Legacy and alternative per- and polyfluoroalkyl substances in the U.S. general population: Paired serum-urine data from the 2013-2014 National Health and Nutrition Examination Survey.
Legacy and alternative per- and polyfluoroalkyl substances in the U.S. general population: Paired serum-urine data from the 2013-2014 National Health and Nutrition Examination Survey.
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DOI：
10.1016/j.envint.2019.105048
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发表时间：
2019-10
影响因子：
11.8
通讯作者：
Wong LY
中科院分区：
文献类型：
--
作者：
Calafat AM;Kato K;Hubbard K;Jia T;Botelho JC;Wong LY
在世界各地的饮用水系统中检测到具有环境持久性的人造全氟烷基和多氟烷基物质（PFAS），引起了人们的高度关注。许多全氟辛烷磺酸，包括全氟辛烷磺酸（PFOS）和全氟辛酸（PFOA），在人体内存在多年。自1999-2000年以来，对美国普通人群接触全氟辛烷磺酸、全氟辛酸和其他特定全氟辛烷磺酸的评估一直依赖于对全国健康和营养检查调查参与者血清中全氟辛烷磺酸浓度的测量。制造商已经用具有较短生物半衰期的PFAS（例如，GenX，全氟丁酸盐[PFBA]），可有效地在尿液中消除。然而，关于暴露于这些化合物的知识是有限的。我们分析了2013-2014年NHANES参与者中年龄≥6岁的17名传统和替代PFAS的2，682份尿液样本。先前在来自相同的NHANES参与者的配对血清样本中测量的这些全氟辛烷磺酸的浓度表明普遍暴露于全氟辛烷磺酸和全氟辛酸，并且很少或没有暴露于两种短链全氟辛烷磺酸，全氟丁烷磺酸和全氟庚酸。然而，在尿液中，PFAS很少被检测到; 17种PFAS中任何一种都检测不到浓度的频率为67.5%。在超过1.5%的人群中只检测到两种：PFBA（13.3%）和全氟己酸酯（PFHxA，22.6%）;第90百分位尿液浓度为0.1 μg/L（PFBA）和0.3 μg/L（PFHxA）。这些结果表明，短链PFAS的暴露并不常见，或者暴露水平低于尿液中可检测浓度的水平。因此，这些发现并不支持在普通人群中使用尿液对短链全氟辛烷磺酸或氟化替代品进行生物监测，并强调了选择适当生物监测矩阵的重要性。
Concerns are heightened from detecting environmentally persistent man-made per- and polyfluoroalkyl substances (PFAS) in drinking water systems around the world. Many PFAS, including perfluorooctane sulfonate (PFOS) and perfluorooctanoate (PFOA), remain in the human body for years. Since 1999–2000, assessment of exposure to PFOS, PFOA, and other select PFAS in the U.S. general population has relied on measuring PFAS serum concentrations in participants of the National Health and Nutrition Examination Survey (NHANES). Manufacturers have replaced select chemistries (“legacy” PFAS) with PFAS with shorter biological half-lives (e.g., GenX, perfluorobutanoate [PFBA]) which may efficiently eliminate in urine. However, knowledge regarding exposure to these compounds is limited. We analyzed 2,682 urine samples for 17 legacy and alternative PFAS from 2013–2014 NHANES participants ≥6 years of age. Concentrations of some of these PFAS, measured previously in paired serum samples from the same NHANES participants, suggested universal exposure to PFOS and PFOA, and infrequent or no exposure to two short-chain PFAS, perfluorobutane sulfonate and perfluoroheptanoate. Yet, in urine, PFAS were seldom detected; the frequency of not having detectable concentrations of any of the 17 PFAS was 67.5%. Only two were detected in more than 1.5% of the population: PFBA (13.3%) and perfluorohexanoate (PFHxA, 22.6%); the 90th percentile urine concentrations were 0.1 μg/L (PFBA), and 0.3 μg/L (PFHxA). These results suggest that exposures to short-chain PFAS are infrequent or at levels below those that would result in detectable concentrations in urine. As such, these findings do not support biomonitoring of short-chain PFAS or fluorinated alternatives in the general population using urine, and highlight the importance of selecting the adequate biomonitoring matrix.
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