近60 年ENSO 事件对鄂尔多斯北部地区气候的影响

通过对鄂尔多斯北部的乌拉特中旗、呼和浩特和包头三个城市近60 年来的降水资料和 气温资料的整理和搜集,研究了ENSO 事件对鄂尔多斯北部地区的气候与灾害的影响。分析数据 得出,自1952 年来,鄂尔多斯北部地区的气候呈变暖变干趋势。1952 年以来鄂尔多斯北部地区 年平均气温增长率为0.48℃ ·10a?1,高于全国的平均气温增长率（0.22℃ ·10a?1）;年降水量则处 于略下降趋势,下降率约为5.5 mm·10a?1,低于全国的平均降水下降率（12.69 mm·10a?1）。厄尔 尼诺年年平均气温高出正常年份0.2℃,而拉尼娜年的平均气温比正常年低0.14℃。厄尔尼诺年 的平均降水量比正常年减少29.2 mm,拉尼娜年的平均降水比正常年减少23.9 mm。厄尔尼诺事 件对鄂尔多斯北部地区的灾害影响比拉尼娜事件更为显著和强烈,厄尔尼诺年鄂尔多斯北部地区 更易发生高温干旱灾害。小波分析指示,鄂尔多斯北部降水周期变化在30 a 尺度内存在2 a、4 a、 8 a 和14 a 的变化周期。     

微波消解ICP—OES法同时测定总悬浮颗粒物中多种重金属

采用微波消解前处理与电感耦合等离子光谱联用技术,初步建立了一套大气总悬浮颗粒物（TSP）中重金属元素的检测方法。研究了不同的滤膜材料、消解方式、波长选择等对分析方法的影响。用所建立的方法测定长沙市火车站采集的大气总悬浮颗粒物中的重金属As、Cd、Co、Cr、Cu、Mn、Mo、Ni、Pb、Zn的含量,检测结果令人满意。最低检出浓度为0．0001～0．005μg／m2,相对标准偏差为0．9％～11．4％,加标回收率为90．9％～106．7％。     

冻融对污染场地土壤重金属稳定化性能的影响

为了分析冻融对污染场地土壤重金属稳定化性能的影响,采用赤泥和硫化钠作为添加剂,对土壤中的Pb、Zn和Cd进行稳定化处理,并通过模拟冻融过程,分析冻融循环后重金属的浸出毒性、生物可给性、土壤pH和土壤结构的变化,探讨冻融循环对稳定化处理土壤中重金属长期稳定性能的影响. 结果表明:稳定化处理后土壤中Pb、Zn和Cd的浸出毒性比原始供试土壤分别降低了98.5%、99.8%和99.7%. 养护30 d后,稳定化处理土壤中Zn和Cd的生物可给性分别由28.8%、49.5%降至11.5%、21.8%,Pb的生物可给性由52.9%升至57.9%. 经过30 d冻融循环后,冻融土壤中Pb、Zn和Cd的浸出毒性比原始供试土壤中相应重金属质量分数分别增加了4.27、2.47、89.65 mg/L. 经过冻融循环后,土壤中重金属的生物可给性比未冻融土壤略有升高. 随着养护时间和冻融时间的延长,土壤pH呈升高趋势. 不同阶段土壤扫描电镜结果显示,冻融循环致使土壤空隙变大、结构松散,说明冻融循环对稳定化土壤结构有一定损伤. 分析结果表明,冻融过程增加了Pb、Zn和Cd释放的环境风险.      

长江经济带市域生态文明建设现状及发展潜力初探

生态文明建设是长江经济带下一阶段的工作重点之一。从生态文明和发展潜力的内涵出发,构建了耦合协调度模型和发展潜力模型,并对长江经济带生态文明建设情况进行分析。研究发现:(1)长江经济带东中西部生态文明特征差异明显,东部为经济、社会系统优势区,中部为相对协调区,西部为自然系统相对优势区;(2)当前长江经济带生态文明格局主要受经济因素的影响;(3)协调发展地区整体上表现出最佳的生态文明发展潜力,协调发展应成为长江经济带生态文明建设的重要途径。     

Linking Cellulose Fiber Sediment Methyl Mercury Levels to Organic Matter Decay and Major Element Composition

Methylation of mercury (Hg) to highly toxic methyl Hg (MeHg), a process known to occur when organic matter (OM) decomposition leads to anoxia, is considered a worldwide threat to aquatic ecosystems and human health. We measured temporal and spatial variations in sediment MeHg, total Hg (THg), and major elements in a freshwater lagoon in Sweden polluted with Hg-laden cellulose fibers. Fiber decomposition, confined to a narrow surface layer, resulted in loss of carbon (C), uptake of nitrogen (N), phosphorus (P), and sulfur (S), and increased MeHg levels. Notably, fiber decomposition and subsequent erosion of fiber residues will cause buried contaminants to gradually come closer to the sediment–water interface. At an adjacent site where decomposed fiber accumulated, there was a gain in C and a loss of S when MeHg increased. As evidenced by correlation patterns and vertical chemical profiles, reduced S may have fueled C-fixation and Hg methylation at this site.     

液液萃取-HPLC-ICPMS联用技术测定水体中甲基汞

建立了二氯甲烷萃取,半胱氨酸-乙酸铵溶液反萃取,液相色谱-电感耦合等离子体质谱法测定水中甲基汞的方法。取样量为1 L时,方法检出限为0.1 ng/L,相对标准偏差为6.6%~13%,地表水、生活污水和工业废水3种实际水样的加标回收率分别为45.6%~70.5%、37.0%~65.6%、18.4%~61.8%。与5种甲基汞测定方法的前处理过程、分析仪器和检出限进行了比较,并讨论了无机汞的干扰情况及如何降低体系空白和消除无机汞干扰的质量控制手段。     

高分辨电感耦合等离子体质谱法测定地下水中稀土元素

采用高分辨电感耦合等离子体质谱法测定地下水中14种稀土元素,并选择Rh作内标,可消除测定中的质谱干扰和非质谱干扰,使方法在0μg/L~100μg/L范围内线性良好。方法检出限为0.002μg/L~0.005μg/L,实际水样的加标回收率为80.0%~117%,RSD为2.1%~3.8%。     

In vivo and in vitro metabolism of tobacco-specific nitrosamine, 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), by the freshwater planarian, Dugesia japonica

Cigarette smoke is a risk factor for human health, and many studies were conducted to investigate its adverse effects on humans and other mammals. However, since large amounts of cigarette products are produced and consumed, it is possible that tobacco chemicals can end up in aquatic environments through several routes, thus influencing aquatic organisms. In this study, the presence of tobacco-specific nitrosamine (TSNA), 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), in aquatic environment was demonstrated. Since toxic effects on and distribution patterns of tobacco chemicals in aquatic organisms were rarely studied, after results of an acute toxicity pretest were obtained, experiment was conducted to investigate the bioaccumulation pattern of NNK and distribution patterns of its metabolites, mainly 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL), in NNK-treated freshwater planarians, Dugesia japonica. Results from in vivo and in vitro studies showed that NNK was readily converted to NNAL through the carbonyl reduction in bodies of NNK-treated planarians. Tissue concentrations of both chemicals increased in time- and dose-dependent manners. Furthermore, we examined the end products of NNK/NNAL α-hydroxylation in NNK-treated planarians, but only 1-(3-pyridyl)-1,4-butanediol was detected, suggesting that NNK metabolism in planarians partially differs from that in mammalian systems. This is the first report on NNK metabolism in an aquatic organism and can be used as a foundation for developing freshwater planarians as a new in vivo model for the study of NNK toxicology in the future.     

Polymer coating of copper oxide nanoparticles increases nanoparticles uptake and toxicity in the green alga Chlamydomonas reinhardtii

Copper oxide nanoparticles (CuO NPs) are frequently used in a polymer-coated form, to be included in paints or fabrics for antimicrobial properties. Their application in antifouling paints may lead to the contamination of aquatic ecosystems. However, the toxicological risk of NPs in the environment is hard to evaluate due to a lack of knowledge on the mechanisms of NP interaction with biological systems. In this study, we investigated the effect of polymer coating on CuO NP toxicity in the green alga Chlamydomonas reinhardtii by comparing bare and polymer-coated CuO NPs prepared from the same CuO nanopowder. Both CuO NP suspensions were toxic to C. reinhardtii after 6 h treatment to concentrations of 0.005-0.04 g L⁻¹. Bare and polymer-coated CuO NPs induced a decrease of Photosystem II activity and the formation of reactive oxygen species. Polymer-coated CuO NP was found to be more toxic than the uncoated CuO NP. The higher toxicity of CS-CuO NP was mainly associated with the increased capacity of polymer-coated CuO NP to penetrate the cell compared to bare CuO NPs. These results indicates that the high toxicity of polymer-coated CuO NPs in algal cells results of intracellular interactions between NPs and the cellular system.