蜂窝煤燃烧氟污染的控制

以碳酸钙为固氟添加剂,以炉渣及粉煤灰等低氟材料取代全部或部分粘土作为粘结剂来制作蜂窝煤,进行了燃煤降氟的试验研究.结果表明,添加碳酸钙能有效降低蜂窝煤燃烧时候的氟排放,当煤:粘土:CaCO3的质量比为70:17:13时,碳酸钙的固氟效果最佳,氟的排放率可降低64.1%.以炉渣为粘结剂制作蜂窝煤能够显著降低燃烧时向外界排放的氟化物量,当煤:炉渣:CaCO3为80:8:12时,蜂窝煤燃烧排氟量较小且趋于稳定.已拌有一定剂量粉煤灰粘结剂的煤中添加15%的粘土后碳酸钙的固氟效果明显改善,当煤:粘土:粉煤灰:CaCO3为70:15:9:6时固氟效果最佳,此时蜂窝煤氟逸出率仅为18.2%,氟的减排率达到77.9%,显著优于未添加粘土时碳酸钙的固氟效果,蜂窝煤添加碳酸钙固氟剂进行高效固氟时,需同时适当增加粉煤灰加入量,以稳定固氟剂的高温固氟效果.     

基于生态安全的DAT-IAT城市污水处理工艺改进研究

通过正交试验,得到了DAT-IAT工艺和A/DAT-IAT工艺处理城市污水的常规指标去除和生态毒理指标削减的最优运行条件。结果表明,在正交试验的同一工艺中,COD去除最优运行条件的出水COD值优于生态毒性削减最优运行条件的出水COD值,但前者出水的生态毒性较大。由于厌氧池的水解酸化作用,A/DAT-IAT工艺对COD和生态毒性的处理效果均优于DAT-IAT工艺,并且回流总能耗低于DAT-IAT工艺,但是出水COD仍不达标。为了降低进入工艺的COD的总量,以絮凝沉淀做为预处理工艺,并采用Al残留量最小的絮凝剂投药量以降低出水中残留Al带来的生态风险。结果表明,在COD去除最优运行条件下,具有絮凝预处理的工艺对COD的去除效果优于没有絮凝预处理的工艺。絮凝-A/DAT-IAT工艺在COD去除最优运行条件下出水COD为104.46 mg/L,满足排放标准。在毒性削减最优运行条件下,具有絮凝预处理的工艺的出水生态毒性有所上升,但是污染物的总量得到了大幅削减。絮凝-A/DAT-IAT工艺与DAT-IAT工艺相比,在污染物去除效率得到大幅增加的同时,生态毒性得到有效控制,生态安全得到了有效的保障。     

含磁粉生物反应器处理苯酚废水

采用含磁粉生物反应器对质量浓度为120～350 mg/L的苯酚模拟废水进行强化生物处理.实验结果表明:添加适量磁粉可使废水中DO提高约10%;与不含磁粉生物反应器比较,含磁粉生物反应器工艺使填料挂膜时间缩短1～2 d,填料上附着微生物量增多;质量浓度为350 mg/L的苯酚模拟废水在20 h内的苯酚去除率可达80%,降解时间缩短了10 h.初步分析了添加磁粉提高生物反应器处理废水效率的机理.实验证实了含磁粉生物反应器工艺的合理运用是强化处理含酚废水的有效途径.     

重金属吸附剂壳聚糖的改性研究进展

综述了重金属吸附剂壳聚糖改性研究的新进展,介绍了交联与接枝等改性方式对壳聚糖稳定性的影响及改性后的壳聚糖对水体中重金属离子吸附性能的改善.针对壳聚糖改性中仍然存在的一些问题,指出今后研究中值得关注的方向.     

混凝法深度处理印染废水中试研究

采用"高效混凝沉淀-过滤"深度处理工艺处理印染废水二级生化出水,并将混凝沉淀污泥回流.实验结果表明,混凝剂聚合氯化铝加入量为160 mg/L时,COD去除率平均可达34.6%,TP去除率平均达到87.9%,平均出水TP为0.3 mg/L.气相色谱-质谱分析和元素分析结果表明混凝沉淀工艺对有机物和TP的去除效果良好.     

林业生物灾害的监测调查技术研究进展

介绍了航天遥感、航空遥感、地面调查等技术在林业生物灾害监测中的应用现状与发展历程,在分析上述三项技术优缺点的基础上,提出了在我国建立树木、林分、景观等尺度综合监测技术体系,开展林业生物灾害监测与调查的方法及相关建议.     

电石渣－铁屑法去除硫酸废水中的氟和砷

对各种处理含氟、砷废水的方法进行了探讨，选择了以电石渣和废铁屑为药剂去除硫酸废水中氟和砷的方法，取得了较好的效果。该法以废治废、工艺简便、运行费用低，处理后的废水可达排放标准。     

Effect of acute exposure to PFOA on mouse liver cells in vivo and in vitro

Increasingly, epidemiological evidences indicate chemosynthetic perfluorooctanoic acid (PFOA), an environmental pollutant, induces potential adverse effect on human health after long-term exposure. However, less study has been performed for assessment of acute effect of PFOA exposure on metabolic homeostasis. In experimental designs, PFOA-exposed liver cells in vivo and in vitro were used to discuss underlying mechanism related to PFOA-induced metabolic dysfunction. In serological tests, PFOA-exposed mice showed increased treads of liver functional enzymes in alanine transaminase (ALT), aspartate transaminase (AST), and total bilirubin (T-BIL), trypsinase, low density lipoprotein-cholesterol (LDL-C), and insulin, while blood glucose, high density lipoprotein-cholesterol (HDL-C), and glucagon levels were reduced. In histocytological observations, PFOA-exposed liver showed visible cytoplasmic vesicles, and intact pancreatic islets were observed in PFOA-exposed pancreas. Additionally, increased insulin-positive cells and reduced glucagon-positive cells were detected in PFOA-exposed islets. As shown in immunoassays, PFOA-exposed liver resulted in elevations of cluster of differentiation 36 (CD36)-labeled cells and CD36 protein. In mouse liver cell study, PFOA-exposed cells showed increased cell apoptotic count, and increased phosphorylated levels of Bcl-2 and Bad in the cells. Furthermore, PFOA-exposed liver cells exhibited elevations of CD36-labeled cells and CD36 protein. Taken together, the present data demonstrate that acute exposure to PFOA-impaired liver function is associated with inducting CD36 expression and apoptosis, as well as disrupting key hormones in the pancreas.     

A dynamic modelling of nutrient metabolism in a cyclic activated sludge technology (CAST) for treating low carbon source wastewater

Environmental Science and Pollution Research - A new mathematical model incorporating biopolymer kinetics and the process of the simultaneous storage and growth are established for the treatment of...