Visual event-related potentials were measured in lead-exposed and control subjects, while they were performing a target detection as well as a memory scanning task. Blood lead and urinary delta-aminolevulinic acid (delta-ALA) were determined in samples taken on the same day. Lead exposure did not affect the memory scanning P300 latency, but it did delay the target detection P300 latency in a dose-dependent fashion. The P300 amplitude of lead-exposed subjects was significantly reduced for both tasks, but not in a dose-dependent fashion. The target detection, but not the memory scanning, P300 latency correlated with urinary delta-ALA. No correlation of P300 with age was found, even though the subjects ranged from 20 to 60 years of age. The difference in the effect of lead exposure on the target detection and memory scanning P300 adds to the evidence that the P300 for the two tasks arises from different generators. The absence of a correlation of the measured P300 latency for each task with age in the present study raises the possibility that this extensively reported observation might, in part, be due to inappropriately matched younger and older subjects. This study indicates that evaluation of subjects exposed to toxic substances can increase our basic understanding of evoked potentials, as well as providing evidence of their toxic manifestations.