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.
Environmental distribution conflicts (EDCs) related to the construction and operation of waste incinerators have become commonplace in China. This article presents a detailed case study of citizen opposition to an incinerator in the village of Panguanying, Hebei Province. Drawing on in-depth fieldwork, we show how this case was notable, because it transcended the local arena to raise bigger questions about environmental justice, particularly in relation to public participation in siting decisions, after villagers exposed fraudulent public consultation in the environmental impact assessment. An informal network between villagers and urban environmental activists formed, enabling the Panguanying case to exert influence far beyond the village locality. This network was critical in creating wider public debate about uneven power and substandard public participation in siting disputes, a central feature in many Chinese EDCs. By transcending local specificities and exposing broader, systemic inadequacies, this case became instrumental in supporting “strong sustainability”. 相似文献
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. 相似文献