The P300 brain potential is reduced in smokers

Rationale: Tobacco smoking is the most prevalent type of substance abuse, y et its biobehavioral etiology is little understood. Identification of diffe rences between smokers and non-smokers on basic characteristics of neurocog nitive functioning may help to elucidate the mechanisms of tobacco dependen ce. Objectives. This study assessed the relationship between smoking status and the P300 component of event-related potential (ERP) while controlling for potential confounders such as alcoholism, drug abuse, and psychopatholo gy. Methods: The ERP responses elicited by a visual oddball task were measu red at the mid-parietal site in 905 current smokers, 463 ex-smokers, and 97 9 never smokers. Results: P300 amplitude was significantly lower in current cigarette smokers compared to never-smokers. Ex-smokers did not differ sig nificantly from never-smokers. P300 reduction was also associated with alco holism, drug dependence, and family density of alcoholism. However, after c ontrolling for smoking, only family density of alcoholism remained a signif icant predictor of P300 amplitude. Conclusions: The results indicate a sign ificant effect of smoking status on P300 amplitude which is additive to fam ily history of alcoholism and suggest that either (1) long-term tobacco smo king may produce a reversible change in brain function, or (2) reduced P300 may be a marker of risk for nicotine dependence.