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Neurobehavioral deficits at age 7 years associated with prenatal exposure to toxicants from maternal seafood diet

机译:7年龄与孕产妇海鲜饮食中毒品的7年龄的神经麻烦缺陷

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摘要

To determine the possible neurotoxic impact of prenatal exposure to polychlorinated biphenyls (PCBs), we analyzed banked cord blood from a Faroese birth cohort for PCBs. The subjects were born in 1986–1987, and 917 cohort members had completed a series of neuropsychological tests at age 7 years. Major PCB congeners (118, 138, 153, and 180), the calculated total PCB concentration, and the PCB exposure estimated in a structural equation model showed weak associations with test deficits, with statistically significant negative associations only with the Boston Naming test. Likewise, neither hexachlorobenzene nor p,p'-dichlorodiphenyldichloroethylene showed clear links to neurobehavioral deficits. Thus, these associations were much weaker than those associated with the cord-blood mercury concentration, and adjustment for mercury substantially attenuated the regression coefficients for PCB exposure. When the outcomes were joined into motor and verbally mediated functions in a structural equation model, the PCB effects remained weak and virtually disappeared after adjustment for methylmercury exposure, while mercury remained statistically significant. Thus, in the presence of elevated methylmercury exposure, PCB neurotoxicity may be difficult to detect, and PCB exposure does not explain the methylmercury neurotoxicity previously reported in this cohort.
机译:为了确定产前暴露于多氯联苯(PCB)的可能神经毒性的影响,我们分析了来自Faroese Tails Cohort的储存脐带血。受试者出生于1986年至1987年,917名队员于7年龄完成了一系列神经心理学检验。主要PCB同一(118,138,153和180),计算出的总PCB浓度,并且在结构方程模型中估计的PCB曝光显示出与测试缺陷的薄弱关联,仅具有统计上显着的负关联,只有波士顿命名测试。同样地,六氯苯和P的P'-二氯二苯基二氯乙烯都没有显示出与神经兽性缺陷的明显环节。因此,这些关联比与脐带血汞浓度相关的关联较弱,并且汞的调整基本上衰减了PCB暴露的回归系数。当结果与结构方程模型中的电动机和口头介导的功能连接时,PCB效应在调整甲基汞暴露后保持弱,几乎消失,而汞仍然存在统计学意义。因此,在升高的甲基汞暴露的情况下,PCB神经毒性可能难以检测,并且PCB暴露不解释此前在该队列中报道的甲基汞神经毒性。

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