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The impacts of pH and dissolved organic carbon (DOC) on the acute toxicity of Cu to larval fathead minnow (Pimephales promelas) were determined using natural soft water from two Precambrian Shield lakes in south-central Ontario. By artificially manipulating the pH and DOC levels of the water, we demonstrated that both acidification and the removal of DOC increased the toxicity of Cu. The 96-h Cu LC50s were determined over a pH range from 5.4 to 7.3 and a DOC concentration range from 0.2 to 16 mg∙L−1. The LC50s ranged from a low of 2 μg∙L−1 (pH 5.6, DOC 0.2 mg∙L−1) to a high of 182 μg∙L−1 (pH 6.9, DOC 15.6 mg∙L−1). A multiple regression model (log1096-h Cu LC50 = −0.308 + 0.192 pH + 0.136 (pH∙log10DOC)) was used to describe the relationship between Cu toxicity, pH, and DOC. The model was significant (p < 0.00001) and explained 93% of the variability in the toxicity data. These results suggest that current water quality objectives for Cu, and possibly for other metals, may not be sufficiently protective of aquatic life in soft, moderately acidic water containing low levels of DOC.

Exposure to 0.8 mg Zn2+/L in natural soft water for up to 72 h was toxic to rainbow trout, Salmo gairdneri, causing an acid–base disturbance and net branchial ion losses. Mean arterial pH fell from 7.78 to 7.58. Both [Formula: see text] and lactate rose, indicating a mixed respiratory and metabolic acidosis, despite maintenance of high [Formula: see text] Net branchial uptake of Na+ and Cl− became a net loss immediately following exposure to Zn2+, and this continued during 60 h of exposure. Net K+ loss was exacerbated, and net Ca2+ uptake was abolished. Unidirectional flux measurements with 22Na+ and 36Cl− indicated an increased efflux immediately following zinc exposure. Both influx and efflux of Na+ and Cl− were stimulated after 48–60 h in Zn2+. Both net branchial ammonia excretion and net branchial uptake of acidic equivalents from the water (=base loss) were greatly stimulated, the latter contributing to metabolic acidosis. Kidney function, as measured by urine flow rate and excretion of ammonia, acidic equivalents, Na+, Cl−, K+, and Zn2+, was relatively insensitive to the effects of zinc. The only renal component to be affected was Ca2+ excretion, which decreased during a single flux period, possibly in response to the reduced entry of Ca2+ at the gill. We conclude that toxic concentrations of zinc are capable of altering gill function so as to cause ionoregulatory and acid–base disturbances without disturbance of [Formula: see text].

Rainbow trout, Salmo gairdneri, were fed purified diets with zinc concentrations ranging from deficient to excessive (1, 90, 590 μg Zn∙g−1) and simultaneously exposed to a range of waterborne [Zn] (7, 39, 148, 529 μg Zn∙L−1). After 1 wk, fish fed the deficient diet, at ambient waterborne [Zn], had low plasma [Zn] which decreased further during the 16-wk experiment. Growth ceased after 12 wk; hematocrit and plasma protein were depressed. Both whole body [Zn] and body burden decreased by 16 wk, but most other elements were elevated. Increasing waterborne [Zn] alone increased plasma [Zn], whole body [Zn], and growth in a graded manner and normalized hematocrit, plasma protein, and other whole body elements. Increasing dietary [Zn] to 90 μg Zn∙g−1 at ambient waterborne [Zn] prevented depression of plasma [Zn] and permitted normal growth and whole body [Zn]. Zinc uptake from water, probably across the gills, was independent of uptake from the diet since at any dietary [Zn], increasing the waterborne [Zn] resulted in increased whole body [Zn]. Even when dietary [Zn] was adequate, the waterborne contribution was as high as 57%, and 100% when the dietary [Zn] was deficient. There were no toxic effects on any of the variables measured.

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The activity of erythrocyte δ-amino levulinic acid dehydratase (ALA-D) of fish is easily measured under a variety of experimental conditions. Exposure of rainbow trout (Salmo gairdneri), brook trout (Salvelinus fontinalis), goldfish (Carassius auratus), and pumpkinseeds (Lepomis gibbosus) to lead consistently inhibited ALA-D within 2 wks at concentrations as low as 10, 90, 470, and 90 μg/ℓ, respectively. In rainbow and brook trout these concentrations were closely related to the published minimum effective concentrations causing sublethal harm. There was a significant linear relationship between ALA-D activity and log of blood lead concentration, between ALA-D activity and log of lead in water, and between blood lead and lead in water. Near lethal exposures to cadmium, copper, zinc, and mercury did not significantly inhibit ALA-D activity. Recovery of ALA-D activity of rainbow trout after transfer from 120 μg/ℓ lead to clean water occurred in 8 wk. This enzyme provides fast, consistent, specific, and sensitive estimates of lead concentrations causing sublethal harm to fish and may help to relate sources of lead to degree of exposure of fish populations in the field. Key words: lead, sublethal toxicity, fish, indicator enzyme, δ-amino levulinic acid dehydratase

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