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Prenatal exposure to glycol ethers and response inhibition in 6-year-old children: The PELAGIE cohort study

机译:6岁儿童的肾上腺醚和反应抑制的产前暴露:Pelagie Cohort研究

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摘要

Background: Exposure to glycol ethers (GEs) is suspected of impairing neurodevelopment in children, but the specific impact on their inhibitory capacity, a central deficit of ADHD, has never been studied. We aimed to assess the impact of prenatal exposure to GEs on the response inhibition of children aged six years. Methods: In total, 169 mother-child pairs from the French cohort PELAGIE (2002-2006) were studied. Maternal urinary concentrations of six GE metabolites (alkoxycarboxylic acids) were measured during pregnancy. Multiple imputation by quantile regression was used to handle non-detected values and the data were then classified into quartiles. Inhibition of children was evaluated by the Rhythmic Continuous Performance Test 90 (R-CPT90). The inhibition score (percentage of correct responses to non-target stimuli) was corrected for compliance with the instructions (percentage of correct responses to target stimuli). The analysis used a multiple linear regression model, adjusting for confounding factors for each metabolite. Results: Median concentrations of metabolites ranged from 0.02 mg/L (Ethoxyacetic acid, EAA) to 0.39 mg/L (Phenoxyacetic acid, PhAA). The median corrected inhibition score was 37.9% [first quartile: 29.8 - third quartile: 47.9]. We found a negative and statistically significant association between the inhibition score and prenatal urinary EAA concentration (p-trend = 0.03), with a significant β coefficient for the third quartile (β = -0.064; 95% confidence interval: -0.121, -0.007). There were no statistically significant associations for the other five metabolites. Conclusion: These results are consistent with the hypothesis of possible impact of prenatal environmental exposure on inhibitory capacity among children. Data about the GEs metabolized to EAA (history of exposure sources and toxicokinetics) should be gathered to further interpret these results and guide precautionary measures.
机译:背景:涉嫌对乙二醇醚(GES)接触儿童的神经发育损害,但从未研究过,对其抑制能力的具体影响从未研究过。我们旨在评估产前暴露对GES对六年儿童的反应抑制的影响。方法:研究了来自法国队队(2002-2006)的169人母婴对。在妊娠期间测量六种Ge代谢物(烷氧基羧酸)的母尿浓度。使用量子回归多重归批用于处理未检测到的值,然后将数据分为四分位数。通过节奏连续性性能试验90(R-CPT90)评估儿童的抑制。纠正抑制得分(对非目标刺激的正确响应的百分比)符合指令(对目标刺激的正确反应的百分比)。分析使用多元线性回归模型,调整每个代谢物的混杂因子。结果:代谢物中位浓度范围为0.02mg / L(乙氧基乙酸,EA)至0.39mg / L(苯氧乙酸,PHAA)。中位矫正抑制得分为37.9%[第一个四分位数:29.8-第三四分位数:47.9]。我们发现抑制得分和产前尿液EAA浓度(p趋势= 0.03)之间的阴性和统计学性质,具有显着的β系数(β= -0.064; 95%置信区间:-0.121,-0.007 )。其他五种代谢物没有统计学上显着的关联。结论:这些结果与产前环境暴露对儿童抑制能力的可能影响的假设一致。应收集关于代谢到EAA的GE的数据(曝光源和毒物动力学的历史),以进一步解释这些结果并指导预防措施。

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  • 来源
    《Environmental research》 |2020年第2期|108950.1-108950.8|共8页
  • 作者单位

    Univ Rennes CHU Rennes Inserm EHESP Irset Institut de Recherche en Sante Environnement et Travail UMR_S 1085 Rennes France;

    Univ Rennes CHU Rennes Inserm EHESP Irset Institut de Recherche en Sante Environnement et Travail UMR_S 1085 Rennes France;

    Univ Rennes LP3C Laboratoire de Psychologie Cognition Comportement et Communication EA 1285 Rennes France;

    Univ Rennes CHU Rennes Inserm EHESP Irset Institut de Recherche en Sante Environnement et Travail UMR_S 1085 Rennes France;

    Univ Rennes Inserm EHESP Irset Institut de Recherche en Sante Environnement et Travail UMR_S 1085 France ISGlobal Doctor Aiguader 88 08003 Barcelona Spain Universitat Pompeu Fabra (UPF) Barcelona Spain CIBER Epidemiologa y Salud Publica (CIBERESP) Madrid Spain;

    ISGlobal Doctor Aiguader 88 08003 Barcelona Spain;

    LABOCEA Laboratory Plouzane France;

    Univ Rennes Inserm EHESP Irset Institut de Recherche en Sante Environnement et Travail UMR_S 1085 France;

    Univ Rennes CHU Rennes Inserm EHESP Irset Institut de Recherche en Sante Environnement et Travail UMR_S 1085 Rennes France;

    Univ Rennes Inserm EHESP Irset Institut de Recherche en Sante Environnement et Travail UMR_S 1085 France;

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  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
  • 关键词

    Solvents; Glycol ethers; Neurodevelopment; Response inhibition; Prenatal exposure;

    机译:溶剂;乙二醇醚;神经发作;反应抑制;产前暴露;

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