Department of Epidemiology and Environmental Health, School of Public Health and Health Professions, The State University of New York (SUNY) at Buffalo, NY, USA.
Department of Neurocognition, Catholic University of Uruguay, Montevideo, Uruguay.
Environ Int. 2020 Sep;142:105883. doi: 10.1016/j.envint.2020.105883. Epub 2020 Jun 26.
Arsenic is a known childhood neurotoxicant, but its neurotoxicity at low exposure levels is still not well established. The aim of our cross-sectional study was to test the association between low-level arsenic exposure and executive functions (EF) among children in Montevideo. We also assessed effect modification by arsenic methylation capacity, a susceptibility factor for the health effects of arsenic, and by B-vitamin intake, which impacts arsenic methylation.
Arsenic exposure was assessed as the specific gravity-adjusted sum of urinary arsenic metabolites (U-As) among 255 ~ 7 year-old children, and methylation capacity as the proportion of urinary monomethylarsonic acid (%MMA). Arsenic concentrations from kitchen water samples at participants' homes were assessed. B-vitamin intake was calculated from the average of two 24-hour dietary recalls. EF was measured using three tests from the Cambridge Neuropsychological Test Automated Battery- Stockings of Cambridge (SOC), Intra-dimensional/extra-dimensional shift task (IED), and Spatial Span (SSP). Generalized linear models assessed the association between U-As and EF measures; models were adjusted for age, sex, maternal education, possessions score, Home Observation for Measurement of the Environment Inventory score, season, and school clusters. Additional analyses were conducted to address issues of residual confounding and sample size. A "B-vitamin index" was calculated using principal component analysis. Effect modification by the index and urinary %MMA was assessed in strata split at the respective medians of these variables.
The median (range) U-As and water arsenic levels were 9.9 µg/L (2.2, 47.7) and 0.45 µg/L (0.1, 18.9) respectively, indicating that exposure originated mainly from other sources. U-As was inversely associated with the number of stages completed (β = -0.02; 95% CI: -0.03, -0.002) and pre-executive shift errors (β = -0.08; 95% CI: -0.14, -0.02) of the IED task, and span length of the SSP task (β = -0.01; 95% CI: -0.02, -0.004). There was no clear pattern of effect modification by B-vitamin intake or urinary %MMA.
Low-level arsenic exposure may adversely affect executive function among children but additional, including longitudinal, studies are necessary to confirm these findings.
砷是一种已知的儿童神经毒物，但在低暴露水平下的神经毒性仍未得到充分证实。本横断面研究的目的是检测蒙得维的亚儿童中低水平砷暴露与执行功能（EF）之间的关联。我们还评估了砷甲基化能力（砷健康影响的易感因素）和 B 族维生素摄入（影响砷甲基化）的效应修饰。
在 255 至 7 岁儿童中，通过尿砷代谢物（U-As）的比重调整总和评估砷暴露情况，并通过尿单甲基砷酸（%MMA）的比例评估甲基化能力。还评估了参与者家中厨房水样的砷浓度。B 族维生素摄入量是从两次 24 小时饮食回忆的平均值计算得出的。EF 通过剑桥神经心理学测试自动电池-剑桥袜子（SOC）、内维/外维转换任务（IED）和空间跨度（SSP）的三个测试进行测量。广义线性模型评估了 U-As 与 EF 测量值之间的关联；模型调整了年龄、性别、母亲教育、财产评分、家庭观察测量环境库存评分、季节和学校聚类。进行了额外的分析以解决残留混杂和样本量的问题。使用主成分分析计算了“B 族维生素指数”。根据这些变量的中位数，在各自的分层中评估了该指数和尿 %MMA 的效应修饰。
U-As 和水砷水平的中位数（范围）分别为 9.9μg/L（2.2，47.7）和 0.45μg/L（0.1，18.9），表明暴露主要来自其他来源。U-As 与 IED 任务中完成的阶段数（β=-0.02；95%CI：-0.03，-0.002）和前执行转换错误（β=-0.08；95%CI：-0.14，-0.02）以及 SSP 任务的跨度长度（β=-0.01；95%CI：-0.02，-0.004）呈负相关。B 族维生素摄入或尿 %MMA 无明显的修饰效应模式。
低水平砷暴露可能会对儿童的执行功能产生不利影响，但需要进一步包括纵向研究来证实这些发现。
