Abstract

Objective To determine possible exposure-associated delays in auditory brainstem evoked potential latencies as an objective measure of neurobehavioral toxicity in 14-year-old children with developmental exposure to methylmercury (MeHg) from seafood. Study design Prospective study of a birth cohort in the Faroe Islands, where 878 of eligible children (87%) were examined at age 14 years. Latencies of brainstem evoked potential peaks I, III, and V at 20 and 40 Hz constituted the outcome variables. Mercury concentrations were determined in cord blood and maternal hair, and in the child's hair at ages 7 and 14. Results Latencies of peaks III and V increased by about 0.012 ms when the cord blood mercury concentration doubled. As seen at age 7 years, this effect appeared mainly within the I–III interpeak interval. Despite lower postnatal exposures, the child's hair mercury level at age 14 years was associated with prolonged III–V interpeak latencies. All benchmark dose results were similar to those obtained for dose-response relationships at age 7 years. Conclusions The persistence of prolonged I–III interpeak intervals indicates that some neurotoxic effects from intrauterine MeHg exposure are irreversible. A change in vulnerability to MeHg toxicity is suggested by the apparent sensitivity of the peak III–V component to recent MeHg exposure.

Highlights

  • The brainstem evoked potential (BAEP) latencies were similar to the results obtained at age 7,5,18,21 and again differed as expected[16] between boys and girls

  • Prolonged BAEP latencies have been reported as an effect of exposure to MeHg 13-15 and other neurotoxicants, such as lead.[17,25]

  • We report that BAEP latency assessments were highly reproducible and that several latencies at age 14 years showed a positive association with MeHg exposure

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Summary

Introduction

From the Division of Environmental Health Sciences, Akita University School of Medicine, Akita, Japan; the Department of Occupational Medicine and Public Health, Faroese Hospital System, Tórshavn, Faroe Islands; the Department of Biostatistics, Institute of Public Health, University of Copenhagen, Copenhagen, Denmark; the Institutes of Clinical Research and Public Health, University of Southern Denmark, Odense, Denmark; and the Department of Environmental Health, Harvard University School of Public Health, Boston. Supported by the National Institute of Environmental Health Sciences (ES09797), the Danish Medical Research Council and the Nissan Science Foundation. Reprint requests: Philippe Grandjean, MD, Department of Environmental Health, Harvard School of Public Health, Landmark Center East room 3-110, 665, P.O.Box 15967, Boston, MA 02115

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