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2015

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In the context of reducing CO2 emissions to the atmosphere, chemical absorption with amines is emerging as the most advanced technology for post-combustion CO2 capture from exhaust gases of fossil fuel power plants. Despite amine solvent recycling during the capture process, degradation products are formed and released into the environment, among them aliphatic nitramines, for which the environmental impact is unknown. In this study, we determined the acute and chronic toxicity of two nitramines identified as important transformation products of amine-based carbon capture, dimethylnitramine and ethanolnitramine, using a multi-trophic suite of bioassays. The results were then used to produce the first environmental risk assessment for the marine ecosystem. In addition, the in vivo genotoxicity of nitramines was studied by adapting the comet assay to cells from experimentally exposed fish. Overall, based on the whole organism bioassays, the toxicity of both nitramines was considered to be low. The most sensitive response to both compounds was found in oysters, and dimethylnitramine was consistently more toxic than ethanolnitramine in all bioassays. The Predicted No Effect Concentrations for dimethylnitramine and ethanolnitramine were 0.08 and 0.18 mg/L, respectively. The genotoxicity assessment revealed contrasting results to the whole organism bioassays, with ethanolnitramine found to be more genotoxic than dimethylnitramine by three orders of magnitude. At the lowest ethanolnitramine concentration (1 mg/L), 84% DNA damage was observed, whereas 100 mg/L dimethylnitramine was required to cause 37% DNA damage. The mechanisms of genotoxicity were also shown to differ between the two compounds, with oxidation of the DNA bases responsible for over 90% of the genotoxicity of dimethylnitramine, whereas DNA strand breaks and alkali-labile sites were responsible for over 90% of the genotoxicity of ethanolnitramine. Fish exposed to > 3 mg/L ethanolnitramine had virtually no DNA left in their red blood cells.

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Elevated nutrient concentrations in streams in the Norwegian agricultural landscape may occur due to faecal contamination. Escherichia coli (E. coli) has been used conventionally as an indicator of this contamination; however, it does not indicate the source of faecal origin. This work describes a study undertaken for the first time in Norway on an application of specific host-associated markers for faecal source tracking of water contamination. Real-time quantitative polymerase chain reaction (qPCR) on Bacteroidales host-specific markers was employed for microbial source tracking (MST) to determine the origin(s) of faecal water contamination. Four genetic markers were used: the universal AllBac (Bacteroidales) and the individual specific markers BacH (humans), BacR (ruminants) and Hor-Bac (horses). In addition, a pathogenicity test was carried out to detect the top seven Shiga toxin-producing E. coli (STEC) serogroups. The ratio between each individual marker and the universal one was used to: (1) normalise the markers to the level of AllBac in faeces, (2) determine the relative abundance of each specific marker, (3) develop a contribution profile for faecal water contamination and (4) elucidate the sources of contamination by highlighting the dominant origin(s). The results of the qPCR MST analyses indicated the actual contributions of humans and animals to faecal water contamination. The pathogenicity test revealed that water samples were STEC positive at a low level, which was in proportion to the concentration of the ruminant marker. The outcomes were verified statistically by coupling the findings of major contamination sources with observations in the field regarding local land use (residential or agricultural). Furthermore, clear correlations between the human marker and E. coli counts as well as the ruminant marker and STEC quantity in faecally contaminated water were observed. The results of this study have the potential to help identify sources of pollution for targeted mitigation of nutrient losses.