Azolla filiculoides has been evaluated for the adsorption of trace toxic metals from aqueous solution. The adsorption performance of the material was compared with commercial resins and fitted using the Langmuir and Freundlich models. The Freundlich model described the adsorption of copper and cadmium. Whilst the Langmuir isotherm had the better fit of the mercury data. The assumptions of the Freundlich model include multi-layer adsorption and different functional group binding. Conversely the Langmuir model suggests mono-layer adsorption and can infer single group reactivity. The pH effect on the uptake of the metals was investigated and an increase in removal was observed at higher pH with all the metals studied. The material has been thoroughly characterised using physical methods, such as, scanning electron microscopy X-ray photoelectron spectroscopy and electrophoretic mobility measurements. This enabled conclusions to be made regarding the surface functionality of the solid. Chemical characterisation included direct titrations, revealing a gradual dissociation of acidic groups as the pH increased within the experimental range. Kjeldahl nitrogen and amino acid analysis of several biological materials that have been used in metal sorption experiments showed A. filiculoides as having a large proportion of these cell constituents. The kinetics of metal ion uptake by the biosorbent was investigated and compared with commercially available resins. The kinetics are slower than conventional ion exchange resins and carbon adsorbents but entirely adequate for utilisation in a column process. The mechanism hypothesized for metal ion removal by the biosorbent is primarily attributed to ionogenic groups exchanging ions for copper and cadmium removal. Mercury on the other hand is said to be predominantly involved in a reduction-precipitation reaction on the surface of the adsorbent. Regeneration was successfully accomplished for copper and cadmium after minicolumn trials, with greater than 95 % elution of the metals using 0.1M HCI. The mini column trials showed a sharp breakthrough for these metals singularly and a dynamic equilibrium was observed during multi-metal processing. Mercury removal was much slower and more difficult with the same eluant, achieving a maximum of 50% removal. A method for a semi-continuous biosorbent process has been evaluated and proven to be successful in processing metal laden solution.

Cadmium (Cd) is a nonessential metal present in sublethal concentrations within the aquatic environment. Cd is an endocrine disruptor and high concentrations of this metal suppress stressor-induced cortisol production in fish. However, few studies have examined the effect of Cd at concentrations that are environmentally relevant on the functioning of the hypothalamus-pituitary-interrenal (HPI) axis. The HPI axis activity is essential in the stressor-induced cortisol production, a highly conserved adaptive response to stress in vertebrates. Elevation of plasma glucose in response to a rise in plasma cortisol is mediated through steroid activation of glucocorticoid receptors (GRs), but the mechanism of action of Cd in disrupting target tissue cortisol action is not known in fish. The overall objective of this thesis was to examine the impact of sublethal and environmentally relevant levels of Cd on the stress response and target tissue metabolic capacities, and to investigate the mechanisms of action of this metal in disrupting cortisol production and target tissue cortisol action in rainbow trout (Oncorhynchus mykiss). The impact of subchronic exposure to environmentally relevant levels of Cd on metabolic capacity and stress performance was identified through a 28 day (d) in vivo exposure of juvenile rainbow trout to either of two Cd concentrations (0.75 µg/L or 2.0 µg/L). During the exposure period, juvenile rainbow trout accumulated Cd within the liver, kidney and gills, but were able to adapt to exposure concentrations as no changes were observed in plasma cortisol, glucose and lactate levels. However, changes in abundance of mRNAs encoding proteins involved in corticosteroidogenesis, including melanocortin 2 receptor (MC2R), steroidogenic acute regulatory protein (StAR) and P450 side chain cleavage enzyme (P450scc), and liver GR protein expression suggesting endocrine disruption over the 28 d period. Also, target tissue metabolic capacities, including lower liver glycogen content and changes in intermediary metabolic enzyme activities in the liver and gill, were compromised by the 28 d exposure to Cd. The response to a secondary handling stressor at either 7 or 28 d exposure was attenuated suggesting that subchronic exposure to low levels of Cd disrupts the highly conserved adaptive stress response in rainbow trout. Upon further investigation using in vitro head kidney slices exposed to 0, 10, 100 or 1000 nM of Cd and stimulated with adrenocorticotropic hormone (ACTH), a similar inhibition of cortisol production was observed, as demonstrated in vivo, suggesting that Cd disrupts interrenal corticosteroidogenesis in fish. The impact of Cd on ACTH-stimulated cortisol production involved the suppression in the abundances of MC2R, StAR and P450scc transcripts. This response was also mimicked when head kidney slices from 7 d Cd exposed fish were incubated ex vivo with ACTH confirming that interrenal tissue is a key target for endocrine disruption by Cd. In both the in vitro and ex vivo incubations of head kidney slices 8-Bromo-cAMP (a cAMP analog) completely abolished the Cd-mediated cortisol inhibition demonstrating for the first time that Cd disruption of corticosteroidogenesis is occurring upstream of cAMP production. Further investigation of Cd-mediated impact on MC2R showed alterations in MC2R mRNA transcripts during in vivo exposure after 7 days and an attenuation of MC2R mRNA levels after Cd-exposed fish were subjected to a handling stressor. Disruptions in the mRNA abundance of MC2R was associated with disruptions of melanocortin receptor accessory protein 1 (MRAP1), but not MRAP2; a phenomenon that was also observed in ex vivo head kidney slices. Cell transfection studies confirmed that rainbow trout MC2R/MRAP1 receptor complex displayed decreased activity in the presence of Cd. Taken together these results suggest that Cd directly targets the MC2R/MRAP1 complex to inhibit ACTH-stimulated cortisol production in juvenile rainbow trout. In addition to Cd inhibiting interrenal steroidogenesis, the results also suggest that Cd may impact the negative feedback regulation of cortisol through the suppression of brain mineralocorticoid receptor (MR), but this requires further investigation. At the target tissue level, Cd by itself did not significantly affect liver metabolism, but inhibited the cortisol-induced glucose production in liver slices. This involved suppression of GR protein expression along with the suppression of GR-responsive genes, including phosphoenolpyruvate carboxykinase (PEPCK) and suppressor of cytokines signaling 1 (SOCS1) and changes in enzyme activities, including hexokinase, glucokinase, pyruvate kinase and PEPCK, pointing to a disruption in liver GR signaling by Cd. Altogether, Cd exposure disrupts the organismal stress responses in juvenile rainbow trout. Furthermore, Cd impairs the ability of juvenile rainbow trout to respond to a secondary stressor, which is a vital adaptive process that is fundamental to successful stress performance. Most importantly, these studies highlight for the first time that disruption of the HPI axis to attenuate cortisol production occurs at the level of the MC2R/MRAP1 complex, suggesting that the mechanism of action for attenuation of cortisol occurs at the level of MC2R activation. Also, GR signaling is a key target for Cd and may be a mechanism leading to altered metabolic capacities in stressed fish from Cd-contaminated sites. Overall environmentally relevant levels of Cd disrupt cortisol production and target tissue action of this steroid in rainbow trout.

Cadmium (Cd) is a nonessential metal present in sublethal concentrations within the aquatic environment. Cd is an endocrine disruptor and high concentrations of this metal suppress stressor-induced cortisol production in fish. However, few studies have examined the effect of Cd at concentrations that are environmentally relevant on the functioning of the hypothalamus-pituitary-interrenal (HPI) axis. The HPI axis activity is essential in the stressor-induced cortisol production, a highly conserved adaptive response to stress in vertebrates. Elevation of plasma glucose in response to a rise in plasma cortisol is mediated through steroid activation of glucocorticoid receptors (GRs), but the mechanism of action of Cd in disrupting target tissue cortisol action is not known in fish. The overall objective of this thesis was to examine the impact of sublethal and environmentally relevant levels of Cd on the stress response and target tissue metabolic capacities, and to investigate the mechanisms of action of this metal in disrupting cortisol production and target tissue cortisol action in rainbow trout (Oncorhynchus mykiss). The impact of subchronic exposure to environmentally relevant levels of Cd on metabolic capacity and stress performance was identified through a 28 day (d) in vivo exposure of juvenile rainbow trout to either of two Cd concentrations (0.75 µg/L or 2.0 µg/L). During the exposure period, juvenile rainbow trout accumulated Cd within the liver, kidney and gills, but were able to adapt to exposure concentrations as no changes were observed in plasma cortisol, glucose and lactate levels. However, changes in abundance of mRNAs encoding proteins involved in corticosteroidogenesis, including melanocortin 2 receptor (MC2R), steroidogenic acute regulatory protein (StAR) and P450 side chain cleavage enzyme (P450scc), and liver GR protein expression suggesting endocrine disruption over the 28 d period. Also, target tissue metabolic capacities, including lower liver glycogen content and changes in intermediary metabolic enzyme activities in the liver and gill, were compromised by the 28 d exposure to Cd. The response to a secondary handling stressor at either 7 or 28 d exposure was attenuated suggesting that subchronic exposure to low levels of Cd disrupts the highly conserved adaptive stress response in rainbow trout. Upon further investigation using in vitro head kidney slices exposed to 0, 10, 100 or 1000 nM of Cd and stimulated with adrenocorticotropic hormone (ACTH), a similar inhibition of cortisol production was observed, as demonstrated in vivo, suggesting that Cd disrupts interrenal corticosteroidogenesis in fish. The impact of Cd on ACTH-stimulated cortisol production involved the suppression in the abundances of MC2R, StAR and P450scc transcripts. This response was also mimicked when head kidney slices from 7 d Cd exposed fish were incubated ex vivo with ACTH confirming that interrenal tissue is a key target for endocrine disruption by Cd. In both the in vitro and ex vivo incubations of head kidney slices 8-Bromo-cAMP (a cAMP analog) completely abolished the Cd-mediated cortisol inhibition demonstrating for the first time that Cd disruption of corticosteroidogenesis is occurring upstream of cAMP production. Further investigation of Cd-mediated impact on MC2R showed alterations in MC2R mRNA transcripts during in vivo exposure after 7 days and an attenuation of MC2R mRNA levels after Cd-exposed fish were subjected to a handling stressor. Disruptions in the mRNA abundance of MC2R was associated with disruptions of melanocortin receptor accessory protein 1 (MRAP1), but not MRAP2; a phenomenon that was also observed in ex vivo head kidney slices. Cell transfection studies confirmed that rainbow trout MC2R/MRAP1 receptor complex displayed decreased activity in the presence of Cd. Taken together these results suggest that Cd directly targets the MC2R/MRAP1 complex to inhibit ACTH-stimulated cortisol production in juvenile rainbow trout. In addition to Cd inhibiting interrenal steroidogenesis, the results also suggest that Cd may impact the negative feedback regulation of cortisol through the suppression of brain mineralocorticoid receptor (MR), but this requires further investigation. At the target tissue level, Cd by itself did not significantly affect liver metabolism, but inhibited the cortisol-induced glucose production in liver slices. This involved suppression of GR protein expression along with the suppression of GR-responsive genes, including phosphoenolpyruvate carboxykinase (PEPCK) and suppressor of cytokines signaling 1 (SOCS1) and changes in enzyme activities, including hexokinase, glucokinase, pyruvate kinase and PEPCK, pointing to a disruption in liver GR signaling by Cd. Altogether, Cd exposure disrupts the organismal stress responses in juvenile rainbow trout. Furthermore, Cd impairs the ability of juvenile rainbow trout to respond to a secondary stressor, which is a vital adaptive process that is fundamental to successful stress performance. Most importantly, these studies highlight for the first time that disruption of the HPI axis to attenuate cortisol production occurs at the level of the MC2R/MRAP1 complex, suggesting that the mechanism of action for attenuation of cortisol occurs at the level of MC2R activation. Also, GR signaling is a key target for Cd and may be a mechanism leading to altered metabolic capacities in stressed fish from Cd-contaminated sites. Overall environmentally relevant levels of Cd disrupt cortisol production and target tissue action of this steroid in rainbow trout.

No description available.

Extraction, production, utilization and disposal of material resources have been undertaken continuously for much of human histories. Unavoidably, all of these activities have disturbed our environment, and subsequently have been harmful to humans and ecosystems in this and future generations. Due to time lag associated with both environment impact and the effects of measures taken to reduce this impact, existing approaches (i.e. monitoring and reacting) do not give sufficiently rapid feedback for effective environmental management. With regard to the complexity and concern related to environment-health chain effects, there is currently no environmental tool or approach that can provide comprehensive information and indicators covering all major environment and health themes, to enable decision makers to make informed judgements about regional policies and plans, relating to the sustainable use and disposal of material resources. Consequently, there is a need for developing a new approach by taking account of a multidisciplinary concept used in this thesis. Substance Flow Analysis (SFA) has been mainly applied in order to provide input information for Health Risk Assessment (HRA). The SFA approach provides the quantity of the substance that is transported (flows) and stored in the system (stock), and of which sub-system, flow, and process is the greatest concern. The HRA approach provides estimates of human health risk associated with site, activity and facility. An environmental fate and transport model is another key knowledge area incorporated into the HRA process. An integrating method of SFA, environmental fate and transport, and HRA is developed and illustrated by a case study of cadmium in Australia. This thesis shows that this new integration of existing stand-alone methods can provide holistic information and useful indicators covering all significant economic activities, environment, flows, and health risk assessment for selected substances. This enables better decision making on the use and disposal of substances at a range of levels in the economy, from corporations to regions and nations.

Agriculture currently faces a number of environmental sustainability issues. Three key issues that are the focus of this study are greenhouse gas emissions, depletion of mineral phosphorus resources and cadmium contamination in agricultural soil. Biomass can potentially be used as a renewable energy source and can also be returned to improve the nutrient and drainage structure of agricultural soils. Sustainable management of biomass and agriculture can have significant impacts on reducing greenhouse gas emissions from a region. Moreover, it reduces the demand for external energy supply, phosphorous (P) based fertilizer, and it??s associated Cadmium (Cd) impurity which can contaminate the soil, plant and food chains. These three issues have typically been considered separately, and managed by different agencies or organisations. The aim of this thesis is to develop an integrated decision support tool that can be used for evaluating alternative options for management and resource recovery from biomass for enhancing recovery of energy, returning carbon (C) and phosphorus (P) from biomass back to soil, reducing greenhouse gas emissions and also cadmium (Cd) contamination in an agricultural region. This research employed a combination of the tools of Material Flow Analysis (MFA), Geographic Information System (GIS) and Cost-Benefit Analysis (CBA). MFA is used as the primary tool for this research. GIS and CBA are combined with MFA in later stages of the overall procedure to develop an integrated decision support tool. This integrated tool has been applied to the Murrumbidgee Irrigation Area (MIA) in Australia. Tracking the flow of essential substances using MFA has identified current resource management efficiency and substances accumulation across the region. Integrating a spatial analysis tool (GIS) with MFA has provided a feedback driven monitoring tool for evaluating trends of spatial accumulation of substances on agricultural land. This enables the time remaining before acceptable limits are exceeded to be estimated on a spatial basis. Integrated MFA and CBA has been applied to evaluate the tradeoffs and potential synergies of alternative biomass management options. Overall the tool can assist in evaluating the effectiveness of alternative scenarios and visualise the results to stakeholders in a systematic way.

Thesis (Ph. D.)--Ohio University, March, 1993. / Title from PDF t.p.

Thesis (MSc)--University of Stellenbosch, 2007. / Bibliography. Also available via the Internet.

Thesis (Ph.D.)--University of Western Australia, 2005.

Thesis (Ph. D.)--University of North Texas, Dec., 2007. / Title from title page display. Includes bibliographical references.