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Polystyrene micro-/nanoplastics induced hematopoietic damages via the crosstalk of gut microbiota, metabolites, and cytokines

Environment International 2022 141 citations ? Citation count from OpenAlex, updated daily. May differ slightly from the publisher's own count. Score: 60 ? 0–100 AI score estimating relevance to the microplastics field. Papers below 30 are filtered from public browse.
Jiaru Jing, Lei Zhang, Han Lin, Jingyu Wang, Wei Zhang, Ziyan Liu, Ai Gao

Summary

Researchers exposed mice to polystyrene micro- and nanoplastics and found that the particles caused damage to the blood-forming system through disruption of gut bacteria, metabolic changes, and inflammatory signaling. Smaller nanoplastics caused more severe effects than larger microplastics, altering gut microbial communities and triggering systemic inflammation. The study reveals a previously unknown pathway by which ingested plastic particles may harm the body's ability to produce healthy blood cells.

Polymers
Models

Micro-/nanoplastics (MNPLs), novel environmental pollutants, widely exist in the environment and life and bring health risks. Previous studies have shown that NMPLs can penetrate bone marrow, but whether they cause hematopoietic damage remains uncertain. In this study, C57BL/6J mice were treated with polystyrene MNPLs (PS-MNPLs, 10 μm, 5 μm and 80 nm) at 60 μg doses for 42 days by intragastric administration. We evaluated the hematopoietic toxicity induced by MNPLs and potential mechanisms via combining 16S rRNA, metabolomics, and cytokine chips. The results demonstrated that PS-MNPLs induced hematopoietic toxicity, which was manifested by the disorder of bone marrow cell arrangement, the reduction in colony-forming, self-renewal and differentiation capacity, and the increased proportion of lymphocytes. PS-MNPLs also disrupted the homeostasis of the gut microbiota, metabolism, and inflammation, all of which were correlated with hematotoxicity, suggesting that abnormal gut microbiota-metabolite-cytokine axes might be the crucial pathways in MNPLs-induced hematopoietic injury. In conclusion, our study systematically demonstrated that multi-scale PS-MNPLs induced hematopoietic toxicity via the crosstalk of gut microbiota, metabolites, and cytokines and provided valuable insights into MNPLs toxicity, which was conducive to health risk assessment and informed policy decisions regarding PS-MNPLs.

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