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Neurodevelopment of Amazonian children exposed to ethylmercury (from Thimerosal in vaccines) and methylmercury (from fish)

机译:暴露于乙基汞(来自疫苗中的硫柳汞)和甲基汞(来自鱼类)的亚马逊儿童的神经发育

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Few studies have addressed co-occurring methylmercury (MeHg) from maternal origin and ethylmercury (EtHg) from Thimerosal-containing vaccines (TCVs) during infant's neurodevelopment. We studied children (n = 1139) from the Western Amazon based on combined (low, intermediate, and high) exposure to chronic MeHg from fish consumption and acute TCV- EtHg. Neurodevelopment outcomes were age of walking and age of talking, and the Bayley Scale of Infant Development (BSID). The Mental Developmental Index (MDI) and Psychomotor Developmental Index (PDI) were measured at six and 24 months of age. Median hair-Hg (HHg) at birth was 6.4 μg g~(-1) in mothers, and 1.94 μg g~(-1) in newborns; total (pregnancy and infancy) EtHg exposure ranged from 0 to 187.5 μg. The combined (MeHg + EtHg) exposure showed significant differences for MDI but not for PDI; however, there was a significant decrease in both MDI and PDI scores at 24 months. The increase in BSID delays (scores < 80) between six and 24 months was not discernible with regards to EtHg or MeHg exposure. We found a statistically significant increase in neurodevelopmental (BSID) delays related to the combined exposure to Hg (MeHg > EtHg). Neurodevelopment delays due to low-doses of organic mercury (albeit undiscernible) are not predictable but can be avoided by choosing low-Hg fish and providing Thimerosal-free vaccines.
机译:很少有研究针对婴儿神经发育过程中母体来源的甲基汞(MeHg)和含硫柳汞的疫苗(TCVs)的乙基汞(EtHg)同时存在。我们根据来自鱼类消费和急性TCV-EtHg的慢性MeHg的综合(低,中和高)暴露,对西亚马逊地区的儿童(n = 1139)进行了研究。神经发育结果是步行年龄和说话年龄,以及贝利婴儿发育量表(BSID)。分别在6和24个月大时测量了精神发育指数(MDI)和精神运动发育指数(PDI)。母亲出生时的头发Hg(HHg)中位数为6.4μgg〜(-1),新生儿为1.94μgg〜(-1)。 EtHg的总暴露量(妊娠和婴儿期)为0至187.5μg。联合暴露(MeHg + EtHg)对MDI表现出显着差异,而对PDI则无显着差异;但是,在24个月时,MDI和PDI得分均显着下降。对于EtHg或MeHg暴露,BSID延迟的延迟(得分<80)在6到24个月之间没有增加。我们发现与汞的综合暴露(MeHg> EtHg)有关的神经发育(BSID)延迟显着增加。不可预测由于有机汞含量低而引起的神经发育迟缓(尽管无法辨别),但可以通过选择低汞含量的鱼类并提供无硫柳汞的疫苗来避免。

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