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Co-exposure to polystyrene microplastics and di-(2-ethylhexyl) phthalate aggravates allergic asthma through the TRPA1-p38 MAPK pathway
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This mouse study found that polystyrene microplastics combined with DEHP, a common plastic additive, worsened allergic asthma symptoms more than either pollutant alone. The combination activated an inflammatory pathway called TRPA1-p38 MAPK in lung tissue, increasing airway inflammation and mucus production. The findings suggest that real-world exposure to microplastics carrying chemical additives could aggravate respiratory conditions like asthma.
Increasing attention has been paid to the potential impact of microplastics (MPs) pollution on human health. MPs and phthalates coexist in the environment, however, the effects of exposure to MPs alone or to a combination of di-(2-ethylhexyl) phthalate (DEHP) and MPs on allergic asthma are unclear. This study investigates the effects of exposure to polystyrene microplastics (PS-MPs) or co-exposure with DEHP, on allergic asthma, and the underlying molecular mechanisms. We established an allergic asthma model using ovalbumin, and mice were exposed to PS-MPs (5 mg/kg bw/day) alone, or combined with DEHP (0.5, 5 mg/kg bw/day), for 28 days. The results showed that in the presence of ovalbumin (OVA) sensitization, exposure to PS-MPs alone slightly affected airway inflammation, and airway hyperresponsiveness, while co-exposure to PS-MPs and DEHP caused more significant damage. Co-exposure also induced more oxidative stress and Th2 immune responses, and activation of the TRPA1 and p38 MAPK pathways. The aggravation of asthmatic symptoms induced by co-exposure to PS-MPs and DEHP were inhibited by blocking TRPA1 ion channel or p38 MAPK pathway. The results demonstrated that co-exposure to PS-MPs and DEHP exacerbates allergic asthma, by exacerbating oxidative stress and inflammatory responses, and activating the TRPA1-p38 MAPK pathway.
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Co-exposure to polyethylene microplastics and house dust mites aggravates airway epithelial barrier dysfunction and airway inflammation via CXCL1 signaling pathway in a mouse model
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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.
Co-exposure of polystyrene nanoplastics and ozone synergistically induced airway inflammation: Evidence and biomarkers screening
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Researchers discovered that co-exposure to airborne polystyrene nanoplastics and ozone in mice caused significantly worse airway inflammation than either pollutant alone, with the two acting synergistically. They identified specific metabolic pathways and genes involved in the inflammatory response, providing potential biomarkers for monitoring this type of combined exposure. The findings suggest that breathing in nanoplastics alongside common air pollutants like ozone may pose amplified respiratory health risks.
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.
Co-exposure to microplastics enhances the allergenic potentials of house dust mite allergen Der p 1
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This study found that polystyrene microplastics can make common house dust mite allergens more potent, increasing allergic reactions. The microplastics changed the shape of the allergen protein, boosting its ability to trigger immune responses and worsening airway inflammation in mice. This research suggests that indoor microplastic pollution could be contributing to the rising rates of allergies and asthma by making existing allergens more harmful.
Detrimental effects of microplastic exposure on normal and asthmatic pulmonary physiology
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Researchers exposed both healthy and asthmatic mice to airborne microplastics and found significant lung inflammation, immune activation, and increased mucus production in both groups. Microplastic particles were taken up by immune cells called macrophages, and gene analysis revealed changes in immune response, cellular stress, and cell death pathways. The study suggests that inhaling microplastics may worsen respiratory health in both normal and vulnerable populations.
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