Abstract

A study of mine-waste contamination effects on Methow River habitat on the eastern slopes of the north Cascade Mountains in Washington state, U.S.A., revealed impacts at ecosystem, community, population, individual, tissue, and cellular levels. Ore deposits in the area were mined for gold, silver, copper and zinc until the early 1950's, but the mines are now inactive. An above-and-below-mine approach was used to compare potentially impacted to control sites. The concentrations of eleven trace elements (i.e., Al, As, B, Ba, Cd, Cr, Cu, Mn, Pb, Se, and Zn) in Methow River sediments downstream from the abandoned mine sites were higher than background levels. Exposed trout and caddisfly larvae in the Methow River showed reduced growth compared to controls. Samples of liver from juvenile trout and small intestine from exposed caddisfly larvae were examined for evidence of metal accumulation, cytopathological change, and chemical toxicity. Morphological changes that are characteristic of nuclear apoptosis were observed in caddisfly small intestine columnar epithelial and trout liver nuclei where extensive chromatin condensation and margination was observed. Histopathological studies revealed glycogen bodies were present in the cytosol and nuclei, which are indicators of Type IV Glycogen Storage Disease (GSD IV). This suggests 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 resulting in poor growth. Examination of trout hepatocytes by transmission electron microscopy revealed the accumulation of electron dense granules in the mitochondrial matrix. Matrix granules contain mixtures of Cd, Cu, Au, Pb, Ni, and Ti. Contaminated sediments caused adverse biological effects at different levels of biological organization, from the cellular to ecosystem-level responses, even where dissolved metal concentrations in the corresponding surface water met water-quality criteria.

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