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Lung inflammation from repeated airway exposure to washing-machine lint microfibers may be linked to phagocytosis dysfunction: Possible effects on mtDNA replication
Summary
Researchers exposed mice to washing machine lint microfibers for 90 days and observed dose-dependent lung inflammation, including immune cell infiltration, mucous cell hyperplasia, and increased inflammatory mediators. Alveolar macrophages aggregated around the fibrous particles but showed signs of phagocytosis dysfunction, and genomic analysis suggested effects on mitochondrial DNA replication. The study indicates that repeated inhalation of textile microfibers from laundry lint may cause chronic lung inflammation through impaired immune cell function.
Textiles and clothing are a primary source of microplastic pollution, releasing microfibers into the environment. In this study, lint microfibers in the top-loading washing machine lint filter (TWML) were provided by 10 volunteers and pooled into a single sample. The TWML consisted of irregularly shaped or fibrous particles, including heavy metals and microplastics. We dosed mice via oropharyngeal aspiration with TWML (10, 25, and 50 μg/mouse) for 90 days. The number of WBCs and the proportion of neutrophils in WBCs decreased in male and female mice exposed to the highest dose, respectively, and the proportion of RET in RBCs decreased in both sexes of mice. The total number of pulmonary immune cells increased with dose, accompanying an increase in the proportion of lymphocytes. Pulmonary immune cells aggregated around TWML, and among the inflammatory mediators measured in this study, only CXCL-1 and TGF-β levels increased significantly in the lungs of both sexes of mice. Infiltration of inflammatory cells and hyperplasia of mucous cells in the bronchial epithelium were found in the lung tissues of TWML-treated mice. When incubated at 40 μg/mL, alveolar macrophages were aggregated around the fibrous particles, as was observed in the lungs. The production of cell signaling-related secondary mediators increased significantly in TWML-treated cells. NGS analysis also indicated that the plasma membrane, cell periphery, and cell projections were the most affected cellular components, and that genes involved in protein synthesis and mitochondrial DNA replication were most downregulated in TWML-treated cells. Expression of mitochondrial dynamics- and cellular iron uptake-related proteins was inhibited following exposure to TWML, and those of anti-oxidant response-related proteins were clearly enhanced in the cells. Overall, we conclude that TWML-induced inflammatory lesions may be attributable to frustrated phagocytosis of alveolar macrophages. Additionally, TWML may disrupt cellular function through oxidative stress and damage to mitochondrial DNA replication.