环境中全氟有机物的毒性、检测分析及降解

自全氟有机物广泛使用50多年以来,已经在世界范围内发现一定浓度的全氟有机物,各国研究人员针对该类物质特别是全氟辛酸(PFOA)、全氟辛烷基磺酸(PFOS)进行了一定的研究.介绍了该类物质的污染现状,阐述了全氟有机物的毒性、检测分析技术及降解技术,在此基础上提出了今后的研究方向.     

真空紫外光解SO_3~(2-)高效还原降解全氟辛烷磺酸

为消除全氟辛烷磺酸(PFOS)对环境水体带来的不利影响,采用真空紫外(VUV)光解SO_3~(2-)产生水合电子(e_(aq))还原降解PFOS。结果表明,在溶液初始pH为10.59,PFOS为20.0μmol/L,SO_3~(2-)为10.0mmol/L的条件下,反应180min,PFOS的脱氟率为53.5%,高于相同条件下紫外光解SO_3~(2-)体系(40.2%),通过刃天青探针实验证实与体系e_(aq)的生成量有关。动力学分析表明,PFOS脱氟满足平行指数动力学(PEK)模型,其快反应与慢反应分别对应于PFOS支链与直链异构体的降解。液相色谱—串联质谱(LC—MS/MS)监测发现,PFOS降解主要中间产物为短链全氟羧酸(PFCAs),且全氟丙酸(PFPrA)和全氟丁酸(PFBA)浓度较高,表明PFOS在e_(aq)的进攻下除了直接脱除α位氟原子及发生端基断裂外,还能通过中间碳碳键断裂的方式进行降解。     

去除水中全氟辛基磺酸的纳米吸附剂的制备及性能表征

实验研究了去除水中全氟辛基磺酸(PFOS)的纳米吸附剂的制备方法,并对其性能进行表征.研究结果表明:单体(4-乙烯基吡啶)含量对吸附剂去除PFOS的效果影响显著;而聚合状态、聚合液含水率、有机溶剂和交联剂的种类仅对吸附剂形态和比表面积有一定影响,但对吸附剂去除PFOS的效果影响不大.红外光谱揭示了单体和交联剂的有效聚合,ζ电位的测定则证实了单体和PFOS是由于静电作用而结合.     

碳纳米管催化臭氧降解PFOS动力学与过程控制

针对全氟化合物难降解问题通过碳纳米管(CNT)诱导臭氧高级氧化路径研究非均相催化体系对高稳性全氟辛烷磺酸(PFOS)的降解效能与机制。结果表明:CNT介质可催化臭氧通过C-F断键对PFOS强制氧化分解,其准一级降解常数(A=0.O_37 min~(-1),5 mg·L~(-1)CNT)均高于碱式臭氧处理(A:=0.009 min~(-1),pH=11)以及高负荷活性炭颗粒(A:=0.013 min~(-1)3 g·L~(-1)GAC);溶液pH是控制催化过程的重要因素酸性或碱性环境由于PFOS吸附阻隔均不利于CNT表面与溶解O_3的接触催化反应;结合羟基自由基淬灭实验,推测CNT通过表面石墨层促成·OH大量生成并在固/液界面原位降解PFOS。研究结果可为开发利用CNT介质强化臭氧水处理过程提供科学依据。     

改性膨润土助凝消除水体中全氟辛烷磺酸盐

以十六烷基三甲基溴化铵(CTMAB)微波改性膨润土(CTMAB-膨润土)作为助凝剂,采用聚合氯化铝(PAC)联用CTMAB-膨润土进行强化混凝实验,对水体中全氟辛烷磺酸盐(PFOS)的消除进行研究。结果表明:经微波改性后,CTMAB进入到膨润土层间,增大了膨润土层间距;PAC的最佳投加量为15mg/L;强化混凝最佳pH为6~7;PFOS去除率随原水浊度的增大而增大;在同等条件下CTMAB-膨润土对PFOS去除率整体优于粉末活性炭。     

Fe3O4纳米磁性微粒对全氟辛烷磺酸盐的吸附

采用共沉淀法合成Fe3O4纳米磁性颗粒,用透射电子显微镜(TEM)、X射线衍射仪(XRD)以及振动样品磁强计(VSM)对Fe3O4纳米磁性颗粒的粒径、形貌和磁性进行表征并研究Fe3O4纳米磁性微粒对全氟辛磺酸盐的吸附。结果表明:在PFOS初始浓度4 mg/L,pH为3,反应时间24 h,Fe3O4纳米磁性微粒投加量1.25 g/L,对全氟辛磺酸盐去除率达到90%。Fe3O4纳米磁性微粒对PFOS的吸附符合Freundlich吸附方程。     

全氟辛烷磺酸盐(PFOS)在藻渣/小球藻上的吸附行为及机理

为了开发新型廉价生物吸附剂,以高效吸附去除水体中全氟辛烷磺酸盐(PFOS),对小球藻提取生物柴油后的藻渣吸附酸性水体中的PFOS进行了吸附行为及机理的研究。小球藻提取生物质柴油后,比表面积、孔容、孔径几乎没有变化;等电点由3.3降低至2.7;蛋白质含量由51.45%提高到57.35%。在酸性条件下(pH≤3),小球藻和藻渣对PFOS的吸附率均达到99%以上;随着pH值增加至7,二者的吸附去除率迅速降低,但仍保持在22%~26%。小球藻和藻渣对PFOS的最大吸附容量分别为353.69 mg/g和444.83 mg/g。Freundlich模型能较好地拟合二者对PFOS的吸附数据,表明为多层吸附,即小球藻以静电吸引的形式吸附PFOS阴离子,并疏水分配至所含蛋白质中;而藻渣中含量较高的蛋白质对PFOS的疏水性分配作用是导致藻渣吸附量增高的主要原因。     

UV/H2O2/GAC工艺去除水中全氟化合物

全氟化合物(PFCs)持久存在于水环境中,难以通过传统的水处理工艺去除,提高水中PFCs的去除性能具有重要意义。本研究采用快速小柱实验探究了UV、H₂O₂和颗粒活性炭(GAC)组合工艺对水中4种PFCs的去除效果,并探究了UV照射时长和H₂O₂质量浓度对PFCs的直接去除效果及其对后续GAC吸附的影响。结果表明：不同工艺条件下,长链全氟辛酸(PFOA)和全氟辛烷磺酸(PFOS)始终表现出较短链全氟丁酸(PFBA)和全氟丁烷磺酸(PFBS)更高的去除率。单独GAC吸附对长链全氟PFOA和PFOS去除率为59.6%和64.3%,但对短链PFBA和PFBS去除率仅为11.7%和13.1%。单独UV或单独H₂O₂分别与GAC联用时,随着UV照射时长和H2O2质量浓度的增加,4种PFCs的去除率略有增加,且UV照射的增益效果较H₂O₂更优。UV/H₂O₂/GAC联用工艺对水中4种...     

纳滤去除饮用水中的PFOS

全氟辛烷磺酸类物质（PFOS）是一种新型持久性有机污染物，对人类健康存在很大威胁，目前世界范围内的水体中均检测到不同浓度的PFOS。研究如何安全有效去除这类新型污染物十分必要。利用HYDRA—COPe10纳滤膜进行PFOS去除研究，在不同操作压力下研究pH、电解质以及与腐殖酸共存对PFOS截留效果的影响。结果表明，随着pH值的增加，截留率上升；二价盐对PFOS截留率的影响要高于一价盐，并且随着二价盐离子强度的增加，截留率上升；腐殖酸共存时截留效率有显著增加，尤其在1mmol／L钙离子存在条件下，PFOS的截留率可达到95．8％，但会引起膜通量下降及膜污染的发生。     

Fe3O4纳米磁性微粒对全氟辛烷磺酸盐的吸附

采用共沉淀法合成Fe3O4纳米磁性颗粒,用透射电子显微镜（TEM）、X射线衍射仪（XRD）以及振动样品磁强计（VSM）对Fe3O4纳米磁性颗粒的粒径、形貌和磁性进行表征并研究Fe3O4纳米磁性微粒对全氟辛磺酸盐的吸附。结果表明：在PFOS初始浓度4 mg/L,pH为3,反应时间24 h,Fe3O4纳米磁性微粒投加量1.25 g/L,对全氟辛磺酸盐去除率达到90%。Fe3O4纳米磁性微粒对PFOS的吸附符合Freundlich吸附方程。     

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.     

Environmental contamination, human exposure and body loadings of perfluorooctane sulfonate (PFOS), focusing on Asian countries

Perfluorinated compounds (PFCs) are man-made fluorinated hydrocarbons, which are very persistent in the environment. Since the early 1980s, the usage of PFCs has sharply increased for a wide array of industrial and commercial applications. Being the most important PFC, perfluorooctane sulfonate (PFOS) has received much attention. In the past decades, increasing surveys have been focused on this compound, to study its sources, fates and effects in the environment. According to the large production volume and wide usage in industrial and commercial products in the past, PFOS can be detected in various environmental media and matrix, even in human tissues. This article attempted to review the current status of PFOS contaminations in Asia, focusing on water systems, sediments, wide animals and human tissues. A special section is devoted to examine the pathways of human exposure to this compound, as well as human body loadings of PFOS and their possible association with diseases.     

Perfluorooctane sulfonate-induced apoptosis of cerebellar granule cells is mediated by ERK 1/2 pathway

Perfluorooctane sulfonate (PFOS), a ubiquitous environmental pollutant, is considered as a neurotoxicant to mammalian species. However, the underlying mechanism of its neurotoxicity is largely unknown. In the present study, we examined roles of mitogen-activated protein kinases (MAPKs) in PFOS-induced apoptosis of neuronal cells to elucidate the molecular mechanism. Cerebellar granule cells were isolated from 7-d old rats and maintained in culture for additional 7 d. Cells were exposed to PFOS and caspase-3 activity and nuclear morphology were evaluated by enzyme activity assay and Hoechst 33342 staining, respectively, to determine its effects on apoptosis. The treatment with PFOS resulted in caspase-3 activation and nuclear condensation and fragmentation. PFOS exposure selectively increased activation of ERK that remained above control over 6 h. The inhibitor of ERK pathway, PD98059, substantially blocked caspase-3 activation induced by PFOS, whereas inhibitors of JNK and p38 MAPK, SP600125 and SB203580, respectively, had no effect. PKC inhibitors, bisindolylmaleimide I and Gö6976, dampened caspase-3 activity and ERK activation induced by PFOS. Collectively, it is suggested that PKC and ERK play proapoptotic roles in PFOS-induced apoptosis of cerebellar granule cells and PKC act as an upstream regulator of ERK activation.     

Perfluorooctane Sulfonate Increases the Genotoxicity of Cyclophosphamide in the Micronucleus Assay with V79 Cells: Further Proof of Alterations in Cell Membrane Properties Caused by PFOS (3 pp)

Background, Aim and Scope Perfluorooctane sulfonate (PFOS; C8F17SO3-) is a fully fluorinated organic compound which has been manufactured for decades and was used widely in industrial and commercial products. The recent toxicological knowledge of PFOS mainly concerns mono-substance exposures of PFOS to biological systems, leaving the potential interactive effects of PFOS with other compounds as an area where understanding is significantly lacking. However, a recent study, reported the potential of PFOS to enhance the toxicity of two compounds by increasing cell membrane permeability. This is of particular concern since PFOS has been reported to be widely distributed in the environment where contaminants are known to occur in complex mixtures. In this study, PFOS was evaluated alone and in combination with cyclophosphamide (CPP) to investigate whether a presence of PFOS leads to an increased genotoxic potential of CPP towards hamster lung V79 cells. Genotoxicity was investigated using the micronucleus (MN) assay according to the recent draft ISO/DIS 21427-2 method. PFOS alone demonstrated no genotoxicity up to a concentration of 12.5 mg/L. However, PFOS combined with two different concentrations of CPP, with metabolic activation, caused a significant increase in the number of micronucleated cells compared to treatments with CPP only. These results provide a first indication that PFOS has the potential to enhance the genotoxic action of CPP towards V79 cells, suggesting that together with the alterations in cell membrane properties shown previously, that genotoxicity of complex mixtures may be increased significantly by changes in chemical uptake. Together with an earlier study performed by the own working group it can be concluded that PFOS alone is not genotoxic in this bioassay using V79 cells up to 12.5 mg/L, but that further investigations are needed to assess the potential interaction between PFOS and other substances, in particular regarding the impact of membrane alterations on the uptake of toxic substances. Materials and Methods: - Results: - Discussion: - Conclusions: - Recommendations and Perspectives: -     

Sorption of perfluorooctane sulfonate to carbon nanotubes in aquatic sediments

To date, sorption of organic compounds to nanomaterials has mainly been studied for the nanomaterial in its pristine state. However, sorption may be different when nanomaterials are buried in sediments. Here, we studied sorption of Perfluorooctane sulfonate (PFOS) to sediment and to sediment with 4% multiwalled carbon nanotubes (MWCNTs), as a function of factors affecting PFOS sorption; aqueous concentration, pH and Ca²⁺ concentration. Sorption to MWCNT in the sediment–MWCNT mixtures was assessed by subtracting the contribution of PFOS sorption to sediment-only from PFOS sorption to the total sediment–MWCNT mixture. PFOS Log K_D values ranged 0.52–1.62 L kg^?1 for sediment and 1.91–2.90 L kg^?1 for MWCNT present in the sediment. The latter values are relatively low, which is attributed to fouling of MWCNT by sediment organic matter. PFOS sorption was near-linear for sediment (Freundlich exponent of 0.92 ± 0.063) but non-linear for MWCNT (Freundlich exponent of 0.66 ± 0.03). Consequently, the impact of MWCNT on sorption in the mixture was larger at low PFOS aqueous concentration. Effects of pH and Ca²⁺ on PFOS sorption to MWCNT were statistically significant. We conclude that MWCNT fouling and PFOS concentration dependency are important factors affecting PFOS–MWCNT interactions in sediments.     

Preliminary screening of perfluorooctane sulfonate (PFOS) and other fluorochemicals in fish, birds and marine mammals from Greenland and the Faroe Islands

Extensive screening analyses of perfluorooctane sulfonate (PFOS) and related perfluorinated compounds in biota samples from all over the world have identified PFOS as a global pollutant and have shown its bioaccumulation into higher trophic levels in the food chain. Perfluorinated compounds have been found in remote areas as the Arctic. In this study a preliminary screening of PFOS and related compounds has been performed in liver samples of fish, birds and marine mammals from Greenland and the Faroe Islands. PFOS was the predominant fluorochemical in the biota analyzed, followed by perfluorooctane sulfonamide (PFOSA). PFOS was found at concentrations above LOQ (10 ng/g wet weight) in 13 out of 16 samples from Greenland and in all samples from the Faroe Islands. The results from Greenland showed a biomagnification of PFOS along the marine food chain (shorthorn sculpin < ringed seal < polar bear). The greatest concentration of PFOS was found in liver of polar bear from east Greenland (mean: 1285 ng/g wet weight, n = 2). The geographical distribution of perfluorinated compounds in Greenland was similar to that of persistent organohalogenated compounds (OHCs), with the highest concentrations in east Greenland, indicating a similar geographical distribution to that of OHCs, with higher concentrations in east Greenland than in west Greenland.     

Effects of perfluorinated compounds on development of zebrafish embryos

Perfluorinated compounds (PFCs) have been widely used in industrial and consumer products and frequently detected in many environmental media. Potential reproductive effects of perfluorooctanesulfonate (PFOS), perfluorooctanoic acid (PFOA) and perfluorononanoic acid (PFNA) have been reported in mice, rats and water birds. PFOS and PFOA were also confirmed developing toxicants towards zebrafish embryos; however, the reported effect concentrations were contradictory. Polyfluorinated alkylated phosphate ester surfactants (including FC807) are precursor of PFOS and PFOA; however, there is no published information about the effects of FC807 and PFNA on zebrafish embryos. Therefore, this study was conducted to determine the effects of these four PFCs on zebrafish embryos. Normal fertilized zebrafish embryos were selected to be exposed to several concentrations of PFOA, PFNA, PFOS or FC807 in 24-well cell culture plates. A digital camera was used to image morphological anomalies of embryos with a stereomicroscope. Embryos were observed through matching up to 96-h post-fertilization (hpf) and rates of survival and abnormalities recorded. PFCs caused lethality in a concentration-dependent manner with potential toxicity in the order of PFOS > FC807 > PFNA > PFOA based on 72-h LC(50). Forty-eight-hour post-fertilization pericardial edema and 72- or 96-hpf spine crooked malformation were all observed. PFOA, PFNA, PFOS and FC807 all caused structural abnormalities using early stages of development of zebrafish. The PFCs all retarded the development of zebrafish embryos. The toxicity of the PFCs was related to the length of the PFC chain and functional groups.     

Perfluorooctane sulfonate increases β-oxidation of palmitic acid in chicken liver

Purpose

Perfluorooctane sulfonate (PFOS) belongs to a group of chemicals called perfluoroalkyl acids that have been extensively used in various applications such as stain and oil resistant treatments for fabrics, fire-fighting foams, and insecticides. These chemicals present an environmental and health risk being present in many samples both in wildlife and humans. In this study, we investigate the effect of PFOS on fatty acid ??-oxidation in developing chicken embryos.

Methods

Fertilized chicken eggs were exposed in ovo to PFOS at day?4 of incubation. On day?10, the eggs were dissected and livers were incubated in vitro with ³H-palmitic acid for 2?h. The media were collected, and after clean up, the amount of tritiated water was measured with liquid scintillation counting to determine the rate of palmitic acid ??-oxidation.

Results

PFOS was found to induce fatty acid ??-oxidation at doses starting from a lowest observed effect level (LOEL) of 0.1???g/g egg weight. Maximum induction of 77?% compared to control was seen at 0.3???g/g.

Conclusions

The administered doses in which effects are seen are around and even lower than the levels that can be found in wild populations of birds. General population human levels are a factor of two to three times lower than the LOEL value of this study. The environmental contamination of PFOS therefore presents a possibility of effects in wild populations of birds.     

Lipophilic organic pollutants induce changes in phospholipid and membrane protein composition leading to Vero cell morphological change

Membrane damage related to morphological change in Vero cells is a sensitive index of the composite biotoxicity of trace lipophilic chemicals. However, judging whether the morphological change in Vero cells happens and its ratio are difficult because it is not a quantitative characteristic. To find biomarkers of cell morphological change for quantitatively representing the ratio of morphological changed cell, the mechanism of cell membrane damage driven by typical lipophilic chemicals, such as trichlorophenol (TCP) and perfluorooctanesulphonate (PFOS), was explored. The ratio of morphologically changed cells generally increased with increased TCP or PFOS concentrations, and the level of four major components of phospholipids varied with concentrations of TCP or PFOS, but only the ratio of phosphatidylcholine (PC)/phosphatidylethanolamine (PE) decreased regularly as TCP or PFOS concentrations increased. Analysis of membrane proteins showed that the level of vimentin in normal cell membranes is high, while it decreases or vanishes after TCP exposure. These variations in phospholipid and membrane protein components may result in membrane leakage and variation in rigid structure, which leads to changes in cell morphology. Therefore, the ratio of PC/PE and amount of vimentin may be potential biomarkers for representing the ratio of morphological changed Vero cell introduced by trace lipophilic compounds, thus their composite bio-toxicity.