Effects of Mine Waste Contamination on Fish and Wildlife Habitat at Multiple Levels of Biological Organization in the Methow River, 2001-2002 Annual Report.

A three-year multidisciplinary study was conducted on the relationship between mine waste contamination and the effects on aquatic and terrestrial habitats in the Methow River below abandoned mines near Twisp in Okanogan County, Washington (U.S.A.). Ore deposits in the area were mined for gold, silver, copper and zinc until the early 1950's. An above-and-below-mine approach was used to study potentially impacted sites. Although the dissolved metal content of water in the Methow River was below the limits of detection, eleven chemicals of potential environmental concern were identified in the tailings, mine effluents, groundwater, streamwater and sediments (Al, As, B, Ba, Cd, Cr, Cu, Mn, Pb, Se and Zn). The potential for ecosystem level impacts was reflected in the risk of contamination in the mine waste to communities and populations that are valued for their functional properties related to energy storage and nutrient cycling. Dissolved and sediment metal contamination changed the benthic insect community structure in a tributary of the Methow River below Alder Mine, and at the population level, caddisfly larval development in the Methow River was delayed. Arsenic accumulation in bear hair and Cd in fish liver suggest top predators are effected. In situ exposure of juvenile triploid trout (Oncorhynchus mykiss) to conditions at the downstream site resulted in reduced growth and increased mortality among exposed individuals. Histopathological studies of their tissues revealed extensive glycogen inclusions suggesting food is being converted into glycogen and stored in the liver but the glycogen is not being converted back normally into glucose for distribution to other tissues in the body. Subcellular observations revealed mitochondrial changes including a decrease in the number and increase in the size of electron-dense metrical granules, the presence of glycogen bodies in the cytoplasm, and glycogen nuclei in exposed trout hepatocytes, which are signs that Type IV Glycogen Storage disease is occurring. GSD IV is caused by either a deficiency or inactivation of the glycogen branching enzyme that results in the synthesis of an abnormal glycogen molecule that is insoluble and has decreased branch points and increased chain length. These results show that the effects of mine waste contaminants can be expressed at all levels of organization from molecular to ecosystem-level responses