In smoking cessation studies, the levels of several biomarkers are considered in order to evaluate the people’s exposure to tobacco smoke. The well-known nicotine is typically considered as one of these biomarkers, but it has a half-life of only two hours in the human body. It is therefore not appropriate for the determination of tobacco smoke exposure after several hours or even days. Cotinine is the main metabolite of nicotine and has a half- life of about eighteen hours. Due to its higher stability, it is one of the widely investigated biomarkers related to tobacco products. However, when patients undergo smoking cessation and replace nicotine with nicotine gums and patches, their cotinine levels are the same as smokers.
Therefore, more universal biomarkers for this kind of studies are typically evaluated. 4-(methylnitrosamino)-1-(3-pyridyl)- 1-butanol (NNAL) is a metabolite of the lung carcinogen NNK (4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone) and a tobacco-specific nitrosamine. Due to its much longer half-life (10–40 days) compared to nicotine and cotinine, it can still be detected after several days up to a few weeks making it a better marker for long-term studies. During tobacco smoke consumption human cells are submitted to oxidative stress. As a result, 8-hydroxy- 2'-deoxyguanosine (8-OHdG), a specific stress marker related to carcinogenesis, is produced in the human body. In addition to DNA oxidation, the exposure to tobacco smoke can also lead to DNA methylation which is indicated by the biomarker 7-methylguanine (m7Gua). In studies, both markers have been found at higher levels among smokers than non-smokers and are typically used to evaluate the DNA damage.
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