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Co-Exposure of airborne microplastics and chromium: Impairment of pulmonary surfactant monolayer
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Researchers investigated what happens when airborne polypropylene microplastics carrying chromium reach the lungs and interact with pulmonary surfactant, the protective lining that helps us breathe. They found that the microplastics disrupted the surfactant layer's ability to function properly, and that chromium was partially released and chemically reduced upon contact. The study suggests that inhaling microplastics contaminated with heavy metals may pose compounding risks to lung health.
Airborne microplastics (AMPs) and their interactions with heavy metals have attracted global concern, however, little is known about their combined effects in the lung environment. In this study, the adverse effects of polypropylene (PP, as representative AMPs)-chromium (Cr) co-exposure on natural pulmonary surfactant (PS) monolayer function was investigated. It was found that upon contact with PS, the desorption of Cr carried by inhaled PP-Cr increased and partially was (∼60 %) reduced to Cr(III). The phase behaviour of PS monolayer in co-exposure scenarios was PP dominated due to the insertion of particulates. Effects among the lipid components were observed that saturated phospholipids suffered the combined effects of Cr(VI) and Cr(III) that impaired its ability to regulate surface pressure, and unsaturated phospholipids were susceptible to infiltration by PP due to their lax structure, leading to a reduction in monolayer compressibility. Co-exposure also led to changes in lipid composition along with metabolic disturbances, and protein contained in PS tended to fold and destabilize. These findings provided front-line evidence of changes in air-liquid interface properties for PS upon PP-Cr co-exposure, suggest targets for the traceability of PS dysfunction, which is helpful for deeply understanding the unfavorable physicochemical effects of AMPs on lung health.
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Researchers examined how aged microplastics that have been weathered in the environment interact with lung surfactant, the thin liquid layer that lines the airways and aids breathing. They found that aged microplastics disrupted surfactant function more severely than pristine particles, potentially impairing the lungs' ability to expand and protect against inhaled pollutants. The study suggests that the weathering process makes airborne microplastics more hazardous to respiratory health over time.
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Researchers investigated how oligomeric plastic particles interact with lung surfactant bilayers to understand inhalation risks, proposing that as plastics break down to oligomeric sizes through environmental degradation they may penetrate and disrupt the protective surfactant layer lining the lungs.
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Researchers investigated how polystyrene microplastics interact with lung surfactant extracted from porcine lungs. The study found that microplastics altered the surface tension and membrane structure of lung surfactant, preferentially adsorbed phospholipid components, and accelerated the production of reactive oxygen species, suggesting potential risks to respiratory health from inhaled microplastics.
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