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Article ? AI-assigned paper type based on the abstract. Classification may not be perfect — flag errors using the feedback button. Tier 2 ? Original research — experimental, observational, or case-control study. Direct primary evidence. Human Health Effects Nanoplastics Sign in to save

Polystyrene nanoplastics amplify the toxic effects of PFOA on the Chinese mitten crab (Eriocheir sinensis)

Journal of Hazardous Materials 2025 19 citations ? Citation count from OpenAlex, updated daily. May differ slightly from the publisher's own count. Score: 68 ? 0–100 AI score estimating relevance to the microplastics field. Papers below 30 are filtered from public browse.
Peng Huang, Liping Cao, Haojun Zhu, Liping Cao, Liping Cao, Liping Cao, Jinliang Du, Jinliang Du, Jiancao Gao, Gangchun Xu Haojun Zhu, Jiancao Gao, Jiancao Gao, Jiancao Gao, Yi Sun, Yi Sun, Gangchun Xu Gangchun Xu Gangchun Xu Gangchun Xu Yiqing Guo, Yiqing Guo, Haojun Zhu, Quanjie Li, Haojun Zhu, Yi Sun, Yi Sun, Gangchun Xu Gangchun Xu Yi Sun, Gangchun Xu Yi Sun, Yi Sun, Haojun Zhu, Haojun Zhu, Quanjie Li, Haojun Zhu, Haojun Zhu, Gangchun Xu Gangchun Xu Gangchun Xu Jiancao Gao, Gangchun Xu

Summary

Nanoplastics amplified the toxic effects of PFOA (a "forever chemical") in Chinese mitten crabs, worsening oxidative stress, immune disruption, and intestinal inflammation beyond what either pollutant caused alone. The combination disrupted fat metabolism and triggered cell death pathways, demonstrating how two common environmental contaminants can interact to create greater health risks in organisms that humans consume as food.

Polymers

Nanoplastics (NPs), the final form of degraded microplastics in the environment, can adsorb PFOA (an emerging organic pollutant in recent years) in several ways. Current research on these has focused on bony fishes and mollusks, however, the combined toxicity of PFOA and NPs remains unknown in Eriocheir sinensis. Therefore, the effects of single or combined exposure to PFOA and NPs were investigated. The results showed that NPs aggravated PFOA exposure-induced oxidative stress, serum lipid disorders, immune responses, and morphological damage. DEGs altered by NPs-PFOA exposure were predominantly enriched in GO terms for cell lumen, and organelle structure, and KEGG terms for spliceosome and endocrine disorders-related diseases. Notably, the apoptotic pathway plays a central role enriched under different exposure modes. PFOA or NPs-PFOA exposure disrupted the levels of lipids molecules-related metabolites by mediating the glycerophospholipid pathway, and the NPs mediated the ferroptosis pathway to exacerbate PFOA-induced metabolic toxicity. In addition, NPs exacerbated the inflammatory response and metabolic imbalance by mediating Fusobacterium ulcerans in the intestinal. In conclusion, this study provides a valuable reference for the characterization of NPs-PFOA combined pollution and a scientific basis for the development of environmental protection policies and pollution management strategies.

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