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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.
Polyethylene terephthalate (PET) is a major source of microplastic (MP) exposure through textiles, packaging, and medical devices, yet its immunological effects in controlled experimental models of respiratory and internal exposure remain incompletely characterized. We investigated PET MPs (median 2.7 µm; D90 < 6.5 µm) and their effects in in vivo mouse models of respiratory and intraperitoneal exposure, with and without allergen co-exposure. PET MPs remained detectable in the lung for 14 days, and induced airway inflammation with lymphocyte and eosinophil recruitment. Co-exposure with ragweed pollen amplified pulmonary inflammation at intermediate doses but reduced allergen-specific IgG1 at higher doses. Systemic Intraperitoneal exposure revealed allergen- and timing-dependent modulation of peritoneal inflammation, accompanied by enhanced antibody responses, particularly Th1-associated IgG2a. Splenocyte recall assays showed altered cytokine production. Together, these findings identify PET MPs as biologically active particles that alter airway inflammation and immune responses in a dose- and context-dependent manner under controlled experimental conditions, including high-dose conditions. These findings support the inclusion of immune endpoints while emphasizing the need for cautious extrapolation to real-world exposure scenarios.
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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.
Harmful effects of true-to-life nanoplastics derived from PET water bottles in human alveolar macrophages.
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Researchers tested nanoplastics derived from actual PET water bottles on mouse lung immune cells, focusing specifically on cells that had internalized the particles. Even though the nanoplastics were taken up by 100% of cells at the highest dose, they did not cause outright cell death. However, they did trigger significant increases in reactive oxygen species and shifted the immune cells toward a pro-inflammatory state, suggesting that inhaled nanoplastics from everyday plastic products could promote chronic lung inflammation.
Pulmonary toxicity of micro- and nano polyethylene particles following intratracheal instillation in rats.
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When rats breathed in tiny plastic particles (the same polyethylene used in plastic bags and bottles) over several weeks, their lungs showed inflammation, tissue damage, and elevated markers linked to disease — even at the lowest doses tested. This suggests there may be no truly "safe" amount of inhaled plastic particles, though more research is needed to know exactly what this means for humans, since we're regularly exposed to microplastics in air, dust, and everyday products.
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.
Impact of Microplastic Exposure on Airway Inflammation in an Acute Asthma Murine Model
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Mouse experiments found that microplastic exposure worsened inflammatory responses in healthy lungs but did not further aggravate airway inflammation in mice with pre-existing asthma, suggesting the lung's response to microplastics depends on baseline immune state.
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