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Nanoplastics Impair Neuroimmune Integrity Via Cellular Retention and Multiple Organelle Stress

Journal of Hazardous Materials Advances 2026
Chman Shahzadi, Pathik Parekh, Buyandelger Batsaikhan, David Tweedie, Erica Costantini, Elliot J. Glotfelty, Piero Di Carlo, Marcella Reale, Nigel H. Greig

Summary

Scientists found that tiny plastic particles (nanoplastics) don't kill brain and immune cells outright, but they get stuck inside them and build up over time, stressing out the cell's internal "cleanup" and energy-making systems. Immune cells called macrophages, whose job is to gobble up foreign particles, were especially affected, and even nerve cells showed signs of low-level inflammation. This suggests that everyday plastic exposure could quietly accumulate in our cells and contribute to long-term brain and immune problems—something researchers are just beginning to understand.

Polymers
Body Systems

The biological persistence of nanoplastics (NPs) has raised growing concern regarding their potential to accumulate in human tissues yet their impact on neuroimmune cellular function remains largely undefined. Here, we investigated the neuroimmune effects of polystyrene NPs (100, 200, and 1000nm; 10 and 100µg/mL) across neuronal (SH-SY5Y, PCNs) and immune cells (THP1, macrophages). Cellular responses were assessed through analyses of cytotoxicity, immunocytochemistry and cytokine profiling. NPs exposure did not induce acute cytotoxicity but promoted persistent intracellular retention accompanied by lysosomal dysfunction, dysregulated autophagic flux, ER stress, and constrained mitochondrial function, thereby inducing a sublethal multi-organelle stress response. Macrophages exhibited greater vulnerability consistent with phagocytic burden, while inflammatory challenge further enhanced NPs uptake, reinforcing intracellular persistence. In contrast, neurons showed limited extracellular cytokine secretion yet accumulated intracellular IL-1β, suggesting low-grade inflammatory activation. Such responses were recapitulated in PCNs, supporting translational relevance across neuronal models. The cumulative nature of these observations suggests that NPs exposure may give rise to previously unrecognized accumulation-related pathologies, a phenomenon we term “plasticoma” as a conceptual framework, to describe the preferential deposition of non-degradable plastic particles within cells, to frame and stimulate future investigations into NP accumulation and pathology. These findings position NPs as potential determinant of neuroimmune dysfunction and highlight the importance of strategies aimed at mitigating their biological accumulation. Environmental Implications NPs are increasingly present in the environment, yet their biological effects remain poorly understood. This study demonstrates that NPs can biological barriers and reach and accumulate in cells to disrupt key cellular processes across neuroimmune systems. These findings highlight potential risks associated with chronic environmental exposure and underscore the need to develop targeted strategies to mitigate NPs associated neuroimmune dysfunction and related human health impacts.

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