Abstract

The effects assessment of metals is mainly based on data of single metals on single species, thereby not accounting for effects of metal mixtures or effects of species interactions. Both of these effects were tested in combination, thereby hypothesizing that the sensitivity of a community to synergistic mixture toxicity depends on the correlation of single-species sensitivities among the single metals. Single-metal and metal-mixture effects were tested in full concentration–response experiments (fixed ray of 1:1:3 and 5:1:13 mass ratio Ni:Cu:Zn) on eight single freshwater algal species and 14 algal communities of four species each. The mean correlation of single-species median effect concentrations among the single metals (Ni–Cu, Cu–Zn, and Zn–Ni) for all species in a community (r ̅ $\mathop{r}\limits^{̅}$) ranged from −0.4 to 0.9 among the communities; most of these (12/14) were positive. Functional endpoints (total biomass) were overall less sensitive than structural endpoints (Bray-Curtis similarity index) for communities with positively correlated single-species sensitivities among the single metals (r ̅ > 0.33 $\mathop{r}\limits^{̅}\gt 0.33$), suggesting that such correlations indicate functional redundancy under metal-mixture stress. Antagonistic metal-mixture interactions were predominantly found in single species, whereas metal-mixture interactions were antagonistic and surprisingly synergistic for the communities, irrespective of the reference mixture model used (concentration addition or independent action). The mixture interactions close to the carrying capacity (day 7) of communities gradually shifted from antagonism to more noninteractions with increasing correlation of single-species sensitivities among the single metals. Overall, this suggests that functional redundancy under mixed-metal stress comes at the cost of reduced biodiversity and that synergisms can emerge at the community level without any synergisms on the single-species level. Environ Toxicol Chem 2023;00:1–18. © 2023 SETAC.

ABSTRACT

Five metal mixture dose-response models are used to predict toxicity of porewater to young sturgeon at areas of interest in the Upper Columbia River and to evaluate these models as tools for risk assessments. Dose components of metal mixture models include exposure to free metal ion activities or metal accumulation by biotic ligands or humic acid, whereas links of dose to response use logistic equations, independent joint action equations, or additive toxicity functions. Laboratory bioassay studies of single metal exposures to juvenile sturgeon, porewater collected in-situ in the fast-flowing Upper Columbia River, and metal mixture models are used to evaluate toxicity.

The five metal mixture models are very similar in their predictions of adverse response of juvenile sturgeon and in identifying copper (Cu) as the metal responsible for the most toxic conditions. Although the modes of toxic action and EC20 values are different among the dose models, predictions of adverse response are consistent among models because all doses are tied to the same biological responses. All models indicate that 56+5% of 122 porewater samples are predicted to have <20% adverse response, 25+5% of samples are predicted to have 20-80% adverse response, and 20+4% are predicted to have >80% adverse response of juvenile sturgeon.

The approach of combining bioassay toxicity data, compositions of field porewater, and metal mixture models to predict lack of growth and survival of aquatic organisms due to metal toxicity is an important tool that can be integrated with other information (e.g., survey studies of organism populations, lifecycle and behavior characteristics, sediment geochemistry, and food sources) to assess risks to aquatic organisms in metal-enriched ecosystems.

ABSTRACT

The mechanisms of acute (96 h) and sub-chronic (28-d) toxicity of the waterborne trace metal thallium (Tl) to rainbow trout (Oncorhynchus mykiss) were investigated. Specifically, effects on branchial and renal ionoregulatory enzymes (sodium/potassium ATPase and proton ATPase) and hepatic oxidative stress endpoints (protein carbonylation, glutathione content and activities of catalase and glutathione peroxidase) were examined. Fish (19-55 g) were acutely exposed to 0 (control), 0.9 (regulatory limit), 2004 (half the acute median lethal concentration) or 4200 (acute median lethal concentration) µg Tl L^-1 or sub-chronically exposed to 0, 0.9 or 141 (an elevated environmental concentration) µg Tl L^-1. The only effect following acute exposure was a stimulation of renal H⁺-ATPase activity at the highest Tl exposure concentration. Similarly, the only significant effect of sub-chronic Tl exposure was an inhibition of branchial NKA activity at 141 µg Tl L^-1, an effect that may reflect the interaction of Tl with potassium ion handling. Despite significant literature evidence for effects of Tl on oxidative stress, there were no effects of Tl on any such endpoint in rainbow trout, regardless of exposure duration or exposure concentration. Elevated basal levels of antioxidant defences may explain this finding. These data suggest that ionoregulatory perturbance is a more likely mechanism of Tl toxicity than oxidative stress in rainbow trout, but is an endpoint of relevance only at elevated environmental Tl concentrations.