引调水河道氮的迁移转化及微生物群落结构特征——以望虞河为例

以引江济太调水工程-望虞河为研究对象,探究引调水河道氮素的迁移转化规律及微生物群落结构特征.于2020年10月、12月以及2021年1月在望虞河沿程布设监测点位并采集水样,分析其水体理化性质、氮的形态分布及含量、微生物群落结构变化特征.结果 表明:①硝酸盐氮是望虞河沿程水体中氮素的主要存在形态,占总氮浓度的75.3％～...     

反硝化细菌、硝酸钙和锆改性沸石联用对底泥中氮磷迁移转化的影响及硝态氮释放风险评估

本文考察了基于反硝化细菌、硝酸钙和锆改性沸石的组合技术（CN+DB+ZZ）对底泥中氮磷迁移转化的影响,并探讨了该技术的硝态氮释放风险.结果发现,单一的硝酸钙处理（CN）虽然可以有效地抑制底泥中磷的释放,但是会造成上覆水体的氨氮和硝态氮污染.硝酸钙和反硝化细菌联合处理（CN+DB）尽管可以有效地抑制底泥中磷的释放,并降低上覆水体的硝态氮二次污染风险,可是却无法有效地控制底泥中氨氮的释放.硝酸钙和锆改性沸石联合处理（CN+ZZ）虽然可以有效地抑制底泥中磷和氨氮向上覆水体的释放,但却会造成上覆水体硝态氮的二次污染.CN+DB+ZZ组合处理技术不仅可以有效地控制底泥中磷的释放,而且可有效降低底泥中氨氮的释放速率,并且与CN和CN+ZZ技术相比还可降低上覆水的硝态氮二次污染风险.CN+DB+ZZ组合技术对底泥中磷与铁同步释放的抑制、对底泥中氧化还原敏感态磷的削减、以及对底泥吸附磷酸盐和氨氮能力的增强,对于其控制底泥中磷和氨氮的释放是至关重要的.以上结果说明,CN+DB+ZZ组合技术是一种非常有希望的用于控制水体底泥中磷和氨氮释放的方法.     

底泥扰动下藻类对不同形态磷在水体中分布的影响

研究了反复扰动与藻类共存条件下,水体中溶解性磷、颗粒态磷、生物有效磷的分布规律,并分析了颗粒物质物理化学吸附与藻类生物利用对水体中磷消失的贡献率.结果表明,扰动抑制了水体中藻类生长,叶绿素a增加量仅为3.53μg/L(初始30μg/L)和4.80μg/L(初始120μg/L),而无扰动下该值分别为21.36μg/L (初始30μg/L)和14.49μg/L (初始120μg/L).并且,溶解氧水平和pH值均低于无扰动状态.扰动导致水体中总磷和颗粒态磷显著增加,但溶解性总磷(DTP)和溶解性磷酸盐(DIP)均有所降低.对于DTP而言,扰动状态下,颗粒物质吸附占90%,而无扰动下,则降低至60%,相应地,藻类生物利用则增加至40%.无论扰动与否,BAP基本处于稳定状态,而BAPP占BAP的百分比则有所增加.扰动状态下BAPP占PP的百分比明显低于无扰动状态.这暗示了扰动对水体中磷迁移和转化的作用大于藻.     

湿热水解预处理对餐厨废弃物液相物质转化的影响

设计湿热水解预处理温度(80、120、150和200 ℃)、时间(40、50、60和70 min)、加水量(40%、60%、80%和100%)的三因素四水平正交试验,研究湿热水解预处理对餐厨废弃物液相可浮油脱出量、ρ(COD_Cr)、糖类、ρ(VFA)(VFA为挥发性脂肪酸)等的影响. 结果表明:餐厨废弃物经湿热水解预处理后可浮油脱出量明显提高. 在150 ℃、加水量40%、处理60 min的湿热水解条件下,可浮油脱出量(67.7 mL/kg)最高,比未经预处理的对照组提高了2.65倍;同时,ρ(还原糖)和ρ(总糖)也达到最高,分别比对照组增加了16.29%和38.92%.随着温度升高和处理时间的延长,ρ(COD_Cr)不断升高,在200 ℃、加水量40%、处理70 min的湿热水解条件下,ρ(COD_Cr)最高为109.729 g/L,比对照组提高了1.39倍. 经湿热水解预处理后,ρ(VFA)也呈显著增加,在200 ℃、加水量100%、处理40 min的湿热水解条件下,ρ(VFA)达到最高,比对照组增加了66.26%.预处理后,ρ(乙酸)、ρ(丁酸)升高,ρ(乙醇)降低. 方差、极差综合分析表明,在湿热水解过程中,温度是影响餐厨废弃物液相物质转化的主控因子,其次是加水量和时间.      

沸石覆盖原位控制湖泊内源中等活性有机磷迁移转化

为揭示湖泊内源中等活性有机磷(MLOP)控制与释放发生机制,采用室内模拟试验,研究沸石覆盖原位控制湖泊内源MLOP迁移转化影响因子.结果表明:酸性水体促进内源MLOP迁移,碱性条件下抑制其转化,不同pH值试验水体沉积物中内源MLOP相对浓度为:[MLOP/TP]pH8>[MLOP/TP]pH7>[MLOP/TP]pH6;温度明显提高内源MLOP迁移水平,低温水体相对高温水体沉积物中内源MLOP含量较低,5℃条件下内源MLOP迁移表观量最大,其随时间迁移量呈幂函数关系,可表示为[MLOP/TP]=0.2823T0.657(R2为0.9709);好氧或厌氧条件下,内源MLOP均发生迁移,且迁移特征和影响效能高度一致,迁移平衡后好氧环境内源MLOP和厌氧内源MLOP相对浓度呈线性相关,可表示为[MLOP/TP]好氧环境=1.0884[MLOP/TP]厌氧环境 -0.0271(R2为99895);光照因子促使内源MLOP迁移,而避光和沸石粒径因素对内源MLOP迁移影响较小;底栖生物颤蚓通过爬行、摄食、掘穴、栖所建造及分泌排泄等一系列活动影响内源MLOP迁移.沸石原位控制湖泊内源MLOP迁移转化效能较弱.     

多种政策对经济-环境系统的综合作用分析

提出了一套分析多种政策手段对社会经济系统物质流和价值流变化的综合作用的理论概念,弥补了现有不足.在理论概念的基础上,构建了由7个子模块组成的具体模型框架,以反映多种政策手段共同实施对物质流和价值流变化的综合作用.以我国为案例,利用提出的模型框架评估了我国7类典型环境经济政策对我国经济增长和物质流变化的综合和单独作用,证明了综合分析的必要性.     

土壤-植物系统中多溴联苯醚(PBDEs)的迁移与转化研究进展

多溴联苯醚(PBDEs)是一类重要的新型持久性有机污染物,因其具有亲脂和难降解特性,易在土壤和沉积物等环境介质以及生物体内累积,同时会发生脱溴还原代谢和氧化代谢,生成毒性更大的低溴代PBDEs、羟基PBDEs(OH-PBDEs)和甲氧基PBDEs(MeO-PBDEs).研究PBDEs在土壤-植物系统的迁移转化对于认识PBDEs的陆生生态环境行为,评价其生态风险以及对食物链的潜在暴露风险都具有重要的意义.本文从土壤中PBDEs的代谢与转化行为,PBDEs的植物吸收与传输特征及其关键影响因素,以及植物体内PBDEs的脱溴、羟基化和甲氧基化代谢行为几个方面总结了PBDEs在土壤-植物系统迁移转化的最新研究进展,并就将来的研究方向提出一些思考和展望,有助于深入认识PBDEs及其代谢产物的环境归趋.     

经济转型中的中国废钢铁投资市场

废钢铁产业是我国再生资源产业的主体,其节能减排、低碳环保和不可替代的钢铁原料功效十分显著。阐述了我国废钢铁产业在经济转型中的主导地位、应用价值、投资环境及今后的发展战略。指出我国经济发展方式的转变,赋予了废钢铁产业良好的发展机遇和重大的历史使命,中国废钢产业具有良好的投资市场和巨大的发展空间。     

Comments on the Carcinogenicity and Mutagenicity of metals and their compounds†

The carcinogenicity of metals has received extensive study, both epidemiologically and in the laboratory. These have included case reports of occasional human occurrence or clusters of cancer cases as well as extensive epidemiologic studies; in addition, there has been significant laboratory research on the whole animals and in vitro systems. This body of information will be examined selectively.

I will not in this paper attempt a comprehensive review of the mutagenicity and carcinogenicity of metals and their compounds. Rather, I will attempt to set forth some historical perspectives, and to comment on some current gaps and needs.

Other papers in this workshop have presented thorough and very current reviews of most of the topics briefly noted in this presentation and do not require repetition here.

The cancer issue has been studied and reported on far more extensively than that relating to heritable mutations. There has been in recent years increasing interest in the use of short term tests for mutagenicity and cell transformation. These, however, are primarily with respect to their relationship to cancer production rather than to germ cell injury. Interest in cancer from metal compounds goes back a long time; in fact, one of the earliest reports was on the carcinogenicity of arsenic not many decades after the pioneering report of Sir Perceval Pott on cancer in chimney sweeps. Since then cancer has been definitely associated in humans with chromium compounds, nickel, and with less assurance but probably definitely with beryllium and cadmium. The confirmation of these findings in laboratory animals has been uneven. In the case of arsenic, for example, there has been only limited success in the production of cancer in laboratory animals with arsenic.

Many other metals have been found in laboratory studies to produce cancer, although with most of these, evidence of production of cancer in humans is either absent or extremely uncertain.

The extensive body of recent information relating to the testing of metals with a variety of short term tests will be briefly reviewed.     

Occupational exposures,delivered doses and exposure limits for chromium and nickel†

The interaction of HCH (50 mg/kg) and dietary protein levels on microsomal drug metabolizing enzymes system and liver lipids were studied in the rats for 90 days. The results indicated that rats fed a lower protein diet and HCH has a higher rate of mortality, lower rate of growth and an increased liver weight. A significant induction in the hepatic microsomal aminopyrine‐N‐demethylase, p‐nitroanisole‐O‐dealkylase, benzo(a)pyrene hydroxylase and glutathione‐S‐transferase activity was observed in pesticide treated animals as compared to control animals. The pathological changes observed in liver of HCH treated animals consisted mainly of necrosis and fatty degeneration of hepatocytes. HCH also induced the significant accumulation of cholesterol, triglycerides, phospholipid and total lipid in liver in low protein diet animals. Protein accelerates the metabolism of HCH, resulting in a decrease of HCH concentration with the increase of dietary protein level. A close correlation existed between lipid accumulation, induction of drug metabolizing enzyme system and deposition of HCH in liver.