957 resultados para OZONE EXPOSURE


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This study examines the potential effects of ocean acidification on countries and fisheries of the Mediterranean Sea. The implications for seafood security and supply are evaluated by examining the sensitivity of the Mediterranean to ocean acidification at chemical, biological, and macro-economic levels. The limited information available on impacts of ocean acidification on harvested (industrial, recreational, and artisanal fishing) and cultured species (aquaculture) prevents any biological impact assessment. However, it appears that non-developed nations around the Mediterranean, particularly those for which fisheries are increasing, yet rely heavily on artisanal fleets, are most greatly exposed to socioeconomic consequences from ocean acidification.

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Polar Oceans are natural CO2 sinks because of the enhanced solubility of CO2 in cold water. The Arctic Ocean is at additional risk of accelerated ocean acidification (OA) because of freshwater inputs from sea ice and rivers, which influence the carbonate system. Winter conditions in the Arctic are of interest because of both cold temperatures and limited CO2 venting to the atmosphere when sea ice is present. Earlier OA experiments on Arctic microbial communities conducted in the absence of ice cover, hinted at shifts in taxa dominance and diversity under lowered pH. The Catlin Arctic Survey provided an opportunity to conduct in situ, under-ice, OA experiments during late Arctic winter. Seawater was collected from under the sea ice off Ellef Ringnes Island, and communities were exposed to three CO2 levels for 6 days. Phylogenetic diversity was greater in the attached fraction compared to the free-living fraction in situ, in the controls and in the treatments. The dominant taxa in all cases were Gammaproteobacteria but acidification had little effect compared to the effects of containment. Phylogenetic net relatedness indices suggested that acidification may have decreased the diversity within some bacterial orders, but overall there was no clear trend. Within the experimental communities, alkalinity best explained the variance among samples and replicates, suggesting subtle changes in the carbonate system need to be considered in such experiments. We conclude that under ice communities have the capacity to respond either by selection or phenotypic plasticity to heightened CO2 levels over the short term.

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The response of the benthic microbial community to a controlled sub-seabed CO2 leak was assessed using quantitative PCR measurements of benthic bacterial, archaeal and cyanobacteria/chloroplast 16S rRNA genes. Samples were taken from four zones (epicentre; 25 m distant, 75 m distant and 450 m distant) during 6 time points (7 days before CO2 exposure, after 14 and 36 days of CO2 release, and 6, 20 and 90 days after the CO2 release had ended). Changes to the active community of microphytobenthos and bacteria were also assessed before, during and after CO2 release. Increases in the abundance of microbial 16S rRNA were detected after 14 days of CO2 release and at a distance of 25 m from the epicentre. CO2 related changes to the relative abundance of both major and minor bacterial taxa were detected: most notably an increase in the relative abundance of the Planctomycetacia after 14 days of CO2 release. Also evident was a decrease in the abundance of microbial 16S rRNA genes at the leak epicentre during the initial recovery phase: this coincided with the highest measurements of DIC within the sediment, but may be related to the release of potentially toxic metals at this time point.

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Substantial variations are reported for egg production and hatching rates of copepods exposed to elevated carbon dioxide concentrations (pCO2). One possible explanation, as found in other marine taxa, is that prior parental exposure to elevated pCO2 (and/or decreased pH) affects reproductive performance. Previous studies have adopted two distinct approaches, either (1) expose male and female copepoda to the test pCO2/pH scenarios, or (2) solely expose egg-laying females to the tests. Although the former approach is more realistic, the majority of studies have used the latter approach. Here, we investigated the variation in egg production and hatching success of Acartia tonsa between these two experimental designs, across five different pCO2 concentrations (385–6000 µatm pCO2). In addition, to determine the effect of pCO2 on the hatching success with no prior parental exposure, eggs produced and fertilized under ambient conditions were also exposed to these pCO2 scenarios. Significant variations were found between experimental designs, with approach (1) resulting in higher impacts; here >20% difference was seen in hatching success between experiments at 1000 µatm pCO2 scenarios (2100 year scenario), and >85% at 6000 µatm pCO2. This study highlights the potential to misrepresent the reproductive response of a species to elevated pCO2 dependent on parental exposure.

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Food is one of the main exogenous sources of genotoxic compounds. In heated food products, polycyclic aromatic hydrocarbons (PAHs) represent a priority group of genotoxic, mutagenic and/or carcinogenic chemical pollutants with adverse long-term health effects. People can be exposed to these compounds through different environments and via various routes: inhalation, ingestion of foods and water and even percutaneously. The presence of these compounds in food may be due to environmental contamination, to industrial handling and processing of foods and to oil processing and refining. The highest levels of these compounds are found in smoked foods, in seafood which is found in polluted waters, in grilled meats and, to a lesser extent, in vegetable fats and oils. Lower levels of PAHs are found in vegetables and in cereals and its products.

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This study examined the effect of exogenous benzo[ a ]pyrene (BaP), an important constituent of cigarette smoke, on cultured bovine retinal pigment epithelial (RPE) cells. Evidence is presented for its metabolic conversion into benzo[ a ]pyrene diol epoxide (BPDE) and the consequent formation of potentially cytotoxic nucleobase adducts in DNA. Cultured RPE cells were treated with BaP at concentrations in the range of 0–100 µm. The presence of BaP was found to cause inhibition of cell growth and replication. BaP induced the expression of a phase I drug metabolizing enzyme which was identified as cytochrome P450 1A1 (CYP 1A1) by RT–PCR and by Western blotting. Coincident with the increased expression of CYP 1A1, covalent adducts between the mutagenic metabolite BPDE and DNA could be detected within RPE cells by immunocytochemical staining. Additional support for their formation was afforded by nuclease P1 enhanced 32P-postlabelling assays on cellular DNA. Single-cell gel electrophoresis (comet) assays showed that exposure of RPE cells to BaP rendered them markedly more susceptible to DNA damage induced by broad band UVB or blue light laser irradiation. In the case of UVB, this is consistent with the photosensitization of DNA cleavage by nucleobase adducts of BPDE. Collectively, these findings imply that BaP has a significant impact on RPE cell pathophysiology and suggest mechanisms whereby exposure to cigarette smoke might cause RPE dysfunction and cell death, thus possibly contributing to degenerative disorders of the retina.

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