In the process of smoking, thousands of chemicals, including carcinogenic polycyclic aromatic hydrocarbons (PAHs) and nitrosamines, are released into the human body [32]. Further downstream, nicotine exerts reinforcing effects in the CNS before being metabolized [33]. Interestingly, the presence of monoamine oxidase inhibitors (MAOIs) has also been demonstrated in tobacco [34], but the magnitude of their psychoactive effects and contribution to patterns of tobacco consumption remain unclear. Despite its widespread effects throughout the body, existing biomarkers for smoking have significant limitations. Exhaled carbon monoxide is detectable only for 3–4 h after smoking [6,7]. Cotinine, a metabolite of nicotine, can be assayed in serum or saliva, but can only be detected for approximately 48 h after last use [7], and the preferred method of detection, enzyme linked immunoassay (ELISA) is expensive and time consuming.
