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Route-dependent immune modulation and long-term lung retention after polypropylene microplastic exposure in mice
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When mice breathed in polypropylene microplastics (a common plastic found in food packaging and textiles), it triggered lung inflammation and made allergy symptoms worse, but when the same plastic entered the body a different way, it affected the immune system differently. This suggests how microplastics enter our bodies (through breathing vs. other routes) may matter a lot for their health effects, and even brief exposures were enough to cause noticeable immune changes, raising questions about the impact of repeated, everyday exposure to plastic pollution.
Polypropylene microplastics (PP MPs) are among the most widely used synthetic polymers and represent a major component of global microplastic (MP) pollution, yet their immunological and environmental health effects remain poorly understood. We investigated immune responses to pristine PP MPs in mouse models using short-term airway and internal exposure models across defined dose ranges designed to assess hazard-relevant immune effects. Intranasally administered PP MPs induced pulmonary inflammation in naïve mice and further potentiated ragweed pollen-induced allergic airway inflammation, demonstrating that PP MPs possess intrinsic inflammatory activity while also modifying ongoing allergic immune responses. Following epithelial barrier bypass, intraperitoneal administration of PP MPs differentially modulated antigen-specific immune responses, producing allergen- and timing-dependent reductions in peritoneal leukocyte accumulation and altering antigen-specific cytokine and antibody responses. These data demonstrate that pristine PP MPs are biologically active and that their immunological effects depend on exposure route, biological compartment, allergen context, and the timing of exposure. Even short-term exposures at controlled doses were sufficient to elicit measurable immune modulation, suggesting the potential for biologically relevant effects following repeated or cumulative exposure. These findings highlight the importance of immunological endpoints and particle persistence when evaluating the hazard potential of micro- and nanoplastic particles across different exposure routes.
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Investigation of Pulmonary Inflammatory Responses Following Intratracheal instillation of and Inhalation exposure to Polypropylene Microplastics
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Researchers conducted short-term pulmonary toxicity studies by exposing mice to polypropylene microplastics via intratracheal instillation and inhalation, finding dose-dependent inflammatory responses in lung tissue that confirm inhalation as a significant exposure route of concern.
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.
Investigation of pulmonary inflammatory responses following intratracheal instillation of and inhalation exposure to polypropylene microplastics
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Rats exposed to polypropylene microplastics through both inhalation and direct lung delivery developed inflammatory responses in their lungs, including increased immune cells and tissue changes. Even at relatively low concentrations, the microplastics triggered pulmonary inflammation, supporting concerns that breathing in airborne microplastics could contribute to respiratory health problems in humans.
Respirable polyethylene terephthalate microplastics modulate airway inflammation and immune responses in murine allergen co-exposure models
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Scientists exposed mice to tiny plastic particles from PET (a common plastic in bottles and polyester clothing) and found the particles stuck around in the lungs for two weeks and triggered inflammation, especially when combined with allergens like ragweed pollen. This suggests breathing in these ultra-small plastic fragments could worsen allergic reactions or immune responses, though this was tested in mice at controlled doses, so more research is needed before we know exactly what this means for people breathing in everyday microplastics.
Pulmonary Toxicity of Polystyrene, Polypropylene, and Polyvinyl Chloride Microplastics in Mice
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Researchers tested the lung toxicity of three common microplastic types (polystyrene, polypropylene, and polyvinyl chloride) in mice and found that all three caused pulmonary inflammation, but through different mechanisms. Polyvinyl chloride produced the most severe inflammatory response, while polystyrene and polypropylene showed distinct patterns of immune activation. The study suggests that the type of plastic inhaled matters for understanding respiratory health risks from airborne microplastics.
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