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Combined PM2.5 and microplastics exposure exacerbates allergic asthma via OPA1/SLC7A11-mediated airway epithelial ferroptosis
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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.
This study aimed to investigate whether PM2.5 and microplastics (MPs) aggravate ovalbumin (OVA)-induced allergic airway injury and to elucidate the role of mitochondrial dysfunction-associated ferroptosis in this process. An OVA-induced murine asthma model and OVA-stimulated MRE cells were established and exposed to PM2.5 and/or MPs. Histopathological, biochemical, molecular, and functional analyses were performed to evaluate pulmonary injury, oxidative stress, ferroptosis, mitochondrial dysfunction, and inflammatory responses. In addition, OPA1 knockdown and ferrostatin-1 (Fer-1) intervention were used to verify the mechanistic involvement of ferroptosis. Exposure to PM2.5 or MPs further aggravated OVA-induced pulmonary damage, as evidenced by enhanced inflammatory infiltration, increased inflammation score, total cell counts and goblet cell percentage, and impaired lung function. In parallel, co-exposure to PM2.5 and MPs markedly intensified oxidative stress in lung tissue and MRE cells, as shown by increased ROS and MDA levels and decreased T-AOC, CAT, and SOD. Moreover, PM2.5 and MPs enhanced ferroptosis by increasing Fe 2 + accumulation, lipid peroxidation, and NCOA4, FTH1, and ACSL4 expression, while suppressing SLC7A11, GPX4, GCLC, and GSS. These effects were accompanied by profound mitochondrial dysfunction, including altered expression of mitochondria-related genes, loss of mitochondrial membrane potential, ATP depletion, reduced mitochondrial respiratory complex activities, impaired oxygen consumption rate, and decreased NADPH and GSH-related antioxidant capacity. Importantly, OPA1 silencing or Fer-1 treatment markedly attenuated PM2.5 +MPs-enhanced ferroptotic and inflammatory injury in OVA-treated MRE cells. Collectively, these findings suggest that PM2.5 and MPs co-exposure may exacerbate allergic airway injury by promoting mitochondrial dysfunction-associated ferroptosis via the OPA1/SLC7A11 pathway.
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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.
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In a mouse model of asthma, co-exposure to inhaled polyethylene microplastics and house dust mite allergens caused worse airway inflammation than either pollutant alone. The microplastics damaged the airway lining and amplified allergic reactions through a specific inflammatory signaling pathway called CXCL1. This finding suggests that breathing in airborne microplastics could make allergies and asthma worse by helping allergens penetrate deeper into the lungs.
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Scientists exposed lab-grown human airway cells to air pollution particles and microplastic fibers, and found the combo was more damaging when the cells were already stressed—whether from allergies, smoking-related damage, or infection. This suggests that people with existing lung conditions like asthma or COPD may be especially vulnerable to the health effects of breathing in pollution and microplastics, since their airway cells have a harder time repairing themselves under this "double hit."
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Mice that inhaled polystyrene microplastics for 60 days developed lung scarring, reduced lung function, and weakened lung barriers. The microplastics increased harmful bacteria in the lungs, which triggered an iron-related cell death process called ferroptosis -- revealing a new mechanism by which breathing in microplastics could cause lasting lung damage.
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This study found that polystyrene microplastics combined with cadmium caused more severe liver damage in mice than either pollutant alone. The microplastics absorbed cadmium on their surface, increasing the amount of the toxic metal delivered to liver cells, and triggered a type of cell death called ferroptosis. This is concerning because microplastics in the environment commonly carry heavy metals, meaning the combined exposure people face may be more harmful than we thought.
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