Golding Jean, Gregory Steven, Iles-Caven Yasmin, Hibbeln Joseph, Emond Alan, Taylor Caroline M
Centre for Child and Adolescent Health, School of Social & Community Medicine, University of Bristol, Bristol, UK.
National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, MD, USA.
Neurotoxicology. 2016 Mar;53:215-222. doi: 10.1016/j.neuro.2016.02.006. Epub 2016 Feb 12.
There is evidence that high levels of mercury exposure to the pregnant woman can result in damage to the brain of the developing fetus. However there is uncertainty as to whether lower levels of the metal have adverse effects on the development of the infant and whether components of fish consumption and/or the selenium status of the woman is protective.
In this study we analysed data from the Avon Longitudinal Study of Parents and Children (ALSPAC) (n=2875-3264) to determine whether levels of total blood mercury of pregnant women collected in the first half of pregnancy are associated with the development of the offspring at ages 6, 18, 30 and 42 months. The developmental measures used maternal self-reported scales for individual types of development (fine and gross motor, social and communication skills) and total scores. Multiple and logistic regression analyses treated the outcomes both as continuous and as suboptimal (the lowest 15th centile). The statistical analyses first examined the association of prenatal mercury exposure with these developmental endpoints and then adjusted each for a number of social and maternal lifestyle factors; finally this model was adjusted for the blood selenium level.
Total maternal prenatal blood mercury and selenium ranged from 0.17 to 12.76 and 17.0 to 324μg/L respectively. We found no evidence to suggest that prenatal levels of maternal blood mercury were associated with adverse development of the child, even when the mother had consumed no fish during pregnancy. In general, the higher the mercury level the more advanced the development of the child within the range of exposure studied. For example, the fully adjusted effect sizes for total development at 6 and 42 months were +0.51 [95%CI +0.05, +1.00] and +0.43 [95%CI +0.08, +0.78] points per SD of mercury. For the risk of suboptimal development the ORs at these ages were 0.90 [95%CI 0.80, 1.02] and 0.88 [95%CI 0.77, 1.02]. In regard to the associations between blood mercury and child development there were no differences between the mothers who ate fish and those who did not, thus implying that the benefits were not solely due to the beneficial nutrients in fish.
We found no evidence of adverse associations between maternal prenatal blood mercury and child development between 6 and 42 months of age. The significant associations that were present were all in the beneficial direction.
有证据表明,孕妇接触高水平汞会损害发育中胎儿的大脑。然而,较低水平的这种金属是否会对婴儿发育产生不利影响,以及鱼类消费的成分和/或女性的硒状态是否具有保护作用尚不确定。
在本研究中,我们分析了阿冯父母与儿童纵向研究(ALSPAC)(n = 2875 - 3264)的数据,以确定孕期前半段采集的孕妇全血汞水平是否与后代在6、18、30和42个月时的发育有关。发育指标采用母亲自我报告的个体发育类型(精细和粗大运动、社交和沟通技能)量表及总分。多元和逻辑回归分析将结局视为连续变量和次优情况(最低第15百分位数)。统计分析首先检查产前汞暴露与这些发育终点的关联,然后针对一些社会和母亲生活方式因素进行调整;最后对该模型进行血硒水平调整。
孕妇产前全血汞和硒水平分别为0.17至12.76μg/L和17.0至324μg/L。我们没有发现证据表明孕妇产前血汞水平与儿童发育不良有关,即使母亲在孕期未食用鱼类。总体而言,在所研究的暴露范围内,汞水平越高,儿童发育越超前。例如,6个月和42个月时总体发育的完全调整效应量分别为每标准差汞增加 +0.51 [95%置信区间 +0.05, +1.00] 和 +0.43 [95%置信区间 +0.08, +0.78] 分。对于次优发育风险,这些年龄的比值比分别为0.90 [95%置信区间0.80, 1.02] 和0.88 [95%置信区间0.77, 1.02]。关于血汞与儿童发育之间的关联,吃鱼的母亲和不吃鱼的母亲之间没有差异,这意味着益处并非仅仅归因于鱼类中的有益营养成分。
我们没有发现证据表明孕妇产前血汞与6至42个月大儿童的发育之间存在不良关联。存在的显著关联均为有益方向。