37 research outputs found

    Coal mine water pollution and ecological impairment of one of Australia’s most 'protected' high conservation-value rivers

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    The environmental regulation of a coal mine in the greater Sydney area has failed to recognise the importance of and protect a high conservation-value river located in a World Heritage listed area. This study measured the water quality and ecological health (using macroinvertebrates) of the Wollangambe River and its tributaries near the point of the waste water discharge of a coal mine and assessed the longitudinal impact for 22 km downstream. The investigation revealed two important aspects. The first is the significant impact of the waste water discharge when compared to the otherwise near-pristine condition of the high conservation-value river system. The second is the spatial extent of the pollution from the mine that extends at least 22 km downstream from the outflow of coal mine wastes. The resulting water pollution is causing major impairment of the aquatic ecosystem, with reduced abundance, taxonomic richness and loss of pollution-sensitive macroinvertebrate groups. Water pollution from the mine includes thermal pollution, increased salinity and increased concentrations of zinc and nickel. The mine’s waste discharge also strongly modified the river’s ionic composition. The study also highlights the failure of the regulatory and governance systems that enable the mine to operate in a manner that causes major environmental impacts

    Impact of a coal mine waste discharge on water quality and aquatic ecosystems in the Blue Mountains World Heritage area

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    Disposal of coal mine wastewater to the headwaters of a high conservation value waterway caused water pollution and ecological degradation of a World Heritage listed upland river. Below the mine, macroinvertebrate family richness decreased by 65% and abundance by 90%. Upstream of the waste discharge had very low electrical conductivity (EC) of 30 μS/cm and pH was acidic (5.6) in contrast to that below the mine which showed EC 11 times higher (342 μS/cm) and a shift in pH to 7.2. The concentration of zinc below the mine was 101.5 μg/L and while below the permitted discharge level of 2500 μg/L as set in the environmental protection license (EPL), was 10 times greater than the recommended ANZECC guidelines for aquatic ecosystems. Nickel is not regulated under the mine EPL yet a concentration of more than double the recommended guideline was reported. The mine discharge also increased water temperature in the Wollangambe River by more than 2.5° C. The data clearly points to a need to review both the operation of the mine and the enabling regulatory system that currently allows pollution of zinc 200 times greater than recommended by the ANZECC guideline and generally does not adequately consider the impacts of the mine on the downstream National Park and World Heritage listed waterways

    Eco-servicing South Creek catchment : a case study from Australia's largest urban growth precincts

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    Assessing the health of catchments and creeks is often underpinned by application of water quality guidelines. Monitoring programs in New South Wales traditionally compare results to default ANZECC water quality guidelines are based on wide geographic areas and do not cater for localised conditions or include an assessment of biota. We outline an alternate framework for assessing catchment health by combining ecosystem services, community values and iconic species and ecological communities. The focus for this study is South Creek catchment which is Sydney’s largest urban freshwater stream and by 2031 will be home to an additional one million residents. To accommodate this growth the landscape and ecosystems will be drastically modified. In this study we explore opportunities to manage the South Creek catchment to maintain liveability values and ecosystem services for future communities through the use of iconic species. We suggest a locally based iconic species can provide a framework and serve as ecological indicators to assess future ecosystem and development scenarios. By following the steps outlined in this paper, catchment managers can develop their own locally based framework grounded on community and catchment specific metrics incorporating iconic species. This approach will provide multiple lines of evidence to identify catchment pressures and responses over time which will provide a more complete picture of catchment health than the use of water quality guidelines alone

    Increased synaptic excitation and abnormal dendritic structure of prefrontal cortex layer V pyramidal neurons following prolonged binge-like consumption of ethanol

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    Long-term alcohol use causes a multitude of neurochemical changes in cortical regions that facilitate the transition to dependence. Therefore, we used a model of long-term, binge-like ethanol consumption in rats to determine the effects on morphology and synaptic physiology of medial prefrontal cortex (mPFC) layer V pyramidal neurons. Following 10 weeks of ethanol consumption, we recorded synaptic currents from mPFC neurons and used neurobiotin filling to analyze their morphology. We then compared these data to measurements obtained from age-matched, water-drinking control rats. We found that long-term ethanol consumption caused a significant increase in total dendrite arbor length of mPFC layer V pyramidal neurons. Dendritic restructuring was primarily observed in basal dendrite arbors, with mPFC neurons from animals engaged in long-term ethanol drinking having significantly larger and more complex basal arbors compared with controls. These changes were accompanied by significantly increased total spine densities and spontaneous postsynaptic excitatory current frequency, suggesting that long-term binge-like ethanol consumption enhances basal excitatory synaptic transmission in mPFC layer V pyramidal neurons. Our results provide insights into the morphological and functional changes in mPFC layer V pyramidal neuronal physiology following prolonged exposure to ethanol and support changes in mPFC activity during the development of alcohol dependence
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