Potentiation of copper toxicity to rainbow trout by potassium and implications for environmental risk assessment

Copper (Cu) toxicity to aquatic organisms is influenced by various water chemistry parameters, including known relationships with hardness, pH and dissolved organic carbon (DOC). Comparatively less is known about the influence of potassium (K) on Cu toxicity, and ambient K levels are rarely considered when evaluating the potential for Cu toxicity. However, Cu toxicity influences the regulation of both sodium (Na) and K. Acute toxicity tests with juvenile rainbow trout (Oncorhynchus mykiss) were conducted to further explore the relationship between K and Cu effect levels. Mixture toxicity tests demonstrated a more-than-additive response between the K and Cu. Tests with Cu conducted at four sub-lethal K concentrations (0.2 to 100 mg K/L) reduced median lethal concentrations (LC50s) of Cu in very soft water from 40 to < 10 µg Cu/L, with the increase in Cu toxicity correlated with K concentration (p=0.001). The increase in Cu toxicity as a result of K occurred regardless of whether the K salt contained an inorganic (chloride) or organic (acetate) counter-ion, and was observed in two low-hardness waters with different mineral compositions. Estimation of Cu risk based on Biotic Ligand (CuBLM) and Multiple Linear Regression (CuMLR) models were unchanged by elevated K, introducing uncertainty in Cu risk characterization, and were further confounded by DOC originating from acetate, which did not empirically modify Cu toxicity. Environmental concentrations of K, and corresponding ratios of Na/K, at which Cu risk may increase were identified and contextualized using real-world examples, including applications of potassium acetate (e.g., to mitigate ice buildup) and potassium chloride (e.g., to control invasive mussels).