陈垃圾反应床＋芦苇人工湿地处理垃圾渗滤液

研究了陈垃圾反应床与芦苇人工湿地串联对垃圾渗滤液中污染物的去除效果, 并探讨了湿地中芦苇生长和对渗滤液中总氮的吸收能力。结果表明： 在进水负荷为0.1 m³/（m²·d）的条件下,经过3个月的运行,陈垃圾反应床与芦苇人工湿地对陈年渗滤液中COD、氨氮、总氮及总磷的最大去除率分别达到90.3%、95.0%、79.3%和99.8%。通过对人工湿地中芦苇的分析表明,芦苇在6—8月份生长迅速,地上部分生物量与其氮含量增加较快,最大值均出现在8月底,植株总含氮量可以达到28.5 g/m²。此时收割芦苇可从湿地中最大限度除氮。如能增加芦苇种植密度,陈垃圾床与芦苇湿地串联处理渗滤液污染物以及深度去氮是可行的。     

乌梁素海表层沉积物重金属分布特征及生态风险评价

采样分析了内蒙古乌梁素海表层沉积物中Cu、Zn、Pb、Cr、Cd、Hg和As的含量、分布特征和富集状况,分别以现代工业化前正常颗粒沉积物中重金属含量的最高背景值和河套地区土壤中重金属含量背景值为参照,采用瑞典科学家Lars Hakanson的潜在生态危害指数法对7种重金属的富集系数和生态危害系数以及各采样点的生态危害指数进行了评价。结果表明,乌梁素海表层沉积物中As和Pb的空间变异性较大;以2种背景值为参比得出的重金属污染水平顺序相近,Hg和As为对乌梁素海生态环境具有潜在影响的主要重金属元素;同时表明,以河套地区土壤重金属背景值为参照更能直观地反映出乌梁素海表层沉积物中重金属的污染程度。     

生态修复综合技术在杭州虾龙圩河的应用

杭州虾龙圩河由于多年污染,河道水质严重黑臭,自净能力遭到破坏。本研究通过综合利用底泥污染物削减、生物接触氧化水质净化、造流曝气及水生生态系统修复等技术对虾龙圩河进行治理。结果显示,此项综合技术对城市河流污水具有良好的污染物去除性能,COD、NH3-N和TP的去除率分别可达到73．3％、80．1％和81．7％。通过1年的运行与养护,虾龙圩河治理段的水质、生态环境等有了明显改善,没有发生过水华及黑臭现象,河道水体具备了较强的自净能力。     

光辅助下TiO2-蒙脱土复合材料抑杀蓝藻

以TiCl4和钠基蒙脱土为原料,采用水解法制备了TiO2-蒙脱土复合材料,采用XRD、IR和TEM对其结构和性质进行表征;通过藻细胞的内含物含量、生长代谢活性和形态的变化以及藻细胞膜脂质过氧化分析,研究了TiO2-蒙脱土复合材料在光辅助下去除颤藻的性能.结果表明,TiO2-蒙脱土复合材料中一部分TiO2插入蒙脱层间,增加了蒙脱土的层间距,另一部分以锐钛矿相均匀分散在蒙脱土上;在紫外光辅助下,TiO2-蒙脱土的用量为50.0 mg/L,lh后颤藻的除藻率可达94.58％;TiO2-蒙脱土通过光催化作用破坏藻细胞膜、降解藻细胞内含物、降低藻细胞代谢活性和破坏藻细胞形态,从而产生抑藻作用.     

亚铁氰化铜的制备及其对铯的吸附

以亚铁氰化钠和硝酸铜为原料,采用水热合成法制备出亚铁氰化铜(CuFC)吸附剂,对其进行了表征,并考察了CuFC对模拟放射性废水中铯的吸附性能。表征结果显示:产物的分子式为Cu2Fe(CN)6·7H2O,外观为具有清晰几何形状的颗粒物,粒径约为30 nm。25℃下的静态吸附实验结果表明:当初始铯质量浓度为98.01μg/L、CuFC加入量为0.08 g/L、吸附时间为90 min时,达到吸附平衡,铯的去污系数达到1.13×104;用拟二级动力学模型可准确描述CuFC对铯的吸附过程,相关系数为1.000 0;吸附等温线符合Freundlich等温吸附模型。     

光催化降解内分泌干扰物双酚A的响应面分析与优化

对光催化降解内分泌干扰物双酚A进行了研究,使用响应面方法(RSM)结合中心组合设计(CCD),对光催化过程中的影响因素(光强、Ti O2浓度、初始双酚A浓度)进行了探讨和分析,构建响应面模型,并对反应条件进行了优化。此响应面模型能够较好地模拟实验结果,可以用于探索设计空间。优化的最佳反应条件为:Ti O2浓度1.80 g/L、初始双酚A浓度41.08 mg/L、UV光强6.61 m W/cm2,预测和实验最大双酚A去除率分别为81.5%和82.3%,数值比较接近,说明此响应面模型能够有效描述光催化反应过程,优化光催化反应条件,为光催化技术工程应用和光反应器设计提供技术参考。     

交流变频磁化聚合硫酸铁混凝处理造纸废水

采用交流变频磁场预处理聚合硫酸铁(PFS),用于混凝处理造纸废水。考察了有无磁化作用、PFS加入量、磁化强度、磁化频率、磁化时间等因素对造纸废水的COD去除率和色度去除率的影响。实验结果表明:磁化PFS对造纸废水的处理效果较未磁化时明显提高;在PFS加入量为1 000 mg/L、磁化强度为6 mT、磁化频率为90 Hz、磁化时间为3 min的条件下,处理初始COD为650 mg/L、初始色度为180倍的造纸废水,COD去除率为93.22%,色度去除率为88.89%。     

Oxidative stress in the kidney injury of mice following exposure to lanthanides trichloride

Environmental pollution from lanthanides (Ln) has been recognized as a major problem due to a grab exploitation of Ln mine in China. Exposure to Ln has been demonstrated to cause the nephrotoxicity, very little is known about the mechanism of oxidative damage to kidney in animals. In order to understand Ln-induced nephrotoxicity, various biochemical and chemical parameters were assayed in mouse kidney. Intragastric exposures of LaCl₃, CeCl₃, and NdCl₃ at doses of 2, 5, and 10 mg kg⁻¹ BW for 90 consecutive days caused nephritis or epithelial cell necrosis and oxidative stress to kidney. An increase in coefficients of the kidney, La, Ce, and Nd accumulation and histopathological changes in the kidney could be observed, followed by increased reactive oxygen species production and peroxidation levels of lipid, protein and DNA, and decreased activities of superoxide dismutase, catalase, glutathione-S-transferase and glutathione reductase as well as antioxidants such as glutathione, ascorbic acid and thiol contents. Furthermore, La, Ce, and Nd significantly suppressed expression of genes and proteins of these antioxidative enzymes in mouse kidney. In addition, kidney functions were disrupted, including an increase of the creatinine, and reductions of uric acid, urea nitrogen, calcium and phosphonium. These findings suggest that nephritis generation or epithelial cell necrosis in mice following exposure to Ln is closely associated with oxidative stress. Of these damages, the most severe was in the Ce³⁺-exposed kidneys, next in the Nd³⁺-exposed kidneys, and the least in the La³⁺-exposed kidneys, which may be attributed to the 4f electron of Ln.     

PCB 77 dechlorination products modulate pro-inflammatory events in vascular endothelial cells

Persistent organic pollutants such as polychlorinated biphenyls (PCBs) are associated with detrimental health outcomes including cardiovascular diseases. Remediation of these compounds is a critical component of environmental policy. Although remediation efforts aim to completely remove toxicants, little is known about the effects of potential remediation byproducts. We previously published that Fe/Pd nanoparticles effectively dechlorinate PCB 77 to biphenyl, thus eliminating PCB-induced endothelial dysfunction using primary vascular endothelial cells. Herein, we analyzed the toxic effects of PCB congener mixtures (representative mixtures of commercial PCBs based on previous dechlorination data) produced at multiple time points during the dechlorination of PCB 77 to biphenyl. Compared with pure PCB 77, exposing endothelial cells to lower chlorinated PCB byproducts led to improved cellular viability, decreased superoxide production, and decreased nuclear factor kappa B activation based on duration of remediation. Presence of the parent compound, PCB 77, led to significant increases in mRNA and protein inflammatory marker expression. These data implicate that PCB dechlorination reduces biological toxicity to vascular endothelial cells.