Between 1999 and 2006, a plateau interrupted the otherwise continuous increase of atmospheric methane concentration [CH4] since preindustrial times. Causes could be sink variability or a temporary reduction in industrial or climate-sensitive sources. We reconstructed the global history of [CH4] and its stable carbon isotopes from ice cores, archived air, and a global network of monitoring stations. A box-model analysis suggests that diminishing thermogenic emissions, probably from the fossil-fuel industry, and/or variations in the hydroxyl CH4 sink caused the [CH4] plateau. Thermogenic emissions did not resume to cause the renewed [CH4] rise after 2006, which contradicts emission inventories. Post-2006 source increases are predominantly biogenic, outside the Arctic, and arguably more consistent with agriculture than wetlands. If so, mitigating CH4 emissions must be balanced with the need for food production.
During the Bremerhaven Workshop, effects of contaminants along a well characterised North Sea contaminant gradient heading northwest of the port of Bremerhaven in the German Bight were determined in dab Limanda lirnanda using i n vitro techniques on isolated hepatocytes. Results demonstrated that lysosomal membrane integrity was impaired following contaminant exposure which resulted in an inability to retain the supravital dye neutral red and in reduced lysosomal uptake of the fluorescent probe acridine orange. There was an improvement in the condition of exposed hepatocytes in samples taken further offshore, and away from the source of the contaminant, however, this trend was reversed in samples taken from the furthermost station on the northeast tail of the Dogger Bank. These findings are related to the histopathological evidence of abnormal lysosomal enlargement and disturbance of liver cell structure.
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