Brainstem neural conduction biomarkers in lead-exposed children of Andean lead-glaze workers.

Abstract

Pediatric lead (Pb) intoxication remains a major medical challenge in some developing countries where Pb is used in glazing industries. Pb exposure is reported to induce neurophysiological and neurocognitive impairment in children. However, the threshold and level of Pb intoxication necessary to induce neuropathology have not been established. Brainstem auditory evoked responses (BAERs) have been used widely as a sensitive biomarker for Pb-induced neurotoxicity. In this field study, BAER neural conduction time was used as a biomarker for central nervous system impairment in Andean children living in areas of high Pb contamination from Pb-glazing cottage industries. The mean Pb level in blood (PbB) for 112 Pb-exposed children was 49.25 microg/dL (SD, 270 microg/dL range, 4.4-119.1 microg/dL). Although BAERs in some children showed prolongations in neural conduction times, regression analyses revealed no significant correlation between PbB levels and BAER interpeak conduction times for 112 replicate recordings (I-III, r = 0.008, P = 0.93; II-V, r = 0.13, P = 0.16; I-V, r = 0.09, P = 0.35; and I-VI, r = 0.14, P = 0.27). A subgroup of 69 children in the study area with PbB levels in the United States Centers for Disease Control and Prevention (CDC) medical intervention-emergency classifications (CDC IV and V; mean, 67.0 microg/dL, SD, 15.8 microg/dL; range, 45.1-119.1 microg/dL) showed no significant correlation between PbB and BAER interpeak interval and no significant differences in BAER than a normal subgroup (t test, P > 0.05). The results demonstrate some evidence of abnormal possibly Pb-induced neural conduction delays in some individual children but a remarkable overall neurobiological functioning in severe, chronic pediatric Pb intoxication without measurable impairment of brainstem auditory nuclei and tracts, as evidenced by neurophysiological conduction times. The findings also demonstrate the variability in the threshold level and duration of Pb exposure necessary to induce brainstem neuropathology.