The effects of mine waste contamination at multiple levels of biological organization

Abstract

This study shows that metal-contaminated sediments cause adverse biological effects at all levels of biological organization, from cellular to ecosystem-level responses, even where the corresponding surface water meets water-quality-based criteria. We studied the effects of contamination from the abandoned Alder Mine, Alder Mill, and Red Shirt Mill located near the town of Twisp on the eastern slopes of the north Cascade Mountains in Okanogan County, Washington (U.S.A.) on fish and wildlife habitat in the Methow River. Ore deposits in the area were mined for gold, silver, copper and zinc until the early 1950s. An up-gradient and down-gradient approach was used to compare impacted sites to control sites. Although the dissolved metal concentrations in the Methow River were below the limits of detection, eight elements were identified as contaminants of potential environmental concern (COPECs) in sediments. Results revealed contamination impacts at ecosystem, community, population, individual, cellular, subcellular, and molecular levels. Metal contaminants in forest soils around the mines were present at concentrations toxic to soil bacteria suggesting that functional properties related to nutrient cycling and energy flow have been effected. Exposed trout in the Methow River showed reduced growth compared to controls. Histopathological evidence is consistent with copper-induced metabolic disease. Glycogen bodies were present in trout hepatocyte cytosol and nuclei and the presence of glycogen inclusions was pathognomic of Type IV glycogen storage disease (GSD IV). This condition suggests food is being converted into glycogen and stored in the liver and that the glycogen is not being converted back normally into glucose for distribution to other tissues in the body, which is a likely cause for the poor growth and development observed in fish and macroinvertebrates. Glycogen storage disease is caused by either a deficiency or inactivation of the glycogen branching enzyme, which results in the synthesis of an abnormal glycogen molecule that is insoluble due to a decreased number of branch points and increased chain length. Further examination of hepatocytes by transmission electron microscopy also revealed the accumulation of electron-dense metal-granules in the mitochondrial matrix.