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儿童接触全氟烷基酸 - 一种建模方法。

Children's exposure to perfluoroalkyl acids - a modelling approach.

机构信息

Department of Environmental Science and Analytical Chemistry (ACES), Stockholm University, Svante Arrhenius väg 8c, 10691 Stockholm, Sweden.

出版信息

Environ Sci Process Impacts. 2019 Nov 1;21(11):1875-1886. doi: 10.1039/c9em00323a. Epub 2019 Sep 24.

Abstract

Adults are mainly exposed to per- and polyfluoroalkyl substances (PFASs) via ingestion of food, inhalation of air and ingestion of dust, whereas for children the exposure to PFASs is largely unknown. This study aimed to reconstruct the serum concentrations of perfluorooctanoic acid (PFOA), perfluorooctane sulfonic acid (PFOS) and perfluorohexane sulfonic acid (PFHxS) in children after infancy up to 10.5 years of age and to test if dietary intake is the major exposure pathway for children to PFOA, PFOS and PFHxS after infancy. For this work, a dataset from a Finnish child cohort study was available, which comprised serum concentrations of the studied perfluoroalkyl acids (PFAAs) and PFAS concentration measurements in dust and air samples from the children's bedrooms. The calculated PFAA intakes were used in a pharmacokinetic model to reconstruct the PFAA serum concentrations from 1 to 10.5 years of age. The calculated PFOA and PFOS intakes were close to current regulatory intake thresholds and diet was the major exposure medium for the 10.5 year-olds. The one-compartment PK model reconstructed median PFOA and PFOS serum concentrations well compared to corresponding measured median serum concentrations, while the modelled PFHxS serum concentrations showed a constant underestimation. The results imply that children's exposure to PFOA and PFOS after breastfeeding and with increasing age resembles the exposure of adults. Further, the children in the Finnish cohort experienced a rather constant exposure to PFOA and PFOS between 1 and 10.5 years of age. The PFHxS exposure sources and respective pharmacokinetic parameter estimations need further investigation.

摘要

成年人主要通过摄入食物、吸入空气和摄入灰尘来接触全氟和多氟烷基物质 (PFAS),而儿童接触 PFAS 的情况则知之甚少。本研究旨在重建婴儿期后至 10.5 岁儿童体内全氟辛酸 (PFOA)、全氟辛烷磺酸 (PFOS) 和全氟己烷磺酸 (PFHxS) 的血清浓度,并检验儿童在婴儿期后通过饮食摄入是否是接触 PFOA、PFOS 和 PFHxS 的主要途径。为此,我们使用了一项芬兰儿童队列研究的数据,该数据集包含研究中涉及的全氟烷基酸 (PFAAs) 的血清浓度以及儿童卧室空气中灰尘样本中的 PFAS 浓度测量值。所计算的 PFAA 摄入量被用于一个药代动力学模型,以重建 1 至 10.5 岁儿童的 PFAA 血清浓度。所计算的 PFOA 和 PFOS 摄入量接近当前监管摄入量阈值,而饮食是 10.5 岁儿童的主要暴露途径。与相应的实测血清浓度相比,单室 PK 模型很好地重建了 PFOA 和 PFOS 血清浓度的中位数,而模型化的 PFHxS 血清浓度则一直存在低估。研究结果表明,母乳喂养后和年龄增长后儿童对 PFOA 和 PFOS 的暴露与成人的暴露相似。此外,芬兰队列中的儿童在 1 至 10.5 岁之间经历了相对稳定的 PFOA 和 PFOS 暴露。还需要进一步研究 PFHxS 的暴露源和相应的药代动力学参数估计。

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