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Incorporating low-dose epidemiology data in a chlorpyrifos risk assessment

机译：将低剂量流行病学数据纳入毒死rif风险评估中

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摘要

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.
机译：美国环保局（USEPA）评估了流行病学数据是否表明胎儿或生命毒死exposure暴露会引起神经发育影响，如果是的话，它们是否以低于当前最敏感终点的暴露发生，会抑制10％的血液乙酰胆碱酯酶（AChE）。我们先前进行了基于假设的证据权重分析，发现在没有AChE抑制的情况下，毒死rif暴露与神经发育作用之间的拟定因果关系在现有动物或体外研究中没有实质性依据，并且没有在低得多的暴露水平下对人类产生此类影响的合理依据。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接触，并且许多数值均在或低于定量限。但是，当与药代动力学数据一起考虑时，这些生物标志物可提供相对于实验研究中的暴露水平的信息，并表明至少有1,000的暴露裕度。由于动物数据考虑了最敏感的生命周期，因此使用AChE抑制作为调节终点可保护敏感人群的不良反应。

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