Microplastics and nanoplastics, emerging pollutants, increased the risk of pulmonary fibrosis in vivo and in vitro: A comparative evaluation of their potential toxicity effects with different polymers and size

Oct 11, 2025Toxicology

Microplastics and nanoplastics raise the risk of lung scarring in living organisms and cells: Comparing toxicity of different plastic types and sizes

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Abstract

Microplastics (MPs) and nanoplastics (NPs) exposure may elevate the risk of pulmonary fibrosis.

Intratracheal injection of MPs/NPs in mice caused significant pulmonary histopathological changes and increased expression of fibrosis-related proteins.
The PS-NPs group showed the highest levels of pro-inflammatory cytokine secretion and recruitment of immune cells.
Cytotoxicity was observed in human lung epithelial cells, with MPs/NPs up-regulating markers associated with fibrosis and inflammation.
In mice and human cells, PS-NPs increased YAP1 expression while inhibiting FXR expression, indicating a potential toxic mechanism.
Manipulating the FXR-YAP1 axis with specific antagonists and agonists altered the expression of fibrosis-related proteins.

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With the increasing consumption of plastic products, microplastics (MPs) and nanoplastics (NPs), as new environmental pollution, pose a huge potential threat to human health. The different polymers and sizes of MPs and NPs are important factors determining the distribution and pathways of particulate organisms, thereby affecting their toxicity. The study explored the pulmonary toxicity and potential mechanism of MPs (1 μm) and NPs (100 nm) of polystyrene (PS), polyethylene (PE), or polypropylene (PP) in vivo and in vitro. Intratracheal injection of MPs/NPs (10 mg/kg, once every six days, continued four times) in mice induced pulmonary histopathological changes, raised α-SMA and collagen I expressions, the TIMP-1/MMP13 ratio, epithelial-mesenchymal transition (EMT)-related proteins, recruited immune cells and increased pro-inflammatory cytokine secretion, especially in PS-NPs group. MPs/NPs (PS, PE or PP) exhibited cytotoxicity in human lung epithelial BEAS-2B, and MPs/NPs (50 μg/mL, 8 h) up-regulated α-SMA, Vimentin, and IL-1β expressions. PS-NPs raised YAP1 and inhibited FXR expression in mice or BEAS-2B, compared with other polymers or diameters. In PS-NPs-induced BEAS-2B, Verteporfin (YAP1 antagonist, 0.2 μM) or GW4064 (FXR agonist, 2 μM) reduced α-SMA, Vimentin, and IL-1β expressions, while Gugglesterone (FXR antagonist, 50 μM) increased above protein expressions. Meanwhile, FXR deficiency increased YAP1 activity and fibrogenesis in PS-NPs-induced BEAS-2B. Collectively, MPs/NPs exposure elevates the risk of pulmonary fibrosis, and FXR-YAP1 axis dysregulation may underlie their toxicity mechanisms. Among the tested polymers, PS exhibits stronger pulmonary toxicity and cytotoxicity compared to PE or PP, and NPs of the same polymer demonstrate greater pulmonary toxicity than MPs.

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Microplastics and nanoplastics, emerging pollutants, increased the risk of pulmonary fibrosis in vivo and in vitro: A comparative evaluation of their potential toxicity effects with different polymers and size

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