高效液相色谱在环境监测中的应用

论述了高效液相色谱法适于环境样品中分子量大、挥发性低、热稳定性差的有机污染物的分析与分离。参阅了国内外文献，例举了用高效液相色谱法测定环境样品中多环芳烃、酚类、多氯联苯、酞酸酯类、联苯胺类、阴离子和非离子表面活性剂、有机农药等有机污染物的测定条件及分离结果。     

环境中汞的污染状况及监测

本文主要介绍环境中汞污染的来源；汞及其化合物的毒性，并且着重说明甲基汞对人类健康的损害状况；同时也介绍对环境中的无机汞和有机汞的监测分析方法，其中几种比较常用的甲基汞的分析方法。     

电化学强化低能耗废水生物处理技术研究

以碳布为阴阳极材料构建一种新型的生物电化学系统（BES）,研究该系统在不曝气条件下对城市污水的处理效果,并与传统的厌氧和好氧处理方法进行比较。结果表明,该BES处理城市污水是可行的,与传统曝气法相比能够显著降低能耗。在进水CODcr,为350mg／L、NH3-N为15mg／L、水力停留时间（HRT）为24h时,电化学强化生物处理系统对CODcr和NH3-N的去除率达84％和80％,优于同等条件下的厌氧、好氧生物处理方法。BES的输出电压最高为211mV。     

啤酒行业涉氨环境风险特征、评估及防控对策

为了解和掌握啤酒行业涉氨环境风险状况,分析了啤酒行业液氨在运输、贮存和使用过程中的环境风险单元和特征。以典型啤酒厂为例,对其环境风险进行评估,确定环境风险等级,并利用环境风险评价系统(RiskSystem)模型对其在不同风速条件下发生液氨泄漏的环境风险进行了预测分析,进而提出有针对性的环境风险防控对策。研究结果表明:啤酒行业在液氨贮存和运输环节存在较大的环境风险,阀门、法兰、接口等连接部位腐蚀和操作不当是氨泄漏的主要原因。根据典型案例环境风险评估和模拟预测结果,在受体敏感区域环境风险较大,风速对氨泄漏事故的影响范围有较大作用,需要严格预防和加强风险控制。建议国家和地方尽快出台相应的环境风险防范技术规范;涉氨单位应以预防为主,加强环境风险单元和重点环节的隐患排查力度,严格落实风险防控措施和要求。     

脉冲电晕低温等离子体提高一氧化氮氧化效率的实验研究

提高一氧化氮（NO）的氧化效率对于提高生物法处理该类废气的净化效率具有重要意义。实验研究了低温等离子体在脉冲电晕条件下氧化废气中NO的过程,考察了不同峰值电压、氧气含量、气体停留时间和添加有机物等因素对提高NO氧化效率的影响。结果表明：低温等离子法可有效地提高NO的氧化效率,主要产物为NO₂;室温条件下,当进气NO浓度590 mg/m³、脉冲频率50 Hz时,增大峰值电压、气体停留时间和进气中的氧气含量可提高NO的氧化效率;在最适峰值电压15 kV,气体停留时间5 s时,NO氧化效率为20%;在进气NO中添加甲苯、乙醇后,NO氧化效率可增加至30%以上,甲苯的效果要好于乙醇。     

环保疏浚底泥干化技术研究

环保疏浚过程中产生的大量污染底泥堆放在底泥堆场,不能快速干化,长时间占用土地资源,增加工程投资。在总结分析国内外环保疏浚底泥干化技术的基础上,系统地介绍不同底泥干化技术及其应用现状,并分析存在的问题,探讨了今后的发展趋势。     

突变灰盖鬼伞过氧化物酶降解刚果红的响应面法优化分析简

酶法降解偶氮染料刚果红是一个复杂的过程,受温度、pH、酶量、刚果红浓度和双氧水浓度显著影响。为研究各因素及因素间交互作用对刚果红降解影响,提高刚果红的降解率,分别使用单因素法和响应面分析法对刚果红降解条件进行了优化。单因素实验结果显示灰盖鬼伞过氧化物酶降解刚果红的最适条件为：pH 5.0、32℃、酶量4.98 U、双氧水0.1 mmol/L、刚果红20 mg/L,此时刚果红最高降解率为34.84%。然后选双氧水浓度、刚果红浓度和灰盖鬼伞过氧化物酶量作为3个因素,通过中心组合设计实验,用响应面法对刚果红降解进行优化分析,最后得到一个拟合度良好的二次多项方程模型（R²=0.9900）。方差分析结果显示,刚果红浓度和酶量是影响最显著的因素,双氧水与酶以及染料与酶之间的交互作用极显著。响应面分析优化后的反应体系为：双氧水浓度0.15 mmol/L,刚果红浓度为27.21 mg/L,酶为2.0 7 U,在此条件下,刚果红降解率达58.13%。     

Emission factors and particulate matter size distribution of polycyclic aromatic hydrocarbons from residential coal combustions in rural Northern China

Coal consumption is one important contributor to energy production, and is regarded as one of the most important sources of air pollutants that have considerable impacts on human health and climate change. Emissions of polycyclic aromatic hydrocarbons (PAHs) from coal combustion were studied in a typical stove. Emission factors (EFs) of 16 EPA priority PAHs from tested coals ranged from 6.25 ± 1.16 mg kg^?1 (anthracite) to 253 ± 170 mg kg^?1 (bituminous), with NAP and PHE dominated in gaseous and particulate phases, respectively. Size distributions of particulate phase PAHs from tested coals showed that they were mostly associated with particulate matter (PM) with size either between 0.7 and 2.1 μm or less than 0.4 μm (PM_0.4). In the latter category, not only were more PAHs present in PM_0.4, but also contained higher fractions of high molecular weight PAHs. Generally, there were more than 89% of total particulate phase PAHs associated with PM_2.5. Gas-particle partitioning of freshly emitted PAHs from residential coal combustions were thought to be mainly controlled by absorption rather than adsorption, which is similar to those from other sources. Besides, the influence of fuel properties and combustion conditions was further investigated by using stepwise regression analysis, which indicated that almost 57 ± 10% of total variations in PAH EFs can be accounted for by moisture and volatile matter content of coal in residential combustion.     

中国显示器件行业VOCs排放特征及控制对策

为掌握和了解我国电子行业VOCs的排放特征,以显示器件行业为研究对象,梳理和分析其生产工艺及排污环节;通过典型企业有机废气的实际排放监测,掌握其VOCs排放水平;利用排放因子法,核算了2011-2016年我国显示器件行业VOCs的排放量,分析其排放量的变化趋势及空间分布特征.结果表明:受产量和污染控制效率变化的双重影响,2011-2016年我国显示器件行业VOCs排放量（文中涉及"全国"的各要素范围均未包含港澳台地区）呈先增后降的趋势,2015年达到最大值（15 605 t）,此后在产量增长放缓和污染控制效率提高的作用下,2016年的排放量有所下降;从排放占比来看,显示器件行业无组织VOCs排放占比从2011年的45%升至2016年的53%,车间无组织VOCs逸散,以及废水处理过程、有机原辅料和有机废液储运等环节的VOCs无组织排放是行业污染控制的重点和难点.研究显示,我国显示器件行业VOCs无组织排放量占比逐年上升,为控制未来行业VOCs排放,企业应将无组织排放转化为有组织排放,之后再通过高效的末端处理装置来减少VOCs排放量.      

Blood concentrations of lead,cadmium, mercury and their association with biomarkers of DNA oxidative damage in preschool children living in an e-waste recycling area

Reactive oxygen species (ROS)-induced DNA damage occurs in heavy metal exposure, but the simultaneous effect on DNA repair is unknown. We investigated the influence of co-exposure of lead (Pb), cadmium (Cd), and mercury (Hg) on 8-hydroxydeoxyguanosine (8-OHdG) and human repair enzyme 8-oxoguanine DNA glycosylase (hOGG1) mRNA levels in exposed children to evaluate the imbalance of DNA damage and repair. Children within the age range of 3–6 years from a primitive electronic waste (e-waste) recycling town were chosen as participants to represent a heavy metal-exposed population. 8-OHdG in the children’s urine was assessed for heavy metal-induced oxidative effects, and the hOGG1 mRNA level in their blood represented the DNA repair ability of the children. Among the children surveyed, 88.14% (104/118) had a blood Pb level >5 μg/dL, 22.03% (26/118) had a blood Cd level >1 μg/dL, and 62.11% (59/95) had a blood Hg level >10 μg/dL. Having an e-waste workshop near the house was a risk factor contributing to high blood Pb (r _s  = 0.273, p < 0.01), while Cd and Hg exposure could have come from other contaminant sources. Preschool children of fathers who had a college or university education had significantly lower 8-OHdG levels (median 242.76 ng/g creatinine, range 154.62–407.79 ng/g creatinine) than did children of fathers who had less education (p = 0.035). However, we did not observe a significant difference in the mRNA expression levels of hOGG1 between the different variables. Compared with children having low lead exposure (quartile 1), the children with high Pb exposure (quartiles 2, 3, and 4) had significantly higher 8-OHdG levels (β _Q2 = 0.362, 95% CI 0.111–0.542; β _Q3 = 0.347, 95% CI 0.103–0.531; β _Q4 = 0.314, 95% CI 0.087–0.557). Associations between blood Hg levels and 8-OHdG were less apparent. Compared with low levels of blood Hg (quartile 1), elevated blood Hg levels (quartile 2) were associated with higher 8-OHdG levels (β _Q2 = 0.236, 95% CI 0.039–0.406). Compared with children having low lead exposure (quartile 1), the children with high Pb exposure (quartiles 2, 3, and 4) had significantly higher 8-OHdG levels.