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Polystyrene particles induces asthma-like Th2-mediated lung injury through IL-33 secretion
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Researchers found that inhaled polystyrene microplastic particles triggered asthma-like inflammation in the lungs of mice, with smaller particles causing more severe responses. The particles stimulated the release of IL-33, a signaling molecule that activates a specific type of immune response associated with allergic airway disease. The study identifies a potential mechanism by which airborne microplastics could contribute to respiratory inflammation.
Plastics, particularly polystyrene (PS), are extensively used worldwide, especially in disposable packaging, which contributes to environmental pollution by generating microplastic particles. Herein, we investigated the pulmonary toxic effects of PS microplastics, focusing on airway inflammation and immune response. PS microplastic (50 nm to 1 μm) exposure was more likely to cause a severe pulmonary inflammatory response, particularly with smaller particle sizes. PS microplastic nose-only inhalation led to pulmonary toxic effects, which is specifically focusing on airborne microplastic exposure via inhalation in humans. We demonstrated that PS microplastic exposure in mice led to significant asthma-like symptoms, including airway inflammation, airway hyperresponsiveness, bronchial epithelial mucus cell hyperplasia, and Th2 immune responses through the IL-33 signalling pathway. Additionally, spatial transcriptome analysis indicated that epithelial cells drive the IL-33 signalling pathway and Th2 cell activation within PS-induced lung injury. PS-stimulated primary epithelial cells with the conditioned medium treatment in C57BL/6 mouse-derived splenocytes increased the Th2 immune response, including cytokine levels and mRNA expression. Meanwhile, Th2-mediated lung inflammation induced by PS exposure was effectively regulated by an IL-33 inhibitor or dexamethasone treatment. These findings enhance our understanding of the toxicological implications of microplastic exposure in the respiratory system and assist in developing potential mitigation strategies.
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Exposure to polystyrene microplastics triggers lung injury via targeting toll-like receptor 2 and activation of the NF-κB signal in mice
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This mouse study found that inhaling polystyrene microplastics caused serious lung damage, including inflammation, cell death, and scar tissue buildup. Smaller microplastics (1-5 micrometers) caused more harm than larger ones, and the damage worsened with longer exposure. The study identified a specific immune pathway (TLR2/NF-kB) through which inhaled microplastics trigger lung injury, raising concerns about the respiratory effects of airborne microplastics on humans.
Sterile inflammation induced by respirable micro and nano polystyrene particles in the pathogenesis of pulmonary diseases
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Researchers exposed human lung and immune cells to polystyrene micro and nanoparticles and found they triggered a type of inflammation that does not require infection, called sterile inflammation. Aged (oxidized) particles and those that interacted with immune cells were especially potent at activating inflammatory pathways including the NLRP3 inflammasome. This suggests that breathing in airborne microplastics could cause chronic lung inflammation over time.
Polystyrene Microplastics Induce Inflammatory Responses and Promote M2‐Associated Cytokine Expression in Mouse Lung Tissues
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Mice were given 10-50 µm polystyrene microplastics orally at 2,000 mg/kg and lung tissue was examined for biodistribution and immune response. PS-MPs accumulated in lung tissue and triggered inflammatory responses with elevated M2-associated cytokines (IL-4, IL-10), suggesting microplastic inhalation may promote an immunosuppressive rather than pro-inflammatory lung phenotype.
Polystyrene nanoplastics aggravate house dust mite induced allergic airway inflammation through EGFR/ERK-dependent lung epithelial barrier dysfunction
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In mice with allergic asthma triggered by house dust mites, exposure to polystyrene nanoplastics significantly worsened airway inflammation and lung damage. The nanoplastics disrupted the protective barrier of lung cells by activating a specific signaling pathway (EGFR/ERK), allowing more allergens and immune cells to penetrate lung tissue. This finding suggests that airborne nanoplastics could make asthma and allergies worse for the millions of people who already suffer from these conditions.
Inhalation of Environmental Polystyrene Micro/Nanoplastics Induces Pulmonary Toxicity and Synergistically Exacerbates Acute Lung Injury in Male Mice
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Breathing in tiny plastic particles—like those found in air pollution—caused lung inflammation and breathing problems in mice, even without any other health issues. Even more concerning, mice that had already inhaled these plastic particles got much sicker when exposed to a bacterial infection afterward, suggesting that everyday plastic pollution in the air we breathe could make our lungs more vulnerable to future illness. Smaller "microplastic" particles (as opposed to even tinier "nanoplastics") seemed to cause the most damage, highlighting that size matters when it comes to how harmful these particles are.
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