The immunotoxic effects of some anthropogenic pollutants on aquatic organisms are among the causes of concern over the presence of these pollutants in the marine environment. The immune system is part of an organism’s biological defense necessarily for homeostasis. Thus, the immunotoxicological impacts on aquatic organisms are important to understand the effects of pollutant chemicals in the aquatic ecosystem. When aquatic organisms are exposed to pollutant chemicals with immunotoxicity, it results in poor health. In addition, aquatic organisms are exposed to pathogenic bacteria, viruses, parasites, and fungi. Exposure to pollutant chemicals has reportedly caused aquatic organisms to show various immunotoxic symptoms such as histological changes of lymphoid tissue, changes of immune functionality and the distribution of immune cells, and changes in the resistance of organisms to infection by pathogens. Alterations of immune systems by contaminants can therefore lead to the deaths of individual organisms, increase the general risk of infections by pathogens, and probably decrease the populations of some species. This review introduced the immunotoxicological impact of pollutant chemicals in aquatic organisms, including invertebrates, fish, amphibians, and marine mammals; described typical biomarkers used in aquatic immunotoxicological studies; and then, discussed the current issues on ecological risk assessment and how to address ecological risk assessment through immunotoxicology. Moreover, the usefulness of the population growth rate to estimate the immunotoxicological impact of pollution chemicals was proposed.

To investigate the effects of salinity on the toxicity of silver nanocolloids (SNCs, 28.4 nm in diameter) in aquatic environments (freshwater, brackish water, and seawater), we exposed 15 medaka eggs in triplicate to SNCs at 10 mg L⁻¹ in different salinities of embryo-rearing medium (ERM) (1×, 5×, 10×, 15×, 20×, and 30×) until hatching (1× ERM and 30× ERM have osmotic pressures equivalent to freshwater and seawater, respectively). With increasing concentration of ERM, SNCs aggregated to 437.3 nm in diameter in 30× ERM solution. Simultaneously, soluble silver chloro complexes (various combinations of [AgCl]⁰, [AgCl₂]¹⁻, [AgCl₃]²⁻, and [AgCl₄]³⁻) were calculated to have been formed. The patterns of the absorption spectra of SNCs and AgNO₃ (a reference compound) differed markedly in ERM at different salinities, indicating that different soluble silver complexes were present in each solution. With increasing salinity, the chorion resistance decreased, and the salinity in the medaka eggs, as indicated by the osmotic pressure, increased. Simultaneously, uptake of SNCs or other silver complexes into the embryos also increased compared with that of AgNO₃ in 20× and 30× ERM. In the presence of SNCs in 20× ERM, embryo hatching rate and full body lengths of post-hatch larvae were significantly lower than those with AgNO₃. The toxic effects of SNCs on the hatching rate increased significantly in media of high salinity and were greater than those of AgNO₃. SNCs and related silver chloro complexes exhibited higher bioavailability and medaka embryo toxicity in saline conditions than did AgNO₃. SNCs pose greater ecological risks to fish embryos in high-salinity aquatic environments than in freshwater environments.

Fish embryo toxicology is important because embryos are considered more susceptible than adult fish to the effects of toxic chemicals. Recently, fish embryo bioassay was proposed to replace the conventional fish acute toxicity chemical test of the Organization for Economic Cooperation and Development guidelines because it offers the advantages of fewer reagents, easy handling, and efficient data production. To accelerate the establishment of a chemical toxicity database for the protection of environmental and human health, we need to determine whether the conventional toxicity test can safely be replaced by such fish embryo toxicity tests. For instance, it is unclear how the presence of the chorion moderates the toxic effects of some chemicals. If such chemical toxicities do differ between embryos and, for example, the larval stage, then different toxic effects should appear in later life. We tested the later-life effects of the neurotoxic insecticide carbaryl at sublethal concentrations (0 [control] and 5 and 10 mg/L) in embryos and posthatch larvae of the freshwater fish medaka, Oryzias latipes. Although embryos exposed until hatching showed multiple developmental malformations and reductions in subsequent survival rates over three months, no significant reduction was observed in tolerance to starvation for 7 d and in intrinsic population growth rate (r). Exposure of larvae for 96 h resulted in dose-responsive vertebral fracture, significant reduction in tolerance to starvation for 7 d, and reduced three-month survival rate; r was reduced significantly and consistently. These results suggested that posthatch larvae were more susceptible than embryos to carbaryl exposure and that the toxic cascades may differ between larvae and embryos. The influences of carbaryl exposure on population growth rate differed significantly with developmental stage.