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Toxicity and antagonistic effects of the combined exposure to di(2-ethylhexyl) phthalate and polyvinyl chloride nanoplastics on the early developmental stage of zebrafish
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Zebrafish embryos exposed to PVC nanoplastics alone showed activated detoxification and antioxidant responses, while the chemical DEHP alone caused oxidative damage and lower expression of neurodevelopment genes. When combined, PVC nanoplastics reduced DEHP's neurotoxic effects, possibly because DEHP stuck to the plastic particles' surfaces.
Possessing prominent polarity and an extensive specific surface area, nanoplastics (NPs) act as efficient transport vectors for diverse contaminants in aquatic ecosystems. Given that di(2-ethylhexyl) phthalate (DEHP), a widespread plastic additive, is prone to leach out and co-exist with polyvinyl chloride (PVC) in aquatic phases, this study artificially pulverized bulk PVC raw materials to generate nano-sized plastic particles that closely match the morphological features of environmental nanoplastic pollutants. A series of experiments were conducted to investigate alterations in embryonic hatching success and cardiac rhythm, as well as the underlying molecular pathways governing xenobiotic detoxification, antioxidant responses, cellular apoptosis and neurodevelopment in zebrafish ( Danio rerio ) upon single and co-exposure to PVC-NPs and DEHP. Experimental results revealed that PVC-NPs at a concentration of 1 ppm (98.18%) induced significantly lower lethal toxicity to zebrafish compared with microplastic particles (33.77%) at an identical dosage. Exposure to 1 ppm PVC-NPs activated aryl hydrocarbon receptors, antioxidant cascades and associated signaling axes, demonstrating that zebrafish initiate xenobiotic metabolic reactions to cope with nanoplastic stress. By contrast, DEHP exposure elicited severe oxidative damage in zebrafish tissues. Downregulated transcription of neurodevelopment-related genes indicated that DEHP interfered with the proliferation and population maintenance of neurons and astrocytes, thereby exerting evident neurotoxicity. Notably, co-exposure to PVC-NPs and DEHP exhibited an antagonistic interaction that mitigated DEHP-induced neurotoxicity, may be attributable to the robust sorption of DEHP onto PVC-NPs surfaces, which reduced the freely dissolved fraction of DEHP available for cellular uptake. These findings challenge the conventional assumption that nanoplastic carriers inevitably exacerbate co-pollutant toxicity, highlighting the necessity of distinguishing between the “vector effect” and the “shielding effect” in future ecological risk assessment models for co-occurring plastic additives.
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