ABSTRACT
Biomarkers of tobacco smoke exposure are related to lung cancer and cardiovascular diseases (Hecht, 2003), in which specic carcinogens are responsible for lung cancer and their contribution to risk is less clear. It makes them attractive surrogate end points to evaluate the effectiveness of smoking reduction interventions at improving health. For example, the polycyclic aromatic hydrocarbons (PAHs) and tobaccospecic carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) present in tobacco smoke are believed to be the major causative chemicals for lung cancer in smokers (Hecht, 1999). A PAH metabolite 1-hydroxypyrene (1-HOP) and NNK metabolite 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL), its glucuronide (NNAL-Gluc) are biomarkers of smoking-related PAHs and TSNAs exposure (Hecht et al., 2004a,b). Such biomarkers could ultimately become part of a predictive model for identifying those smokers most likely to get lung cancer and cardiovascular diseases. Furthermore, doing so could improve understanding of lung cancer etiology in smokers and provide a basis for rational approaches to prevention and even therapy. This model, which has evaded researchers to date, could serve not only to identify long-term smokers needing more vigorous intervention or surveillance but also perhaps to identify among smokers newly acquiring the habit those with demonstrably increased susceptibility, in hopes that the increased risk may help motivate them to give up smoking.
