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Inhaled tire-wear microplastic particles induced pulmonary fibrotic injury via epithelial cytoskeleton rearrangement
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Researchers investigated the health effects of inhaling tire-wear microplastic particles in mice and found that exposure caused lung fibrosis and restricted breathing function. The study identified that the particles triggered rearrangement of the structural framework in lung cells, leading to scarring and tissue damage through epigenetic mechanisms. These findings suggest that airborne tire-wear particles, a common but understudied pollutant, may pose a significant risk to respiratory health.
Tire wear microplastic particles (TWMPs) are emerging microplastic pollutants that have gained increasing attention lately. However, the health effect of inhaled airborne TWMPs has never been explored before and may already be included in particulate matter morbidity and mortality. Here, we endeavored to address the preliminary study of TWMP inhalation-induced pulmonary toxic effects and its epigenetic mechanisms in C57BL/6 mice. As a result, restricted ventilatory dysfunction and fibrotic pathological changes were observed in TWMP-treaded mice. Further research found that attenuation of miR-1a-3p plays an important role in TWMP-induced lung injury. Results from in vitro study confirmed that cytoskeleton regulatory gene twinfilin-1 was one of the target genes of miR-1a-3p, and involved in cytoskeleton rearrangement caused by TWMP exposure. Mechanistically, miR-1a-3p inhibited the F-actin formation by targeting cytoskeletal regulatory proteins twinfilin-1, leading to TWMP-induced pulmonary fibrotic injury. While we are in the very early stages of explaining the role of epigenetics in TWMP-induced lung injury, the potential for the use of epigenetic marks as biomarkers is high and discoveries made in this field will likely bring us closer to better understanding this crucial mechanism.
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In a mouse study, inhaled polyethylene microplastics accumulated in lung tissue over 90 days of repeated exposure, causing chronic inflammation, immune changes, and early signs of lung scarring (fibrosis). Even at the lowest doses, the microplastics triggered inflammatory cell buildup and thickening of lung walls. These findings suggest that long-term breathing of airborne microplastics could lead to permanent lung damage, which is concerning given rising levels of plastic particles in indoor and outdoor air.
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Scientists exposed mice to tiny plastic particles found in air pollution and discovered these particles caused serious lung damage and scarring that didn't heal even weeks after exposure stopped. The smallest plastic particles were the most harmful, spreading from the lungs to other organs like the heart and liver. This research suggests that breathing in nanoplastics from everyday sources like car tire wear and plastic waste could pose long-term risks to human lung health.
A particle of concern: explored and proposed underlying mechanisms of microplastic-induced lung damage and pulmonary fibrosis
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This paper explores how inhaled microplastics may cause lung damage and scarring (pulmonary fibrosis) through several biological pathways. The research identifies signaling pathways that could be targeted for future treatments to reduce microplastic-induced lung damage. This is relevant to human health because people regularly breathe in airborne microplastic particles.
Intratracheal administration of polystyrene microplastics induces pulmonary fibrosis by activating oxidative stress and Wnt/β-catenin signaling pathway in mice
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Researchers administered polystyrene microplastics directly into the lungs of mice and found that the particles induced pulmonary fibrosis by triggering oxidative stress and activating the Wnt signaling pathway. The microplastics caused damage to the lung lining cells and promoted the buildup of scar tissue in lung tissue. The study provides evidence that inhaled microplastics may contribute to serious respiratory conditions by driving fibrotic changes in the lungs.
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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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