Acute effects of waterpipe tobacco smoking: A double-blind, placebo-control study

Abstract

Background

Waterpipe tobacco smoking usually involves heating flavored tobacco with charcoal and inhaling the resulting smoke after it has passed through water. Waterpipe tobacco smoking increases heart rate and produces subjective effects similar to those reported by cigarette smokers. These responses are thought to be nicotine-mediated, though no placebo-control studies exist. Accordingly, this double-blind, placebo-control study compared the acute physiological and subjective effects of waterpipe tobacco smoking to those produced when participants used a waterpipe to smoke a flavor-matched, tobacco-free preparation.

Methods

Occasional waterpipe tobacco smokers (n = 37; 2–5 monthly smoking episodes for ≥6 months) completed two double-blind, counterbalanced sessions that differed by product: preferred brand/flavor of waterpipe tobacco or flavor-matched, tobacco-free preparation. For each 45-min, ad lib smoking episode blood and expired air CO were sampled, cardiovascular and respiratory response were measured, and subjective response was assessed.

Results

Waterpipe tobacco smoking significantly increased mean (±SEM) plasma nicotine concentration (3.6 ± 0.7 ng/ml) and heart rate (8.6 ± 1.4 bpm) while placebo did not (0.1 ± 0.0 ng/ml; 1.3 ± 0.9 bpm). For carboxyhemoglobin (COHb) and expired air CO, significant increases were observed for tobacco (3.8 ± 0.4%; 27.9 ± 2.6 ppm) and for placebo (3.9 ± 0.4%; 27.7 ± 3.3 ppm) with no differences across condition. Independent of condition, symptoms of nicotine/tobacco abstinence (e.g., “urges to smoke”, “anxious”) were reduced and direct effects (e.g., “dizzy”, “satisfy”) increased.

Discussion

These results from the first placebo-control study of waterpipe tobacco smoking demonstrate that waterpipe-induced heart rate increases are almost certainly mediated by nicotine though the subjective effects observed in these occasional smokers were not.

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.