ArticleMicroplastics and nanoplastics2025
Size- and polymer-dependent toxicity of amorphous environmentally relevant micro- and nanoplastics in human bronchial epithelial cells.
Article in Microplastics and nanoplastics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Micro- and Nanoplastics and Pulmonary Health: The Current State of Research.Microplastics (Basel, Switzerland) · 2026Article
- Polyamide and polyvinyl chloride microplastics induce cytotoxicity and cytokine release in primary normal human bronchial epithelial cells.Microplastics and nanoplastics · 2026Article
- Potential toxicity of micro- and nanoplastics in primary bronchial epithelial cells of patients with chronic obstructive pulmonary disease.Microplastics and nanoplastics · 2026Article
- Microplastic induced cascades of multiple cell death pathways: inflammation, immune imbalance, and cancer susceptibility.Frontiers in public health · 2026Review
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Authors and funding
11 authors.
Funding
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Abstract
Background: Knowledge of the toxicological impact of micro- and nanoplastics (MNPs) on the human airway epithelium is limited and almost exclusively based on experiments applying high doses of spherical polystyrene (PS) particles. In this study, we investigated the toxicity of a broad size range of amorphous MNPs generated from different environmentally-relevant polymers. Methods: Bronchial epithelial cells (BEAS-2B) were exposed to three different doses of polyvinylchloride (PVC), polypropylene (PP), or polyamide (PA) particles (< 1 μm-10 μm), as well as leachates from these polymers. Toxicity was evaluated by assessment of cytotoxicity, inflammation (IL-8 release and inflammatory gene expression) and oxidative stress (DCFH-DA assay and antioxidant gene expression). Furthermore, the molecular mechanism behind MNP-induced inflammation was investigated by studying activation of two well-known inflammation related transcriptional factors (NF-κB and AP-1). Results: Only PA nanoplastics induced significant cell death, IL-8 secretion and inflammatory gene expression compared to vehicle control. PA-induced inflammation was accompanied by NF-κB, but not AP-1, transcriptional activity. PA did not increase cellular ROS levels; however, it did lead to increased expression of the antioxidant gene superoxide dismutase 2. In addition to PA, exposure to < 1 µm and 1-5 µm PP particles resulted in elevated IL-8 secretion, likely due to the presence of talc added as filler. None of the leachates affected cytotoxicity or inflammation. Conclusion: Toxicity of MNPs to human bronchial epithelial cells was dependent on polymer type, size and dose. Nanoplastics, especially PA, were more toxic to bronchial epithelial cells than microplastics and induced cytotoxicity and an inflammatory response. Graphical Abstract: Supplementary Information: The online version contains supplementary material available at 10.1186/s43591-025-00126-9.
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