We quantified uptake of nicotine in hookah smokers and non-smokers exposed exclusively to hookah tobacco SHS in indoor hookah smoking social events in natural settings: private homes and hookah lounges. Our results demonstrated higher exposures to nicotine post hookah events in both hookah smokers and non-smokers exposed to hookah tobacco SHS in both home and hookah lounge settings. Both before and after hookah events, GM urinary cotinine levels in daily and weekly hookah smokers were significantly higher than in non-smokers. Furthermore, among hookah smokers overall, pre-to-post event change in cotinine levels was positively correlated with number of hookah heads smoked at home events. These results suggest that hookah tobacco smoking is a source of exposure to the addictive drug nicotine and should be included in tobacco control strategies.
We identified only one study in the U.S. that assessed levels of urine cotinine resulting from hookah smoking in a natural setting in a hookah lounge (14). The study reported a significant increase (4 times) in the excretion of cotinine after smoking hookah tobacco in a hookah lounge (n = 47); the urinary cotinine levels were similar to our study in pre-exposure levels (GM, 14.4 ng/mg vs. 14.5 ng/mg), however, post-exposure levels were 2.1 times lower than observed in our study (GM, 59.3 ng/mg vs. 124.7 ng/mg), respectively (14). The overall trend is higher in our study, showing an 8.6-fold increase vs. a 4-fold increase in GMs post a hookah lounge visit (14). This variability may be explained in part in that participants in our study spent more time during the hookah lounge visit (mean, 182 minutes vs. 101 minutes), and smoked more hookah heads (mean, 3.67 heads vs. 1.5 heads) (14, 27).
To date, we did not identify studies in the U.S. that assessed levels of urine cotinine resulting from hookah smoking in private homes. Beside hookah lounges, hookah smokers smoke hookah tobacco while socializing in their homes or in friends’ or relatives’ homes (15, 16). We did not find a significant difference in change in urine cotinine levels pre-to-post hookah event between hookah smokers in hookah lounges vs. in private homes. Therefore, future research and hookah tobacco preventive measures and control should include both natural locations where hookah smoking is allowed in hookah lounges and in homes.
We also were not able to find data on urinary cotinine levels in tobacco smokers and non-tobacco smokers exposed to tobacco SHS in a nationally representative sample of the U.S. population via the National Health and Nutrition Examination Survey (NHANES). NHANES provides serum cotinine levels in tobacco smokers (cigarettes, cigars) (29). Because collecting urine samples are less invasive than blood samples, and in order to compare our results to a representative sample of tobacco smokers and non-tobacco users exposed to SHS in the U.S., we suggest that NHANES and other national surveys that measure plasma cotinine also provide urine cotinine values, and include hookah tobacco smoking in future assessments.
5.1. Hookah Tobacco SHS Exposure
To date, research focusing on the impact of SHS exposure from hookah tobacco smoking on non-smokers, particularly in natural settings is limited (13). We found that passive exposure to hookah tobacco SHS in non-smokers resulted in a significant increase, 3.3 times and 1.8 times, respectively, in GM urinary cotinine levels post hookah social event in hookah lounges and in homes. Urine cotinine levels among non-smokers exposed to hookah tobacco SHS ranged from 0.12 - 25.5 ng/mg post hookah lounge event, and 0.04 - 13.1 ng/mg post home hookah event.
We were also the first to find that GM urinary cotinine levels in children living in daily hookah smoker homes and weekly/monthly hookah smoker homes were significantly 6.5 times and 3.7 times higher, respectively, than those found in children living in non-smoker homes (16). Since there is no level of exposure to tobacco smoke considered to be risk free (30), exposure to SHS should be minimized in order to protect the health of non-smoker adults and children socializing or living with hookah smokers.
Furthermore, optimal cut-off points for biomarker values to distinguish tobacco use versus no tobacco use have been determined for tobacco use other than hookah use. For example, a urinary cotinine of 50 ng/mL and 31.5 ng/mL were determined, respectively, to discriminate smokers from non-smokers, and smokers from non-smokers exposed to SHS (31, 32). We suggest that future research identify urine cotinine cut-off values to distinguish among hookah smokers, non-smokers exposed to hookah tobacco SHS, and non-smokers. Additionally, for disease epidemiology, it will be important to consider investigating the adverse effect of the cumulative dose of low cotinine levels due to chronic exposure to hookah tobacco SHS.
5.2. Multidimensional Stimuli to Dependence
The causes of nicotine dependence among hookah smokers are likely multidimensional (3, 20, 33). Therefore, studies are needed to investigate the effect of chronic nicotine exposure within the context of various stimuli that may induce tobacco dependence in daily hookah smokers versus in occasional hookah smokers with intermittent nicotine exposure. We found that among daily hookah smokers, GM urinary cotinine levels increased 2.7 times post event in daily hookah smokers, as compared to 31.2 times in occasional hookah smokers. This variation by hookah smoking status in changes in GM urinary cotinine levels due to smoking hookah was partly the result of differences in pre hookah event cotinine levels; pre-event GM urinary cotinine levels were 53 times higher in daily hookah smokers than in occasional smokers (106.0 ng/mg vs. 2.0 ng/mg).
We have previously identified stimuli to practice the habit of hookah smoking in hookah lounges, such as the high density of hookah lounges and proximity to colleges and homes, social aspects, and the availability of a variety of hookah tobacco flavors (15). In this paper, we identified stimuli to smoke in private homes, such as socializing while smoking with family and friends who prefer to smoke at home, being more comfortable smoking at home, eating dinner/lunch while smoking hookah (hookah lounges in the U.S. are not allowed to sell foods to their hookah smoking customers), owning a hookah, and saving money by smoking at home instead of going to hookah lounges. These stimuli could be included as points of intervention in public health programs to curb the spread of hookah use in private homes.
A few of our participants tried to save money by smoking in their private homes. Such stimulus that encourages hookah smoking at home suggests raising excise taxes on hookah tobacco products to increase the burden of smoking. A study in Lebanon estimated that a 10% rise in the price of hookah tobacco would result in a 14.5% relative decrease in its home-based consumption (34, 35).
Hookah tobacco smoke inside homes is hazardous to the health of non-smokers who live or socialize with hookah smokers in their homes (16). While previously we suggested curbing the spread of hookah lounges (15, 27), our previous and present findings reported in this paper suggest encouraging banning hookah tobacco smoking inside private homes (27). Efforts to pass regulations to ban smoking in public housing, and to encourage voluntary bans of smoking in private homes (36), should be extended to include hookah tobacco smoking.
5.3. Limitations
Generalizability of this study is limited by convenience sampling. We have a small sample size for daily hookah smokers (n = 20). Additional research is needed with larger sample sizes by smoking frequency status to enable a more rigorous assessment of nicotine exposure from hookah tobacco smoking.
5.4. Conclusions
Hookah tobacco smoke is a source of nicotine exposure. Those attending social smoking events in hookah lounges and private homes are at risk of nicotine intake from exposure to hookah tobacco SHS, and smokers absorb even more nicotine through direct inhalation. GM urinary cotinine levels in hookah smokers and non-smokers increased significantly 8.5 times and 2.5 times, respectively, following a hookah social event. Among hookah smokers, the greatest change in urinary cotinine levels was found in occasional hookah smokers, in which GM levels increased 31.2 times. Our results call for protecting hookah smokers’ and non-smokers’ health by requiring accurate hookah tobacco labels for nicotine content, raising taxes on hookah tobacco, reducing the spread of hookah lounges, and encouraging voluntary bans on smoking hookah tobacco in private homes.
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