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Effects of Atmospheric Aging on the Respiratory Toxicityof Polystyrene Nanoplastic Particles
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Researchers exposed human bronchial epithelial cells to atmospherically aged polystyrene nanoplastics at an air-liquid interface, finding significantly elevated expression of inflammatory genes IL-8, TNF-α, and IL-6 compared to fresh nanoplastics, demonstrating that environmental aging increases respiratory toxicity.
Inhalation exposure to nanoplastic particles (NPPs) can lead to significant pulmonary toxicity; however, the effects of environmental processing on their toxicity remain poorly understood. This study examines the toxicity of polystyrene (PS) NPPs on lung cells following controlled atmospheric aging. Human bronchial epithelial cells (16HBE) were cultured in vitro at the air–liquid interface and acutely exposed to oxidized PS NPPs through electrostatic precipitation. Expression of proinflammatory genes interleukin-8 (IL-8) and tumor necrosis factor alpha (TNF-α) was significantly elevated at 6 and 48 h postexposure to aged NPPs, with corresponding increases in interleukin-6 (IL-6) protein levels supporting an inflammatory response. The oxidative stress marker heme oxygenase-1 (HO-1) also showed significantly increased expression at 6 h postexposure, supported by protein analysis. Atomic force microscopy (AFM) and aerosol mass spectrometry (AMS) revealed increased surface roughness and oxygen to carbon ratios in the atmospherically aged NPPs. Together, these results demonstrate that atmospheric aging alters the chemical composition and surface morphology of PS NPPs, enhancing proinflammatory and oxidative stress responses in bronchial epithelial cells, highlighting the critical role of environmental processing in determining the toxicity of nanoplastics.
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Effects of Atmospheric Aging on the Respiratory Toxicity of Polystyrene Nanoplastic Particles
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Researchers exposed human bronchial epithelial cells to atmospherically aged polystyrene nanoplastics at an air-liquid interface, finding that oxidized particles significantly elevated inflammatory gene expression (IL-8, TNF-α, IL-6) compared to fresh particles, demonstrating that environmental aging enhances respiratory toxicity.
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Researchers found that environmentally aged (oxidised) nano- and microplastics were rapidly taken up by human lung cells and caused significantly greater DNA damage, oxidative stress, and mitochondrial impairment compared to pristine particles, highlighting the heightened health risks of weathered airborne plastics.
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Aged low-density polyethylene (LDPE) micro(nano)plastic particles were found to damage human airway epithelial cells in vitro, causing oxidative stress, inflammation, and cytotoxicity at relevant concentrations. UV-weathered LDPE particles were more toxic than unaged counterparts, highlighting the importance of environmental aging in assessing airborne MP health risks.
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