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41.
Lead (Pb), cadmium (Cd), copper (Cu) and zinc (Zn) have been measured by electrothermal atomic absorption spectrometry in various sections of the 3623 m deep ice core drilled at Vostok, in central East Antarctica. The sections were dated from 240 to 410 kyear BP (Marine Isotopic Stages (MIS) 7.5 to 11.3), which corresponds to the 3rd and 4th glacial-interglacial cycles before present. Concentrations are found to have varied greatly during this 170 kyear time period, with high concentration values during the coldest climatic stages such as MIS 8.4 and 10.2 and much lower concentration values during warmer periods, such as the interglacials MIS 7.5, 9.3 and 11.3. Rock and soil dust were the dominant sources for Pb, whatever the period, and for Zn and Cu and possibly Cd during cold climatic stages. The contribution from volcanic emissions was important for Cd during all periods and might have been significant for Cu and Zn during warm periods.  相似文献   
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Environmental pollutants polychlorinated biphenyls (PCBs), especially dioxin-like PCBs, cause oxidative stress and associated toxic effects, including cancer and possibly atherosclerosis. We previously reported that PCB 126, the most potent dioxin-like PCB congener, not only decreases antioxidants such as hepatic selenium (Se), Se-dependent glutathione peroxidase, and glutathione (GSH) but also increases levels of the antiatherosclerosis enzyme paraoxonase 1 (PON1) in liver and serum. To probe the interconnection of these three antioxidant systems, Se, GSH, and PON1, we examined the influence of varying levels of dietary Se and N-acetylcysteine (NAC), a scavenger of reactive oxygen species (ROS) and precursor for GSH synthesis, on PON1 in the absence and presence of PCB 126 exposure. Male Sprague–Dawley rats, fed diets with differing Se levels (0.02, 0.2, or 2 ppm) or NAC (1 %), were treated with a single intraperitoneal injection of corn oil or various doses of PCB 126 and euthanized 2 weeks later. PCB 126 significantly increased liver PON1 mRNA, protein level and activity, and serum PON1 activity in all dietary groups but did not consistently increase thiobarbituric acid levels (thiobarbituric acid reactive substances, TBARS), an indicator of lipid oxidation and oxidative stress, in liver or serum. Inadequate (high or low) dietary Se decreased baseline and PCB 126-induced aryl hydrocarbon receptor (AhR) expression but further increased PCB 126-induced cytochrome P450 1A1 (CYP1A1) expression, the enzyme believed to be the cause for PCB 126-induced oxidative stress. In addition, a significant inverse relationship was observed not only between dietary Se levels and PON1 mRNA and PON1 activity but also with TBARS levels in the liver, suggesting significant antioxidant protection from dietary Se. NAC lowered serum baseline TBARS levels in controls and increased serum PON1 activity but lowered liver PON1 activities in animals treated with 1 μmol/kg PCB 126, suggesting antioxidant activity by NAC primarily in serum. These results also show an unexpected predominantly inverse relationship between Se or NAC and PON1 during control and PCB 126 exposure conditions. These interactions should be further explored in the development of dietary protection regimens.  相似文献   
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Using the GAINS (Greenhouse Gas–Air Pollution Interactions and Synergies) model, we derived Annex I marginal abatement cost curves for the years 2020 and 2030 for three World Energy Outlook baseline scenarios (2007–2009) of the International Energy Agency. These cost curves are presented by country, by greenhouse gas and by sector. They are available for further inter-country comparisons in the GAINS Mitigation Efforts Calculator—a free online tool. We illustrate the influence of the baseline scenario on the shape of mitigation cost curves, and identify key low cost options as well as no-regret priority investment areas for the years 2010–2030. Finally, we show the co-effect of GHG mitigation on the emissions of local air pollutants and argue that these co-benefits offer strong local incentives for mitigation.  相似文献   
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This paper provides an analysis of co-benefits for traditional air pollutants made possible through global climate policies using the Greenhouse Gas and Air Pollution Interactions and Synergies (GAINS) model in the time horizon up to 2050. The impact analysis is based on projections of energy consumption provided by the Prospective Outlook for the Long term Energy System (POLES) model for a scenario without any global greenhouse gas mitigation efforts, and for a 2°C climate policy scenario which assumes internationally coordinated action to mitigate climate change. Outcomes of the analysis are reported globally and for key world regions: the European Union (EU), China, India and the United States. The assessment takes into account current air pollution control legislation in each country. Expenditures on air pollution control under the global climate mitigation regime are reduced in 2050 by 250 billion € when compared to the case without climate measures. Around one third of financial co-benefits estimated world-wide in this study by 2050 occur in China, while an annual cost saving of 35 billion (Euros) € is estimated for the EU if the current air pollution legislation and climate policies are adopted in parallel. Health impacts of air pollution are quantified in terms of loss of life expectancy related to the exposure from anthropogenic emissions of fine particles, as well as in terms of premature mortality due to ground-level ozone. For example in China, current ambient concentrations of particulate matter are responsible for about 40 months-losses in the average life expectancy. In 2050, the climate strategies reduce this indicator by 50 %. Decrease of ozone concentrations estimated for the climate scenario might save nearly 20,000 cases of premature death per year. Similarly significant are reductions of impacts on ecosystems due to acidification and eutrophication.  相似文献   
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