Private drinking water wells as a source of exposure to perfluorooctanoic acid (PFOA) in communities surrounding a fluoropolymer production facility.

Private drinking water wells as a source of exposure to perfluorooctanoic acid (PFOA) in communities surrounding a fluoropolymer production facility.
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DOI:
10.1289/ehp.1002503
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发表时间:
2011-01
影响因子:
10.4
通讯作者:
Vieira VM
Vieira VM
中科院分区:
环境科学与生态学1区
文献类型:
--
作者:
Hoffman K;Webster TF;Bartell SM;Weisskopf MG;Fletcher T;Vieira VM

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C8健康项目成立于2005年,旨在收集俄亥俄州和西弗吉尼亚州社区受含氟聚合物生产设施污染的全氟辛酸(PFOA或C8)和人类健康数据。我们评估了饮用私人威尔斯水的C8健康项目参与者通过受污染的饮用水暴露于PFOA的情况。参与者提供了人口统计信息和居住,职业和病史。进行了实验室分析,以确定血清中的全氟辛酸浓度。从2001年到2005年,从62口私人饮用水威尔斯井中收集了全氟辛酸数据。我们使用稳健的回归方法研究了饮用水和血清中PFOA水平之间的关系。作为与回归模型的比较,我们使用一阶单室药代动力学模型来估计稳态时的血清:饮用水浓度比。108名使用私人威尔斯水井的研究参与者的血清PFOA浓度中位数为75.7 μg/L,约为美国普通人群水平的20倍,但与饮用公共水的当地居民相似。饮用水中的全氟辛酸浓度每增加1微克/升,血清浓度就会增加141.5微克/升(95%置信区间为134.9-148.1)。稳态药代动力学模型的血清:饮用水浓度比为114。受PFOA污染的饮用水是研究人群血清中PFOA水平的重要贡献者。回归方法和药代动力学建模产生了相似的关系估计。
The C8 Health Project was established in 2005 to collect data on perfluorooctanoic acid (PFOA, or C8) and human health in Ohio and West Virginia communities contaminated by a fluoropolymer production facility. We assessed PFOA exposure via contaminated drinking water in a subset of C8 Health Project participants who drank water from private wells. Participants provided demographic information and residential, occupational, and medical histories. Laboratory analyses were conducted to determine serum-PFOA concentrations. PFOA data were collected from 2001 through 2005 from 62 private drinking water wells. We examined the relationship between drinking water and PFOA levels in serum using robust regression methods. As a comparison with regression models, we used a first-order, single-compartment pharmacokinetic model to estimate the serum:drinking-water concentration ratio at steady state. The median serum PFOA concentration in 108 study participants who used private wells was 75.7 μg/L, approximately 20 times greater than the levels in the U.S. general population but similar to those of local residents who drank public water. Each 1 μg/L increase in PFOA levels in drinking water was associated with an increase in serum concentrations of 141.5 μg/L (95% confidence interval, 134.9–148.1). The serum:drinking-water concentration ratio for the steady-state pharmacokinetic model was 114. PFOA-contaminated drinking water is a significant contributor to PFOA levels in serum in the study population. Regression methods and pharmacokinetic modeling produced similar estimates of the relationship.
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