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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]