Rhesus monkeys were exposed to low, chronic levels of lead acetate either pre- or postnatally. Considerable neural and behavioral evidence indicates that the hippocampus is preferentially affected by low-level lead exposure. Hippocampal dysfunction is known to result in disruption of spatial memory. The monkeys in these experiments were tested as juveniles on a spatial memory test, the Hamilton Search Task. The monkeys exposed prenatally to lead did not show a deficit, while those exposed postnatally showed a significant deficit on the Hamilton Search Task. The deficit was not apparent until the monkeys were required to meet the most strict criterion, suggesting that the impairment may be due to the memory rather than the learning components of the task. The fact that the deficit was seen more than 3 years after the end of lead exposure indicates that the lead-induced cognitive effect is quite long-lasting and perhaps permanent.