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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.

Fathead minnows (Pimephales promelas) were exposed to 17 μg Cu∙L−1 or 6 μg Cd∙L−1 in synthetic soft water in the presence of competing ligands. Measured gill metal concentrations correlated with free metal ion concentrations, not with total metal. Langmuir isotherms were used to calculate conditional metal–gill equilibrium constants and the number of binding sites for each metal. Log KCu-gill was estimated to be 7.4 and the number of Cu binding sites on a set of gills (70 mg, wet weight) was ~2 × 10−10 mol (~30 nmol∙g wet weight−1). Log KCd-gill was ~8.6, and the number of Cd binding sites on minnow gills was ~2 × 10−10 mol (~2 nmol∙g wet weight−1). Stability constants for H+ and Ca interactions at metal–gill binding sites and for metal interactions with dissolved organic carbon (DOC) were estimated using these metal–gill constants. All stability constants were entered into the MSNEQL+ aquatic chemistry program, to predict metal accumulation on fish gills using metal, DOC, and Ca concentrations, and water pH. Calculated metal accumulation on gills correlated well with measured gill metal concentrations and with LC50 values. Our approach of inserting biological data into an aquatic chemistry program is useful for modelling and predicting metal accumulation on gills and therefore toxicity to fish.

Adult fathead minnows (Pimephales promelas) were exposed to 17 g Cu∙L−1 or 6 g Cd∙L−1 for 2 to 3 h in synthetic softwater solutions at pH 6.2 containing either naturally-occurring, freeze-dried dissolved organic carbon (DOC) or synthetic ligands such as EDTA. After exposures, gills were assayed for bound Cu or Cd. As a first approximation, lake of origin or molecular size fraction of DOC did not influence Cu binding to gills, while DOC concentration did. DOC concentrations ≥4.8 mg∙L−1 prevented Cu from accumulating on fathead gills. At the relatively low concentrations used, neither Cu nor Cd interfered with binding of the other metal on gills, suggesting different gill binding sites. Cadmium accumulation on gills was more sensitive to increased concentrations of Ca and H+ than was Cu. Surprisingly, Cd bound to gills to the same or greater extent than did Cu: for synthetic ligands, Cd binds less well than Cu. This result corroborates previously published observations that Cd, unlike Cu, is taken up at gills through high affinity Ca channels. Accumulation of Cd on fish gills was never associated with 14C-labelled EDTA or 14C-citrate, indicating that free metal interacts with the gill while metal–ligand complexes usually do not.

Rainbow trout (Oncorhynchus mykiss, 1–3 g) were exposed to ∼0.1 μM silver (Ag) (∼11 μg.L−1 Ag) for 2 to 3 h in synthetic soft water (Ca, Na ∼ 300 μM, pH 6.5–7.5) to which was added Ca, Na, H+, dissolved organic carbon (DOC), CI, or thiosulfate (S2O3). Gills were extracted and gill Ag concentrations were measured using graphite‐furnace atomic absorption spectrophotometry. The concentrations of cations (Ca, Na, H+) and complexing agents (DOC, CI, S2O3) needed to keep Ag off the gills were used to calculate conditional equilibrium binding constants (K) at the gills. Log K for Ag‐gill binding was 10.0, with approximately 1.3 nmol Ag binding sites per fish. All experimentally determined log K values were entered into an aquatic chemistry equilibrium model, MINEQL+, to predict Ag binding at trout gills. For a series of natural waters, model‐predicted gill Ag concentrations correlated well with observed gill Ag concentrations, with one exception, very hard city of Waterloo tapwater. This exception may indicate a kinetic constraint on the thermodynamic basis of the model.

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Abstract-In this review, we outline the physiological and toxicological effects of silver (Ag) in freshwater and marine fish. For freshwater fish, the acute toxicity of Ag appears to be caused solely by ionic Ag ϩ interacting at the gills, inhibiting basolateral Na ϩ ,K ϩ -ATPase activity. Disruption of this enzyme inhibits active Na ϩ and Cl Ϫ uptake and therefore osmoregulation by the fish. Silver is much less toxic to marine fish, mainly because ionic Ag ϩ is complexed by Cl Ϫ , but the mechanisms of acute toxicity and the toxic species of Ag are poorly understood. Osmoregulatory failure occurs in marine fish exposed to high concentrations of Ag, and the intestine appears to be a primary toxic site of action, perhaps along with a gill component. Modeling approaches to calculate Ag interactions at biological surfaces are used to illustrate the effects of water chemistry on Ag speciation and therefore toxicity to freshwater and marine fish. In these models, the most important components affecting Ag speciation are the complexing agents Cl Ϫ and dissolved organic matter followed by the competing agents Na ϩ and Ca 2ϩ , although a particulate component may be important to incorporate into the models in future. More precise knowledge of the actual toxic sites of Ag is necessary if we are to fully understand the effects of waterborne Ag in the environment.

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