Gradient, Cambridge, MA.
Dose Response. 2012 Jul 30;11(2):207-19. doi: 10.2203/doseresponse.12022.Goodman. Print 2013.
USEPA assessed whether epidemiology data suggest that fetal or early-life chlorpyrifos exposure causes neurodevelopmental effects and, if so, whether they occur at exposures below those causing the current most sensitive endpoint, 10% inhibition of blood acetylcholinesterase (AChE). We previously conducted a hypothesis-based weight-of-evidence analysis and found that a proposed causal association between chlorpyrifos exposure and neurodevelopmental effects in the absence of AChE inhibition does not have a substantial basis in existing animal or in vitro studies, and there is no plausible basis for invoking such effects in humans at their far lower exposure levels. The epidemiology studies fail to show consistent patterns; the few associations are likely attributable to alternative explanations. Human data are inappropriate for a dose-response assessment because biomarkers were only measured at one time point, may reflect exposure to other pesticides, and many values are at or below limits of quantification. When considered with pharmacokinetic data, however, these biomarkers provide information on exposure levels relative to those in experimental studies and indicate a margin of exposure of at least 1,000. Because animal data take into account the most sensitive lifestages, the use of AChE inhibition as a regulatory endpoint is protective of adverse effects in sensitive populations.
美国环保署评估了流行病学数据是否表明胎儿或婴儿期接触毒死蜱会导致神经发育影响,以及如果是这样,这些影响是否发生在导致当前最敏感终点(血液乙酰胆碱酯酶的 10%抑制)以下的暴露水平。我们之前进行了基于假设的证据权重分析,发现没有证据表明在没有乙酰胆碱酯酶抑制的情况下,毒死蜱暴露与神经发育影响之间存在因果关系,在人类低得多的暴露水平下,没有合理的理由可以推断出这种影响。流行病学研究未能显示出一致的模式;少数关联可能归因于其他解释。人类数据不适合进行剂量-反应评估,因为生物标志物仅在一个时间点进行测量,可能反映了对其他农药的暴露,并且许多值处于或低于定量限。然而,当与药代动力学数据一起考虑时,这些生物标志物提供了相对于实验研究中暴露水平的信息,并表明暴露水平至少高出 1000 倍。由于动物数据考虑了最敏感的生命阶段,因此将乙酰胆碱酯酶抑制用作监管终点可保护敏感人群免受不良影响。