好氧硝化颗粒污泥膜生物反应器性能和膜污染研究

实验研究了好氧硝化颗粒污泥膜生物反应器AGMBR的处理性能,并将其与活性污泥膜生物反应器ASMBR进行对比,考察了颗粒污泥在减缓膜污染中所起的作用.好氧硝化颗粒污泥膜生物反应器AGMBR连续稳定运行102 d,系统具有良好的去除有机物和同时硝化反硝化能力,在进水COD和NH+4-N浓度分别为500和200 mg/L时,COD、NH+4-N和TN的去除率分别稳定在86%、94%和45%以上.颗粒污泥有效减缓了膜污染,延长了膜清洗的周期,AGMBR中的膜污染以膜孔堵塞为主,占总阻力的64.81%;滤饼层的阻力为2.1×1012m-1,远小于ASMBR中的16.07×10"m-1;膜清洗周期是相同条件下ASMBR的2.43倍以上;而且AGMBR内不断有新颗粒生成,维持了AGMBR系统性能和运行的稳定.     

强化生物通风修复过程中柴油衰减规律及其影响因素研究

强化生物通风技术对于修复因地下储油罐泄漏引起的土壤污染具有很大的应用前景。通过室内土柱模拟柴油泄漏污染土壤,从土柱中总石油烃（total petroleum hydrocarbon,TPH）剖面分布随时间的变化及降解模式角度,分析了其自然衰减和强化生物通风过程。结果表明：初始柴油浓度直接影响着各柱在自然衰减和强化生物通风过程中柱内的残余TPH平衡分布曲线的形状和浓度峰值位置;在前期自然衰减过程中（约1个月）,当土壤中的柴油浓度为5 000～40 000 mg油/kg土时,整个柱内TPH变化的主要原因是重力扩散迁移的结果;当土壤中的柴油浓度≤5 000 mg油/kg土时,其TPH的变化不仅是重力扩散迁移作用的结果,生物降解作用也存在;通风约2个月后,抽提作用对于保持土柱上部柴油浓度稳定变化的意义较为突出。     

高锰酸钾降解地下水中PCE的研究

以氯代有机污染物中常见的PCE为目标污染物,以自制高锰酸钾溶液为氧化剂,采用批实验方法,探讨了高锰酸钾降解PCE的反应动力学、影响因素以及反应机理。反应结果表明,高锰酸钾降解PCE的反应符合一级动力学方程,反应活化能E为57.119 kJ/mol,在30℃条件下,反应速率常数为0.0076 min^-1,半衰期为91.20 min。在pH在3～10,离子强度在0～0.1030 mol/L之间变化时,反应速率不受明显影响。     

TiO2催化高压脉冲放电等离子体降解2，4-二硝基苯酚

采用TiO2催化高压脉冲放电等离子体降解废水中的2,4-二硝基苯酚,对反应进行了动力学研究.研究结果表明,在高压脉冲放电等离子体及TiO2催化高压脉冲放电等离子体反应中,2,4-二硝基苯酚的降解过程均符合表观一级反应动力学方程.加入TiO2催化剂、提高放电电压均可提高2,4-二硝基苯酚的降解反应速率常数.在TiO2加入量为0.15%、放电电压为16 kV时,2,4-二硝基苯酚的降解率为87.4%,TiO2的催化效应增强因子为1.55.     

Ru/γ-Al_2O_3和Ru/AC催化剂的制备及其对氨氧化反应的催化性能

分别以γ-Al_2O_3和活性炭(AC)为载体,采用浸渍法制备了Ru质量分数均为2.0%的Ru/γ-Al_2O_3和Ru/AC催化剂,并用X射线衍射仪和透射电子显微镜等方法对催化剂结构进行了表征.实验结果表明:Ru/AC中Ru沉积在AC表面,分散度较低;而Ru/γ-Al_2O_3中Ru进入到γ-Al_2O_3内部,形成了一种高度分散体系.Ru/γ-Al_2O_3对氨的催化活性高于Ru/AC,氨在Ru/γ-Al_2O_3和Ru/AC上的起活温度分别为200 ℃和266 ℃,T_(90)(氨去除率达90%时的反应温度)分别为267℃和320 ℃.随混合气体空速增大,Ru/γ-Al_2O_3催化剂的T_(90)逐渐升高,气体空速分别为3 600,4 800,5 400 h~(-1)时,T_(90)分别为235,266,303 ℃.随反应前混合气体中氨质量分数增加,氨的去除率降低.     

学龄儿童肺功能水平影响因素的研究

用逐步回归分析方法对与室内、外空气污染和机体状况等有关的因素对广州市学龄儿童肺功能 (FVC、FEV1 、PEFR和 FEF2 5～ 75 )水平的影响进行研究。结果提示 ,影响肺功能水平的主要因素是内因 ,身高的影响最明显 ,呼吸系统疾病或症状发生与肺功能水平下降有关 ;室外空气污染使肺功能水平下降 ,SO2 、NOx 和 PM2 .5 的影响明显 ,PM2 .5 的影响明显大于 PM1 0 和 TSP;居室或厨房通风不良、家庭烹饪用不洁燃料对儿童肺功能的生长不利 ;被动吸烟对女性儿童肺功能有不利影响。对各种影响因素 ,PEFR和 FEF2 5～ 75 比 FVC和 FEV1 更为敏感     

Waste polyvinylchloride derived pitch as a precursor to develop carbon fibers and activated carbon fibers

Polyvinylchloride (PVC) was successfully recycled through the solvent extraction from waste pipe with an extraction yield of ca. 86%. The extracted PVC was pyrolyzed by a two-stage process (260 and 410 degrees C) to obtain free-chlorine PVC based pitch through an effective removal of chlorine from PVC during the heat-treatment. As-prepared pitch (softening point: 220 degrees C) was spun, stabilized, carbonized into carbon fibers (CFs), and further activated into activated carbon fibers (ACFs) in a flow of CO2. As-prepared CFs show comparable mechanical properties to commercial CFs, whose maximum tensile strength and modulus are 862 MPa and 62 GPa, respectively. The resultant ACFs exhibit a high surface area of 1200 m2/g, narrow pore size distribution and a low oxygen content of 3%. The study provides an effective insight to recycle PVC from waste PVC and develop a carbon precursor for high performance carbon materials such as CFs and ACFs.     

建筑火灾烟流运动特性网络模型的求解收敛性

分析了运用网络模型模拟建筑火灾烟流的计算过程,通过总结影响网络模型求解精度及收敛性的关键因素,改进了原烟流预测软件对建筑物各开口的净、正、负质量流量的算法。改进后的模型消除了振荡效应,模拟结果曲线平滑稳定,实现了运用网络模型对多室建筑物烟流特性的模拟计算。     

Soil surface Hg emission flux in coalfield in Wuda,Inner Mongolia,China

Hg emission flux from various land covers, such as forests, wetlands, and urban areas, have been investigated. China has the largest area of coalfield in the world, but data of Hg flux of coalfields, especially, those with coal fires, are seriously limited. In this study, Hg fluxes of a coalfield were measured using the dynamic flux chamber (DFC) method, coupled with a Lumex multifunctional Hg analyzer RA-915+ (Lumex Ltd., Russia). The results show that the Hg flux in Wuda coalfield ranged from 4 to 318 ng m^?2 h^?1, and the average value for different areas varied, e.g., coal-fire area 99 and 177 ng m^?2 h^?1; no coal-fire area 19 and 32 ng m^?2 h^?1; and backfilling area 53 ng m^?2 h^?1. Hg continued to be emitted from an underground coal seam, even if there were no phenomena, such as vents, cracks, and smog, of coal fire on the soil surface. This phenomenon occurred in all area types, i.e., coal-fire area, no coal-fire area, and backfilling area, which is universal in Wuda coalfield. Considering that many coalfields in northern China are similar to Wuda coalfield, they may be large sources of atmospheric Hg. The correlations of Hg emission flux with influence factors, such as sunlight intensity, soil surface temperature, and atmospheric Hg content, were also investigated for Wuda coalfield.

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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.