Postnatal lead exposure has been found to cause long‐term learning and memory deficits in monkeys. Pulse‐chronic exposure, consisting of acute high‐level exposure followed by chronic lower‐level exposure, has been particularly effective in causing these impairments. We investigated possible antecedents of lead‐induced cognitive dysfunction by evaluating the behavioral effects of pulse‐chronic lead exposure in rhesus monkeys during the first 6 months of postnatal life. Blood lead pulse‐chronic lead exposure in rhesus monkeys during the first 6 months of postnatal life. Blood lead concentrations in the monkeys reached a peak of 55.8±7.8 ug/dl during week 5 after birth and then averaged between 33.1 and 42.9 ug/dl during the rest of the first 6 months after birth. Zinc protoporphyrin levels were increased by lead exposure, but hematocrits were unaffected. Significant lead‐related effects were detected on a visual exploration test and a neonatal behavioral assessment battery. Lead‐treated monkeys exhibited decreased looking behavior on the visual exploration test and decereased muscle tonus and increased arousal or agitation on the behaiovral assesment battery. No effectw were seen on a Piagetian object permanence task and ton toxic effects on health on growth were detected. In addition to providing indices of behavioral dysfunction during postnatal lead exposure, performance on these early behavioral tests may predict later lead‐induced cognitive dysfunctionn.
ASJC Scopus subject areas
- Developmental and Educational Psychology
- Developmental Neuroscience
- Developmental Biology
- Behavioral Neuroscience