Environmental Geochemistry and Health - Effective supply of environmental public services (EPS) is important to guarantee the mitigation of residential pollution exposure risk. This study analyzes... 相似文献
采用"自上而下"的能源清单法,研究了长株潭城市群2017年人为热排放量及其时空分布特征;同时,利用中尺度天气预报模式(Weather Research and Forecasting,WRF)及其耦合的UCM对夏冬两季分别进行数值模拟试验,定量分析了不同类型建成区人为热排放增温效应的季节性差异.结果表明:(1)长株潭2017年人为热排放总量为3.49x1017J/a,平均人为热排放强度为14.22 W/m2,工业、建筑、交通和人体新城代谢对人为热的贡献率分别为48.15%、40%、11.3%和0.55%.(2)人为热的引入使得城市群主城区夏季和冬季的平均温度分别升高了约0.7℃和1.5℃;冬季增温效果是夏季的2倍.(3)不同密度分区人为热排放导致的增温效果不同,总的来说,工业/商业区>高密度住宅区>低密度住宅区. 相似文献
Plastic pollution is a major environmental issue worldwide, calling for advanced methods to recycle waste plastics in the context of the circular economy. Here we review methods and strategies to convert waste plastics into value-added carbon materials, with focus on sources, properties, pretreatment of waste plastics, and on preparation of carbon materials. Pretreatment techniques include mechanical crushing, plastic stabilization and electrospinning. Carbon materials such as carbon nanotubes, graphene, carbon nanosheets, carbon spheres and porous carbon are prepared by oxygen-limited carbonization, catalytic carbonization, the template-based method, and pressure carbonization. We emphasize the conversion of polyethene terephthalate, polyethylene, polypropylene, polystyrene, halogenated plastics, polyurethane and mixed plastics.
AbstractThe roles of PM2.5-induced mitochondrial damage and oxidative stress on mast cell degranulation were examined in vitro. Mast cells were treated with suspensions of PM2.5 in Dulbecco’s modified Eagle’s medium at concentrations from 25 to 200?mg/L in the absence or presence of 10?mmol/L N-acetyl-L-cysteine. Biological effects and mitochondrial function were assessed by determining cell viability, β-hexosaminidase release, interleukin-4 secretion, reactive oxygen species generation, adenosine triphosphate production, potential alteration of mitochondrial membrane, and activities of mitochondrial electron transport chain complexes I and III. Exposure of mast cells to PM2.5 induced reduction of adenosine triphosphate production, collapse of mitochondrial membrane potential, and inhibition of the activity of complex III. Co-treatment of mast cells exposed to PM2.5 with N-acetyl-L-cysteine attenuated cytotoxicity and the production of reactive oxygen species, and decreased the release of β-hexosaminidase and interleukin-4. Evidently, PM2.5-induced oxidative stress plays an essential role in mitochondrial toxicity and mast cell activation. 相似文献