class of carcinogens ( and ). Not surprisingly, as our subjects were not cigarette smokers or occasional cigarette smokers, urine concentrations of PAH metabolites were less than those in smokers by factors ranging from about 1.5 to 5, but about twice those found in non-smokers [13
] The lower concentrations compared to cigarette smokers is presumably due to our subjects smoking only once during the study day, compared to habitual cigarette smokers who may smoke 10–20 cigarettes per day.
A limitation of our study is that subjects smoked an entire waterpipe by themselves in a laboratory environment. Usually a waterpipe is smoked in a social situation, and often many people share a pipe full of tobacco. Our exposure data are likely to exceed what most smokers take in when they share a pipe with others. Data obtained from people smoking waterpipes in their usual social circumstances are needed to determine more usual levels of exposure. Our subjects were primarily waterpipe only smokers, but three were mixed tobacco users. Our data suggest that smoke toxicant exposure is higher in mixed tobacco users, but because of the small number of mixed users our findings must be viewed as tentative.