# Effects of Atmospheric Aging on the Respiratory Toxicity of Polystyrene Nanoplastic Particles

**Authors:** Alana J. Dodero, Olivia C. G. Lampe, Sahir Gagan, Sining Niu, Natalie M. Johnson, Yue Zhang

PMC · DOI: 10.1021/acs.chemrestox.5c00237 · Chemical Research in Toxicology · 2025-11-03

## TL;DR

This study shows that atmospheric aging increases the toxicity of polystyrene nanoplastics to lung cells, causing inflammation and oxidative stress.

## Contribution

The study reveals how environmental aging of nanoplastics enhances their respiratory toxicity through changes in surface and chemical properties.

## Key findings

- Atmospheric aging of polystyrene nanoplastics increases proinflammatory gene expression in bronchial epithelial cells.
- Aged nanoplastics induce oxidative stress, as indicated by elevated heme oxygenase-1 expression.
- Surface roughness and oxygen-to-carbon ratios increase in aged nanoplastics, contributing to toxicity.

## Abstract

Inhalation exposure to nanoplastic particles (NPPs) can lead to
significant pulmonary toxicity; however, the effects of environmental
processing on their toxicity remain poorly understood. This study
examines the toxicity of polystyrene (PS) NPPs on lung cells following
controlled atmospheric aging. Human bronchial epithelial cells (16HBE)
were cultured in vitro at the air–liquid interface and acutely
exposed to oxidized PS NPPs through electrostatic precipitation. Expression
of proinflammatory genes interleukin-8 (IL-8) and
tumor necrosis factor alpha (TNF-α) was significantly
elevated at 6 and 48 h postexposure to aged NPPs, with corresponding
increases in interleukin-6 (IL-6) protein levels supporting an inflammatory
response. The oxidative stress marker heme oxygenase-1 (HO-1) also
showed significantly increased expression at 6 h postexposure, supported
by protein analysis. Atomic force microscopy (AFM) and aerosol mass
spectrometry (AMS) revealed increased surface roughness and oxygen
to carbon ratios in the atmospherically aged NPPs. Together, these
results demonstrate that atmospheric aging alters the chemical composition
and surface morphology of PS NPPs, enhancing proinflammatory and oxidative
stress responses in bronchial epithelial cells, highlighting the critical
role of environmental processing in determining the toxicity of nanoplastics.

## Linked entities

- **Genes:** CXCL8 (C-X-C motif chemokine ligand 8) [NCBI Gene 3576], TNF (tumor necrosis factor) [NCBI Gene 7124], IL6 (interleukin 6) [NCBI Gene 3569], HMOX1 (heme oxygenase 1) [NCBI Gene 3162]
- **Proteins:** IL6 (interleukin 6), TED4 (Plant heme oxygenase (decyclizing) family protein)
- **Species:** Homo sapiens (taxon 9606)

## Full-text entities

- **Genes:** CXCL8 (C-X-C motif chemokine ligand 8) [NCBI Gene 3576] {aka GCP-1, GCP1, IL8, LECT, LUCT, LYNAP}, TNF (tumor necrosis factor) [NCBI Gene 7124] {aka DIF, IMD127, TNF-alpha, TNFA, TNFSF2, TNLG1F}, HMOX1 (heme oxygenase 1) [NCBI Gene 3162] {aka HMOX1D, HO-1, HSP32, bK286B10}, IL6 (interleukin 6) [NCBI Gene 3569] {aka BSF-2, BSF2, CDF, HGF, HSF, IFN-beta-2}
- **Diseases:** inflammatory (MESH:D007249), pulmonary toxicity (MESH:D008171), toxicity (MESH:D064420), Respiratory Toxicity (MESH:D012140)
- **Chemicals:** carbon (MESH:D002244), oxygen (MESH:D010100), PS (MESH:D011137)
- **Species:** Homo sapiens (human, species) [taxon 9606]
- **Cell lines:** 16HBE — Homo sapiens (Human), Transformed cell line (CVCL_0112)

## Full text

_Full body text omitted from this summary view._ Fetch the complete paper as Markdown: https://tomesphere.com/paper/PMC12956272/full.md

## Figures

6 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12956272/full.md

## References

72 references — full list in the complete paper: https://tomesphere.com/paper/PMC12956272/full.md

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Source: https://tomesphere.com/paper/PMC12956272