Elevated CO2 levels increase the toxicity of ZnO nanoparticles to goldfish (Carassius auratus) in a water-sediment ecosystem.

Concerns about the environmental safety of metal-based nanoparticles (MNPs) in aquatic ecosystems are increasing. Simultaneously, elevated atmospheric CO2 levels are a serious problem worldwide, making it possible for the combined exposure of MNPs and elevated CO2 to the ecosystem. Here we studied the toxicity of nZnO to goldfish in a water-sediment ecosystem using open-top chambers flushed with ambient (400±10μL/L) or elevated (600±10μL/L) CO2 for 30days. We measured the content of Zn in suspension and fish, and analyzed physiological and biochemical changes in fish tissues. Results showed that elevated CO2 increased the Zn content in suspension by reducing the pH value of water and consequently enhanced the bioavailability and toxicity of nZnO. Elevated CO2 led to higher accumulation of Zn in fish tissues (increased by 43.3%, 86.4% and 22.5% in liver, brain and muscle, respectively) when compared to ambient. Elevated CO2 also intensified the oxidative damage to fish induced by nZnO, resulting in higher ROS intensity, greater contents of MDA and MT and lower GSH content in liver and brain. Our results suggest that more studies in natural ecosystems are needed to better understand the fate and toxicity of nanoparticles in future CO2 levels.