Lead effects on the brain stem auditory evoked potential in monkeys during and after the treatment phase

Rhesus monkeys were pre- and postnatally exposed to either 0, 350, or 600 mg lead acetate/kg diet continuously until the age of about 9.75 years. At the age of 8-8.25 years (Experiment 1) and 9.25-9.5 years (Experiment 2) brain stem auditory evoked potentials (BAEPs) were recorded. Blood lead levels at the time of testing were about 5, 35, or 55 micrograms/dl for controls, the 350-mg group and the 600-mg group, respectively. There were no clinical signs of intoxications. Clicks varying in sound pressure level (SPL) and rate were used to elicit BAEPs. In addition, the influence of different levels of masking noise was explored in Experiment 1. Four early prominent waves were detected in accordance with other studies of the monkey BAEP. The most reliable wave was No. II. Latencies in the BAEP exhibited the known dependencies on parametric variation for SPL, stimulus rate, and masking level. The 600-mg group exhibited the longest latencies at all stimulus conditions. Analysis of wave II and IV latencies revealed a significant main effect for lead on wave II. At the rate condition there were also signs of latency decreases in the 350-mg group that did not reach significance. Therefore, repetition rate was varied on all SPLs in Experiment 2 to assess the reliability of this effect because similar observations were reported in lead-exposed children. There was no indication of reduced latencies using this extended design. In contrast, significant lead-induced increases in latencies of waves I, II, and IV were revealed by multivariate ANOVA. The purpose of Experiment 3 was to examine whether these results were dependent on current exposure or persisted after cessation of lead treatment. It started 18 months after the end of lead feeding, when blood lead levels had declined to nearly normal values. The same lead-related effects were detected as in the previous experiments. Taken together, these results indicate consistent prolongations of latencies in the BAEP due to subtoxic lead exposure that are not dependent on current treatment. The results are compared to the effects found in epidemiological studies in lead-exposed children.