This paper provides an overview of the Motueka integrated catchment management (ICM) research programme. This research was based on the thesis that achieving ecosystem resilience at a catchment scale requires active measures to develop community resilience. We define a generic adaptive planning and action process, with associated knowledge management and stakeholder involvement processes, and illustrate those processes with observations from five research themes: (1) water allocation; (2) land use effects on water; (3) land and freshwater impacts on the coast; (4) integrative tools and processes for managing cumulative effects; and (5) building human capital and facilitating community action. Our research clearly illustrates the benefits for effective decision-making of carrying out catchment scale science and management within collaborative processes which patiently develop trusting relationships. We conclude that coastal catchments should be managed as a holistic continuum from ridge tops to the sea and that some processes like floods or loss of community resilience have decadal consequences, which support the need for long-term monitoring and investment.

Microbial contamination of New Zealand's rivers, lakes and coastal waters can pose a risk to human health through both recreational contact and the consumption of contaminated shellfish. Microbial source tracking (MST) methods provide a means to identify potential contaminant sources, which can lead to high faecal indicator bacteria concentrations and elevated human health risk because of associated pathogens. Eight MST markers, including general, ruminant and human-associated Bacteroidales markers, a duck-associated E2 marker, a gull-associated Catellicoccus marimammalium marker and three additional human markers [Enterococcus faecium esp gene, Methanobrevibacter smithii nifH gene, and human polyomaviruses (HPyVs)] were tested for host specificity and sensitivity using an array of animal faecal samples of known origin and wastewater samples. The cross-reactivity identified for some of the markers, although limited, signals a need to validate overseas markers further in New Zealand before employing them in field studies. Application of MST markers on water samples collected from an urbanised section of the Maitai River (Nelson, New Zealand) identified the presence of faecal contamination originating from humans, ruminants and birds. Human faecal contamination was present in the lower section of the Matai River, and in stormwater drains entering the river, in association with elevated faecal coliform concentrations. Application of the markers to the rural Little Sydney Stream (near Motueka, Tasman district, NZ) identified faecal contamination derived from ruminants, which is consistent with the agricultural (pasture) use of the catchment. This study indicates that some of the markers developed overseas can be used effectively to track sources of microbial contamination in New Zealand watersheds.

Hydrographic and water quality surveys of the Motueka River and its river plume were conducted during a moderate flood event (peak flow of 420 m 3

Progress towards development of a river plume ecosystem basis for management of coastal resources requires a thorough understanding of the nature and spatial extent of terrestrial influences on receiving water and seabed characteristics. As a case study, we estimate suspended sediment (SS) loading rates from the Motueka River catchment into Tasman Bay, New Zealand and describe benthic characteristics along a series of transects encompassing the coastal river plume. A mineral-rich geological formation in the headwaters of the river was identified as a storm-generated source of highly elevated concentrations of nickel and chromium in river margin sediments, and coastal sediments extending !5 km offshore. A major storm in 2005, focused in the upper catchment, resulted in an estimated SS discharge of 161,000 tonnes into the Bay. Spatial gradients of a suite of sediment trace metal signatures, organic content and infauna community structure were used to define a river plume depositional footprint of c. 180 km 2. We suggest that the boundaries of the Motueka catchment be redefined to include this area in order to facilitate engagement of marine stakeholders in management decisions that may affect coastal biological resources.

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Rationale: Since there is a well−established association between inhaled ambient ultrafine particles and increased risk of cardiopulmonary disease, it has been suggested that inhaled engineered nanoparticles (NPs) may also induce adverse effects on the cardiovascular system. We hypothesized that inhaled nickel (Ni) NPs could induce not only pulmonary but also systemic inflammation, which could ultimately contribute to progression of atherosclerosis in a susceptible mouse model. Methods: Male ApoE knockout mice were exposed either to filtered air or Ni NPs at around 100 microgram per cubic meter for 5h/d, 5d/wk for either 1 week or 5 months. Various indicators of inflammation were measured at the end of the exposures, and the degree of plaque formation on the aorta was determined after the 5m−exposure. Results: The analyses using bronchoalveolar lavage fluid revealed significant pulmonary inflammation at both time points and these results were consistent with gene expression analyses showing up−regulation of various pro−inflammatory cytokine genes in the lung. Some of the cytokines were also up−regulated in the spleen and heart following the 5m−exposure and that is, along with increased expression of an acute phase protein in the liver, indicative of systemic inflammation induced by inhaled Ni NPs. After 5−month exposure, the mice exposed to Ni NPs developed significantly more plaque around the aortic arch area. Conclusions: These results suggest that inhaled Ni NPs, at occupationally relevant levels, can induce significant acute and chronic pulmonary inflammation, systemic inflammation, and in the long term, exacerbation of atherosclerosis. Further studies will be needed to investigate mechanisms in which inhaled NPs could affect the cardiovascular system. This abstract is funded by: NIH grant (RO1−ES015495). Am J Respir Crit Care Med 179;2009:A5256 Internet address: www.atsjournals.org Online Abstracts Issue