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接触乙基汞(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

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

作者信息

Marques Rejane C, Abreu Luciana, Bernardi José V E, Dórea José G

机构信息

Universidade Federal do Rio de Janeiro, Rio de Janeiro CEP 27930-560, RJ, Brazil.

Statistika Consultoria, Campinas, SP, Brazil.

出版信息

Environ Res. 2016 Aug;149:259-265. doi: 10.1016/j.envres.2015.12.022. Epub 2016 Jan 7.

Abstract

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 6.4µgg(-1) in mothers, and 1.94µgg(-1) in newborns; total (pregnancy and infancy) EtHg exposure ranged from 0 to 187.5µg. 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.

摘要

很少有研究探讨婴儿神经发育过程中母体来源的甲基汞(MeHg)和含硫柳汞疫苗(TCV)中的乙基汞(EtHg)共同存在的情况。我们对来自亚马逊西部的1139名儿童进行了研究,这些儿童因食用鱼类而长期接触(低、中、高)甲基汞,并同时接触急性TCV-乙基汞。神经发育指标包括开始走路的年龄、开始说话的年龄以及贝利婴儿发育量表(BSID)。在6个月和24个月大时测量心理发育指数(MDI)和精神运动发育指数(PDI)。母亲分娩时头发汞(HHg)中位数为6.4µg/g,新生儿为1.94µg/g;总(孕期和婴儿期)乙基汞暴露量范围为0至187.5µg。甲基汞和乙基汞联合暴露对MDI有显著差异,但对PDI没有;然而,在24个月时MDI和PDI评分均显著下降。关于乙基汞或甲基汞暴露,6个月至24个月期间BSID延迟(评分<80)的增加并不明显。我们发现,与汞联合暴露(甲基汞>乙基汞)相关的神经发育(BSID)延迟有统计学意义的增加。低剂量有机汞导致的神经发育延迟(尽管不明显)无法预测,但可以通过选择低汞鱼类和提供无硫柳汞疫苗来避免。

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