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In coastal waters, particulate metals constitute a substantial fraction of the total metals; however, the prevalent water quality criteria are primarily based on dissolved metals, seemingly neglecting the contribution of particulate metals. Here we developed a method to quantify the toxicity risk of particulate metals, and proposed a way to calculate modifying factors (MFs) for setting site-specific criteria in turbid waters. Specifically, we used a side-by-side experimental design to study copper (Cu) bioaccumulation and toxicity in an estuarine clam, Potamocorbula laevis , under the exposure to "dissolved only" and "dissolved + particulate" 65 Cu. A toxicokinetic-toxicodynamic model (TK-TD) was used to quantify the processes of Cu uptake, ingestion, assimilation, egestion, and elimination, and to relate mortality risk to tissue Cu. We find that particulate Cu contributes 40-67% of the Cu bioaccumulation when the suspended particulate matter (SPM) ranges from 12 to 229 mg L -1 . The Cu-bearing SPM also increases the sensitivity of organisms to internalized Cu by decreasing the internal threshold concentration ( C IT ) from 141 to 76.8 μg g -1 . MFs were derived based on the TK-TD model to consider the contribution of particulate Cu (in the studied SPM range) for increasing Cu bioaccumulation (MF = 1.3-2.2) and toxicity (MF = 2.3-3.9). Water quality criteria derived from dissolved metal exposure need to be lowered by dividing by an MF to provide adequate protection. Overall, the method we developed provides a scientifically sound framework to manage the risks of metals in turbid waters.

Numerous studies have reported that the toxicity differences among metals are widespread; however, little is known about the mechanism of differences in metal toxicity to aquatic organisms due to the lack of quantitative understanding of their adverse outcome pathway. Here, we investigated the effects of Cd and Cu on bioaccumulation, gene expression, physiological responses, and apical effects in zebrafish larvae. RNA sequencing was conducted to provide supplementary mechanistic information for the effects of Cd and Cu exposure. On this basis, we proposed a quantitative adverse outcome pathway (qAOP) suitable for metal risk assessment of aquatic organisms. Our work provides a mechanistic explanation for the differences in metal toxicity where the strong bioaccumulation of Cu enables the newly accumulated Cu to reach the threshold that causes different adverse effects faster than Cd in zebrafish larvae, resulting in a higher toxicity of Cu than that of Cd. Furthermore, we proposed a parameter C IT /BCF (the ratio of internal threshold concentration and bioaccumulation factor) that helps to understand the toxicity differences by combining the information of bioaccumulation and internal threshold of adverse effects. This work demonstrated that qAOP is an effective quantitative tool for understanding the toxicity mechanism and highlight the importance of toxicokinetics and toxicodynamics at different biological levels in determining the metal toxicity.

Given the persistence and toxic potencies of metal contaminants in ecosystems, animals, and human beings, they are considered to be hazardous global pollutants. While the lethality of metal toxicities (e.g., LC 50 ) can significantly vary, even within the same species, the underlying mechanisms are less well-understood. In this study, we developed a subcellular two-compartment toxicokinetic-toxicodynamic (TK-TD) model for zebrafish larvae when exposed to four metals (cadmium, lead, copper, and zinc) to reveal whether differences in metal toxicity (LC 50 values) were dominated by the TK or TD processes. Results showed that the subcellular TK and TD parameters of the four metals were significantly different, and the bioconcentration factor (BCF) value of copper was higher than those of the other metals. We also found that the TD parameter internal threshold concentration ( C IT ) was significantly positively correlated to the LC 50 values ( R 2 = 0.7), suggesting a dominant role of TD processes in metal toxicity. Furthermore, the combined parameter C IT /BCF for a metal-sensitive fraction (BCF MSF ), which linked exposure to effects through the TK-TD approach, explained up to 89% of the variation in toxicity to the four metals. The present study suggests that the observed variation in toxicity of these four metals was mainly determined by TD processes but that TK processes should not be ignored, especially for copper.