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    Inferring arsenic anomalies indirectly using airborne hyperspectral imaging – Implication for gold prospecting along the Rise and Shine Shear Zone in New Zealand
    (Elsevier B V, 2024-08-01) Chakraborty R; Kereszturi G; Pullanagari R; Craw D; Durance P; Ashraf S
    Well-exposed mineral deposits are scarce at a global level and presently potential mineral-rich sites are underlying vegetation cover and topsoil, which are suboptimal for direct remote sensing based exploration techniques. This study aims to implement an indirect approach to arsenic (As) distribution mapping using the surface manifestations of the subsurface geology and link it to the known gold mineralisation in the study area. Rise and Shine Shear Zone (RSSZ) in New Zealand is broadly a part of the Otago schist hosting lower to upper green-schist facies rocks manifesting mesothermal gold mineralisation. The area has several surficial geological imprints separating mineralised and non-mineralised zones, but these are dominated by topographic ruggedness, soil moisture and vegetation (mainly grass/tussock) spectra in the hyperspectral data. Initially, a band selection using Recursive Feature Elimination (RFE) was executed. The bands generated were tallied with the field and geological understanding of the area. The resultant 85 bands were then further put through Orthogonal Total Variation Component Analysis (OTVCA) to concise the information in 10 bands. OTVCA output was then classified using Random Forest classifier to map three levels of As concentration (<20 ppm, between 20 and 100 ppm and >100 ppm). The potentially high As concentration zones are likely to be related to the gold mineralisation. The geology of the area correlates with soil exposure which is captured by the classification in some parts, this increases the accuracy but also makes the classification analysis challenging.
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    Investigations into the uptake and effects of long-term cadmium and arsenic exposure on the earthworm Eisenia fetida : a thesis presented in partial fulfilment of the requirements for the degree of Doctor of Philosophy at Massey University, Wellington, New Zealand
    (Massey University, 2020) Dharmadasa, Lokugama
    Cadmium (Cd) and arsenic (As) are trace elements that differ in their chemistries but are both highly toxic, and common soil contaminants in agricultural land and contaminated sites. Their potential impacts range from adverse effects on soil-dwelling organisms to uptake into food and leading to human exposures. This study examines the uptake and effects of Cd and As individually and in mixtures primarily on the earthworm Eisenia fetida on up to three consecutive generations, and the potential for recovery when exposure ceases. Exposure ranges were selected to minimise mortality and permit reproduction. Key variables examined were contaminant concentrations and associated trace elements in worm tissue, growth, reproduction, and levels of gene expression. In worms exposed to Cd-spiked soils, Cd accumulation was rapid. Three key factors determining [Cd] in worm tissue were exposure level, time, and the bioconcentration factor (BCF), which increased with decreasing soil [Cd]. Results indicate that for all exposure conditions, and given enough time, Cd accumulation will continue until a lethal tissue level is reached. This point may be either before or after reproduction has occurred (depending on circumstances), but indicates a need to re-examine standardised approaches to toxicity testing for cumulative and biologically persistent contaminants such as Cd. The biological half-life for Cd loss was 6.5 months. This implies that worms that have been exposed to elevated Cd for more than a few weeks would unable to eliminate much of the accumulated burden over their normal lifetimes. Worms exposed to Cd took longer to reach sexual maturation, and at higher exposures, cocoon production progressively decreased from generation to generation. However, there were differences depending on the exposure level. At the lowest level (30 mg/kg), first generation worms returned to clean soil showed a large rebound effect, and by the third generation there was a recovery in cocoon production. By contrast, for higher (90 and 270 mg/kg) and longer (56 d and 84 d) exposures worms performed more poorly, suggesting that there is a tissue Cd threshold beyond which recovery becomes challenging. Evidence from gene expression results are consistent with the idea that this threshold corresponds to a point at which the Cd-sequestering protein metallothionein (MT) has reached saturation, as can also occur in human kidney tissue. Below this point, worms transferred to clean soils will recover. Above it, they will not. As (spiked as arsenate, AsO₄³⁻) also accumulated in worm tissue with exposure concentration and time, but showed some distinct differences compared to Cd. Modest As exposure extended for longer than 28 d had the unusual effect of stimulating growth and causing excessive cocoon production, an effect likely to be missed in most standardised tests. The effects are not thought to be related to parasite suppression, because they were accompanied by large-scale changes to gene expression. Despite appearing beneficial, by the second generation it was clear that effects of the As exposure were overwhelmingly negative, both in terms of extremely low survival rates and the delayed growth of surviving earthworms. Perhaps more notably, results for both the lower exposure condition (10 mg/kg soil As) and As-exposed worms returned to clean soils, suggest there are circumstances where As may promote its own uptake in a positive feedback loop. If correct such an effect may be linked to an increase in uptake of phosphate (PO₄³⁻) for cellular repair, with co-uptake of arsenate (AsO₄³⁻, which is isomorphous). A parallel mechanism is known for marine fish. Remarkably, results suggest that Cd exposure may have also caused an increase in As uptake, from soils that contained only natural [As]. Though a tentative finding, such an effect would be consistent with the idea that any contaminant that causes cellular damage in an invertebrate may trigger a need for more soil phosphate, presumably with some As co-uptake. This would also imply that many (presumed) single contaminant exposures whether in the laboratory or the field may in fact be As co-exposures. Relevant to this, the adverse impacts of As and Cd co-exposure were found to be more severe than effects of exposure to either contaminant alone; despite the fact the lower amounts of each contaminant were taken up under the co-exposure condition. This result supports an argument that soil guideline values derived from single contaminant toxicity experiments may be insufficiently protective for soil invertebrates in many real-life settings. Gene expression results were useful as an interpretive tool, with numbers and overlaps of differentially expressed genes being more useful than knowledge of the subset of named genes and their putative functions. Exposure to Cd or/and As triggered large-scale changes in gene expression, indicating ‘organism-wide’ biochemical responses and providing circumstantial evidence that supported particular interpretations, such as existence of an MT saturation-threshold, and the existence of substantive biochemical changes between lower and higher As exposures. Analysis of differentially expressed genes in common between Cd-only, As-only and co-exposure suggests existence of both similar and different impacts of toxicity under the three conditions.
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    Arsenic in urban air : sources, health risk and mitigation : a thesis presented in partial fulfilment of the requirements for the degree of Master of Philosophy in Environmental Health, Massey University, Wellington, New Zealand
    (Massey University, 2015) Mitchell, Tamsin A.
    Over recent years, several studies have suggested that high concentrations of arsenic may occur in outdoor air in urban areas of New Zealand on some winter nights. These spikes in arsenic concentrations are presumed to be caused by some householders burning copper-chrome-arsenate (CCA)-treated wood as a fuel for domestic home heating, but detailed examination of the issue has been lacking. The aims of this work are to examine the concentrations and source(s) of arsenic in ambient air in a representative New Zealand wood-burning community, identify and quantify potential health risks linked to both arsenic in air and the activity of burning CCA-treated wood, and undertake an initial exploration of social factors that may contribute to the issue. The town of Wainuiomata in the Wellington region was selected as the representative community. Concentrations of total arsenic in Wainuiomata outdoor air were measured over two years, along with a number of other relevant variables useful for source characterisation, including two size fractions of particulate matter (PM10 and PM2.5), black carbon and other trace elements. Over both years, concentrations of arsenic in Wainuiomata air were indistinguishable from the national ambient air quality guideline of 5.5 ng/m3 expressed as an annual average. Arsenic levels were strongly seasonal and peaked during the winter months, but with significant variability from night to night. The highest 24-hour concentration recorded during winter was 79 ng/m3. Results of correlation analysis and source attribution provide strong support for the idea that the principal source of elevated arsenic in outdoor air is the domestic burning of wood treated with CCA preservative. A detailed exposure model was developed and applied to estimate and contextualise potential arsenic exposures that may be experienced by adults and children living in the community, and quantify relative health risks. Potential community health impacts are estimated not to be significant where exposure is limited to outdoor arsenic, including that which infiltrates into the indoor environment, where “not significant” is defined as an additional lifetime cancer risk of less than 1 in 100,000 and a hazard quotient less than 1. Annual average arsenic in outdoor air would need to be around 15 times higher than the guideline value to increase an individual’s attributable lifetime cancer risk to 1 in 10,000. Of more potential concern are health risks arising from indoor exposure for residents who use CCA-treated timber as supplementary firewood where this may lead to fugitive emissions of arsenic from the firebox into indoor air. Not only does the predicted excess lifetime cancer risk approach 7 in 100,000, but there are also non-cancer health risks to children due to short-term exposure to the relatively higher levels of arsenic during the winter months. Hazard quotients above 1 were found to potentially exist for a small number of children (4%) based on the likelihood of living in a home where CCA-treated timber might be burnt combined with the presence of at least one adult smoker. However, overall greatest potential for acute health risk for children was found to be posed by accidental or incidental ingestion of CCA-wood ash, which contains very high concentrations of arsenic. Results of focus group sessions and community surveying provided useful contextual information about the source activity and identification of some potentially modifiable social factors, along with some understanding about why prohibition of the activity of burning CCA-treated wood may be ineffective. Findings included an upper estimate of the proportion of households that may burn CCA-treated timber (approximately 16%), and identification of the problem that most residents are not able to distinguish treated from untreated wood. A number of recommendations are made. Despite the preliminary nature of the findings due to uncertainties in the modelling and toxicity reference values, it is recommended that efforts should be made to discourage the practice of CCA-wood burning as a precautionary measure to protect against inhalation exposure to indoor sources of arsenic and ingestion of contaminated ash by children. Community education initiatives would need to be developed from the perspective of local residents, most of whom cannot identify CCA-treated wood. It would be ideal if this were complemented with a high-level review of the policy and regulatory framework which permits the manufacture, use and disposal of CCA-treated wood in New Zealand, to determine where risks might be best managed.