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Waterpipe (aka hookah) tobacco smokers are exposed to toxicants that can lead to oxidative DNA and RNA damage, a precursor to chronic disease formation. This study assessed toxicant exposure and biomarkers of DNA [8-oxo-7, 8-dihydro-2′-deoxyguanosine (8-oxodG)] and RNA [8-oxo-7,8-dihydroguanosine (8-oxoGuo)] oxidative damage during smoking of flavored and non-flavored waterpipe tobacco. Thirty waterpipe smokers completed two counterbalanced 2-h lab waterpipe smoking sessions (flavored vs. non-flavored waterpipe tobacco). Urinary concentrations of 8-oxodG and 8-oxoGuo and expired carbon monoxide (eCO) were measured before and after the smoking sessions. A significant increase in the urinary concentrations of 8-oxodG (from 2.12 ± 0.83 to 2.35 ± 0.91 ng/mg creatinine, p = 0.024) and 8-oxoGuo (from 2.96 ± 0.84 to 3.45 ± 0.76 ng/mg creatinine, p = 0.003) were observed after smoking the non-flavored and flavored waterpipe tobacco, respectively. Our results also showed that the mean ± SD of eCO increased significantly after smoking the flavored (from 1.3 ± 1.1 to 20.3 ± 23.6 ppm, p < 0.001) and non-flavored waterpipe tobacco (from 1.8 ± 1.2 to 24.5 ± 26.1 ppm, p < 0.001). There were no significant differences in the means of 8-oxodG (p = 0.576), 8-oxoGuo (p = 0.108), and eCO (p = 0.170) between the flavored and non-flavored tobacco sessions. Smoking non-flavored and flavored waterpipe tobacco leads to oxidative stress and toxicant exposure. Our findings add to the existing evidence about the adverse effects of waterpipe tobacco smoking (WTS) and the need for strong policies to inform and protect young people from the risks of WTS. [ABSTRACT FROM AUTHOR]

Abstract Background Worldwide, smoking is a major public health problem, with exposure to environmental tobacco smoke (ETS) affecting both smokers, and passive smokers, including children. Despite ETS also describing secondhand, and thirdhand smoke (SHS, and THS respectively), the health effects of exposure to passive smoking via these sources are not fully understood, particularly in children. Although cotinine, the primary proximate metabolite of nicotine, has been widely used as a biomarker of ETS exposure, 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL), the metabolite of the tobacco-specific nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), provides a uniquely important contribution, both as a biomarker of exposure, and as a specific risk indicator for pulmonary carcinogenesis. Methods We used LC-MS/MS to study NNK metabolites, cotinine, and 8-oxo-7,8-dihydro-2′-deoxyguanosine (a biomarker of oxidative stress), in the urine of 110 non-smoking adults (age range: 23–62) and 101 children (age range: 9–11), exposed to ETS. Results In our study of passive smoking adults, and children exposed to ETS, we showed that although the children had a similar urinary level of cotinine compared to the adults, the children had approximately two times higher levels of urinary total NNAL (P = 0.002), and free NNAL (P = 0.01), than adults. The children also had three times lower ability to detoxify NNK than adults (P < 0.001). Furthermore, the children showed 1.5 times higher ratio of total NNAL/cotinine than adults (P = 0.01), implying that THS is another important source of ETS in this population. Furthermore, ETS exposure in children appeared to lead to an increase in levels of oxidative stress. Conclusions Taken together, our results demonstrate that, in children, THS may play an important role in the ETS exposure, and that children are at particular risk of ETS-induced health effects. Highlights • Children had a significantly lower ability to detoxify NNK than adults. • Urinary total NNAL:cotinine ratio could inform on the ETS exposure source. • In children, THS might be a more important source of NNK exposure than SHS. • Children have a higher risk of ETS health effects, e.g., oxidative stress. [ABSTRACT FROM AUTHOR]

Chronic obstructive pulmonary disease (COPD) is a disease characterized by chronic inflammation and irreversible airway obstruction. Cigarette smoking is the predominant risk factor for developing COPD. It is well-known that the COPD is also strongly associated with an increased risk of developing lung cancer. Cigarette smoke contains elevated concentrations of oxidants and various carcinogens (e.g., tobacco-derived nitrosamines) that can cause oxidative and alkylating stresses, which can also arise from inflammation. However, it is surprising that, except for oxidative stress, little information is available on the burden of alkylating stress and the detoxification efficiency of tobacco-derived carcinogens in COPD patients. In this study, we used LC-MS/MS to measure the archetypical tobacco-specific carcinogenic 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), its major metabolite, 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL), three biomarkers of oxidative stress (8-oxo-7,8-dihydroguanine, 8-oxoGua; 8-oxo-7,8-dihydro-2′-deoxyguanosine, 8-oxodGuo; 8-oxo-7,8-dihydroguanosine, 8-oxoGuo) and two biomarkers of alkylating stress (N7-methylguanine, N7-MeGua and N3-methyladenine, N3-MeAde), in the urine of smoking and non-smoking COPD patients and healthy controls. Our results showed that not only was oxidative stress significantly elevated in the COPD patients compared to the controls, but also alkylating stress. Significantly, levels of alkylating stress (i.e., N7-MeGua) were highly correlated with the COPD severity and not affected by age and smoking status. Furthermore, COPD smokers had significantly higher ratios of free NNAL to the total NNAL than control smokers, implying a lower detoxification efficiency of NNK in COPD smokers. This ratio was even higher in COPD smokers with stages 3–4 than in COPD smokers with stages 1–2. Taken together, our results demonstrated that the detoxification efficiency of tobacco-derived carcinogens (e.g., NNK) was associated with the pathogenesis and possibly the progression of COPD. In addition to oxidative stress, alkylating stress derived from chronic inflammation appears to be also dominant in COPD patients. Image 1 • Alkylating and oxidative stresses were increased in COPD patients. • Alkylating stress was correlated with COPD severity. • Ratio of free NNAL/total NNAL were determined and increased in COPD smokers. • The higher COPD severity the higher ratio of free NNAL/total NNAL. • Cigarette smoke/chronic inflammation induced oxidative and alkylating stresses. [ABSTRACT FROM AUTHOR]