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Mechanisms of exacerbation of Th2-mediated eosinophilic allergic asthma induced by plastic pollution derivatives (PPD): A molecular toxicological study involving lung cell ferroptosis and metabolomics
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Researchers found that mice exposed to polystyrene microplastics combined with a common plastic additive (dibutyl phthalate) developed significantly worse allergic asthma symptoms, including increased airway inflammation driven by a specific type of immune response. The microplastics triggered a form of cell death called ferroptosis in lung cells, which amplified the allergic reaction. Treatment with an iron-binding drug provided relief, suggesting potential therapeutic approaches for people with asthma who are exposed to plastic pollution.
Polystyrene microplastics (PS-MP) and dibutyl phthalate (DBP) are plastic pollution derivatives (PPDs) commonly found in the natural environment. To investigate the effects of PPD exposure on the risk of allergic asthma, we established a PPD exposure group in a mouse model. The dose administered for PS-MP was 0.1 mg/d and for DBP was 30 mg/kg/d, with a 5-week oral administration period. The pathological changes of airway tissue and the increase of oxidative stress and inflammatory response confirmed that PPD aggravated eosinophilic allergic asthma in mice. The mitochondrial morphological changes and metabolomics of mice confirmed that ferrotosis and oxidative stress played key roles in this process. Treatment with 100 mg/Kg deferoxamine (DFO) provided significant relief, and metabolomic analysis of lung tissue supported the molecular toxicological. Our findings suggest that the increased levels of reactive oxygen species (ROS) in the lungs lead to Th2-mediated eosinophilic inflammation, characterized by elevated IL-4, IL-5, and eosinophils, and reduced INF-γ levels. This inflammatory response is mediated by the NFκB pathway and exacerbates type I hypersensitivity through increased IL-4 production. In this study, the molecular mechanism by which PPD aggravates asthma in mice was elucidated, which helps to improve the understanding of the health effects of PPD and lays a theoretical foundation for addressing the health risks posed by PPD.
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A mouse study found that air pollution particles (PM2.5) and microplastics together made asthma-like lung damage much worse than either one alone, by triggering a harmful form of cell death in airway cells. This suggests that everyday exposure to both pollutants at once could be riskier for people with asthma or allergies than scientists previously realized.
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In a mouse study, exposure to dibutyl phthalate (a plastic additive) and polystyrene microplastics for five weeks caused pneumonia-like lung damage, increased oxidative stress, and triggered inflammation. The researchers found that these plastic pollution byproducts caused a specific type of immune response that leads to eosinophilic inflammation in the airways, connected through the gut-lung axis. The findings suggest that everyday exposure to plastic-derived chemicals and particles could contribute to respiratory disease.
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