Murata K, Weihe P, Araki S, Budtz-Jørgensen E, Grandjean P
Department of Public Health and Occupational Medicine, Graduate School of Medicine, University of Tokyo, Japan.
Neurotoxicol Teratol. 1999 Jul-Aug;21(4):471-2. doi: 10.1016/s0892-0362(99)00026-4.
A study of 7-year-old children from a fishing village on Madeira has suggested that latencies of evoked potentials may be delayed because of increased exposures to methylmercury during development. Data from a previously published prospective study in the Faroe Islands have therefore been reexamined. Because of changes in instrumentation, results obtained during the second year of examination were excluded. After this restriction, the results show significant mercury-associated delays of the peak III latency and the I-III interpeak latency of the auditory brainstem evoked potentials. Mercury concentrations in both maternal hair at parturition and in cord blood indicated this association, whereas no such relationship was apparent with the child's current hair-mercury concentration. Thus, in agreement with the findings from Madeira, a delay of the peak III latency of the brainstem auditory evoked potentials appears to serve as a marker of prenatal methylmercury toxicity from contaminated seafood.
一项针对马德拉岛一个渔村7岁儿童的研究表明，由于发育过程中甲基汞暴露增加，诱发电位的潜伏期可能会延迟。因此，对法罗群岛之前发表的一项前瞻性研究的数据进行了重新审视。由于仪器设备的变化，第二年检查期间获得的结果被排除。经过这一限制后，结果显示听觉脑干诱发电位的III波潜伏期和I-III峰间潜伏期与汞存在显著关联。分娩时母亲头发和脐带血中的汞浓度表明了这种关联，而与孩子目前头发中的汞浓度没有明显关系。因此，与马德拉岛的研究结果一致，脑干听觉诱发电位的III波潜伏期延迟似乎是受污染海鲜中产前甲基汞毒性的一个标志。
