Biomarkers of Secondhand Smoke Exposure in Waterpipe Tobacco Venue Employees in Istanbul, Moscow, and Cairo

Abstract

Smoke-free regulation should be extended to waterpipe venues to protect nonsmoking employees and patrons from the adverse health effects of SHS.

Water Pipe (Hookah) Smoking and Cardiovascular Disease Risk: A Scientific Statement From the American Heart Association

“…6,109 Numerous studies have examined the environmental and health effects of secondhand exposure to water pipe tobacco smoke in various geographic regions, including the United States, Canada, the United Kingdom, Russia, India, and the eastern Mediterranean region. [110][111][112][113][114][115] In terms of environmental air quality indicators, a primary outcome typically assessed is the level of PM 2.5…”

Biomarkers of Exposure to Secondhand and Thirdhand Tobacco Smoke: Recent Advances and Future Perspectives

“…However, nicotine is a useful biomarker for long-term tobacco smoke exposure in hair, where it remains unmetabolized and, consequently, as hair grows over the months, tobacco exposure is “recorded” over long periods of time [74]. As shown in Table 2, nicotine in hair can be found in 10 to 100 times higher concentrations than cotinine typically ranging from 2.01 to 79.3 ng/mg in smokers [35] and from 0.08 to 5.02 ng/mg [23,35,36,37,38,39,40] in a SHS-exposed population. Hair nicotine concentrations also highly correlated with airborne nicotine and cotinine in urine, thus confirming its suitability as an alternative tobacco smoke exposure biomarker.…”

“…The typical urinary cotinine cutoff value is 30 ng/mL. Urinary cotinine concentrations usually range from 34.5 to 489 ng/mL for smokers [46,47], from 0.25 to 30 ng/mL for SHS exposed nonsmokers [22,36,42,45,46,48,49,50], up to 5 ng/mL for THS exposed nonsmokers [41,43,44] and around 0.88 ng/mL in non-exposed nonsmokers [43]. Nevertheless, acute exposure to SHS can raise urinary cotinine concentrations to levels similar to those reported in smokers’ concentrations.…”

“…Salivary cotinine levels were used to categorize the studied population into different groups according to the level of exposure: Low SHS exposure (0.1–0.3 ng/mL), moderate SHS exposure (0.4–0.7 ng/mL) and high SHS (0.8–14.9 ng/mL) [59]. As shown in Table 2, salivary cotinine concentration ranged between 0.04 and 14.9 ng/mL in nonsmokers exposed to SHS [36,38,39,40,59,61,62,63], and reached up to 653 ng/mL in active smokers [38,39,59,60]. Salivary cotinine concentrations increase even after a short time of SHS exposure, thus demonstrating the suitability of salivary cotinine as a short-term SHS exposure biomarker [61].…”

“…Besides, as SHS ages, nicotine levels rapidly decline but NNK levels increase confirming the suitability of urinary NNAL as a more reliable biomarker of THS exposure than nicotine metabolites. Mean urinary NNAL concentrations were 80.9–405.5 pg/mL in active smokers [50,51,58], 5.9–20.1 pg/mL for high SHS exposure [44,48,58,66], 0.95–2.21 pg/mL for low SHS exposure [36,50,51,54,61], 2.7–6.7 pg/mL for THS exposure [42] and 0.81 pg/mL for no exposure [43]. Recently, Benowitz et al estimated a urinary NNAL cutoff value to distinguish between active smokers and nonsmokers exposed to SHS.…”