Nicotine is one of more than 4000 compounds composing the particulate and gas phases of cigarette smoke [5,8,118]. In addition to nicotine, scores of these compounds are bioactive and may affect tissue locally in the oral cavity, the upper and lower respiratory systems, and distally via the systemic circulation. The many potentially cytotoxic compounds in cigarette smoke (e.g., carbon monoxide, aldehydes, ketones, nitrosamines, dihydroxybenzenes) [119] may directly compromise neuronal and cellular membrane function of cerebral tissue. There are several potential mechanisms that may contribute independently, or in concert, to the neurobiological and neurocognitive abnormalities in chronic smokers. These mechanisms may operate in a direct and/or indirect manner. The following overview is based on in vivo and in vitro studies of animals and humans.
