Acute effects of waterpipe tobacco smoking: A double-blind, placebo-control study☆
Introduction
For centuries, millions of people have smoked tobacco using a waterpipe (a.k.a. hookah, narghile, shisha): inhalation of charcoal-heated air passes through tobacco, travels down the body, and bubbles through water in the bowl before reaching smokers’ lungs (World Health Organization, 2005). While often associated with southwest Asia, waterpipe tobacco smoking is now seen worldwide (e.g., Pärna et al., 2008, Jensen et al., 2010). In the U.S., for example, past 30-day waterpipe tobacco smoking has been reported by 9–20% of some college samples (Cobb et al., 2010). A survey of 8745 students from 8 universities revealed that 7.2% reported past 30-day use and 29.5% reported “ever use” (Primack et al., 2010). Past 30-day use among 14–18 year old Arab-Americans may be as high as 16% and non-Arab-Americans as high as 11% (Weglicki et al., 2007).
One reason for the global spread of waterpipe tobacco smoking may involve the oft-reported belief that waterpipes are less risky than cigarettes (Aljarrah et al., 2009, Smith-Simone et al., 2008). This belief seemingly is contradicted by demonstrations that various constituents of waterpipe smoke are known to cause cancer (e.g., polycyclic aromatic hydrocarbons [PAH]; Sepetdjian et al., 2008), lung disease (e.g., volatile aldehydes; Al Rashidi et al., 2008), cardiovascular disease (e.g., carbon monoxide [CO]; Shihadeh and Saleh, 2005), and dependence (i.e., nicotine; Shihadeh, 2003). At least some of these smoke toxicants have been found in waterpipe tobacco smokers during smoking, including CO and nicotine (El-Nachef and Hammond, 2008, Shafagoj and Mohammed, 2002).
While there is a growing literature investigating waterpipe smoke toxicant content and exposure, relatively few studies have examined the acute effects of waterpipe tobacco smoking. In terms of cardiovascular response, two laboratory studies demonstrate that waterpipe tobacco smoking produces clear cardiovascular effects. A single 45-min waterpipe smoking episode has been shown to increase average heart rate (HR) by 6 (Eissenberg and Shihadeh, 2009) or 16 bpm (Shafagoj and Mohammed, 2002), as well as to increase systolic blood pressure (SBP) by 6.7 mmHg, diastolic blood pressure (DBP) by 4.4 mmHg and mean arterial pressure (MAP) by 5.2 mmHg (Shafagoj and Mohammed, 2002). In both studies these cardiovascular effects were attributed to waterpipe-induced increases in plasma nicotine (see also Shafagoj et al., 2002). Subjective effects of waterpipe tobacco smoking have also been observed; the suppression of tobacco abstinence symptoms commonly reported in cigarette smokers (e.g., urges to smoke, craving) were suppressed following a single waterpipe use episode (Maziak et al., 2009). These subjective effects are also thought to be mediated by waterpipe-delivered nicotine.
Importantly, the role of nicotine as a causal factor in the acute effects of waterpipe smoking is speculative, as no study has included a nicotine-free placebo condition using double-blind administration procedures. Without such a study, several non-nicotine factors might explain some effects observed during waterpipe tobacco smoking, including CO intoxication (e.g., Lim et al., 2009), expectancy, or activity associated with the use episode. Therefore, the purpose of this double-blind, placebo-control, within-subject study of waterpipe use was to determine the extent to which the acute effects of waterpipe tobacco smoking were due to nicotine exposure. We hypothesized that cardiovascular and subjective effects reported elsewhere would also be observed when participants used a waterpipe to smoke tobacco that delivered nicotine, but not when participants smoked a tobacco-free herbal waterpipe preparation that did not deliver nicotine.
Section snippets
Participants
Eight women and 29 men were recruited for this university IRB-approved study. These individuals (three African-American, seven Asian, 20 Caucasian, one Hawaiian/Pacific Islander and six mixed/other ethnicity) were healthy, between the ages of 18–50 (mean ± standard error of the mean [SEM] = 20.5 ± 2.1 years) and reported smoking waterpipe tobacco 2–5 times/month (3.8 ± 1.0) for ≥six months (20.2 ± 12.9). Participants’ average expired air CO level at screening was 2.5 ± 1.6 ppm. Exclusion criteria included
Results
Statistical analysis results for all measures except topography are displayed in Table 1. The results of primary interest involve significant condition by time interactions, meaning that changes in outcome measures across time depended upon product smoked.
Discussion
This report details the first double-blind, placebo-control study of the acute effects of waterpipe tobacco smoking with the goal of determining the extent to which the acute effects of a waterpipe smoking episode are due to nicotine exposure. Many results observed when participants smoked tobacco in the waterpipe were similar to those reported elsewhere (Eissenberg and Shihadeh, 2009, Shafagoj et al., 2002, Shafagoj and Mohammed, 2002): significant increases in plasma nicotine (mean pre- to
Conclusions
Overall, results from this double-blind, placebo-control study demonstrate that waterpipe tobacco smoking produces some effects likely due to nicotine (e.g., cardiovascular response) and some effects likely due to other factors (e.g., subjective experience). Importantly, nicotine- and non-nicotine factors may be involved in the development of tobacco dependence in cigarette smokers (e.g., Eissenberg, 2004, Brandon et al., 2004), thus waterpipe tobacco smokers may also be at risk for dependence (
Role of funding source
This work was funded by PHS Grants R01CA120142, R01DA024876 and F31DA028102. The NIH had no further role in study design; in the collection, analysis and interpretation of data; in the writing of the report; or in the decision to submit the paper for publication.
Contributors
Author MB assisted with IRB approval, study set-up, and led the data analysis and manuscript preparation processes. Author BK managed all aspects of study execution (set-up, recruitment, and screening and session completion) and assisted with drafts of select manuscript sections. Author JA assisted with all aspects of study execution (set-up, recruitment, and screening and session completion), maintained study data, and completed a portion of the data analyses. Author MW served as the medical
Conflict of Interest
The authors declare no conflicts of interest.
Acknowledgments
Portions of this work were presented at the 16th Annual Meeting of the Society for Research on Nicotine and Tobacco, Baltimore, MD, February 24–27, 2010.
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All work was performed at Virginia Commonwealth University.