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Aluminum toxicity in coastal and brackish waters

Academic lecture
Year of publication
2003
External websites
Cristin
Contributors
Frode Kroglund, Bjørn Olav Rosseland, M Kroglund, Hans-Christian Teien, Brit Salbu, Tom Hansen

Summary

Fifth Keele Meeting on Aluminium 22nd – 25th February 2003 Aluminum toxicity in coastal/brackish waters Frode Kroglund1, Bjørn O. Rosseland1, Hans C. Teien2, Brit Salbu2, Tom Hansen3 and Marianne Kroglund1 1Norwegian Institute for Water Research, PO Box 173, Kjelsås, N-0411 Oslo, Norway. 2Lab. for Analytical Chem., Agricultural University of Norway, P.O. Box 5026, N-1432 Ås, Norway. e-mail: frode.krodlund@niva.no Inorganic monomeric species of aluminum (Ali) is recognized as the major toxic component in acidified freshwater. Ali is detoxified by increasing pH, where low molecular mass forms of Ali are transformed to colloidal forms of Al through the process of polymerization. Transformation rates are dependent on pH and temperature. During the transformation process, when “unstable” forms of Al are present, Al-toxicity can actually increase. Al becomes non-toxic when Ali is transformed to “stable” forms of colloidal Al. As 3% seawater addition (to 1 ppt salinity) has successfully been used to detoxify acidic water in fish farms, a similar detoxification mechanism was assumed to take place when acid river water mixed with seawater. This hypothesis was tested in a flow through system where acid Al-rich freshwater from River Matre, western Norway was mixed with seawater to obtain salinities ranging from 3 to 17 ppt. Fish were exposed to water immediately following mixing and in subsequent tanks permitting discussion of transformation rates. The toxicity depended on mixing ratio of freshwater to seawater and on salinity. The results suggested that the increase in salinity influenced Al speciation, where toxic forms of Al were remobilized from the non-toxic colloidal forms present in freshwater. Plasma chloride was reduced to concentrations between 120 and 130 mM in dying fish, suggesting that the fish died from hypoxia rather than ionoregulatory disturbance. Fish responses were related to the accumulation of Al onto the gills. The observed responses can explain some of the fish kills that have been described from fish farms holding Atlantic salmon in Norwegian fjords.