The increased use of engineered nanoparticles (ENPs) in consumer products raises the concern of environmental release and subsequent impacts in natural communities. We tested for physiological and demographic impacts of ZnO, a prevalent metal oxide ENP, on the mussel Mytilus galloprovincialis . We exposed mussels of two size classes, <4.5 and ≥4.5 cm shell length, to 0.1–2 mg l −1 ZnO ENPs in seawater for 12 wk, and measured the effect on mussel respiration, accumulation of Zn, growth, and survival. After 12 wk of exposure to ZnO ENPs, respiration rates of mussels increased with ZnO concentration. Mussels had up to three fold more Zn in tissues than control groups after 12 wk of exposure, but patterns of Zn accumulation varied with mussel size and Zn concentrations. Small mussels accumulated Zn 10 times faster than large mussels at 0.5 mg l −1 , while large mussels accumulated Zn four times faster than small mussels at 2 mg l −1 . Mussels exposed to 2 mg l −1 ZnO grew 40% less than mussels in our control group for both size classes. Survival significantly decreased only in groups exposed to the highest ZnO concentration (2 mg l −1 ) and was lower for small mussels than large. Our results indicate that ZnO ENPs are toxic to mussels but at levels unlikely to be reached in natural marine waters.

Cu is an essential trace element but can be highly toxic to aquatic organisms at elevated concentrations. Greater use of CuO engineered nanoparticles (ENPs) may lead to increased concentrations of CuO ENPs in aquatic environments causing potential ecological injury. We examined the toxicity of CuO ENPs to marine mussels and the influence of mussels on the fate and transport of CuO ENPs. We exposed marine mussels to 1, 2, or 3 mg L⁻¹ CuO ENPs for four weeks, and measured clearance rate, rejection, excretion and accumulation of Cu, and mussel shell growth. Mussel clearance rate was 48% less, and growth was 68% less, in mussels exposed to 3 mg L⁻¹ than in control animals. Previous studies show 100% mortality at 1 mg Cu L⁻¹, suggesting that CuO ENPs are much less toxic than ionic Cu, probably due to the slow dissolution rate of the ENPs. Mussels rejected and excreted CuO ENPs in biodeposits containing as much as 110 mg Cu g⁻¹, suggesting the potential for magnification in sediments. Mussels exposed to 3 mg L⁻¹ CuO ENPs accumulated 79.14 ± 12.46 µg Cu g⁻¹ dry weight, which was 60 times more Cu than in control animals. Our results suggest that mussels have the potential to influence the fate and transport of CuO ENPs and potentially cause magnification of CuO ENPs in mussel bed communities, creating a significant source of Cu to marine benthos.