Aluminium in acidic river water causes mortality of farmed Atlantic Salmon (Salmo salar L.) in Norwegian fjords (original) (raw)
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Environmental Pollution, 1997
The present study focuses on the relative sensitivity among freshwater jish species to aqueous aluminium. Seven common Scandinavian fish species were exposed to acidic Al-rich water, acidic Al-poor water, and approximately neutral water as a control. The relative sensitivity among the species to an acute aluminium challenge was documented, and was in the following order: Atlantic salmon, Salmo salar, as the most sensitive; then roach, Rutilus rutilus; minnow, Phoxinus phoxinus; perch, Perca fluviatilis; grayling, Thymallus thymallus; brown trout, Salmo trutta; and Arctic char, Salvelinus alpinus. Substantial mortality was observed in all species when exposed to the Al-rich medium. Some mortality was also observed in minnow, roach, and brown trout exposed to the acidic Al-poor medium and the control medium. A high resistance to aluminium was observed in Arctic char, while perch was found to be more sensiiive to aluminium than expected and, for thejrst time, a toxic response to aqueous aluminium in grayling was documented. Through controlled experimental studies, the results confirm that aluminium is an important,factor in the toxicity of acid@ed waters to ,freshwater fish species.
Estuarine, Coastal and Shelf Science, 2013
Salmo salar acidification acid precipitation aluminium smolt and post-smolt migration telemetry Regional index terms: Europe Norway Møre and Romsdal County Romsdalsfjord a b s t r a c t Short-term Al-exposure and moderate acidification increased initial marine mortality in migrating postsmolts, and can thereby reduce viability of Atlantic salmon stocks. The delayed impact of short-term aluminium (Al) exposure on hatchery-reared Atlantic salmon smolt in moderately acidified freshwater (pH 5.88e5.98) was investigated during the first 37 km of the marine migration. Smolts were tagged with acoustic tags and exposed to low (28.3 AE 4.6 mg l À1 labile Al, 90 h) or high (48.5 AE 6.4 mg l À1 labile Al, 90 or 48 h) Al concentrations within the hatchery. Thereafter their movements, together with a control group, were monitored throughout the marine fjord. Al-exposure resulted in increased gill-Al and compromised hypoosmoregulatory capacity, as shown by elevated mortality in laboratory seawater challenge tests and reduced Na þ , K þ -ATPase activity levels. Further, Al-exposure resulted in decreased plasma concentrations of growth hormone (GH), while the insulin-like growth factor (IGF-I) was unaffected. There was a significant mortality in the 90 h high-Al group during exposure, and those surviving until release died during the first 3.6 km of the marine migration. Physiological stress and mortality were not only a result of the Al-concentrations, but also dependent on exposure duration, as shown by results from the 48 h high-Al group. Elevated mortality was not recorded in freshwater or after entering the sea for this group, which highly contrasts to the 100% mortality in the 90 h high-Al group, despite both groups having similarly high gill-Al levels. The low-Al group showed a 20% higher mortality compared to the control group during the first 10 km of the marine migration, but during the next 28 km, mortality rates did not differ. Hence, post-smolts surviving the first 10 km subsequently showed no differences in mortality compared to controls. At least one third of the mortality in both the low-Al and control groups were due to predation by marine fishes, indicating that the proximate cause for elevated mortality due to Al-exposure may have been predation. Migration speeds over 3.6, 9.6 or 37.1 km from the release site was not affected by Al-exposure.
Water, Air, and Soil Pollution, 1986
Physiological stress, measured as changes in plasma chloride, and mortality were measured on different year-classes of landlocked and migratory Atlantic salmon, two strains of brown trout, and brook trout, in a flow-through system with acidic Al-rich soft water. The oldest year-classes of salmon were smolts. Water from Lake Byglandsfjord (pH = 5.9), was enriched with inorganic AI (as AICI3) ~nd H2SO 4 to pH = 5.1, total AI = 225 ug L-I, and labile AI = 135 ug L-~. As a reference, lake water was limed by means of a shellsan~ filter to pH = 6.2, increasing Ca-concentration from 1.0 to 1.5 mg L-~. During the 83 hr experiment, neither mortality nor physiological stress occurred in any species or year-class in the limed water. In the acid water, no mortality occurred on any stage of brown trout or brook trout. Among the migratory and landlocked salmon, however, 5% of the alevins died after 49 and 70 hr, respectively. All smolts of both the landlocked and the migratory salmon died after 83 and 35 hr, respectively, the co~responding loss rate of plasma chloride was-0.76 and-1.26 meq CI hr-~. Brook trout, however, increased plasma ion concentration during the experimental period, and hence showed no stress.
Exposure to moderate acid water and aluminum reduces Atlantic salmon post-smolt survival
Aquaculture, 2007
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 N 6.5 and b 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 N 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.
The effect of aluminium in Atlantic salmon (Salmo salar) with special emphasis on alkaline water
Journal of Inorganic Biochemistry, 2003
Atlantic salmon (Salmo salar) parr were exposed to aluminium under both steady state and non-steady state chemical conditions in 21 2 alkaline water. Under alkaline (pH 9.5) steady state conditions, |350 mg Al l (predominantly aluminate, Al(OH)) had no acute toxic 4 effect on the salmon. The fish, however, showed a physiological response after 3 weeks of exposure (|300% increase in blood glucose 2 concentration, about 30% increase in blood haematocrit, and about 15% decrease in plasma Cl concentration). No increase in toxicity was evident under non-steady state conditions, i.e. lowering Al solubility as pH was lowered from 9.5 to 7.5. The results indicate that the 2 toxicity of the aluminate ion (Al(OH)) is low, and particularly lower than the corresponding toxicity of cationic Al hydroxides. The 4 effects observed in fish exposed to Al-rich water at pH 9.5 were counteracted as Al solubility was decreased by lowering pH to 7.5. This is contrary to previous observations where Al solubility has been lowered by increasing pH from 5.0 to 6.5.
Effects of exposure to aluminium on fish in acidic waters
2003
Abstract Aluminium (Al) is one of the important factors in the toxicity of acidified waters to freshwater fish species because low pH and high concentrations of Al have been of particular concern in affected waters. Al mobilization in its soluble forms from soil to aquatic ecosystems is an important consequence of acidification of lakes and steams.
Aquatic Toxicology, 1991
The present study is mainly focusing on the effect of tempe~ture on Al-chemistry and the resulting toxicity to fish. Atlantic salmon (Salmo salar L.) fingerlings were exposed to water at defmed combinations of temperature, pH and Al-concentration, and mortality was recorded. Mortality was correlated to the concentration of inorganic aluminium, and increased systematically with increasing temperature. The dzgree of ongoing Al-polymerization is thought to be the most important factor for the temperature dependent Al-toxicity observed.
Water, Air, and Soil Pollution, 1988
The respiratory, acid-base, and ionoregulatory responses of juvenile rainbow trout (Salmo gairdneri) were monitored during exposure of the fish in the laboratory to inorganic A1 (2.8 rtM) over the pH range 4.0 to 6.5. Responses to A1 were most severe at pH 6.1 and 4.5, mortality being primarily due to asphyxia at pH 6.1 and to electrolyte loss at pH 4.5. Competition between the H+-ion and A1 for binding at the gill surface is offered as an explanation for the decreased toxicity of A1 at pH 4.0, one which is compatible with the free-ion toxicity model that has been developed for other metals. The physiologically distinct response of S. gairdneri to A1 at pH 6.1 is less amenable to unambiguous interpretation. If a mixed ligand hydroxo-At complex is incorporated in the free-ion model, and if it is assumed that the two A1 species, [A1-L-gill] and [HO-A1-L-giU], provoke distinct toxicological responses, then a bimodal toxicological response to A1 is indeed predicted. An alternative explanation of the apparent toxic action of A1 at pH 6.1, i.e., at pH values close to that of minimum AI solubility, is the precipitation of solid AI(OH)3 at the gill surface, i.e., a 'physical' effect rather than a biochemical one.