Gosselink I F, Leonhardt P, Höppener E M, Smelt R, Drittij M J, Davigo M, van den Akker G G H, Kooter I M, Welting T J M, van Schooten F J, Remels A H V
Department of Pharmacology and Toxicology, Institute of Nutrition and Translational Research in Metabolism (NUTRIM), Maastricht University, Universiteitssingel 50, 6629 ER Maastricht, the Netherlands.
Netherlands Organisation for Applied Scientific Research, TNO, 3584 CB Utrecht, the Netherlands.
Microplast nanoplast. 2025;5(1):19. doi: 10.1186/s43591-025-00126-9. Epub 2025 May 16.
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.
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).
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.
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.
The online version contains supplementary material available at 10.1186/s43591-025-00126-9.
关于微塑料和纳米塑料（MNPs）对人类气道上皮细胞的毒理学影响的了解有限，且几乎完全基于应用高剂量球形聚苯乙烯（PS）颗粒的实验。在本研究中，我们调查了由不同环境相关聚合物产生的广泛尺寸范围的无定形MNPs的毒性。
将支气管上皮细胞（BEAS-2B）暴露于三种不同剂量的聚氯乙烯（PVC）、聚丙烯（PP）或聚酰胺（PA）颗粒（<1μm - 10μm）以及这些聚合物的浸出液中。通过评估细胞毒性、炎症（IL-8释放和炎症基因表达）和氧化应激（DCFH-DA测定和抗氧化基因表达）来评估毒性。此外，通过研究两种著名的炎症相关转录因子（NF-κB和AP-1）的激活来探究MNP诱导炎症背后的分子机制。
与载体对照相比，只有PA纳米塑料诱导了显著的细胞死亡、IL-8分泌和炎症基因表达。PA诱导的炎症伴随着NF-κB的转录活性，但不伴随AP-1的转录活性。PA没有增加细胞内活性氧水平；然而，它确实导致了抗氧化基因超氧化物歧化酶2的表达增加。除了PA，暴露于<1μm和1 - 5μm的PP颗粒也导致IL-8分泌增加，这可能是由于添加了滑石粉作为填充剂。没有一种浸出液影响细胞毒性或炎症。
MNPs对人支气管上皮细胞的毒性取决于聚合物类型、大小和剂量。纳米塑料，尤其是PA，对支气管上皮细胞的毒性比微塑料更大，并诱导细胞毒性和炎症反应。
在线版本包含可在10.1186/s43591-025-00126-9获取的补充材料。
