Exposure to moderate acid water and aluminum reduces Atlantic salmon post-smolt survival

Acidification is acknowledged as the cause for extinction or catch reductions in numerous Atlantic salmon (Salmo salar L.) populations in Norway. In freshwater, labile (cationic/inorganic) forms of Al (LAl) accumulate in fish gills, where high concentrations result in mortality due to respiratory and ionoregulatory dysfunction. At lower concentrations, Al may still have population effects by inhibiting gill Na+,K+-ATPase activity, thereby reducing hypoosmoregulatory capacity and marine survival. Over the years 1999 to 2003 we exposed groups of 1150 to 1200 one-year old hatchery reared, Carlin tagged Atlantic salmon smolts of the Imsa strain (South-Western Norway) to moderately acidified water (pH 5.8; 5–15 μg LAl L− 1) from 3 (short term exposure) to 60 (long term exposure) days. Fish exposed to Lake Imsa water (pH > 6.5 and < 5 μg LAl L− 1) acted as controls. Control fish had gill-Al concentrations in the range of 5 to 10 μg Al g− 1 gill dry weight (dw), while Al-exposed fish had gill-Al concentrations exceeding 20 μg Al g− 1 gill dw prior to seawater release. The physiological responses measured as plasma Cl− and glucose were related to the LAl concentration in water and to the accumulation of Al onto the gills. Gill Na+,K+-ATPase activity was depressed in all groups having > 25 μg Al g− 1 gill dw. Following exposure, the smolts were released into River Imsa to monitor downstream migration and ocean return rates. Acid exposed smolts migrated out of the river together with controls. Adult return rates were reduced by 20 to 50% in all Al-exposed groups relative to the control groups, although marine growth was unaffected. The results suggest that even moderately and/or episodically acidified rivers containing 5–15 μg LAl L− 1 can cause substantial reductions in returns of Atlantic salmon.