The mixing zone between limed and acidic river waters: complex aluminium chemistry and extreme toxicity for salmonids

Rosseland, Bjørn Olav; Blakar, Inggard Arne; Bulger, Arthur J.; Kroglund, Frode; Kvellstad, A.; Lydersen, Espen; Oughton, Deborah; Salbu, Brit; Staurnes, Magne; Vogt, Rolf D.

doi:10.1016/0269-7491(92)90003-s

Cited by 156 publications

(113 citation statements)

References 18 publications

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“…A wide spectrum of metals and ions was determined (Fe, Mn, Zn, Ni, Cu, Pb, Ca, Mg, Na, K, C1 SO4, NO3, F) but only A1 levels were in the toxic range. In previous articles of our group reporting on the mixing zone phenomenon a causal relationship between the toxicity and the process of Al-polymerization has been suggested (Rosseland et al, 1992;Salbu et al, 1995). The proposed mechanism was a combination of suffocation by Al-precipitates on the gills and loss of plasma Na § and C1-by the acidification (Poleo et al, 1994).…”

Section: Discussionmentioning

confidence: 89%

“…In field experiments with Atlantic salmon and brown trout, higher mortality has been observed in the mixing zone (0-20 sec after mixing of water of an acid inlet with that of a neutral lake) than in the acid inlet, which has been attributed to transient products of Al-polymerization (Rosseland et al, 1992;Poleo et al, 1994). In this study we aimed to gain more insight in the toxic effects of such mixing zones on brown trout by electron microscopy of the gills in combination with measurements of plasma CI-levels and blood haematocrit.…”

Section: Introductionmentioning

confidence: 99%

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The toxic mixing zone of neutral and acidic river water: Acute aluminium toxicity in brown trout (Salmo trutta L.)

Verbost

Berntssen

Kroglund

et al. 1995

Water Air Soil Pollut

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Abstract. Mixing of acid river water containing aluminium (pH 5.1, AI 345 btg.1 "I) with neutral water of a lake (pH 7.0, A173 p.g.1 "~) resulted in water (pH 6.4, A1 245 p.g.l "x) with a pH (6.4) and A1 concentration (245 p.g.1 "l) expected to have low toxicity to fish on the basis of current AI toxicity models. However, under semi-field conditions the freshly mixed water (a few sec. after mixing) proved to be highly toxic to brown trout. The fish were exposed to the water at different places along a 30 m channel. At the beginning of the channel acid and neutral water were continuously mixed; the mixed water left the channel atter 340 sec. The cells of the gills showed a highly increased rate of cell death by apoptosis and necrosis. Intercellular spaces were enlarged, and many leucocytes penetrated in these spaces. Mucus release was stimulated to depletion. Plasma chloride levels were hardly affected. There was a clear gradient in the deleterious effects on the fish along the channel. The fish at the beginning of the channel (about 12 sec. after mixing of the water), were severely affected, whereas the fish kept at the end of the channel (340 sec. after mixing) were only mildly affected. In the natural situation fish will relatively quickly pass through a mixing zone. In our study we therefore focused on the effects on fish after a 60 min exposure to a mixing zone (5 sec after mixing), with subsequent recovery in a region downstream of the confluence and in neutral water with low AI. The recovery in the downstream area (at the end of the channel, i.e. 5 min after mixing) was clearly hampered when compared to the recovery in neutral water with low aluminium. Thus, a short exposure to the toxic mixing zone followed by a stay in water downstream of this zone, as may occur in nature, is detrimental to migrating trout. We conclude that freshly mixed acid and neutral water contain toxic components during the first seconds to minutes after mixing, that can not be explained by current models on aluminium toxicity.

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Section: Discussionmentioning

confidence: 89%

Section: Introductionmentioning

confidence: 99%

The toxic mixing zone of neutral and acidic river water: Acute aluminium toxicity in brown trout (Salmo trutta L.)

Verbost

Berntssen

Kroglund

et al. 1995

Water Air Soil Pollut

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“…These results agree with the study of Rosseland et al (1986a), who documented plasma Clloss (from 110 to 85 mmol-L"1) for Atlantic salmon smolts exposed to 21.5 mg labile AI L" 1 at pH 6.6 and 2.68 mg Ca*L-1. The mixing of acid-rich tap water with neutral river water in the supplementary tanks implies that we cannot ex clude a possible toxic influence from ongoing Al polymerisa tion (Rosseland et al 1992). However, this is unlikely because no toxic effects were observed in brown trout (Salmo trutta) exposed to a 5.6-min aged mixing zone (Verbost et al 1995).…”

Section: Discussionmentioning

confidence: 90%

“…However, recently it has been established that Al toxicity can also be high at high pH when Al-rich acid water mixes with neutral water. The rapid increase in pH in such a mixing zone causes Al polymerisation and subsequently severe stress and mortality in fish (Rosseland et al 1992). For anadromous spe cies such as the Atlantic salmon (Salmo salar), the smolt stage is considered particularly sensitive to low pH/Al exposure (Rosseland and Skogheim 1984;Rosseland et al 19866;Skogheim and Rosseland 1986) because of the extensive changes in physiology for preadaptating them to marine life (Staumes et al 1993).…”

Section: Introductionmentioning

confidence: 99%

Responses of skin mucous cells to aluminium exposure at low pH in Atlantic salmon (Salmo salar) smolts

Berntssen¹,

Kroglund²,

Rosseland³

et al. 1997

Can. J. Fish. Aquat. Sci.

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Atlantic salmon (Sahtio salar) smolts were exposed for 80 h to seven water qualities: pH 5.6 with 31 and 46 |ig labile AI L-1, pH 6.0 with 18 and 24 jig labile AI L-1, and pH 6.2 with 12 and 18 jig labile AI L-1 and control water at pH 6.8 and <10 fig labile AI L-1. The three groups with the highest concentrations of labile A1 (31 and 46 jig labile AI L-1 at pH 5.6 and 24 jig labile AI L-1 at pH 6.0) suffered high mortalities and showed a disturbance in osmoregulation and a massive secretion of mucus, as seen from a decrease in number of skin mucous cells. Furthermore, an increase in skin mucous cells containing acidic mucosubstances was observed. The loss of plasma chloride and skin mucous cells showed a significant linear correlation (R2 = 0.68,/? < 0.001). The increased secretion of mucus on skin and gills and the increase in acidity of mucosubstances are consistent with their prior presumed defensive role in binding of Al. Résumé

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“…A 245 µg · L -1 Al solution at pH 6.4 is clearly oversaturated with Al, so either Al precipitation or Al polymerization mechanisms could have been responsible for the gill damage seen, and either process would be more severe right after mixing. Witters et al (1996) set out to simulate in more controlled laboratory conditions the mixing situations studied by Rosseland et al (1992) and Verbost et al (1995). Brown trout (~60 g) were exposed to a pH 6.4, 2.8 µM Al solution (75 µg · L -1 Al) that was produced 1.5 or 6.5 min earlier from an acidic, Al-rich solution (pH 4.0, 200 µg · L -1 Al) mixed with pH 6.7 soft water containing no Al (Witters et al, 1996; see also the summary of these experiments in Witters, 1998).…”

Section: Respiratory Disturbances In Fish: Precipitation and Polymerimentioning

confidence: 99%

The Bioavailability and Toxicity of Aluminum in Aquatic Environments

Gensemer

Playle

1999

Critical Reviews in Environmental Science and Technology

618

435

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ABSTRACT:In this article we review the biological effects of Al, primarily with respect to the chemical factors controlling Al bioavailability and toxicity, and how its biological effects are best predicted. Our intent is not to duplicate recent reviews on Al chemistry or toxicity, but rather to update the literature since these reviews were published, and to focus on Al speciation and other external chemical influences on Al bioavailability to freshwater biota. Briefly, we first review Al chemistry, with a specific focus on understanding, as well as measuring, Al chemical species of importance to aquatic biota. Next we more comprehensively review Al toxicity and bioavailability to freshwater algae, with a thorough analysis of the relationships between speciation and toxicity, the role of important chemical complexing agents such as P, Si, and organic carbon, as well as the potential for Al to impact algal community structure. A third section reviews the more sparse literature on aquatic higher plants; the fourth section reviews a somewhat more abundant literature of Al toxicity to freshwater invertebrates. We close with an updated review of Al toxicity to fish, again with a focus on mechanisms of toxicity, and the role of Al speciation in controlling bioavailability.

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The mixing zone between limed and acidic river waters: complex aluminium chemistry and extreme toxicity for salmonids

Cited by 156 publications

References 18 publications

The toxic mixing zone of neutral and acidic river water: Acute aluminium toxicity in brown trout (Salmo trutta L.)

The toxic mixing zone of neutral and acidic river water: Acute aluminium toxicity in brown trout (Salmo trutta L.)

Responses of skin mucous cells to aluminium exposure at low pH in Atlantic salmon (Salmo salar) smolts

The Bioavailability and Toxicity of Aluminum in Aquatic Environments

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