Opportunities and challenges of integrating ecological restoration into assessment and management of contaminated ecosystems.

Ecosystem restoration planning near the beginning of the site assessment and management process ("early integration") involves consideration of restoration goals from the outset in developing solutions for contaminated ecosystems. There are limitations to integration that stem from institutional barriers, few successful precedents, and limited availability of guidance. Challenges occur in integrating expertise from various disciplines and multiple, sometimes divergent interests and goals. The more complex process can result in timing, capacity, communication, and collaboration challenges. On the other hand, integrating the 2 approaches presents new and creative opportunities. For example, integration allows early planning for expanding ecosystem services on or near contaminated lands or waters that might otherwise have been unaddressed by remediation alone. Integrated plans can explicitly pursue ecosystem services that have market value, which can add to funds for long-term monitoring and management. Early integration presents opportunities for improved and productive collaboration and coordination between ecosystem restoration and contaminant assessment and management. Examples exist where early integration facilitates liability resolution and generates positive public relations. Restoration planning and implementation before the completion of the contaminated site assessment, remediation, or management process ("early restoration") can facilitate coordination with offsite restoration options and a regional approach to restoration of contaminated environments. Integration of performance monitoring, for both remedial and restoration actions, can save resources and expand the interpretive power of results. Early integration may aid experimentation, which may be more feasible on contaminated lands than in many other situations. The potential application of concepts and tools from adaptive management is discussed as a way of avoiding pitfalls and achieving benefits in early integration. In any case, there will be challenges with early integration of restoration concepts for contaminated ecosystems, but the benefits are likely to outweigh them.

Attempts to identify the source of avian vacuolar myelinopathy for waterbirds.

Attempts were made to reproduce avian vacuolar myelinopathy (AVM) in a number of test animals in order to determine the source of the causative agent for birds and to find a suitable animal model for future studies. Submerged vegetation, plankton, invertebrates, forage fish, and sediments were collected from three lakes with ongoing outbreaks of AVM and fed to American coots (Fulica americana), mallard ducks and ducklings (Anas platyrhynchos), quail (Coturnix japonica), and laboratory mice either via gavage or ad libitum. Tissues from AVM-affected coots with brain lesions were fed to ducklings, kestrels (Falco sparverius), and American crows (Corvus brachyrhynchos). Two mallards that ingested one sample of Hydrilla verticillata along with any biotic or abiotic material associated with its external surface developed brain lesions consistent with AVM, although neither of the ducks had clinical signs of disease. Ingestion of numerous other samples of Hydrilla from the AVM affected lakes and a lake with no prior history of AVM, other materials (sediments, algae, fish, invertebrates, and water from affected lakes), or tissues from AVM-affected birds did not produce either clinical signs or brain lesions in any of the other test animals in our studies. These results suggest that waterbirds are most likely exposed to the causative agent of AVM while feeding on aquatic vegetation, but we do not believe the vegetation itself is the agent. We hypothesize that the causative agent of AVM might either be accumulated by aquatic vegetation, such as Hydrilla, or associated with biotic or abiotic material on its external surfaces. In support of that hypothesis, two coots that ingested Hydrilla sampled from a lake with an ongoing AVM outbreak in wild birds developed neurologic signs within 9 days (ataxia, limb weakness, and incoordination), and one of two coots that ingested Hydrilla collected from the same site 13 days later became sick and died within 38 days. None of these three sick coots had definitive brain lesions consistent with AVM by light microscopy, but they had no gross or histologic lesions in other tissues. It is unclear if these birds died of AVM. Perhaps they did not ingest a dose sufficient to produce brain lesions or the lesions were ultrastructural. Alternatively, it is possible that a separate neurotoxic agent is responsible for the morbidity and mortality observed in these coots.