Size- and polymer-dependent toxicity of amorphous environmentally relevant micro- and nanoplastics in human bronchial epithelial cells

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 r...

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Main Authors: I. F. Gosselink, P. Leonhardt, E. M. Höppener, R. Smelt, M. J. Drittij, M. Davigo, G. G. H. van den Akker, I. M. Kooter, T. J. M. Welting, F. J. van Schooten, A. H. V. Remels
Format: Article
Language:English
Published: SpringerOpen 2025-05-01
Series:Microplastics and Nanoplastics
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Online Access:https://doi.org/10.1186/s43591-025-00126-9
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author I. F. Gosselink
P. Leonhardt
E. M. Höppener
R. Smelt
M. J. Drittij
M. Davigo
G. G. H. van den Akker
I. M. Kooter
T. J. M. Welting
F. J. van Schooten
A. H. V. Remels
author_facet I. F. Gosselink
P. Leonhardt
E. M. Höppener
R. Smelt
M. J. Drittij
M. Davigo
G. G. H. van den Akker
I. M. Kooter
T. J. M. Welting
F. J. van Schooten
A. H. V. Remels
author_sort I. F. Gosselink
collection DOAJ
description 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
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spelling doaj-art-9f2b3a9681d0492b902ea600b29469d42025-08-20T02:32:00ZengSpringerOpenMicroplastics and Nanoplastics2662-49662025-05-015111710.1186/s43591-025-00126-9Size- and polymer-dependent toxicity of amorphous environmentally relevant micro- and nanoplastics in human bronchial epithelial cellsI. F. Gosselink0P. Leonhardt1E. M. Höppener2R. Smelt3M. J. Drittij4M. Davigo5G. G. H. van den Akker6I. M. Kooter7T. J. M. Welting8F. J. van Schooten9A. H. V. Remels10Department of Pharmacology and Toxicology, Institute of Nutrition and Translational Research in Metabolism (NUTRIM), Maastricht UniversityDepartment of Pharmacology and Toxicology, Institute of Nutrition and Translational Research in Metabolism (NUTRIM), Maastricht UniversityNetherlands Organisation for Applied Scientific Research, TNODepartment of Pharmacology and Toxicology, Institute of Nutrition and Translational Research in Metabolism (NUTRIM), Maastricht UniversityDepartment of Pharmacology and Toxicology, Institute of Nutrition and Translational Research in Metabolism (NUTRIM), Maastricht UniversityDepartment of Pharmacology and Toxicology, Institute of Nutrition and Translational Research in Metabolism (NUTRIM), Maastricht UniversityLaboratory of Experimental Orthopedics, Department of Orthopedic Surgery, Maastricht UniversityDepartment of Pharmacology and Toxicology, Institute of Nutrition and Translational Research in Metabolism (NUTRIM), Maastricht UniversityLaboratory of Experimental Orthopedics, Department of Orthopedic Surgery, Maastricht UniversityDepartment of Pharmacology and Toxicology, Institute of Nutrition and Translational Research in Metabolism (NUTRIM), Maastricht UniversityDepartment of Pharmacology and Toxicology, Institute of Nutrition and Translational Research in Metabolism (NUTRIM), Maastricht UniversityAbstract 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 Abstracthttps://doi.org/10.1186/s43591-025-00126-9Inhalation toxicologyPolypropylenePolyamidePolyvinylchlorideInflammationNF-ĸB
spellingShingle I. F. Gosselink
P. Leonhardt
E. M. Höppener
R. Smelt
M. J. Drittij
M. Davigo
G. G. H. van den Akker
I. M. Kooter
T. J. M. Welting
F. J. van Schooten
A. H. V. Remels
Size- and polymer-dependent toxicity of amorphous environmentally relevant micro- and nanoplastics in human bronchial epithelial cells
Microplastics and Nanoplastics
Inhalation toxicology
Polypropylene
Polyamide
Polyvinylchloride
Inflammation
NF-ĸB
title Size- and polymer-dependent toxicity of amorphous environmentally relevant micro- and nanoplastics in human bronchial epithelial cells
title_full Size- and polymer-dependent toxicity of amorphous environmentally relevant micro- and nanoplastics in human bronchial epithelial cells
title_fullStr Size- and polymer-dependent toxicity of amorphous environmentally relevant micro- and nanoplastics in human bronchial epithelial cells
title_full_unstemmed Size- and polymer-dependent toxicity of amorphous environmentally relevant micro- and nanoplastics in human bronchial epithelial cells
title_short Size- and polymer-dependent toxicity of amorphous environmentally relevant micro- and nanoplastics in human bronchial epithelial cells
title_sort size and polymer dependent toxicity of amorphous environmentally relevant micro and nanoplastics in human bronchial epithelial cells
topic Inhalation toxicology
Polypropylene
Polyamide
Polyvinylchloride
Inflammation
NF-ĸB
url https://doi.org/10.1186/s43591-025-00126-9
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