Mu-Rong Chao1, Marcus S Cooke2, Chung-Yih Kuo3, Chih-Hong Pan4, Hung-Hsin Liu5, Hao-Jan Yang3, Szu-Chieh Chen3, Yi-Chen Chiang6, Chiung-Wen Hu7. 1. Department of Occupational Safety and Health, Chung Shan Medical University, Taichung 402, Taiwan; Oxidative Stress Group, Department of Environmental Health Sciences, Florida International University, Miami, FL 33199, USA. 2. Oxidative Stress Group, Department of Environmental Health Sciences, Florida International University, Miami, FL 33199, USA; Biomolecular Sciences Institute, Florida International University, Miami, FL 33199, USA. 3. Department of Public Health, Chung Shan Medical University, Taichung 402, Taiwan. 4. Institute of Labor, Occupational Safety and Health, Ministry of Labor, New Taipei City 221, Taiwan. 5. Department of Occupational Safety and Health, Chung Shan Medical University, Taichung 402, Taiwan. 6. State Key Laboratory of Molecular Vaccinology and Molecular Diagnostics, School of Public Health, Xiamen University, Xiamen, Fujian 361102, China. 7. Department of Public Health, Chung Shan Medical University, Taichung 402, Taiwan; Department of Family and Community Medicine, Chung Shan Medical University Hospital, Taichung 402, Taiwan. Electronic address: cwhu0823@gmail.com.
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.
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.
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