The Influence of pH, Water Hardness, and Alkalinity on the Acute Lethality of Zinc to Rainbow Trout (Salmo gairdneri)

1985 ◽  
Vol 42 (4) ◽  
pp. 731-736 ◽  
Author(s):  
R. W. Bradley ◽  
J. B. Sprague
Keyword(s):  
Rainbow Trout ◽  
Water Hardness ◽  
Salmo Gairdneri ◽  
Total Hardness ◽  
Zinc Toxicity ◽  
Carbonate Alkalinity ◽  
Effects Of Ph ◽  
Order Of Magnitude ◽  
Low Toxicity ◽  
Influence Of Ph

The acute lethality of dissolved zinc to rainbow trout (Salmo gairdneri) was significantly increased at higher pH and lower hardness levels. Changes in pH from 5.5 to 7.0 increased zinc toxicity by factors of 2 to 5, depending on total hardness levels. A decrease in hardness from 386 to 31 mg CaCO3/L increased zinc toxicity by more than an order of magnitude at both pH levels. These effects of pH and hardness were not caused by changes in the chemical speciation of zinc. An increase in carbonate alkalinity from 8.4 to 24 mg CaCO3/L at pH 7.0 did not significantly alter zinc toxicity at either hardness level. Thus, carbonate alkalinity is not an important factor at or below pH 7.0. At low hardness, dissolved zinc was more than 10 times as toxic at pH 9.0 as at pH 5.5. Two competing mechanisms appear to operate: as the pH rises, dissolved zinc becomes increasingly toxic, but at higher pH levels it is increasingly replaced by zinc precipitate, which is of very low toxicity to fish.

Influence of Water Hardness, pH, and Alkalinity on the Mechanisms of Copper Toxicity in Juvenile Rainbow Trout, Salmo gairdneri

1986 ◽  
Vol 43 (8) ◽  
pp. 1488-1496 ◽  
Author(s):  
Darrel Jon Laurén ◽  
D. G. McDonald
Keyword(s):  
Rainbow Trout ◽  
Pure Copper ◽  
Copper Toxicity ◽  
Water Hardness ◽  
Salmo Gairdneri ◽  
Sodium Efflux ◽  
Juvenile Rainbow Trout ◽  
Influence Of Water ◽  
Effects Of Ph ◽  
High Alkalinity

Juvenile rainbow trout were exposed to 25–400 μg copper∙L−1 for 24 h. Water hardness, pH, and alkalinity were varied independently at a constant [Na+]. Net and unidirectional sodium fluxes were measured in hard and soft, low-alkalinity water and in hard, high-alkalinity water at neutral pH and pH 5.0. In low alkalinity water, Na+ uptake (Jin) was inhibited at copper concentrations as low as 25 μg∙L−1, and sodium efflux (Jout) was stimulated above 100 μg∙L−1. High-alkalinity water significantly reduced the effects of copper on Jin and Jout, but there was no significant effect of increasing water hardness. The effects of pH 5.0 and copper were additive from 25 to 100 μg∙L−1, but a pure copper effect was found from 200 to 400 μg∙L−1. Fish died when they had lost about 50–55% of their exchangeable Na+ pool. Water hardness and alkalinity had no effect on the apparent uptake of copper, but copper uptake was reduced by about 50% at pH 5.0.

Toxicity of TFM (Lampricide) to Six Early Life Stages of Rainbow Trout (Salmo gairdneri)

1973 ◽  
Vol 30 (8) ◽  
pp. 1047-1052 ◽  
Author(s):  
L. E. Olson ◽  
L. L. Marking
Keyword(s):  
Rainbow Trout ◽  
Early Life ◽  
Natural Waters ◽  
Life Stage ◽  
Water Hardness ◽  
Salmo Gairdneri ◽  
Life Stages ◽  
Early Life Stages ◽  
Margin Of Safety ◽  
Coexisting Species

The lampricide TFM (3-trifluoromethyl-4-nitrophenol) was tested against the following life stages of rainbow trout (Salmo gairdneri): green eggs, eyed eggs, sac fry, swim-up fry, fry, and fingerlings in four water hardnesses (12, 44, 170, and 320 mg/liter as CaCO3). The eyed-egg stage was one of the most resistant stages tested, and the sac-fry stage was one of the least resistant. Increased water hardness decreases toxicity to all stages. The LC50’s range from 0.532 mg/liter to 40.0 mg/liter depending upon life stage, water hardness, and duration of exposure. The margin of safety for coexisting species exposed to TFM ranges from 3.2 to 4.1 in natural waters. The margin of safety for early life stages of rainbow trout and larval lamprey under controlled laboratory conditions ranges from 4.2 to 12.2. Therefore, all six early life stages of rainbow trout are safe in minimum lampricidal concentrations of TFM.

Influence of pH on the Acute Lethality of Fenitrothion, 2,4-D, and Aminocarb and Some pH-Altered Sublethal Effects of Aminocarb on Rainbow Trout (Salmo gairdneri)

1988 ◽  
Vol 45 (2) ◽  
pp. 287-293 ◽  
Author(s):  
K. G. Doe ◽  
W. R. Ernst ◽  
W. R. Parker ◽  
G. R. J. Julien ◽  
P. A. Hennigar
Keyword(s):  
Rainbow Trout ◽  
Sublethal Effects ◽  
Acetylcholinesterase Activity ◽  
Whole Body ◽  
Toxicity Tests ◽  
Salmo Gairdneri ◽  
Control Range ◽  
Decreasing Ph ◽  
Influence Of Ph ◽  
Brain Acetylcholinesterase

Three pesticides, fenitrothion, 2,4-D, and aminocarb, were tested in static 96-h acute lethal toxicity tests using fingerling rainbow trout (Salmo gairdneri) at pH 4.6, 5.6, 6.9, and 8.5. The toxicity of aminocarb, a base, increased significantly with increasing pH. Conversely, the toxicity of the acidic pesticide 2,4-D increased with decreasing pH. The toxicity of the neutral pesticide fenitrothion did not change significantly with changing pH. Subsequent tests were performed on trout fingerlings with aminocarb to determine the effect of two exposure pH's on brain acetylcholinesterase activity and whole-body aminocarb residue. Brain acetylcholinesterase was found to be inversely proportional to whole-body aminocarb content of fish. In fish exposed at pH 4.6, brain acetylcholinesterase was maximally depressed at 6 h, after which it recovered to within the control range. Whole-body aminocarb concentrations rose to a maximum within 6 h and subsequently declined to low levels. In fish exposed at pH 8.2, brain acetylcholinesterase dropped below the control range by 1 h and remained low until all fish died by 72 h. A maximum whole-body aminocarb concentration was reached within 1 h and remained elevated until the fish died. Several explanations for the observed results are presented.

Acute Zinc Toxicity to Rainbow Trout (Salmo gairdneri): Confirmation of the Hypothesis that Death is Related to Tissue Hypoxia

1972 ◽  
Vol 29 (10) ◽  
pp. 1463-1466 ◽  
Author(s):  
Dennis T. Burton ◽  
Alma H. Jones ◽  
John Cairns Jr.
Keyword(s):  
Rainbow Trout ◽  
Gas Exchange ◽  
Exchange Process ◽  
Physiological Mechanism ◽  
Tissue Level ◽  
Tissue Hypoxia ◽  
Salmo Gairdneri ◽  
Zinc Toxicity ◽  
Oxygen Requirements ◽  
Gas Exchange Process

Acute heavy metal toxicity to fish has been attributed to the coagulation or precipitation of mucus on the gills and/or to cytological damage to the gills. The physiological mechanism of death by either of the above causes is related to a breakdown in gas exchange at the gills. This study of acute zinc toxicity to rainbow trout (Salmo gairdneri) supports an earlier hypothesis that modification of the gas exchange process at the gills creates hypoxia at the tissue level. Tissue hypoxia appears to be a major physiological change preceding death once the gas exchange process at the gills is no longer sufficient to supply the oxygen requirements of the fish.

Acute Toxicity of Nitrite to Rainbow Trout (Salmo gairdneri): Effects of pH, Nitrite Species, and Anion Species

1981 ◽  
Vol 38 (4) ◽  
pp. 387-393 ◽  
Author(s):  
Rosemarie C. Russo ◽  
Robert V. Thurston ◽  
Kenneth Emerson
Keyword(s):  
Rainbow Trout ◽  
Ph Dependence ◽  
Salmo Gairdneri ◽  
Aquatic Life ◽  
Nitrite Toxicity ◽  
Effects Of Ph ◽  
Chloride Sulfate ◽  
Ph Dependent ◽  
Nitrate Anions ◽  
Anion Species

The toxicity of nitrite to rainbow trout is pH-dependent within the range considered acceptable to most freshwater aquatic life (pH 6.5–9.0). Both of the nitrite species, NO2− and HNO2, are toxic. It is recommended that nitrite criteria to protect freshwater aquatic life be based on total nitrite, and that such criteria reflect the pH dependence of nitrite toxicity. Variation in the toxicity of nitrite in the presence of chloride, sulfate, phosphate, and nitrate anions has also been demonstrated. It is concluded that the toxicity of nitrite to fishes, in addition to being pH-dependent, is also dependent in varying degrees upon many of the anions that are commonly found in natural aquatic environments.Key words: nitrite, pH, chloride, phosphate, sulfate, toxicity, rainbow trout, Salmo gairdneri

Toxicity of environmental acid to the rainbow trout: interactions of water hardness, acid type, and exercise

1981 ◽  
Vol 59 (8) ◽  
pp. 1518-1526 ◽  
Author(s):  
Mark S. Graham ◽  
Chris M. Wood
Keyword(s):  
Rainbow Trout ◽  
Water Hardness ◽  
Low Ph ◽  
Soft Water ◽  
Activity Level ◽  
Salmo Gairdneri ◽  
Physiological Mechanisms ◽  
Acid Type ◽  
Influence Of Water ◽  
Acid Toxicity

Classical 7-day lethality tests were used to establish the influence of water hardness [Formula: see text], acid type (HCl versus H2SO4) and activity level (rest versus exhaustive exercise) on acid toxicity to fingerling rainbow trout (Salmo gairdneri) at 15 °C. Seven-day mean lethal concentration (LC50) pH's ranged from 4.1 to 4.5. Hardness reduced H2SO4 toxicity at all pH levels during both rest and exericise, but reduced HCl toxicity only at very low pH levels. Hardness increased HCl toxicity at pH's > 3.8. H2SO4 was generally less toxic than HCl, except at pH's > 3.8 in soft water. Exchaustive exercise markedly potentiated H2SO4 toxicity in both hard and soft water except at very low pH levels. Below pH = 4.4–4.6, critical swimming speed declined linearly by about 4% per 0.1 pH unit. Possible physiological mechanisms responsible for these modifying influences and their ecological significance are discussed.

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