Ten adult non-smokers and 10 tobacco smokers of mixed gender were studied. The non-smokers were asked to avoid secondhand smoke; the tobacco smokers were asked to abstain from tobacco products for 6-15 h before one abstinent session and to maintain their usual smoking behavior before one smoking session. All subjects were studied twice about 1 week apart in a counterbalanced design. The tobacco smokers smoked their own brand of cigarettes in the smoking session. Auditory event-related potential recordings were begun shortly after the last puff in the smoking session. The potential recordings were repeated three times. The non-smokers had no significant change in their late and long-latency auditory evoked potentials except that about 1 week later the P2 response to irrelevant tones was slightly enhanced. During tobacco abstinence, the P2 amplitude of the smokers was similar to that of the non-smokers, but was diminished after tobacco smoking. During tobacco abstinence, the P3 amplitude to relevant tones was decreased. After smoking, it was increased to that of non-smokers. Tobacco smoking also decreased the amplitude of the P2 response to frequent tones. The data support the hypothesis that tobacco smoking enhances the "protective shield" or "stimulus barrier" to irrelevant and increases attention to relevant auditory stimuli.

Topographic brain EEG mapping techniques indicate that frontal brain beta 1 EEG activity may be useful as an objective brain index of propofol conscious sedation.

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The shorter latencies of the middle latency brain wave components in the smoking session suggest faster processing of sensory information after cigarette smoking. Larger Pa amplitudes after cigarette smoking suggest a higher arousal level than that among partially abstinent smokers and nonsmokers.