全氟化合物以及典型异构体的人体暴露和肾排泄研究
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摘要
由于长期生产和使用,全氟化合物(perfluoroalkyl substances, PFASs)在环境中广泛存在并在世界各国人体样本中检出。全氟辛烷磺酸(perfluorooctanesulfonate, PFOS)和全氟辛酸(perfluorooctanoate, PFOA)是环境中检出频率最高的两种PFASs. PFASs具有持久性和生物累积性,可能导致多种不良健康结果。历史上主要有两种生产方式用来生产PFASs及其前体物,即调聚法(telomerization)和电氟化法(electrochemical fluorination, ECF)早在1947和1949年,电氟化法就应用于生产PFOA和PFOS,该方法的最终产品一般含有稳定比例的直链(约70%PFOS和80%PFOA)和支链(约30%PFOS和20%PFOA)异构体。而由杜邦公司于1970年开发了调聚法生产的产品通常是纯的直链结构。由于PFOS和PFOA异构体的环境行为、药代动力学、毒性等具有一定的差异,研究人体中PFASs异构体的组成和清除效率对于追溯人体暴露来源和评估健康风险具有重要意义。
本文首次应用一种新的PFASs异构体分析方法对来自我国典型城市(石家庄、邯郸和天津)的229名志愿者提供的血清样本进行分析。目标是分析我国人体中的PFASs以及PFOS和PFOA异构体,阐明性别和年龄对典型异构体累积的影响,评估这些人群中的PFOS和PFOA来源。随后,为了评估PFASs以及PFOS和PFOA异构体在人体中的肾排泄能力,对来自石家庄和邯郸的86对血样和尿样进行了分析,对肾清除率和半衰期进行了估算。最后,对30对来自石家庄的夫妇提供的60个成对全血和血清样本进行分析,用于研究PFASs以及PFOS和PFOA异构体在全血和血清中的分布。
在石家庄和邯郸的129个血清样本中,PFOS (平均值33.3ng/mL)是最主要的PFAS,依次是全氟己烷磺酸(PFHxS,2.95ng/mL), PFOA (2.38ng/mL)和全氟壬酸(PFNA,0.51ng/mL)。PFOS的平均水平比近些年北美地区的人群还要高。石家庄市区(59.0ng/mL)和邯郸市区(35.6ng/mL)人群中PFASs的总浓度显著(p<0.001和p=0.041)高于石家庄农村地区人群(24.3ng/mL);青年女性组主要PFASs的浓度比男性、老年女性组都低。石家庄和邯郸(n=129)人群中的全氟烷基磺酸(perfluoroalkane sulfonates, PFSAs)比天津(n=100)人群中高,而天津人群中全氟羧酸(perfluoroalkyl carboxylates, PFCAs)则高于石家庄和邯郸人群。这些暗示着不同地区PFASs不同的暴露源和暴露途径。
石家庄和邯郸人群中的直链PFOS平均比例(n-PFOS)仅占48.1%,比天津人群低(59.2%),都低于历史上主要PFOS生产商的工业品(约70%直链)。此外,在229个样本中,n-PFOS比例随着PFOS总浓度的增加而显著下降。所得数据支持之前的推论：i)人体血液中高比例支链PFOS异构体是PFOS前体物(PreFOS)的生物标记物；ii)高暴露水平人群中PFOS来源于高浓度的PreFOS不等比例的暴露。石家庄和邯郸人群血清中的直链PFOA (n-PFOA)比例为96.1%,明显高于工业品(约75-80%直链),但是低于2007-2008年的美国人群(接近100%直链),这说明我国仍然存在ECF方式生产的PFOA的使用。
建立了高灵敏度的分析尿液中PFASs及异构体的方法,并首次在尿液中发现了多种PFASs。大多数PFASs在尿液中的浓度与血液中的浓度有较强的正相关性(p<0.05),因此尿液可以用于监测人体中PFASs的暴露水平。短链的PFCAs比长链的更容易排泄,而同等碳链长度的PFCAs比PFSAs排泄更快。但是,PFOS (C8)比PFHxS (C6)排泄更快。在PFOS和PFOA的异构体中,除一个PFOS的支链异构体(lm-PFOS)外,各主要支链异构体都比直链异构体更易排泄。尿液中的直链全氟辛基磺酰胺(perfluorooctane sulfonamide, PFOSA)(中位值,84%)显著(p<0.001)高于血液中(65%),说明直链PFOSA相对其支链异构体优先通过尿液排泄,这与PFOS和PFOA的异构体肾排泄方式相反。通过一室药代动力学模型估算PFASs的生物半衰期从0.5±0.1年(5m-PFOA)到90±11年(lm-PFOS)。肾排泄是PFOA的主要排泄方式,但是对于PFOS和PFHxS(以及一些其他长链的PFCAs)来说,月经或者其他排泄途径可能对整体排泄有贡献。
除了PFHxA和PFNA外,大多数PFASs在全血和成对血清中有很好的正相关性(n=60, r=0.49-0.87,p<0.001). PFHxA在血清中的浓度显著(p<0.001)低于成对全血；PFOA (p=0.105)和PFNA (p=0.237)没有显著差异；对于更长碳链的PFCAs,全氟癸酸(perfluorodecanoate, PFDA)和全氟十一酸(perfluoroundecanoate, PFUdA)在血清中的浓度显著(p<0.001)高于全血。这说明短链的PFCA更倾向于分布于血细胞中。与PFHxA (C6)和PFOA(C8)不同,尽管有相同的碳链长度,PFHxS (C6)和PFOS (C8)在血清中的浓度显著(p<0.001)高于全血,说明官能团(羧酸和磺酸基团)在血清和全血分配中也起着重要作用。
血清/全血分配率的中位数如下,PFHxS (1.67), PFOS (1.68), PFHxA (0.34), PFOA (1.24), PFNA (0.85), PFDA (1.39)和PFUdA (1.60)。对于PFOS的异构体,除iso-PFOS外,其他单支链的PFOS异构体的分配率中位数接近或者大于2(1.94～2.69);n-PFOS,iso-PFOS和2-PFOS的分配率中位数都低于2(1.40-1.54)。对于PFOA的异构体,支链的PFOA分配率中位数都低于1,n-PFOA的为1.29。说明PFOS和PFOA异构体在血清和全血中分布具有较大的差异。把全血中的PFASs浓度直接乘以2转为血清中的浓度,会导致绝大多数的PFASs高估。采用血细胞比容计算的比率(女性1.69和男性1.85)去转化数据,对于PFSAs(PFHxS和PFOS)和长碳链的PFCAs(PFUdA)是合适的,但是对于其他的PFASs也会对结果产生偏高估算。
After decades of production and applications, perfluoroalkyl substances (PFASs) are ubiquitous present in the environment and have been widely detected in human samples. The most commonly detected PFASs in human samples are perfluorooctanesulfonate (PFOS) and perfluorooctanoate (PFOA). PFASs are persistent and bioaccumulative and display adverse effects to human health. Historically, two major manufacturing methods, namely telomerization and electrochemical fluorination (ECF), have been used to produce PFASs and their precursors. ECF was used to produce PFOA beginning in1947and PFOS and its precursors in1949. This process was known to yield a complex, yet rather consistent, mixture of linear (ca.70%for PFOS,80%for PFOA) and branched isomers (ca.30%for PFOS,20%for PFOA) in final products. However, the telomerization method, which was developed by Dupont in the1970s, produces typically pure linear isomer. The isomers of PFOS and PFOA display different environmental behaviors, pharmacokinetics and toxicity. Thus, it is of great importance to study the distribution and elimination effciency of isomers for human exposure source analysis and health risk assessment.
In the present thesis, a new isomer-specific PFAS analytial method was developed for the first time to analyze229serum samples collected in three typical cities (Shijiazhuang, Handan and Tianjin) in North China. The objectives were to quantify PFASs and the isomer profiles of PFOS and PFOA in general Chinese people, to elucidate the impacts of gender and age on the isomer-specific accumulation pattern, and to try to evaluate the sources of PFOS and PFOA exposure in these populations. Subsequently, to estimate the renal excretion of PFASs and isomers of PFOS and PFOA, paired blood and urine samples (n=86) from adults in Shijiazhuang and Handan were analyzed, and rates of renal clearance and half-lives were estimated. At last, to study the ditribution of PFASs and the isomers of PFOS and PFOA in whole blood and serum, sixty paired samples from thirty couples in Shijiazhuang were analyzed.
Among the129serum samples from Shijiazhuang and Handan, total PFOS (∑PFOS, mean33.3ng/mL) was the predominant PFAS followed by perfluorohexanesulfonate (PFHxS,2.95ng/mL), total PFOA (∑PFOA,2.38ng/mL), and perfluorononanoate (PFNA,0.51ng/mL). The level of∑PFOS appeared to be higher than in people from North America in recent years. The mean concentrations of∑PFASs in the participants living in urban Shijiazhuang (59.0ng/mL) and urban Handan (35.6ng/mL) were significantly higher (p<0.001and p=0.041, respectively) than those living in the rural district of Shijiazhuang (24.3ng/mL). The young female sub-population had the lowest∑PFAS concentrations compared with males and older females. The mean concentration of perfluoroalkane sulfonates (PFSAs) in people (n=129) from Shijiazhuang and Handan was higher than in people (n=100) from Tianjin, while, people in Tianjin displayed higher level of perfluoroalkyl carboxylates (PFCAs) than in Shijiazhuang and Handan. These suggest that the people in different regions may have different exposure sources of PFASs.
The proportion of linear PFOS (n-PFOS) inFOS was only48.1%for people in Shijiazhuang and Handan, which is lower than people in Tianjin (59.2%). They are both much lower than what was present in technical PFOS from the major historical manufacturer (ca.70%linear). Moreover, the proportion of n-PFOS decreased significantly with increasing∑PFOS concentration in the229serum samples. The results may have two implications:i) high content of branched PFOS isomers in serum is a biomarker of exposure to PFOS-precursors (PreFOS), and ii) that people with the highest∑PFOS concentrations are exposed disproportionately to high concentrations of PreFOS. On average, linear PFOA (n-PFOA) contributed96.1%of∑PFOA in serum samples from Shijiazhuang and Handan, significantly higher than in technical PFOA (ca.75-80%linear), but lower than in Americans (close to100%) in2007-2008, suggesting ECF PFOA was still be used in China.
A newly sensitive isomer-specific method was developed to analyze PFASs in human urine, which permitted the detection of many PFASs in human urine for the first time. The levels of most PFASs in urine correlated positively with their levels in paired blood (p<0.05). Thus, urine could be used to monitor PFASs exposure in humans. In general, shorter PFCAs were excreted more efficiently than longer ones, and PFCAs were excreted more efficiently than PFSAs of the same carbon chain-length. However, PFOS (a C8compound) was excreted more efficiently than PFHxS (a C6compound). Among PFOS and PFOA isomers, major branched isomers were more efficiently excreted than the corresponding linear isomer except1m-PFOS. The proportion of linear perfluorooctane sulfonamide (PFOSA) was significantly higher (p<0.001) in urine (median84%) than in blood (65%), demonstrating that linear PFOSA is preferentially excreted via urine relative to branched isomers; opposite to the findings for renal excretion of PFOS and PFOA isomers. A one-compartment model was used to estimate the biological elimination half-lives of PFASs. Among all PFASs, the estimated arithmetic mean with standard error elimination half-lives ranged from0.5±0.1years (5m-PFOA) to90±11years (1m-PFOS). Renal excretion was the major elimination route for PFOA, but for PFOS and PFHxS (and possibly other long-chain PFCAs) menstruation and other routes of excretion likely contribute to overall elimination.
For most PFASs, the levels in the whole blood correlated positively with the levels in paired serum samples (n=60, r=0.49-0.87,p<0.001) except PFHxA and PFNA. PFHxA in serum samples was significantly lower (p<0.001) than in the paired whole blood samples, while, for PFOA (p=0.105) and PFNA (p=0.237), no significantly differences were found, but for the longer chain-length PFCAs, perfluorodecanoate (PFDA) and perfluoroundecanoate (PFUdA) in serum samples was significantly higher (p<0.001) than in the paired whole blood samples. These suggested that shorter chain-length PFCAs preferrd to distribute in the blood corpuscles. Unlike PFHxA (C6) and PFOA (C8), althrough kept the same chain-length, PFHxS (C6) and PFOS (C8) in serum samples were significantly higher (p<0.001) than in the paired whole blood samples, which implied functional groups (carboxyl group and sulfonic group) also played an important role in the ditribution of serum and whole blood.
The median serum/whole blood distribution ratios were showed as follows, PFHxS (1.67), PFOS (1.68), PFHxA (0.34), PFOA (1.24), PFNA (0.85), PFDA (1.39) and PFUdA (1.60). For PFOS isomers, the median serum/whole blood distribution ratios for all the monomethyl branched PFOS were close to or greater than2(1.94～2.69) except iso-PFOS, while, the median ratios for n-PFOS, iso-PFOS and2-PFOS were similar and lower than2(1.40～1.54). For PFOA isomers, the median ratios for branched PFOA were lower than1, and was1.29for n-PFOA. These suggested the isomers distribution in serum and whole blood were different. When transfer PFASs concentration from whole blood samples to serum samples, using the factor2would lead to overestimation for most PFASs except some branched PFOS isomers. Using haematocrit calculated ratios (1.69for female and1.85for male) to transfer, would be suitable for PFSAs (PFHxS and PFOS) and long chain-length PFCA (PFUdA), but also overestimation for other PFASs.
本文首次应用一种新的PFASs异构体分析方法对来自我国典型城市(石家庄、邯郸和天津)的229名志愿者提供的血清样本进行分析。目标是分析我国人体中的PFASs以及PFOS和PFOA异构体,阐明性别和年龄对典型异构体累积的影响,评估这些人群中的PFOS和PFOA来源。随后,为了评估PFASs以及PFOS和PFOA异构体在人体中的肾排泄能力,对来自石家庄和邯郸的86对血样和尿样进行了分析,对肾清除率和半衰期进行了估算。最后,对30对来自石家庄的夫妇提供的60个成对全血和血清样本进行分析,用于研究PFASs以及PFOS和PFOA异构体在全血和血清中的分布。
在石家庄和邯郸的129个血清样本中,PFOS (平均值33.3ng/mL)是最主要的PFAS,依次是全氟己烷磺酸(PFHxS,2.95ng/mL), PFOA (2.38ng/mL)和全氟壬酸(PFNA,0.51ng/mL)。PFOS的平均水平比近些年北美地区的人群还要高。石家庄市区(59.0ng/mL)和邯郸市区(35.6ng/mL)人群中PFASs的总浓度显著(p<0.001和p=0.041)高于石家庄农村地区人群(24.3ng/mL);青年女性组主要PFASs的浓度比男性、老年女性组都低。石家庄和邯郸(n=129)人群中的全氟烷基磺酸(perfluoroalkane sulfonates, PFSAs)比天津(n=100)人群中高,而天津人群中全氟羧酸(perfluoroalkyl carboxylates, PFCAs)则高于石家庄和邯郸人群。这些暗示着不同地区PFASs不同的暴露源和暴露途径。
石家庄和邯郸人群中的直链PFOS平均比例(n-PFOS)仅占48.1%,比天津人群低(59.2%),都低于历史上主要PFOS生产商的工业品(约70%直链)。此外,在229个样本中,n-PFOS比例随着PFOS总浓度的增加而显著下降。所得数据支持之前的推论：i)人体血液中高比例支链PFOS异构体是PFOS前体物(PreFOS)的生物标记物；ii)高暴露水平人群中PFOS来源于高浓度的PreFOS不等比例的暴露。石家庄和邯郸人群血清中的直链PFOA (n-PFOA)比例为96.1%,明显高于工业品(约75-80%直链),但是低于2007-2008年的美国人群(接近100%直链),这说明我国仍然存在ECF方式生产的PFOA的使用。
建立了高灵敏度的分析尿液中PFASs及异构体的方法,并首次在尿液中发现了多种PFASs。大多数PFASs在尿液中的浓度与血液中的浓度有较强的正相关性(p<0.05),因此尿液可以用于监测人体中PFASs的暴露水平。短链的PFCAs比长链的更容易排泄,而同等碳链长度的PFCAs比PFSAs排泄更快。但是,PFOS (C8)比PFHxS (C6)排泄更快。在PFOS和PFOA的异构体中,除一个PFOS的支链异构体(lm-PFOS)外,各主要支链异构体都比直链异构体更易排泄。尿液中的直链全氟辛基磺酰胺(perfluorooctane sulfonamide, PFOSA)(中位值,84%)显著(p<0.001)高于血液中(65%),说明直链PFOSA相对其支链异构体优先通过尿液排泄,这与PFOS和PFOA的异构体肾排泄方式相反。通过一室药代动力学模型估算PFASs的生物半衰期从0.5±0.1年(5m-PFOA)到90±11年(lm-PFOS)。肾排泄是PFOA的主要排泄方式,但是对于PFOS和PFHxS(以及一些其他长链的PFCAs)来说,月经或者其他排泄途径可能对整体排泄有贡献。
除了PFHxA和PFNA外,大多数PFASs在全血和成对血清中有很好的正相关性(n=60, r=0.49-0.87,p<0.001). PFHxA在血清中的浓度显著(p<0.001)低于成对全血；PFOA (p=0.105)和PFNA (p=0.237)没有显著差异；对于更长碳链的PFCAs,全氟癸酸(perfluorodecanoate, PFDA)和全氟十一酸(perfluoroundecanoate, PFUdA)在血清中的浓度显著(p<0.001)高于全血。这说明短链的PFCA更倾向于分布于血细胞中。与PFHxA (C6)和PFOA(C8)不同,尽管有相同的碳链长度,PFHxS (C6)和PFOS (C8)在血清中的浓度显著(p<0.001)高于全血,说明官能团(羧酸和磺酸基团)在血清和全血分配中也起着重要作用。
血清/全血分配率的中位数如下,PFHxS (1.67), PFOS (1.68), PFHxA (0.34), PFOA (1.24), PFNA (0.85), PFDA (1.39)和PFUdA (1.60)。对于PFOS的异构体,除iso-PFOS外,其他单支链的PFOS异构体的分配率中位数接近或者大于2(1.94～2.69);n-PFOS,iso-PFOS和2-PFOS的分配率中位数都低于2(1.40-1.54)。对于PFOA的异构体,支链的PFOA分配率中位数都低于1,n-PFOA的为1.29。说明PFOS和PFOA异构体在血清和全血中分布具有较大的差异。把全血中的PFASs浓度直接乘以2转为血清中的浓度,会导致绝大多数的PFASs高估。采用血细胞比容计算的比率(女性1.69和男性1.85)去转化数据,对于PFSAs(PFHxS和PFOS)和长碳链的PFCAs(PFUdA)是合适的,但是对于其他的PFASs也会对结果产生偏高估算。
After decades of production and applications, perfluoroalkyl substances (PFASs) are ubiquitous present in the environment and have been widely detected in human samples. The most commonly detected PFASs in human samples are perfluorooctanesulfonate (PFOS) and perfluorooctanoate (PFOA). PFASs are persistent and bioaccumulative and display adverse effects to human health. Historically, two major manufacturing methods, namely telomerization and electrochemical fluorination (ECF), have been used to produce PFASs and their precursors. ECF was used to produce PFOA beginning in1947and PFOS and its precursors in1949. This process was known to yield a complex, yet rather consistent, mixture of linear (ca.70%for PFOS,80%for PFOA) and branched isomers (ca.30%for PFOS,20%for PFOA) in final products. However, the telomerization method, which was developed by Dupont in the1970s, produces typically pure linear isomer. The isomers of PFOS and PFOA display different environmental behaviors, pharmacokinetics and toxicity. Thus, it is of great importance to study the distribution and elimination effciency of isomers for human exposure source analysis and health risk assessment.
In the present thesis, a new isomer-specific PFAS analytial method was developed for the first time to analyze229serum samples collected in three typical cities (Shijiazhuang, Handan and Tianjin) in North China. The objectives were to quantify PFASs and the isomer profiles of PFOS and PFOA in general Chinese people, to elucidate the impacts of gender and age on the isomer-specific accumulation pattern, and to try to evaluate the sources of PFOS and PFOA exposure in these populations. Subsequently, to estimate the renal excretion of PFASs and isomers of PFOS and PFOA, paired blood and urine samples (n=86) from adults in Shijiazhuang and Handan were analyzed, and rates of renal clearance and half-lives were estimated. At last, to study the ditribution of PFASs and the isomers of PFOS and PFOA in whole blood and serum, sixty paired samples from thirty couples in Shijiazhuang were analyzed.
Among the129serum samples from Shijiazhuang and Handan, total PFOS (∑PFOS, mean33.3ng/mL) was the predominant PFAS followed by perfluorohexanesulfonate (PFHxS,2.95ng/mL), total PFOA (∑PFOA,2.38ng/mL), and perfluorononanoate (PFNA,0.51ng/mL). The level of∑PFOS appeared to be higher than in people from North America in recent years. The mean concentrations of∑PFASs in the participants living in urban Shijiazhuang (59.0ng/mL) and urban Handan (35.6ng/mL) were significantly higher (p<0.001and p=0.041, respectively) than those living in the rural district of Shijiazhuang (24.3ng/mL). The young female sub-population had the lowest∑PFAS concentrations compared with males and older females. The mean concentration of perfluoroalkane sulfonates (PFSAs) in people (n=129) from Shijiazhuang and Handan was higher than in people (n=100) from Tianjin, while, people in Tianjin displayed higher level of perfluoroalkyl carboxylates (PFCAs) than in Shijiazhuang and Handan. These suggest that the people in different regions may have different exposure sources of PFASs.
The proportion of linear PFOS (n-PFOS) inFOS was only48.1%for people in Shijiazhuang and Handan, which is lower than people in Tianjin (59.2%). They are both much lower than what was present in technical PFOS from the major historical manufacturer (ca.70%linear). Moreover, the proportion of n-PFOS decreased significantly with increasing∑PFOS concentration in the229serum samples. The results may have two implications:i) high content of branched PFOS isomers in serum is a biomarker of exposure to PFOS-precursors (PreFOS), and ii) that people with the highest∑PFOS concentrations are exposed disproportionately to high concentrations of PreFOS. On average, linear PFOA (n-PFOA) contributed96.1%of∑PFOA in serum samples from Shijiazhuang and Handan, significantly higher than in technical PFOA (ca.75-80%linear), but lower than in Americans (close to100%) in2007-2008, suggesting ECF PFOA was still be used in China.
A newly sensitive isomer-specific method was developed to analyze PFASs in human urine, which permitted the detection of many PFASs in human urine for the first time. The levels of most PFASs in urine correlated positively with their levels in paired blood (p<0.05). Thus, urine could be used to monitor PFASs exposure in humans. In general, shorter PFCAs were excreted more efficiently than longer ones, and PFCAs were excreted more efficiently than PFSAs of the same carbon chain-length. However, PFOS (a C8compound) was excreted more efficiently than PFHxS (a C6compound). Among PFOS and PFOA isomers, major branched isomers were more efficiently excreted than the corresponding linear isomer except1m-PFOS. The proportion of linear perfluorooctane sulfonamide (PFOSA) was significantly higher (p<0.001) in urine (median84%) than in blood (65%), demonstrating that linear PFOSA is preferentially excreted via urine relative to branched isomers; opposite to the findings for renal excretion of PFOS and PFOA isomers. A one-compartment model was used to estimate the biological elimination half-lives of PFASs. Among all PFASs, the estimated arithmetic mean with standard error elimination half-lives ranged from0.5±0.1years (5m-PFOA) to90±11years (1m-PFOS). Renal excretion was the major elimination route for PFOA, but for PFOS and PFHxS (and possibly other long-chain PFCAs) menstruation and other routes of excretion likely contribute to overall elimination.
For most PFASs, the levels in the whole blood correlated positively with the levels in paired serum samples (n=60, r=0.49-0.87,p<0.001) except PFHxA and PFNA. PFHxA in serum samples was significantly lower (p<0.001) than in the paired whole blood samples, while, for PFOA (p=0.105) and PFNA (p=0.237), no significantly differences were found, but for the longer chain-length PFCAs, perfluorodecanoate (PFDA) and perfluoroundecanoate (PFUdA) in serum samples was significantly higher (p<0.001) than in the paired whole blood samples. These suggested that shorter chain-length PFCAs preferrd to distribute in the blood corpuscles. Unlike PFHxA (C6) and PFOA (C8), althrough kept the same chain-length, PFHxS (C6) and PFOS (C8) in serum samples were significantly higher (p<0.001) than in the paired whole blood samples, which implied functional groups (carboxyl group and sulfonic group) also played an important role in the ditribution of serum and whole blood.
The median serum/whole blood distribution ratios were showed as follows, PFHxS (1.67), PFOS (1.68), PFHxA (0.34), PFOA (1.24), PFNA (0.85), PFDA (1.39) and PFUdA (1.60). For PFOS isomers, the median serum/whole blood distribution ratios for all the monomethyl branched PFOS were close to or greater than2(1.94～2.69) except iso-PFOS, while, the median ratios for n-PFOS, iso-PFOS and2-PFOS were similar and lower than2(1.40～1.54). For PFOA isomers, the median ratios for branched PFOA were lower than1, and was1.29for n-PFOA. These suggested the isomers distribution in serum and whole blood were different. When transfer PFASs concentration from whole blood samples to serum samples, using the factor2would lead to overestimation for most PFASs except some branched PFOS isomers. Using haematocrit calculated ratios (1.69for female and1.85for male) to transfer, would be suitable for PFSAs (PFHxS and PFOS) and long chain-length PFCA (PFUdA), but also overestimation for other PFASs.
引文
[1]. Hekster F M, Laane R, de Voogt P. Environmental and toxicity effects of perfluoroalkylated substances. Rev. Environ. Contam. Toxicol.2003,179:99-121.
[2]. Buck R C, Franklin J, Berger U, et al. Perfluoroalkyl and polyfluoroalkyl substances in the environment:Terminology, classification, and origins. Integr. Environ. Assess. Manage. 2011,7:513-541.
[3]. Deng S, Zhang Q, Nie Y, et al. Sorption mechanisms of perfluorinated compounds on carbon nanotubes. Environ. Pollut.2012,168:138-144.
[4]. Prevedouros K, Cousins I T, Buck R C, et al. Sources, fate and transport of perfluorocarboxylates. Environ. Sci. Technol.2006,40:32-44.
[5]. Kissa E. Fluorinated surfactants and repellents.2nd ed.; Marcel Dekker:NewYork.2005.
[6]. Drakesmith F. Electrofluorination of organic compounds. Organofluorine Chemistry.1997, 197-242.
[7], Benskin J P, De Silva A O, Martin J W. Isomer profiling of perfluorinated substances as a tool for source tracking:A review of early findings and future applications. Rev. Environ. Contam. Toxicol.2010,208:111-160.
[8]. Rayne S, Forest K, Friesen K J. Congener-specific numbering systems for the environmentally relevant C4 through C8 perfluorinated homologue groups of alkyl sulfonates, carboxylates, telomer alcohols, olefins, and acids, and their derivatives. J Environ Sci Health A Tox Hazard Subst Environ Eng.2008,43:1391-1401.
[9]. Paul A G, Jones K C, Sweetman A J. A first global production, emission, and environmental inventory for perfluorooctane sulfonate. Environ. Sci. Technol.2009,43:386-392.
[10].3M C. Phase-out plan for posf-based products, specialty materials markets group, US epa administrative, record docket ar 226-0600, U.S. Environmental Protection Agency, Washington, DC,2000.
[11]. Xie S, Wang T, Liu S, et al. Industrial source identification and emission estimation of perfluorooctane sulfonate in China. Environ. Int.2013,52:1-8.
[12]. Trier X, Granby K, Christensen J H. Polyfluorinated surfactants (PFS) in paper and board coatings for food packaging. Environ Sci Pollut Res.2011,18:1108-1120.
[13]. Lau C, Anitole K, Hodes C, et al. Perfluoroalkyl acids:A review of monitoring and toxicological findings. Toxicol. Sci.2007,99:366-394.
[14]. Wang B, Huang J, Deng S, et al. Addressing the environmental risk of persistent organic pollutants in China. Front Environ Sci Engin China.2012,6:2-16.
[15]. Reagen W K, Lindstrom K R, Jacoby C B, et al. Environmental characterization of 3M electrochemical fluorination derived perfluorooctanoate and perfluorooctanesulfonate. Society of environmental toxicology and chemistry 28th North American meeting, Milwaukee, WI, USA.2007,11-15 Nov.
[16]. Benskin J P, Bataineh M, Martin J W. Simultaneous characterization of perfluoroalkyl carboxylate, sulfonate, and sulfonamide isomers by liquid chromatography-tandem mass spectrometry. Anal. Chem.2007,79:6455-6464.
[17]. Taves D. Evidence that there are two forms of fluoride in human serum. Nature.1968,217: 1050-1051.
[18].3M C. Fluorochemical isomer distribution by 19F NMR spectroscopy. US EPA Public Docket AR-226-0564.1997.
[19]. Bastos J K, Freitas L A P, Pagliarussi R S, et al. A rapid quantitative method for the analysis of sulfluramid and its isomers in ant bait by capillary column gas chromatography. J. Sep. Sci. 2001,24:406-410.
[20]. Stevenson L A. U.S. Environmental Protection Agency Public Docket AR-2261150: Comparative analysis of fluorochemicals in human serum samples obtained commercially. U.S. Environmental Protection Agency, Office of Pollution Prevention and Toxic Substances, Washington, DC.2002.
[21]. De Silva A O, Mabury S A. Isolating isomers of perfluorocarboxylates in polar bears (Ursus maritimus) from two geographical locations. Environ. Sci. Technol.2004,38: 6538-6545.
[22], Chu S, Letcher R. Linear and branched perfluorooctane sulfonate isomers in technical product and environmental samples by in-port derivatization-gas chromatography-mass spectrometry. Anal. Chem.2009,81:4256-4262.
[23]. Langlois I, Oehme M. Structural identification of isomers present in technical perfluorooctane sulfonate by tandem mass spectrometry. Rapid Commun. Mass Spectrom. 2006,20:844-850.
[24]. Benskin J P, Ikonomou M G, Woudneh M B, et al. Rapid characterization of perfluoralkyl carboxylate, sulfonate, and sulfonamide isomers by high-performance liquid chromatography-tandem mass spectrometry.J. Chromatogr. A.2012,1247:165-70.
[25]. Riddell N, Arsenault G, Benskin J P, et al. Branched perfluorooctane sulfonate isomer quantification and characterization in blood serum samples by HPLC/ESI-MS(/MS). Environ. Sci. Technol.2009,43:7902-7908.
[26]. Benskin J P, Yeung L W Y, Yamashita N, et al. Perfluorinated acid isomer profiling in water and quantitative assessment of manufacturing source. Environ. Sci. Technol.2010,44: 9049-9054.
[27]. Kestner T. U.S. Environmental Protection Agency Public Docket AR226-0564: Fluorochemical isomer distribution by F-NMR spectroscopy. U.S. Environmental Protection Agency, Office of Pollution Prevention and Toxic Substances, Washington, DC. 1997.
[28]. Arsenault G, Chittim B, McAlees A, et al. Some issues relating to the use of perfluorooctanesulfonate (PFOS) samples as reference standards. Chemosphere.2008,70: 616-625.
[29]. De Silva A O, Mabury S A. Isomer distribution of perfluorocarboxylates in human blood: Potential correlation to source. Environ. Sci. Technol.2006,40:2903-2909.
[30]. De Silva A O, Muir D C G, Mabury S A. Distribution of perfluorocarboxylate isomers in select samples from the North American environment. Environ. Toxicol. Chem.2009,28: 1801-1814.
[31]. De Silva A O, Benskin J P, Martin L J, et al. Disposition of perfluorinated acid isomers in Sprague-Dawley rats; part 2:Subchronic dose. Environ. Toxicol. Chem.2009,28:555-567.
[32]. De Silva A 0, Tseng P J, Mabury S A. Toxicokinetics of perfluorocarboxylate isomers in rainbow trout. Environ. Toxicol. Chem.2009,28:330-337.
[33]. Langlois I, Berger U, Zencak Z, et al. Mass spectral studies of perfluorooctane sulfonate derivatives separated by high-resolution gas chromatography. Rapid Commun. Mass Spectrom.2007,21:3547-3553.
[34]. O'Brien J M, Kennedy S W, Chu S, et al. Isomer-specific accumulation of perfluorooctane sulfonate in the liver of chicken embryos exposed in ovo to a technical mixture. Environ. Toxicol. Chem.2010,30:226-231.
[35]. Langlois I. Mass spectrometric isomer characterization of perfluorinated compounds in technical mixture, water and human blood. PhD Thesis, Department of Chemistry, University of Basel, Switzerland.2006.
[36]. Karrman A, Langlois I, van Bavel B, et al. Identification and pattern of perfluorooctane sulfonate (PFOS) isomers in human serum and plasma. Environ. Int.2007,33:782-788.
[37]. Furdui V, Helm P, Crozier P, et al. Temporal trends of perfluoroalkyl compounds with isomer analysis in lake trout from Lake Ontario (1979-2004). Environ. Sci. Technol.2008, 42:4739-4744.
[38]. Beesoon S, Webster G M, Shoeib M, et al. Isomer profiles of perfluorochemicals in matched maternal, cord, and house dust samples:Manufacturing sources and transplacental transfer. Environ. Health Perspect.2011,119:1659-1664.
[39]. Benskin J P, De Silva A O, Martin L J, et al. Disposition of perfluorinated acid isomers in Sprague-Dawley rats; part 1:Single dose. Environ. Toxicol. Chem.2009,28:542-554.
[40]. Benskin J P, Holt A, Martin J W. Isomer-specific biotransformation rates of a perfluorooctane sulfonate (PFOS)-precursor by cytochrome P450 isozymes and human liver microsomes. Environ. Sci. Technol.2009,43:8566-8572.
[41]. Ross M S, Wong C S, Martin J W. Isomer-specific biotransformation of perfluorooctane sulfonamide in Sprague-Dawley rats. Environ. Sci. Technol.2012,46:3196-3203.
[42]. Benskin J, Yeung L, Yamashita N, et al. Perfluorinated acid isomer profiling in water and quantitative assessment of manufacturing source. Environ. Sci. Technol.2010,44: 9049-9054.
[43]. Benskin J P, Ahrens L, Muir D C G, et al. Manufacturing origin of perfluorooctanoate (PFOA) in Atlantic and Canadian Arctic seawater. Environ. Sci. Technol.2011,46: 677-685.
[44]. Benskin J P, Phillips V, St. Louis V L, et al. Source elucidation of perfluorinated carboxylic acids in remote alpine lake sediment cores. Environ. Sci. Technol.2011,45: 7188-7194.
[45]. Loveless S E, Finlay C, Everds N E, et al. Comparative responses of rats and mice exposed to linear/branched, linear, or branched ammonium perfluorooctanoate (APFO). Toxicology. 2006,220:203-217.
[46]. White S, Kato K, Jia L, et al. Effects of perfluorooctanoic acid on mouse mammary gland development and differentiation resulting from cross-foster and restricted gestational exposures. Reprod. Toxicol.2009,27:289-298.
[47]. Wellington-Lab. Certificate of analysis/documentation for TPFOA. Obtained Jun 2011 from Wellington laboratories, Guelph, ON, Canada.2011.
[48]. Vyas S M, Kania-Korwel I, Lehmler H-J. Differences in the isomer composition of perfluoroctanesulfonyl (PFOS) derivatives. J Environ Sci Health A Tox Hazard Subst Environ Eng.2007,42:249-255.
[49]. Wellington-Lab. Certificate of analysis/documentation for br-PFOSK. Obtained Dec 2010 from Wellington laboratories, Guelph, ON, Canada.2008.
[50]. Korkowski P, Kestner T. Chemical characterization of FOSA & PFOSA samples by 1H and 19F NMR spectroscopy. Provided by 3M co.1999.
[51]. Olsen G W, Hansen K J, Stevenson L A, et al. Human donor liver and serum concentrations of perfluorooctanesulfonate and other perfluorochemicals. Environ. Sci. Technol. 2003,37:888-891.
[52]. Kannan K, Corsolini S, Falandysz J, et al. Perfluorooctanesulfonate and related fluorochemicals in human blood from several countries. Environ. Sci. Technol.2004,38: 4489-4495.
[53]. Yeung L W Y, So M, Jiang G, et al. Perfluorooctanesulfonate and related fluorochemicals in human blood samples from China. Environ. Sci. Technol.2006,40:715-720.
[54]. Olsen G W, Lange C C, Ellefson M E, et al. Temporal trends of perfluoroalkyl concentrations in American Red Cross adult blood donors,2000-2010. Environ. Sci. Technol.2012,46:6330-6338.
[55]. Zhang T, Sun H, Lin Y, et al. Perfluorinated compounds in human blood, water, edible freshwater fish and seafood in China:Daily intake and regional differences in human exposures. J. Agric. Food. Chem.2011,59:11168-11176.
[56]. Zhang T, Wu Q, Sun H, et al. Perfluorinated compounds in whole blood samples from infants, children, and adults in China. Environ. Sci. Technol.2010,44:4341-4347.
[57]. Zhang W, Lin Z, Hu M, et al. Perfluorinated chemicals in blood of residents in Wenzhou, China. Ecotoxicol. Environ. Saf.2011,74:1787-1793.
[58]. Guo F, Zhong Y, Wang Y, et al. Perfluorinated compounds in human blood around Bohai Sea, China. Chemosphere.2011,85:156-162.
[59]. Liu J, Li J, Luan Y, et al. Geographical distribution of perfluorinated compounds in human blood from Liaoning province, China. Environ. Sci. Technol.2009,43:4044-4048.
[60]. Pan Y, Shi Y, Wang J, et al. Concentrations of perfluorinated compounds in human blood from twelve cities in China. Environ. Toxicol. Chem.2010,29:2695-2701.
[61]. Yeung L W Y, Miyake Y, Taniyasu S, et al. Perfluorinated compounds and total and extractable organic fluorine in human blood samples from China. Environ. Sci. Technol. 2008,42:8140-8145.
[62]. Jin Y, Saito N, Harada K, et al. Historical trends in human serum levels of perfluorooctanoate and perfluorooctane sulfonate in Shenyang, China. Tohoku J. Exp. Med. 2007,212:63-70.
[63]. Olsen G W, Huang H Y, Helzlsouer K J, et al. Historical comparison of perfluorooctanesulfonate, perfluorooctanoate, and other fluorochemicals in human blood. Environ. Health Perspect.2005,113:539-545.
[64]. Kato K, Wong L-Y, Jia L T, et al. Trends in exposure to polyfluoroalkyl chemicals in the U.S. Population:1999-2008. Environ. Sci. Technol.2011,45:8037-8045.
[65]. Karrman A, Mueller J, van Bavel B, et al. Levels of 12 perfluorinated chemicals in pooled Australian serum, collected 2002-2003, in relation to age, gender, and region. Environ. Sci. Technol.2006,40:3742-3748.
[66]. Toms L, Calafat A, Kato K, et al. Polyfluoroalkyl chemicals in pooled blood serum from infants, children, and adults in Australia. Environ. Sci. Technol.2009,43:4194-4199.
[67]. Ingelido A, Marra V, Abballe A, et al. Perfluorooctanesulfonate and perfluorooctanoic acid exposures of the italian general population. Chemosphere.2010,80:1125-1130.
[68]. Lindh C H, Rylander L, Toft G, et al. Blood serum concentrations of perfluorinated compounds in men from Greenlandic Inuit and European populations. Chemosphere.2012, 88:1269-75.
[69], Kubwabo C, Vais N, Benoit F. A pilot study on the determination of perfluorooctanesulfonate and other perfluorinated compounds in blood of Canadians. J. Environ. Monit.2004,6:540-545.
[70]. Harada K, Yang H, Moon C, et al. Levels of perfluorooctane sulfonate and perfluorooctanoic acid in female serum samples from Japan in 2008, Korea in 1994-2008 and Vietnam in 2007-2008. Chemosphere.2010,79:314-319.
[71]. Harada K, Koizumi A, Saito N, et al. Historical and geographical aspects of the increasing perfluorooctanoate and perfluorooctane sulfonate contamination in human serum in Japan. Chemosphere.2007,66:293-301.
[72]. Karrman A, van Bavel B, J rnberg U, et al. Perfluorinated chemicals in relation to other persistent organic pollutants in human blood. Chemosphere.2006,64:1582-1591.
[73]. Karrman A, Ericson I, Van Bavel B, et al. Exposure of perfluorinated chemicals through lactation:Levels of matched human milk and serum and a temporal trend,1996-2004, in Sweden. Environ. Health Perspect.2007,115:226-230.
[74]. Midasch O, Schettgen T, Angerer J. Pilot study on the perfluorooctanesulfonate and perfluorooctanoate exposure of the German general population. Int. J. Hyg. Environ. Health. 2006,209:489-496.
[75]. Fromme H, Midasch O, Twardella D, et al. Occurrence of perfluorinated substances in an adult German population in southern Bavaria. Int. Arch. Occup. Environ. Health.2007,80: 313-319.
[76]. Ericson I, Gomez M, Nadal M, et al. Perfluorinated chemicals in blood of residents in Catalonia (Spain) in relation to age and gender:A pilot study. Environ. Int.2007,33: 616-623.
[77]. Fei C, McLaughlin J K, Tarone R E, et al. Perfluorinated chemicals and fetal growth:A study within the Danish National Birth Cohort. Environ. Health Perspect.2007,115: 1677-1682.
[78]. Eriksen K, Sorensen M, McLaughlin J, et al. Perfluorooctanoate and perfluorooctanesulfonate plasma levels and risk of cancer in the general Danish population. J. Natl Cancer Inst.2009,101:605-609.
[79]. Monroy R, Morrison K, Teo K, et al. Serum levels of perfluoroalkyl compounds in human maternal and umbilical cord blood samples. Environ. Res.2008,108:56-62.
[80]. Rylander C, Brustad M, Falk H, et al. Dietary predictors and plasma concentrations of perfluorinated compounds in a coastal population from Northern Norway. J. Environ. Pub. Health.2009, doi:10.1155/2009/268219.
[81]. Hemat H, Wilhelm M, V lkel W, et al. Low serum levels of perfluorooctanoic acid (PFOA), perfluorooctane sulfonate (PFOS) and perfluorohexane sulfonate (PFHxS) in children and adults from Afghanistan. Sci. Total Environ.2010,408:3493-3495.
[82]. Olsen G W, Burris J M, Ehresman D J, et al. Half-life of serum elimination of perfluorooctanesulfonate, perfluorohexanesulfonate, and perfluorooctanoate in retired fluorochemical production workers. Environ. Health Perspect.2007,115:1298-1305.
[83]. Hanssen L, Roellin H, Odland J O, et al. Perfluorinated compounds in maternal serum and cord blood from selected areas of South Africa:Results of a pilot study. J. Environ. Monit. 2010,12:1355-1361.
[84]. Rylander C, Duong Trong P, Odland J O, et al. Perfluorinated compounds in delivering women from south central Vietnam. J. Environ. Monit.2009,11:2002-2008.
[85]. Haug L S, Huber S, Becher G, et al. Characterisation of human exposure pathways to perfluorinated compounds-comparing exposure estimates with biomarkers of exposure. Environ. Int.2011,37:687-693.
[86]. Thomsen C, Haug L S, Stigum H, et al. Changes in concentrations of perfluorinated compounds, polybrominated biphenyl ethers, and polychlorinated biphenyls in Norwegian breast-milk during twelve months of lactation. Environ. Sci. Technol.2010,44:9550-9556.
[87]. Haug L S, Thomsen C, Bechert G. Time trends and the influence of age and gender on serum concentrations of perfluorinated compounds in archived human samples. Environ. Sci. Technol.2009,43:2131-2136.
[88]. Kudo N, Katakura M, Sato Y, et al. Sex hormone-regulated renal transport of perfluorooctanoic acid. Chem. Biol. Interact.2002,139:301-316.
[89]. Butenhoff J L, Kennedy G L, Hinderliter P M, et al. Phannacokinetics of perfluorooctanoate in cynomolgus monkeys. Toxicol. Sci.2004,82:394-406.
[90]. Harada K, Inoue K, Morikawa A, et al. Renal clearance of perfluorooctane sulfonate and perfluorooctanoate in humans and their species-specific excretion. Environ. Res.2005,99: 253-261.
[91]. Perez F, Llorca M, Farre M, et al. Automated analysis of perfluorinated compounds in human hair and urine samples by turbulent flow chromatography coupled to tandem mass spectrometry. Anal. Bioanal. Chem.2012,402:2369-2378.
[92]. Beesoon S, Genuis S J, Benskin J P, et al. Exceptionally high serum concentrations of perfluorohexanesulfonate in a Canadian family are linked to home carpet treatment applications. Environ. Sci. Technol.2012,46:12960-12967.
[93]. Li J, Guo F, Wang Y, et al. Development of extraction methods for the analysis of perfluorinated compounds in human hair and nail by high performance liquid chromatography tandem mass spectrometry. J. Chromatogr. A.2012,1219:54-60.
[94]. Liu W, Xu L, Li X, et al. Human nails analysis as biomarker of exposure to perfluoroalkyl compounds. Environ. Sci. Technol.2011,45:8144-8150.
[95].姚丹,张鸿,柴之芳,等.天津成人头发指甲中有机氟污染物的残留特征.环境科学.2013,718-723.
[96]. Stein C R, Wolff M S, Calafat A M, et al. Comparison of polyfluoroalkyl compound concentrations in maternal serum and amniotic fluid:A pilot study. Reprod. Toxicol.2012, 34:312-316.
[97]. Tittlemier S, Ryan J, Van Oostdam J. Presence of anionic organic compounds in serum collected from northern Canadian populations. Organohalogen Compd.2004,66: 4009-4014.
[98]. Inoue K, Okada F, Ito R, et al. Perfluorooctane sulfonate (PFOS) and related perfluorinated compounds in human maternal and cord blood samples:Assessment of PFOS exposure in a susceptible population during pregnancy. Environ. Health Perspect.2004,112:1204-1207.
[99]. Apelberg B, Goldman L, Calafat A, et al. Determinants of fetal exposure to polyfluoroalkyl compounds in Baltimore, Maryland. Environ. Sci. Technol.2007,41:3891-3897.
[100]. Liu J, Li J, Zhao Y, et al. The occurrence of perfluorinated alkyl compounds in human milk from different regions of China. Environ. Int.2010,36:433-438.
[101]. Karrman A, Domingo J, Llebaria X, et al. Biomonitoring perfluorinated compounds in Catalonia, Spain:Concentrations and trends in human liver and milk samples. Environ Sci Pollut Res.2010,17:750-758.
[102]. Tao L, Ma J, Kunisue T, et al. Perfluorinated compounds in human breast milk from several Asian countries, and in infant formula and dairy milk from the United States. Environ. Sci. Technol.2008,42:8597-8602.
[103]. Tao L, Kannan K, Wong C, et al. Perfluorinated compounds in human milk from Massachusetts, USA. Environ. Sci. Technol.2008,42:3096-3101.
[104]. So M, Yamashita N, Taniyasu S, et al. Health risks in infants associated with exposure to perfluorinated compounds in human breast milk from Zhoushan, China. Environ. Sci. Technol.2006,40:2924-2929.
[105]. Voelkel W, Genzel-Boroviczeny O, Demmelmair H, et al. Perfluorooctane sulphonate (PFOS) and perfluorooctanoic acid (PFOA) in human breast milk:Results of a pilot study. Int. J. Hyg. Environ. Health.2008,211:440-446.
[106]. Kim S K, Lee K T, Kang C S, et al. Distribution of perfluorochemicals between sera and milk from the same mothers and implications for prenatal and postnatal exposures. Environ. Pollut.2011,159:169-174.
[107]. Guruge K, Taniyasu S, Yamashita N, et al. Perfluorinated organic compounds in human blood serum and seminal plasma:A study of urban and rural tea worker populations in Sri Lanka. J. Environ. Monit.2005,7:371-377.
[108]. Wang T, Wang Y, Liao C, et al. Perspectives on the inclusion of perfluorooctane sulfonate into the Stockholm Convention on persistent organic pollutants. Environ. Sci. Technol.2009,43:5171-5175.
[109]. Spliethoff H, Tao L, Shaver S, et al. Use of newborn screening program blood spots for exposure assessment:Declining levels of perfluorinated compounds in New York State infants. Environ. Sci. Technol.2008,42:5361-5367.
[110]. Bartell S M, Calafat A M, Lyu C, et al. Rate of decline in serum PFOA concentrations after granular activated carbon filtration at two public water systems in Ohio and West Virginia. Environ. Health Perspect.2010,118:222-228.
[111]. Steenland K, Fletcher T, Savitz D A. Epidemiologic evidence on the health effects of perfluorooctanoic acid (PFOA). Environ. Health Perspect.2010,118:1100-1108.
[112]. Joensen U N, Bossi R, Leffers H, et al. Do perfluoroalkyl compounds impair human semen quality? Environ. Health Perspect.2009,117:923-927.
[113]. Stein C R, Savitz D A, Dougan M. Serum'levels of perfluorooctanoic acid and perfluorooctane sulfonate and pregnancy outcome. Am. J. Epidemiol.2009,170:837-846.
[114]. Maisonet M, Terrell M L, McGeehin M A, et al. Maternal concentrations of polyfluoroalkyl compounds during pregnancy and fetal and postnatal growth in British girls. Environ. Health Perspect.2012,120:1432-7.
[115]. Apelberg B, Witter F, Herbstman J, et al. Cord serum concentrations of perfluorooctane sulfonate (PFOS) and perfluorooctanoate (PFOA) in relation to weight and size at birth. Environ. Health Perspect.2007,115:1670-1676.
[116]. Chen M-H, Ha E-H, Wen T-W, et al. Perfluorinated compounds in umbilical cord blood and adverse birth outcomes. Plos One.2012,7.
[117]. Lopez-Espinosa M-J, Mondal D, Armstrong B, et al. Thyroid function and perfluoroalkyl acids in children living near a chemical plant. Environ. Health Perspect.2012,120: 1036-1041.
[118]. Grandjean P, Andersen E W, Budtz-Jorgensen E, et al. Serum vaccine antibody concentrations in children exposed to perfluorinated compounds. J. Am. Med. Assoc.2012, 307:391-397.
[119]. Gump B B, Wu Q, Dumas A K, et al. Perfluorochemical (PFC) exposure in children: Associations with impaired response inhibition. Environ. Sci. Technol.2011,45: 8151-8159.
[120]. Lopez-Espinosa M-J, Fletcher T, Armstrong B, et al. Association of perfluorooctanoic acid (PFOA) and perfluorooctane sulfonate (PFOS) with age of puberty among children living near a chemical plant. Environ. Sci. Technol.2011,45:8160-8166.
[121]. Hoffman K, Webster T F, Weisskopf M G, et al. Exposure to polyfluoroalkyl chemicals and attention deficit/hyperactivity disorder in US children 12-15 years of age. Environ. Health Perspect.2010,118:1762-1767.
[122]. Halldorsson T I, Rytter D, Haug L S, et al. Prenatal exposure to perfluorooctanoate and risk of overweight at 20 years of age:A prospective cohort study. Environ. Health Perspect.2012,120:668-73.
[123]. Shankar A, Xiao J, Ducatman A. Perfluoroalkyl chemicals and chronic kidney disease in US adults. Am. J. Epidemiol.2011,174:893-900.
[124]. Steenland K, Tinker S, Shankar A, et al. Association of perfluorooctanoic acid (PFOA) and perfluorooctane sulfonate (PFOS) with uric acid among adults with elevated community exposure to PFOA. Environ. Health Perspect.2010,.118:229-233.
[125]. La Rocca C, Alessi E, Bergamasco B, et al. Exposure and effective dose biomarkers for perfluorooctane sulfonic acid (PFOS) and perfluorooctanoic acid (PFOA) in infertile subjects:Preliminary results of the PREVIENI project. Int. J. Hyg. Environ. Health.2012, 215:206-211.
[126]. Melzer D, Rice N, Depledge M H, et al. Association between serum perfluorooctanoic acid (PFOA) and thyroid disease in the US National Health and Nutrition Examination Survey. Environ. Health Perspect.2010,118:686-692.
[127]. Lin C-Y, Lin L-Y, Chiang C-K, et al. Investigation of the associations between low-dose serum perfluorinated chemicals and liver enzymes in US adults. Am. J. Gastroenterol. 2010,105:1354-1363.
[128]. Fei C, McLaughlin J K, Lipworth L, et al. Maternal levels of perfluorinated chemicals and subfecundity. Hum. Reprod.2009,24:1200-1205.
[129]. Steenland K, Tinker S, Frisbee S, et al. Association of perfluorooctanoic acid and perfluorooctane sulfonate with serum lipids among adults living near a chemical plant. Am. J. Epidemiol.2009,170:1268-1278.
[130]. Vanden Heuvel J P, Thompson J T, Frame S R, et al. Differential activation of nuclear receptors by perfluorinated fatty acid analogs and natural fatty acids:A comparison of human, mouse, and rat peroxisome proliferator-activated receptor-alpha,-beta, and-gamma, liver x receptor-beta, and retinoid x receptor-alpha. Toxicol. Sci.2006,92: 476-489.
[131]. O'Brien J M, Austin A J, Williams A, et al. Technical-grade perfluorooctane sulfonate alters the expression of more transcripts in cultured chicken embryonic hepatocytes than linear perfluorooctane sulfonate. Environ. Toxicol. Chem.2011,30:2846-2859.
[132]. Kuklenyik Z, Reich J A, Tully J S, et al. Automated solid-phase extraction and measurement of perfluorinated organic acids and amides in human serum and milk. Environ. Sci. Technol.2004,38:3698-3704.
[133]. Hansen K J, Clemen L A, Ellefson M E, et al. Compound-specific, quantitative characterization of organic:Fluorochemicals in biological matrices. Environ. Sci. Technol. 2001,35:766-770.
[134].吴茵.棉纺织业与城市化进程：1921-1990年——以石家庄市为例.经济与管理2010,70-73.
[135]. Calafat A M, Wong L-Y, Kuklenyik Z, et al. Polyfluoroalkyl chemicals in the US population:Data from the National Health and Nutrition Examination Survey (NHANES) 2003-2004 and comparisons with NHANES 1999-2000. Environ. Health Perspect.2007, 115:1596-1602.
[136]. Wang M, Park J-S, Petreas M. Temporal changes in the levels of perfluorinated compounds in California women's serum over the past 50 years. Environ. Sci. Technol. 2011,45:7510-7516.
[137]. Domingo J L. Health risks of dietary exposure to perfluorinated compounds. Environ. Int. 2012,40:187-195.
[138]. Zhang T, Sun H, Wu Q, et al. Perfluorochemicals in meat, eggs and indoor dust in China: Assessment of sources and pathways of human exposure to perfluorochemicals. Environ. Sci. Technol.2010,44:3572-3579.
[139]. Kannan K, Corsolini S, Falandysz J, et al. Perfluorooctanesulfonate and related fluorochemicals in human blood from several countries. Environ. Sci. Technol.2004,38: 4489-4495.
[140]. Fromme H, Mosch C, Morovitz M, et al. Pre-and postnatal exposure to perfluorinated compounds (PFCs). Environ. Sci. Technol.2010,44:7123-7129.
[141]. Wang Y, Beesoon S, Benskin J P, et al. Enantiomer fractions of chiral perfluorooctanesulfonate (PFOS) in human sera. Environ. Sci. Technol.2011,45: 8907-8914.
[142]. Vestergren R, Cousins I T, Trudel D, et al. Estimating the contribution of precursor compounds in consumer exposure to PFOS and PFOA. Chemosphere.2008,73: 1617-1624.
[143]. Haug L S, Huber S, Schlabach M, et al. Investigation on per-and polyfluorinated compounds in paired samples of house dust and indoor air from Norwegian homes. Environ. Sci. Technol. 2011,45:7991-7998.
[144], Seals R, Bartell S M, Steenland K. Accumulation and clearance of perfluorooctanoic acid (PFOA) in current and former residents of an exposed community. Environ. Health Perspect.2011,119:119-124.
[145]. Sharpe R L, Benskin J P, Laarman A H, et al. Perfluorooctane sulfonate toxicity, isomer-specific accumulation, and maternal transfer in zebrafish (Danio rerio) and rainbow trout (Oncorhynchus mykiss). Environ. Toxicol. Chem.2010,29:1957-1966.
[146]. Cui L, Liao C, Zhou Q, et al. Excretion of PFOA and PFOS in male rats during a subchronic exposure. Arch. Environ. Contam. Toxicol.2010,58:205-213.
[147], Ubel F A, Sorenson S D, Roach D E. Health status of plant workers exposed to fluorochemicals--a preliminary report. Am. Ind. Hyg. Assoc. J.1980,41:584-9.
[148]. Li J, Guo F, Wang Y, et al. Can nail, hair and urine be used for biomonitoring of human exposure to perfluorooctane sulfonate and perfluorooctanoic acid? Environ. Int.2013,53: 47-52.
[149]. Jaffe M. Ueber den niederschlag welchen pikrinsaure in normalen harn erzeugt und uber eine neue reaction des kreatinins [in German]. Z Physiol Chem.1886,10:391-400.
[150]. Borghi L, Meschi T, Amato F, et al. Urinary volume, water and recurrences in idiopathic calcium nephrolithiasis:A 5-year randomized prospective study. J. Urol.1996,155: 839-843.
[151]. Walser M. Creatinine excretion as a measure of protein nutrition in adults of varying age. JPEN. J. Parenter. Enteral Nutr.1987,11:73S-78S.
[152]. Thompson J, Lorber M, Toms L-M L, et al. Use of simple pharmacokinetic modeling to characterize exposure of Australians to perfluorooctanoic acid and perfluorooctane sulfonic acid. Environ. Int.2010,36:390-397.
[153]. Ohmori K, Kudo N, Katayama K, et al. Comparison of the toxicokinetics between perfluorocarboxylic acids with different carbon chain length. Toxicology.2003,184: 135-140.
[154]. Gao J, Zeng S, Sun B L, et al. Menstrual blood loss and hematologic indices in healthy Chinese women. J. Reprod. Med.1987,32:822-826.
[155]. Ge M, Yan Y, Zhang C, et al. Discussion on the relationship between normal hematocrit and geographical factors in China. Clin. Hemorheol. Microcirc.1997,17:459-465.
[156]. Hanssen L, Dudarev A A, Huber S, et al. Partition of perfluoroalkyl substances (PFASs) in whole blood and plasma, assessed in maternal and umbilical cord samples from inhabitants of arctic Russia and Uzbekistan. Sci. Total Environ.2013,447:430-7.
[157]. Kudo N, Suzuki E, Katakura M, et al. Comparison of the elimination between perfluorinated fatty acids with different carbon chain length in rats. Chem. Biol. Interact. 2001,134:203-216.
[158]. Bhhatarai B, Gramatica P. Prediction of aqueous solubility, vapor pressure and critical micelle concentration for aquatic partitioning of perfluorinated chemicals. Environ. Sci. Technol.2011,45:8120-8128.
[159]. Martin J W, Asher B J, Beesoon S, et al. PFOS or PreFOS? Are perfluorooctane sulfonate precursors (PreFOS) important determinants of human and environmental perfluorooctane sulfonate (PFOS) exposure?J. Environ. Monit.2010,12:1979-2004.
[160]. Taniyasu S, Kannan K, Horii Y, et al. A survey of perfluorooctane sulfonate and related perfluorinated organic compounds in water, fish, birds, and humans from Japan. Environ. Sci. Technol.2003,37:2634-2639.
[161]. Ehresman D J, Froehlich J W, Olsen G W, et al. Comparison of human whole blood, plasma, and serum matrices for the determination of perfluorooctanesulfonate (PFOS), perfluorooctanoate (PFOA), and other fluorochemicals. Environ. Res.2007,103:176-184.
[2]. Buck R C, Franklin J, Berger U, et al. Perfluoroalkyl and polyfluoroalkyl substances in the environment:Terminology, classification, and origins. Integr. Environ. Assess. Manage. 2011,7:513-541.
[3]. Deng S, Zhang Q, Nie Y, et al. Sorption mechanisms of perfluorinated compounds on carbon nanotubes. Environ. Pollut.2012,168:138-144.
[4]. Prevedouros K, Cousins I T, Buck R C, et al. Sources, fate and transport of perfluorocarboxylates. Environ. Sci. Technol.2006,40:32-44.
[5]. Kissa E. Fluorinated surfactants and repellents.2nd ed.; Marcel Dekker:NewYork.2005.
[6]. Drakesmith F. Electrofluorination of organic compounds. Organofluorine Chemistry.1997, 197-242.
[7], Benskin J P, De Silva A O, Martin J W. Isomer profiling of perfluorinated substances as a tool for source tracking:A review of early findings and future applications. Rev. Environ. Contam. Toxicol.2010,208:111-160.
[8]. Rayne S, Forest K, Friesen K J. Congener-specific numbering systems for the environmentally relevant C4 through C8 perfluorinated homologue groups of alkyl sulfonates, carboxylates, telomer alcohols, olefins, and acids, and their derivatives. J Environ Sci Health A Tox Hazard Subst Environ Eng.2008,43:1391-1401.
[9]. Paul A G, Jones K C, Sweetman A J. A first global production, emission, and environmental inventory for perfluorooctane sulfonate. Environ. Sci. Technol.2009,43:386-392.
[10].3M C. Phase-out plan for posf-based products, specialty materials markets group, US epa administrative, record docket ar 226-0600, U.S. Environmental Protection Agency, Washington, DC,2000.
[11]. Xie S, Wang T, Liu S, et al. Industrial source identification and emission estimation of perfluorooctane sulfonate in China. Environ. Int.2013,52:1-8.
[12]. Trier X, Granby K, Christensen J H. Polyfluorinated surfactants (PFS) in paper and board coatings for food packaging. Environ Sci Pollut Res.2011,18:1108-1120.
[13]. Lau C, Anitole K, Hodes C, et al. Perfluoroalkyl acids:A review of monitoring and toxicological findings. Toxicol. Sci.2007,99:366-394.
[14]. Wang B, Huang J, Deng S, et al. Addressing the environmental risk of persistent organic pollutants in China. Front Environ Sci Engin China.2012,6:2-16.
[15]. Reagen W K, Lindstrom K R, Jacoby C B, et al. Environmental characterization of 3M electrochemical fluorination derived perfluorooctanoate and perfluorooctanesulfonate. Society of environmental toxicology and chemistry 28th North American meeting, Milwaukee, WI, USA.2007,11-15 Nov.
[16]. Benskin J P, Bataineh M, Martin J W. Simultaneous characterization of perfluoroalkyl carboxylate, sulfonate, and sulfonamide isomers by liquid chromatography-tandem mass spectrometry. Anal. Chem.2007,79:6455-6464.
[17]. Taves D. Evidence that there are two forms of fluoride in human serum. Nature.1968,217: 1050-1051.
[18].3M C. Fluorochemical isomer distribution by 19F NMR spectroscopy. US EPA Public Docket AR-226-0564.1997.
[19]. Bastos J K, Freitas L A P, Pagliarussi R S, et al. A rapid quantitative method for the analysis of sulfluramid and its isomers in ant bait by capillary column gas chromatography. J. Sep. Sci. 2001,24:406-410.
[20]. Stevenson L A. U.S. Environmental Protection Agency Public Docket AR-2261150: Comparative analysis of fluorochemicals in human serum samples obtained commercially. U.S. Environmental Protection Agency, Office of Pollution Prevention and Toxic Substances, Washington, DC.2002.
[21]. De Silva A O, Mabury S A. Isolating isomers of perfluorocarboxylates in polar bears (Ursus maritimus) from two geographical locations. Environ. Sci. Technol.2004,38: 6538-6545.
[22], Chu S, Letcher R. Linear and branched perfluorooctane sulfonate isomers in technical product and environmental samples by in-port derivatization-gas chromatography-mass spectrometry. Anal. Chem.2009,81:4256-4262.
[23]. Langlois I, Oehme M. Structural identification of isomers present in technical perfluorooctane sulfonate by tandem mass spectrometry. Rapid Commun. Mass Spectrom. 2006,20:844-850.
[24]. Benskin J P, Ikonomou M G, Woudneh M B, et al. Rapid characterization of perfluoralkyl carboxylate, sulfonate, and sulfonamide isomers by high-performance liquid chromatography-tandem mass spectrometry.J. Chromatogr. A.2012,1247:165-70.
[25]. Riddell N, Arsenault G, Benskin J P, et al. Branched perfluorooctane sulfonate isomer quantification and characterization in blood serum samples by HPLC/ESI-MS(/MS). Environ. Sci. Technol.2009,43:7902-7908.
[26]. Benskin J P, Yeung L W Y, Yamashita N, et al. Perfluorinated acid isomer profiling in water and quantitative assessment of manufacturing source. Environ. Sci. Technol.2010,44: 9049-9054.
[27]. Kestner T. U.S. Environmental Protection Agency Public Docket AR226-0564: Fluorochemical isomer distribution by F-NMR spectroscopy. U.S. Environmental Protection Agency, Office of Pollution Prevention and Toxic Substances, Washington, DC. 1997.
[28]. Arsenault G, Chittim B, McAlees A, et al. Some issues relating to the use of perfluorooctanesulfonate (PFOS) samples as reference standards. Chemosphere.2008,70: 616-625.
[29]. De Silva A O, Mabury S A. Isomer distribution of perfluorocarboxylates in human blood: Potential correlation to source. Environ. Sci. Technol.2006,40:2903-2909.
[30]. De Silva A O, Muir D C G, Mabury S A. Distribution of perfluorocarboxylate isomers in select samples from the North American environment. Environ. Toxicol. Chem.2009,28: 1801-1814.
[31]. De Silva A O, Benskin J P, Martin L J, et al. Disposition of perfluorinated acid isomers in Sprague-Dawley rats; part 2:Subchronic dose. Environ. Toxicol. Chem.2009,28:555-567.
[32]. De Silva A 0, Tseng P J, Mabury S A. Toxicokinetics of perfluorocarboxylate isomers in rainbow trout. Environ. Toxicol. Chem.2009,28:330-337.
[33]. Langlois I, Berger U, Zencak Z, et al. Mass spectral studies of perfluorooctane sulfonate derivatives separated by high-resolution gas chromatography. Rapid Commun. Mass Spectrom.2007,21:3547-3553.
[34]. O'Brien J M, Kennedy S W, Chu S, et al. Isomer-specific accumulation of perfluorooctane sulfonate in the liver of chicken embryos exposed in ovo to a technical mixture. Environ. Toxicol. Chem.2010,30:226-231.
[35]. Langlois I. Mass spectrometric isomer characterization of perfluorinated compounds in technical mixture, water and human blood. PhD Thesis, Department of Chemistry, University of Basel, Switzerland.2006.
[36]. Karrman A, Langlois I, van Bavel B, et al. Identification and pattern of perfluorooctane sulfonate (PFOS) isomers in human serum and plasma. Environ. Int.2007,33:782-788.
[37]. Furdui V, Helm P, Crozier P, et al. Temporal trends of perfluoroalkyl compounds with isomer analysis in lake trout from Lake Ontario (1979-2004). Environ. Sci. Technol.2008, 42:4739-4744.
[38]. Beesoon S, Webster G M, Shoeib M, et al. Isomer profiles of perfluorochemicals in matched maternal, cord, and house dust samples:Manufacturing sources and transplacental transfer. Environ. Health Perspect.2011,119:1659-1664.
[39]. Benskin J P, De Silva A O, Martin L J, et al. Disposition of perfluorinated acid isomers in Sprague-Dawley rats; part 1:Single dose. Environ. Toxicol. Chem.2009,28:542-554.
[40]. Benskin J P, Holt A, Martin J W. Isomer-specific biotransformation rates of a perfluorooctane sulfonate (PFOS)-precursor by cytochrome P450 isozymes and human liver microsomes. Environ. Sci. Technol.2009,43:8566-8572.
[41]. Ross M S, Wong C S, Martin J W. Isomer-specific biotransformation of perfluorooctane sulfonamide in Sprague-Dawley rats. Environ. Sci. Technol.2012,46:3196-3203.
[42]. Benskin J, Yeung L, Yamashita N, et al. Perfluorinated acid isomer profiling in water and quantitative assessment of manufacturing source. Environ. Sci. Technol.2010,44: 9049-9054.
[43]. Benskin J P, Ahrens L, Muir D C G, et al. Manufacturing origin of perfluorooctanoate (PFOA) in Atlantic and Canadian Arctic seawater. Environ. Sci. Technol.2011,46: 677-685.
[44]. Benskin J P, Phillips V, St. Louis V L, et al. Source elucidation of perfluorinated carboxylic acids in remote alpine lake sediment cores. Environ. Sci. Technol.2011,45: 7188-7194.
[45]. Loveless S E, Finlay C, Everds N E, et al. Comparative responses of rats and mice exposed to linear/branched, linear, or branched ammonium perfluorooctanoate (APFO). Toxicology. 2006,220:203-217.
[46]. White S, Kato K, Jia L, et al. Effects of perfluorooctanoic acid on mouse mammary gland development and differentiation resulting from cross-foster and restricted gestational exposures. Reprod. Toxicol.2009,27:289-298.
[47]. Wellington-Lab. Certificate of analysis/documentation for TPFOA. Obtained Jun 2011 from Wellington laboratories, Guelph, ON, Canada.2011.
[48]. Vyas S M, Kania-Korwel I, Lehmler H-J. Differences in the isomer composition of perfluoroctanesulfonyl (PFOS) derivatives. J Environ Sci Health A Tox Hazard Subst Environ Eng.2007,42:249-255.
[49]. Wellington-Lab. Certificate of analysis/documentation for br-PFOSK. Obtained Dec 2010 from Wellington laboratories, Guelph, ON, Canada.2008.
[50]. Korkowski P, Kestner T. Chemical characterization of FOSA & PFOSA samples by 1H and 19F NMR spectroscopy. Provided by 3M co.1999.
[51]. Olsen G W, Hansen K J, Stevenson L A, et al. Human donor liver and serum concentrations of perfluorooctanesulfonate and other perfluorochemicals. Environ. Sci. Technol. 2003,37:888-891.
[52]. Kannan K, Corsolini S, Falandysz J, et al. Perfluorooctanesulfonate and related fluorochemicals in human blood from several countries. Environ. Sci. Technol.2004,38: 4489-4495.
[53]. Yeung L W Y, So M, Jiang G, et al. Perfluorooctanesulfonate and related fluorochemicals in human blood samples from China. Environ. Sci. Technol.2006,40:715-720.
[54]. Olsen G W, Lange C C, Ellefson M E, et al. Temporal trends of perfluoroalkyl concentrations in American Red Cross adult blood donors,2000-2010. Environ. Sci. Technol.2012,46:6330-6338.
[55]. Zhang T, Sun H, Lin Y, et al. Perfluorinated compounds in human blood, water, edible freshwater fish and seafood in China:Daily intake and regional differences in human exposures. J. Agric. Food. Chem.2011,59:11168-11176.
[56]. Zhang T, Wu Q, Sun H, et al. Perfluorinated compounds in whole blood samples from infants, children, and adults in China. Environ. Sci. Technol.2010,44:4341-4347.
[57]. Zhang W, Lin Z, Hu M, et al. Perfluorinated chemicals in blood of residents in Wenzhou, China. Ecotoxicol. Environ. Saf.2011,74:1787-1793.
[58]. Guo F, Zhong Y, Wang Y, et al. Perfluorinated compounds in human blood around Bohai Sea, China. Chemosphere.2011,85:156-162.
[59]. Liu J, Li J, Luan Y, et al. Geographical distribution of perfluorinated compounds in human blood from Liaoning province, China. Environ. Sci. Technol.2009,43:4044-4048.
[60]. Pan Y, Shi Y, Wang J, et al. Concentrations of perfluorinated compounds in human blood from twelve cities in China. Environ. Toxicol. Chem.2010,29:2695-2701.
[61]. Yeung L W Y, Miyake Y, Taniyasu S, et al. Perfluorinated compounds and total and extractable organic fluorine in human blood samples from China. Environ. Sci. Technol. 2008,42:8140-8145.
[62]. Jin Y, Saito N, Harada K, et al. Historical trends in human serum levels of perfluorooctanoate and perfluorooctane sulfonate in Shenyang, China. Tohoku J. Exp. Med. 2007,212:63-70.
[63]. Olsen G W, Huang H Y, Helzlsouer K J, et al. Historical comparison of perfluorooctanesulfonate, perfluorooctanoate, and other fluorochemicals in human blood. Environ. Health Perspect.2005,113:539-545.
[64]. Kato K, Wong L-Y, Jia L T, et al. Trends in exposure to polyfluoroalkyl chemicals in the U.S. Population:1999-2008. Environ. Sci. Technol.2011,45:8037-8045.
[65]. Karrman A, Mueller J, van Bavel B, et al. Levels of 12 perfluorinated chemicals in pooled Australian serum, collected 2002-2003, in relation to age, gender, and region. Environ. Sci. Technol.2006,40:3742-3748.
[66]. Toms L, Calafat A, Kato K, et al. Polyfluoroalkyl chemicals in pooled blood serum from infants, children, and adults in Australia. Environ. Sci. Technol.2009,43:4194-4199.
[67]. Ingelido A, Marra V, Abballe A, et al. Perfluorooctanesulfonate and perfluorooctanoic acid exposures of the italian general population. Chemosphere.2010,80:1125-1130.
[68]. Lindh C H, Rylander L, Toft G, et al. Blood serum concentrations of perfluorinated compounds in men from Greenlandic Inuit and European populations. Chemosphere.2012, 88:1269-75.
[69], Kubwabo C, Vais N, Benoit F. A pilot study on the determination of perfluorooctanesulfonate and other perfluorinated compounds in blood of Canadians. J. Environ. Monit.2004,6:540-545.
[70]. Harada K, Yang H, Moon C, et al. Levels of perfluorooctane sulfonate and perfluorooctanoic acid in female serum samples from Japan in 2008, Korea in 1994-2008 and Vietnam in 2007-2008. Chemosphere.2010,79:314-319.
[71]. Harada K, Koizumi A, Saito N, et al. Historical and geographical aspects of the increasing perfluorooctanoate and perfluorooctane sulfonate contamination in human serum in Japan. Chemosphere.2007,66:293-301.
[72]. Karrman A, van Bavel B, J rnberg U, et al. Perfluorinated chemicals in relation to other persistent organic pollutants in human blood. Chemosphere.2006,64:1582-1591.
[73]. Karrman A, Ericson I, Van Bavel B, et al. Exposure of perfluorinated chemicals through lactation:Levels of matched human milk and serum and a temporal trend,1996-2004, in Sweden. Environ. Health Perspect.2007,115:226-230.
[74]. Midasch O, Schettgen T, Angerer J. Pilot study on the perfluorooctanesulfonate and perfluorooctanoate exposure of the German general population. Int. J. Hyg. Environ. Health. 2006,209:489-496.
[75]. Fromme H, Midasch O, Twardella D, et al. Occurrence of perfluorinated substances in an adult German population in southern Bavaria. Int. Arch. Occup. Environ. Health.2007,80: 313-319.
[76]. Ericson I, Gomez M, Nadal M, et al. Perfluorinated chemicals in blood of residents in Catalonia (Spain) in relation to age and gender:A pilot study. Environ. Int.2007,33: 616-623.
[77]. Fei C, McLaughlin J K, Tarone R E, et al. Perfluorinated chemicals and fetal growth:A study within the Danish National Birth Cohort. Environ. Health Perspect.2007,115: 1677-1682.
[78]. Eriksen K, Sorensen M, McLaughlin J, et al. Perfluorooctanoate and perfluorooctanesulfonate plasma levels and risk of cancer in the general Danish population. J. Natl Cancer Inst.2009,101:605-609.
[79]. Monroy R, Morrison K, Teo K, et al. Serum levels of perfluoroalkyl compounds in human maternal and umbilical cord blood samples. Environ. Res.2008,108:56-62.
[80]. Rylander C, Brustad M, Falk H, et al. Dietary predictors and plasma concentrations of perfluorinated compounds in a coastal population from Northern Norway. J. Environ. Pub. Health.2009, doi:10.1155/2009/268219.
[81]. Hemat H, Wilhelm M, V lkel W, et al. Low serum levels of perfluorooctanoic acid (PFOA), perfluorooctane sulfonate (PFOS) and perfluorohexane sulfonate (PFHxS) in children and adults from Afghanistan. Sci. Total Environ.2010,408:3493-3495.
[82]. Olsen G W, Burris J M, Ehresman D J, et al. Half-life of serum elimination of perfluorooctanesulfonate, perfluorohexanesulfonate, and perfluorooctanoate in retired fluorochemical production workers. Environ. Health Perspect.2007,115:1298-1305.
[83]. Hanssen L, Roellin H, Odland J O, et al. Perfluorinated compounds in maternal serum and cord blood from selected areas of South Africa:Results of a pilot study. J. Environ. Monit. 2010,12:1355-1361.
[84]. Rylander C, Duong Trong P, Odland J O, et al. Perfluorinated compounds in delivering women from south central Vietnam. J. Environ. Monit.2009,11:2002-2008.
[85]. Haug L S, Huber S, Becher G, et al. Characterisation of human exposure pathways to perfluorinated compounds-comparing exposure estimates with biomarkers of exposure. Environ. Int.2011,37:687-693.
[86]. Thomsen C, Haug L S, Stigum H, et al. Changes in concentrations of perfluorinated compounds, polybrominated biphenyl ethers, and polychlorinated biphenyls in Norwegian breast-milk during twelve months of lactation. Environ. Sci. Technol.2010,44:9550-9556.
[87]. Haug L S, Thomsen C, Bechert G. Time trends and the influence of age and gender on serum concentrations of perfluorinated compounds in archived human samples. Environ. Sci. Technol.2009,43:2131-2136.
[88]. Kudo N, Katakura M, Sato Y, et al. Sex hormone-regulated renal transport of perfluorooctanoic acid. Chem. Biol. Interact.2002,139:301-316.
[89]. Butenhoff J L, Kennedy G L, Hinderliter P M, et al. Phannacokinetics of perfluorooctanoate in cynomolgus monkeys. Toxicol. Sci.2004,82:394-406.
[90]. Harada K, Inoue K, Morikawa A, et al. Renal clearance of perfluorooctane sulfonate and perfluorooctanoate in humans and their species-specific excretion. Environ. Res.2005,99: 253-261.
[91]. Perez F, Llorca M, Farre M, et al. Automated analysis of perfluorinated compounds in human hair and urine samples by turbulent flow chromatography coupled to tandem mass spectrometry. Anal. Bioanal. Chem.2012,402:2369-2378.
[92]. Beesoon S, Genuis S J, Benskin J P, et al. Exceptionally high serum concentrations of perfluorohexanesulfonate in a Canadian family are linked to home carpet treatment applications. Environ. Sci. Technol.2012,46:12960-12967.
[93]. Li J, Guo F, Wang Y, et al. Development of extraction methods for the analysis of perfluorinated compounds in human hair and nail by high performance liquid chromatography tandem mass spectrometry. J. Chromatogr. A.2012,1219:54-60.
[94]. Liu W, Xu L, Li X, et al. Human nails analysis as biomarker of exposure to perfluoroalkyl compounds. Environ. Sci. Technol.2011,45:8144-8150.
[95].姚丹,张鸿,柴之芳,等.天津成人头发指甲中有机氟污染物的残留特征.环境科学.2013,718-723.
[96]. Stein C R, Wolff M S, Calafat A M, et al. Comparison of polyfluoroalkyl compound concentrations in maternal serum and amniotic fluid:A pilot study. Reprod. Toxicol.2012, 34:312-316.
[97]. Tittlemier S, Ryan J, Van Oostdam J. Presence of anionic organic compounds in serum collected from northern Canadian populations. Organohalogen Compd.2004,66: 4009-4014.
[98]. Inoue K, Okada F, Ito R, et al. Perfluorooctane sulfonate (PFOS) and related perfluorinated compounds in human maternal and cord blood samples:Assessment of PFOS exposure in a susceptible population during pregnancy. Environ. Health Perspect.2004,112:1204-1207.
[99]. Apelberg B, Goldman L, Calafat A, et al. Determinants of fetal exposure to polyfluoroalkyl compounds in Baltimore, Maryland. Environ. Sci. Technol.2007,41:3891-3897.
[100]. Liu J, Li J, Zhao Y, et al. The occurrence of perfluorinated alkyl compounds in human milk from different regions of China. Environ. Int.2010,36:433-438.
[101]. Karrman A, Domingo J, Llebaria X, et al. Biomonitoring perfluorinated compounds in Catalonia, Spain:Concentrations and trends in human liver and milk samples. Environ Sci Pollut Res.2010,17:750-758.
[102]. Tao L, Ma J, Kunisue T, et al. Perfluorinated compounds in human breast milk from several Asian countries, and in infant formula and dairy milk from the United States. Environ. Sci. Technol.2008,42:8597-8602.
[103]. Tao L, Kannan K, Wong C, et al. Perfluorinated compounds in human milk from Massachusetts, USA. Environ. Sci. Technol.2008,42:3096-3101.
[104]. So M, Yamashita N, Taniyasu S, et al. Health risks in infants associated with exposure to perfluorinated compounds in human breast milk from Zhoushan, China. Environ. Sci. Technol.2006,40:2924-2929.
[105]. Voelkel W, Genzel-Boroviczeny O, Demmelmair H, et al. Perfluorooctane sulphonate (PFOS) and perfluorooctanoic acid (PFOA) in human breast milk:Results of a pilot study. Int. J. Hyg. Environ. Health.2008,211:440-446.
[106]. Kim S K, Lee K T, Kang C S, et al. Distribution of perfluorochemicals between sera and milk from the same mothers and implications for prenatal and postnatal exposures. Environ. Pollut.2011,159:169-174.
[107]. Guruge K, Taniyasu S, Yamashita N, et al. Perfluorinated organic compounds in human blood serum and seminal plasma:A study of urban and rural tea worker populations in Sri Lanka. J. Environ. Monit.2005,7:371-377.
[108]. Wang T, Wang Y, Liao C, et al. Perspectives on the inclusion of perfluorooctane sulfonate into the Stockholm Convention on persistent organic pollutants. Environ. Sci. Technol.2009,43:5171-5175.
[109]. Spliethoff H, Tao L, Shaver S, et al. Use of newborn screening program blood spots for exposure assessment:Declining levels of perfluorinated compounds in New York State infants. Environ. Sci. Technol.2008,42:5361-5367.
[110]. Bartell S M, Calafat A M, Lyu C, et al. Rate of decline in serum PFOA concentrations after granular activated carbon filtration at two public water systems in Ohio and West Virginia. Environ. Health Perspect.2010,118:222-228.
[111]. Steenland K, Fletcher T, Savitz D A. Epidemiologic evidence on the health effects of perfluorooctanoic acid (PFOA). Environ. Health Perspect.2010,118:1100-1108.
[112]. Joensen U N, Bossi R, Leffers H, et al. Do perfluoroalkyl compounds impair human semen quality? Environ. Health Perspect.2009,117:923-927.
[113]. Stein C R, Savitz D A, Dougan M. Serum'levels of perfluorooctanoic acid and perfluorooctane sulfonate and pregnancy outcome. Am. J. Epidemiol.2009,170:837-846.
[114]. Maisonet M, Terrell M L, McGeehin M A, et al. Maternal concentrations of polyfluoroalkyl compounds during pregnancy and fetal and postnatal growth in British girls. Environ. Health Perspect.2012,120:1432-7.
[115]. Apelberg B, Witter F, Herbstman J, et al. Cord serum concentrations of perfluorooctane sulfonate (PFOS) and perfluorooctanoate (PFOA) in relation to weight and size at birth. Environ. Health Perspect.2007,115:1670-1676.
[116]. Chen M-H, Ha E-H, Wen T-W, et al. Perfluorinated compounds in umbilical cord blood and adverse birth outcomes. Plos One.2012,7.
[117]. Lopez-Espinosa M-J, Mondal D, Armstrong B, et al. Thyroid function and perfluoroalkyl acids in children living near a chemical plant. Environ. Health Perspect.2012,120: 1036-1041.
[118]. Grandjean P, Andersen E W, Budtz-Jorgensen E, et al. Serum vaccine antibody concentrations in children exposed to perfluorinated compounds. J. Am. Med. Assoc.2012, 307:391-397.
[119]. Gump B B, Wu Q, Dumas A K, et al. Perfluorochemical (PFC) exposure in children: Associations with impaired response inhibition. Environ. Sci. Technol.2011,45: 8151-8159.
[120]. Lopez-Espinosa M-J, Fletcher T, Armstrong B, et al. Association of perfluorooctanoic acid (PFOA) and perfluorooctane sulfonate (PFOS) with age of puberty among children living near a chemical plant. Environ. Sci. Technol.2011,45:8160-8166.
[121]. Hoffman K, Webster T F, Weisskopf M G, et al. Exposure to polyfluoroalkyl chemicals and attention deficit/hyperactivity disorder in US children 12-15 years of age. Environ. Health Perspect.2010,118:1762-1767.
[122]. Halldorsson T I, Rytter D, Haug L S, et al. Prenatal exposure to perfluorooctanoate and risk of overweight at 20 years of age:A prospective cohort study. Environ. Health Perspect.2012,120:668-73.
[123]. Shankar A, Xiao J, Ducatman A. Perfluoroalkyl chemicals and chronic kidney disease in US adults. Am. J. Epidemiol.2011,174:893-900.
[124]. Steenland K, Tinker S, Shankar A, et al. Association of perfluorooctanoic acid (PFOA) and perfluorooctane sulfonate (PFOS) with uric acid among adults with elevated community exposure to PFOA. Environ. Health Perspect.2010,.118:229-233.
[125]. La Rocca C, Alessi E, Bergamasco B, et al. Exposure and effective dose biomarkers for perfluorooctane sulfonic acid (PFOS) and perfluorooctanoic acid (PFOA) in infertile subjects:Preliminary results of the PREVIENI project. Int. J. Hyg. Environ. Health.2012, 215:206-211.
[126]. Melzer D, Rice N, Depledge M H, et al. Association between serum perfluorooctanoic acid (PFOA) and thyroid disease in the US National Health and Nutrition Examination Survey. Environ. Health Perspect.2010,118:686-692.
[127]. Lin C-Y, Lin L-Y, Chiang C-K, et al. Investigation of the associations between low-dose serum perfluorinated chemicals and liver enzymes in US adults. Am. J. Gastroenterol. 2010,105:1354-1363.
[128]. Fei C, McLaughlin J K, Lipworth L, et al. Maternal levels of perfluorinated chemicals and subfecundity. Hum. Reprod.2009,24:1200-1205.
[129]. Steenland K, Tinker S, Frisbee S, et al. Association of perfluorooctanoic acid and perfluorooctane sulfonate with serum lipids among adults living near a chemical plant. Am. J. Epidemiol.2009,170:1268-1278.
[130]. Vanden Heuvel J P, Thompson J T, Frame S R, et al. Differential activation of nuclear receptors by perfluorinated fatty acid analogs and natural fatty acids:A comparison of human, mouse, and rat peroxisome proliferator-activated receptor-alpha,-beta, and-gamma, liver x receptor-beta, and retinoid x receptor-alpha. Toxicol. Sci.2006,92: 476-489.
[131]. O'Brien J M, Austin A J, Williams A, et al. Technical-grade perfluorooctane sulfonate alters the expression of more transcripts in cultured chicken embryonic hepatocytes than linear perfluorooctane sulfonate. Environ. Toxicol. Chem.2011,30:2846-2859.
[132]. Kuklenyik Z, Reich J A, Tully J S, et al. Automated solid-phase extraction and measurement of perfluorinated organic acids and amides in human serum and milk. Environ. Sci. Technol.2004,38:3698-3704.
[133]. Hansen K J, Clemen L A, Ellefson M E, et al. Compound-specific, quantitative characterization of organic:Fluorochemicals in biological matrices. Environ. Sci. Technol. 2001,35:766-770.
[134].吴茵.棉纺织业与城市化进程：1921-1990年——以石家庄市为例.经济与管理2010,70-73.
[135]. Calafat A M, Wong L-Y, Kuklenyik Z, et al. Polyfluoroalkyl chemicals in the US population:Data from the National Health and Nutrition Examination Survey (NHANES) 2003-2004 and comparisons with NHANES 1999-2000. Environ. Health Perspect.2007, 115:1596-1602.
[136]. Wang M, Park J-S, Petreas M. Temporal changes in the levels of perfluorinated compounds in California women's serum over the past 50 years. Environ. Sci. Technol. 2011,45:7510-7516.
[137]. Domingo J L. Health risks of dietary exposure to perfluorinated compounds. Environ. Int. 2012,40:187-195.
[138]. Zhang T, Sun H, Wu Q, et al. Perfluorochemicals in meat, eggs and indoor dust in China: Assessment of sources and pathways of human exposure to perfluorochemicals. Environ. Sci. Technol.2010,44:3572-3579.
[139]. Kannan K, Corsolini S, Falandysz J, et al. Perfluorooctanesulfonate and related fluorochemicals in human blood from several countries. Environ. Sci. Technol.2004,38: 4489-4495.
[140]. Fromme H, Mosch C, Morovitz M, et al. Pre-and postnatal exposure to perfluorinated compounds (PFCs). Environ. Sci. Technol.2010,44:7123-7129.
[141]. Wang Y, Beesoon S, Benskin J P, et al. Enantiomer fractions of chiral perfluorooctanesulfonate (PFOS) in human sera. Environ. Sci. Technol.2011,45: 8907-8914.
[142]. Vestergren R, Cousins I T, Trudel D, et al. Estimating the contribution of precursor compounds in consumer exposure to PFOS and PFOA. Chemosphere.2008,73: 1617-1624.
[143]. Haug L S, Huber S, Schlabach M, et al. Investigation on per-and polyfluorinated compounds in paired samples of house dust and indoor air from Norwegian homes. Environ. Sci. Technol. 2011,45:7991-7998.
[144], Seals R, Bartell S M, Steenland K. Accumulation and clearance of perfluorooctanoic acid (PFOA) in current and former residents of an exposed community. Environ. Health Perspect.2011,119:119-124.
[145]. Sharpe R L, Benskin J P, Laarman A H, et al. Perfluorooctane sulfonate toxicity, isomer-specific accumulation, and maternal transfer in zebrafish (Danio rerio) and rainbow trout (Oncorhynchus mykiss). Environ. Toxicol. Chem.2010,29:1957-1966.
[146]. Cui L, Liao C, Zhou Q, et al. Excretion of PFOA and PFOS in male rats during a subchronic exposure. Arch. Environ. Contam. Toxicol.2010,58:205-213.
[147], Ubel F A, Sorenson S D, Roach D E. Health status of plant workers exposed to fluorochemicals--a preliminary report. Am. Ind. Hyg. Assoc. J.1980,41:584-9.
[148]. Li J, Guo F, Wang Y, et al. Can nail, hair and urine be used for biomonitoring of human exposure to perfluorooctane sulfonate and perfluorooctanoic acid? Environ. Int.2013,53: 47-52.
[149]. Jaffe M. Ueber den niederschlag welchen pikrinsaure in normalen harn erzeugt und uber eine neue reaction des kreatinins [in German]. Z Physiol Chem.1886,10:391-400.
[150]. Borghi L, Meschi T, Amato F, et al. Urinary volume, water and recurrences in idiopathic calcium nephrolithiasis:A 5-year randomized prospective study. J. Urol.1996,155: 839-843.
[151]. Walser M. Creatinine excretion as a measure of protein nutrition in adults of varying age. JPEN. J. Parenter. Enteral Nutr.1987,11:73S-78S.
[152]. Thompson J, Lorber M, Toms L-M L, et al. Use of simple pharmacokinetic modeling to characterize exposure of Australians to perfluorooctanoic acid and perfluorooctane sulfonic acid. Environ. Int.2010,36:390-397.
[153]. Ohmori K, Kudo N, Katayama K, et al. Comparison of the toxicokinetics between perfluorocarboxylic acids with different carbon chain length. Toxicology.2003,184: 135-140.
[154]. Gao J, Zeng S, Sun B L, et al. Menstrual blood loss and hematologic indices in healthy Chinese women. J. Reprod. Med.1987,32:822-826.
[155]. Ge M, Yan Y, Zhang C, et al. Discussion on the relationship between normal hematocrit and geographical factors in China. Clin. Hemorheol. Microcirc.1997,17:459-465.
[156]. Hanssen L, Dudarev A A, Huber S, et al. Partition of perfluoroalkyl substances (PFASs) in whole blood and plasma, assessed in maternal and umbilical cord samples from inhabitants of arctic Russia and Uzbekistan. Sci. Total Environ.2013,447:430-7.
[157]. Kudo N, Suzuki E, Katakura M, et al. Comparison of the elimination between perfluorinated fatty acids with different carbon chain length in rats. Chem. Biol. Interact. 2001,134:203-216.
[158]. Bhhatarai B, Gramatica P. Prediction of aqueous solubility, vapor pressure and critical micelle concentration for aquatic partitioning of perfluorinated chemicals. Environ. Sci. Technol.2011,45:8120-8128.
[159]. Martin J W, Asher B J, Beesoon S, et al. PFOS or PreFOS? Are perfluorooctane sulfonate precursors (PreFOS) important determinants of human and environmental perfluorooctane sulfonate (PFOS) exposure?J. Environ. Monit.2010,12:1979-2004.
[160]. Taniyasu S, Kannan K, Horii Y, et al. A survey of perfluorooctane sulfonate and related perfluorinated organic compounds in water, fish, birds, and humans from Japan. Environ. Sci. Technol.2003,37:2634-2639.
[161]. Ehresman D J, Froehlich J W, Olsen G W, et al. Comparison of human whole blood, plasma, and serum matrices for the determination of perfluorooctanesulfonate (PFOS), perfluorooctanoate (PFOA), and other fluorochemicals. Environ. Res.2007,103:176-184.
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