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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.
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 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.
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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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Researchers compared uptake of virgin and oxidized polystyrene nano- and microparticles in human lung cells, finding that photoaged particles showed altered surface chemistry and different cellular internalization patterns relevant to realistic airborne microplastic exposure.
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Researchers investigated the pulmonary toxicity of polystyrene nanoplastics smaller than 100 nm in lung epithelial cells and macrophages, finding that exposure triggered a hierarchical oxidative stress mechanism that drove acute to subacute lung injury through lipid peroxidation and inflammation.
Photoaging of polystyrene microspheres causes oxidative alterations to surface physicochemistry and enhances airway epithelial toxicity
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