Abstract:
Micro(nano)plastics (MNPs) have become persistent and widespread contaminants in aquatic ecosystems, raising concerns about their capacity to impair reproductive success and population renewal in exposed organisms. However, the interpretation of cross-generational reproductive risks remains fragmented because similar offspring phenotypes can arise from nonequivalent causal routes, including direct maternal particle transfer, parental physiological injury, or external exposure at embryonic interfaces.
Here, we propose an evidence hierarchy framework to distinguish true maternal particle transfer from broader cross-generational toxicity, encompassing intergenerational, multigenerational, and transgenerational effects. Our synthesis reveals that transfer pathways differ markedly among aquatic taxa, ranging from brood chamber exposure and gut–ovary–oocyte transfer in cladocerans to ovary–oocyte–yolk/chorion interfaces in fish, yet conclusive evidence for endogenous particle entry into offspring's tissues remains scarce and requires rigorous orthogonal localization and contamination controls. Mechanistically, we link MNP exposure to offspring outcomes through a network of barrier uptake, oxidative and mitochondrial stress, inflammation, apoptosis, endocrine disruption, epigenetic regulation, microbiota dysbiosis, and contaminant vector effects, which collectively compromise gamete quality, embryonic development, and subsequent life history performance.
Our synthesis indicates that offspring toxicity following parental exposure cannot be equated with maternal particle transfer, and that environmentally realistic risk assessment must prioritize particle localization evidence, clean-generation designs, and population-level fitness endpoints over single-generation toxicity descriptions.
