全氟辛烷磺酰基化合物(PFOS)类有机污染物在生物体中的污染现状

以全氟辛烷磺酰基化合物(Perfluorooctanesulphonate,PFOS)为代表的全氟化合物是一类新型持久性环境污染物,因在生产生活中的广泛使用而长期存在于环境中,目前已成为一种全球性污染物.近年来对PFOS等物质的污染检测已经从水土环境转向了生物有机体,在鸟类、鱼类、海洋动物、哺乳动物、人类等各个层次上的生物均已开始了广泛的检测分析.北美、欧洲、日本、中国等国是受此类物质污染程度较高并且研究报道较多的区域.论文总结了PFOS在上述地区不同生物体和不同人群的污染现状及暴露水平,为全面了解并控制PFOS污染提供了基础依据.     

全氟辛烷磺酸盐(PFOS)对其它有机污染物在沉积物上吸附的影响

采用平衡振荡实验方法,研究了不同浓度的全氟辛烷磺酸盐(PFOS)对两种有机污染物(硝基苯和菲)在沉积物上吸附的影响.结果表明,单组分PFOS在沉积物上是非线性吸附;与其它有机污染物共存时,随着PFOS浓度的升高,硝基苯的吸附量先减少后增加,而菲的吸附量则先增加后减少.PFOS对其它有机污染物吸附的影响规律与有机污染物的...     

全氟辛酸和全氟辛基磺酸的光降解技术及机理研究进展

目前,普遍存在于各种环境介质中的全氟辛酸(PFOA)和全氟辛基磺酸(PFOS)造成的环境污染问题已引起全球的广泛关注.PFOA和PFOS具有稳定性、持久性和生物累积性等特点.常规的方法如:超声降解法、电化学氧化法和微生物降解法等,很难将其彻底降解,因此开发有效的PFOA和PFOS降解技术成为了环境领域的研究重点.近年来...     

PFOS对星形胶质细胞表观遗传调控作用初探

脑源性神经营养因子(BDNF)甲基化在全氟辛烷磺酸(PFOS)神经毒性中的作用已证实,但表观遗传修饰中其他调控因子在PFOS对星形胶质细胞毒性中的影响仍有待探索。本文以大鼠原代星形胶质细胞为体外生物体系,建立24 h PFOS(0、25、50和100μmol·L~(-1))暴露模型,通过观察PFOS暴露对星形胶质细胞表观遗传调控主要分子DNA甲基化酶(DNMTs)、组蛋白去乙酰化酶(HDACs)和小泛素化修饰物(SUMOs)的影响,初步明确表观遗传调控机制参与PFOS神经毒性作用。采用Hoechst 33258检测细胞凋亡,利用ELISA试剂盒检测HDACs含量,以实时荧光定量PCR考察DNMTs、HDACs和SUMOs基因表达。结果显示,星形胶质细胞暴露于一定浓度PFOS(≥25μmol·L~(-1))时产生凋亡现象(P0.05),HDACs含量升高(P0.05),且DNMT1、HDAC1/2/4与SUMO-1的基因表达显著升高(P0.05);而当PFOS浓度高于50μmol·L~(-1)时,可显著诱导DNMT3A、SUMO-2的基因表达(P0.05); DNMT3B在PFOS≥25μmol·L~(-1)时,其基因表达具有升高趋势,但不具统计学显著性(P0.05)。结果表明,PFOS可以影响星形胶质细胞的表观遗传修饰;表观遗传修饰可能是PFOS神经毒性作用机制之一。     

维生素B12催化纳米零价铁仿生降解全氟辛磺酸

研究了维生素B₁₂（VB₁₂）催化纳米零价铁（nFe⁰）仿生还原降解工业级全氟辛磺酸（PFOS）.结果表明,VB₁₂催化nFe⁰不仅能够降解支链PFOS,而且也能够同时降解直链PFOS,这是首次报道直链PFOS的仿生还原降解.PFOS降解过程可用准一级动力学模型模拟,且升高温度有利于PFOS的还原降解去除和脱氟.超高效液相色谱-四级杆飞行时间质谱（UPLC-QTOF）定性分析表明,PFOS仿生降解产物包括4种全氟磺酸类（全氟碳链长度为C4~C7）、9种全氟羧酸类（全氟碳链长度为C2~C7、C10、C11和C13）和5种多氟代酸类（即H-全氟己酸、H-全氟庚酸、H-全氟辛酸、H₂-全氟辛酸和H-全氟辛磺酸）化合物.全氟磺酸类和全氟羧酸类化合物首次在VB₁₂仿生催化降解PFOS的产物之中检出,其中全氟十一烷酸（C10）、全氟十二烷酸（C11）和全氟十四烷酸（C13）等长链化合物第一次在降解PFOS过程中被发现.在降解样中检出的H-全氟烷烃（链长为C2~C7、C10、C11和C13）是否是PFOS的仿生降解产物,还有待进一步研究确认.     

Preparation, characterization and performance of poly(m-phenylene isophthalamide)/organically modified montmorillonite nanocomposite membranes in removal of perfluorooctane sulfonate

Nanocomposite membranes containing poly(m-phenylene isophthalamide) (PMIA) and organically modified montmorillonite (OMMT) were prepared by a combination of solution dispersion and wet-phase inversion methods, and the effects of OMMT addition on the properties and performance of fabricated nanofiltration membranes were investigated. The membranes were characterized by contact angle measurements, scanning electron microscopy (SEM), atomic force microscopy (AFM), thermogravimetric analysis, and zeta potential. The performance of the membranes was elucidated by the removal of perfluorooctane sulfonate (PFOS) at neutral pH. Increasing OMMT concentration improved the thermal stability and hydrophilicity of the membranes. The permeation and rejection of PFOS were significantly improved. The performance of fabricated nanofiltration membranes in removal of PFOS varied depending on the solute and membrane properties as well as solution conditions. Finally, a comparison between fabricated membranes and a commercial NF membrane (ESNA1-K1, Hydecanme) proved that the OMMT addition is a convenient procedure for producing nanocomposite membranes with superior properties and performance.     

Dietary exposure of rainbow trout to 8:2 and 10:2 fluorotelomer alcohols and perfluorooctanesulfonamide: Uptake, transformation and elimination

The bioaccumulation of perfluorooctanesulfonamide (PFOSA) and two fluorotelomer alcohols (8:2 FTOH, 10:2 FTOH) by rainbow trout (Oncorhynchus mykiss) through dietary exposure, including depuration rates and metabolism was investigated. Concentrations in the spiked feed ranged from 10.9 μg g⁻¹ wet weight (wet wt) for PFOSA and 6.7 μg g⁻¹ wet wt for 8:2 FTOH to 5.0 μg g⁻¹ wet wt for 10:2 FTOH. Trout was fed at 1.5% body weight per day for 30 d and depuration was followed for up to 30 d following previously published dietary exposure protocols. Perfluorooctanesulfonate (PFOS) was the major perfluoroalkylsulfonate (PFSA) detected in fish following dietary exposure to PFOSA. Half-lives of PFOS and PFOSA were 16.9 ± 2.5 and 6.0 ± 0.4 d, respectively. A biomagnification factor (BMF) of 0.023 was calculated for PFOSA which indicates that dietary exposure to PFOSA does not result in biomagnification in the rainbow trout. PFOS had a BMF of 0.08. The fluorotelomer saturated acids (8:2 FTCA, 10:2 FTCA) and fluorotelomer unsaturated acids (8:2 FTUCA, 10:2 FTUCA) were the major products detected in rainbow trout following dietary exposure to 8:2 FTOH and 10:2 FTOH, respectively. Half-lives were 3.7 ± 0.4, 2.1 ± 0.5, 3.3, and 1.3 d for 10:2 FTCA, 10:2 FTUCA, 8:2 FTCA, and 8:2 FTUCA, respectively. Small amounts of perfluorooctanoate (PFOA) and perfluorodecanoate (PFDA) were also detected in the FTOH exposed fish.     

Spatial distribution and sources of perfluorochemicals in the NW Mediterranean coastal waters (Catalonia, Spain)

This study provides the first evidence of the sources and loads of perfluorochemicals (PFCs) to the NW Mediterranean Sea. Five PFCs were analyzed in 45 seawater samples collected along the Catalan coast. Total PFCs ranged from 0.07 to 13.0 ng/l, being the levels higher in ports than in coastal waters. To determine the sources of PFCs, 8 wastewater treatment plants (WWTPs) effluents and 6 rivers discharging to the sea were also analyzed. WWTP effluents contained total PFCs levels ranging from 3.47 to 132 ng/l but due to the relatively low discharge flows, they contributed to 34.7 g/d to the sea. Total PFCs in rivers ranged from 2.24 to 21.9 ng/l and were the principal PFCs contributors to the sea. Overall, a total load of 190 g/d of PFCs are discharged to the NW Mediterranean coast. The effects and risk of PFCs discharges to the Mediterranean basin are discussed.     

Atmospheric concentrations of PCDD/Fs, dl-PCBs and some pesticides in northern Algeria using passive air sampling

Perfluorooctanesulfonate (PFOS) is the terminal degradation product of many commercially used perfluorinated compounds, and most of the toxicity testing to date has focused on its potential biological effects. While PFOS has been extensively studied, other PFCs including replacement chemicals such as perfluorobutanesulfonate (PFBS) and perfluorobutyric acid (PFBA), have not been well characterized. Despite the relative lack of data available on these other PFCs it has been assumed that they will cause similar or lesser effects than PFOS. This study compared the effects of 10 PFCs routinely found in the environment on mRNA abundance of 7 genes related to processes known to be affected by PFOS, such as fatty acid and cholesterol synthesis, and thyroid development. Rat H4IIE hepatoma cells were exposed and changes in mRNA abundance were quantified by real-time PCR. Significant changes in mRNA abundance were observed. The effects caused by the shorter chain replacement chemicals differed significantly from those caused by PFOS or PFOA. Furthermore, not all of the PFCs caused the same effects, and changes could not simply be attributed to chain-length or functional group. These differences could mean that these replacement chemicals do not act through the same mechanisms as the more studied PFOS and PFOA.