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20 resultsShowing papers similar to Unveiling the Pulmonary Toxicity of Polystyrene Nanoplastics: A Hierarchical Oxidative Stress Mechanism Driving Acute–Subacute Lung Injury
ClearUptake of Breathable Nano- and Micro-Sized Polystyrene Particles: Comparison of Virgin and Oxidised nPS/mPS in Human Alveolar Cells
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.
Polystyrene Nanoplastics Induce Lung Injury via Activating Oxidative Stress: Molecular Insights from Bioinformatics Analysis
Researchers found that polystyrene nanoplastics induce lung cell injury through oxidative stress pathways, identifying key transcription factors and the molecule TNFRSF12A as crucial mediators of nanoplastic-triggered redox imbalance and respiratory damage.
Internalization and toxicity: A preliminary study of effects of nanoplastic particles on human lung epithelial cell
Researchers studied the effects of polystyrene nanoplastic particles on human lung cells and found that the particles were internalized by the cells and caused dose-dependent toxicity. The nanoplastics triggered oxidative stress, inflammation, and disrupted normal cell function. The findings suggest that inhaling airborne nanoplastics may pose risks to respiratory health.
Uptake of Breathable Nano- and Micro-Sized Polystyrene Particles: Comparison of Virgin and Oxidised nPS/mPS in Human Alveolar Cells
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.
Polystyrene nanoplastics mediate oxidative stress, senescence, and apoptosis in a human alveolar epithelial cell line
A cell study found that polystyrene nanoplastics cause dose-dependent damage to human lung cells, triggering oxidative stress, premature cell aging, and cell death. These findings suggest that breathing in nanoplastics could harm lung tissue over time and potentially contribute to cancer risk from air pollution.
In vitro evaluation of nanoplastics using human lung epithelial cells, microarray analysis and co-culture model
Researchers tested polystyrene nanoplastics on two types of human lung cells and found that the particles caused cell damage, oxidative stress, and inflammation-related gene changes at relatively low concentrations. Using a co-culture model that mimics the lung's layered structure, they showed that nanoplastics can trigger immune responses even in cells not directly exposed. The study suggests that inhaled nanoplastics may pose respiratory health risks through both direct toxicity and inflammatory signaling.
Polystyrene microplastic particles: In vitro pulmonary toxicity assessment
Researchers tested the effects of polystyrene microplastics on human lung cells in the laboratory and found that the particles triggered inflammation and oxidative stress. The microplastics also weakened the protective barrier function of lung tissue by depleting key structural proteins. The study suggests that inhaling microplastics may increase the risk of respiratory problems by damaging the lung's natural defenses.
Size-dependent toxicity of polystyrene microplastics in lung cells: An in vivo and in vitro study
Researchers investigated the size-dependent toxicity of polystyrene microplastics in lung cells using both mouse and cell culture models. The study found that smaller 1-micrometer particles accumulated more in lung tissue than larger particles and identified epithelial-mesenchymal transition as a key toxic mechanism, driven by ECM-MMP signaling cascades that contribute to lung injury.
Polystyrene nanoplastics induced lung injury in mice: Insights into lung metabolic disorders
Researchers exposed mice to polystyrene nanoplastics through the airway and found that the particles caused lung inflammation and tissue damage. Using metabolomics analysis, they discovered that the nanoplastics disrupted multiple metabolic pathways in lung tissue, with surface-modified particles causing more severe effects. The study provides evidence that inhaled nanoplastics can alter lung metabolism in ways that may contribute to respiratory health problems.
Microplastics and nanoplastics, emerging pollutants, increased the risk of pulmonary fibrosis in vivo and in vitro: A comparative evaluation of their potential toxicity effects with different polymers and size
Researchers compared the lung toxicity of microplastics and nanoplastics made from polystyrene, polyethylene, and polypropylene in mice and human lung cells. They found that all particle types induced signs of pulmonary fibrosis, inflammation, and tissue remodeling, with polystyrene nanoplastics causing the most severe effects. The study suggests that smaller nanoplastic particles and certain polymer types may pose greater risks to lung health.
Investigation of pulmonary toxicity evaluation on mice exposed to polystyrene nanoplastics: The potential protective role of the antioxidant N-acetylcysteine
Researchers investigated lung damage in mice exposed to inhaled polystyrene nanoplastics and tested whether the antioxidant N-acetylcysteine could offer protection. They found that nanoplastics caused significant lung inflammation, tissue damage, and oxidative stress, but N-acetylcysteine treatment helped reduce these harmful effects. The study suggests that oxidative stress is a key mechanism behind nanoplastic-induced lung injury and points to potential protective strategies.
Pulmonary hazards of nanoplastic particles: a study using polystyrene in in vitro models of the alveolar and bronchial epithelium
Lab tests on human lung cell models found that polystyrene nanoplastics did not cause immediate cell death but did interfere with key lung functions like surfactant and mucus production and immune signaling. This means standard toxicity tests may underestimate the real danger of inhaling nanoplastics, and researchers need to look beyond simple cell survival to understand the true health effects on the lungs.
Polystyrene nanoplastics induce pulmonary oxidative stress and programmed cell death through the cGAS-STING-NLRP3 pathway
Researchers exposed mice to polystyrene nanoplastics through nasal administration and studied the resulting lung damage over seven days. They found that the nanoplastics triggered oxidative stress, programmed cell death, and inflammatory responses in lung tissue through activation of the cGAS-STING-NLRP3 signaling pathway. The study provides evidence that inhaled nanoplastics can cause acute lung injury through specific molecular mechanisms involving both apoptosis and pyroptosis.
Effects of Atmospheric Aging on the Respiratory Toxicityof Polystyrene Nanoplastic Particles
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.
Combined cytotoxicity of polystyrene nanoplastics and phthalate esters on human lung epithelial A549 cells and its mechanism
Researchers investigated the combined toxicity of polystyrene nanoplastics and common plasticizer chemicals (phthalate esters) on human lung cells. At lower nanoplastic concentrations, the particles actually reduced the toxicity of the plasticizers by adsorbing them, but at higher concentrations nanoplastics dominated and worsened overall cell damage. The study identified oxidative stress and inflammation as key mechanisms driving the combined toxic effects on lung tissue.
Effects of Atmospheric Aging on the Respiratory Toxicity of Polystyrene Nanoplastic Particles
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.
Dynamic non-coding RNA biomarker reveals lung injury and repair induced by polystyrene nanoplastics
Researchers found that mice and lung organoids (lab-grown mini-organs) repeatedly exposed to polystyrene nanoplastics suffered lung tissue damage, impaired repair processes, and changes in non-coding RNA molecules that could serve as early warning biomarkers for nanoplastic-induced lung injury.
Sterile inflammation induced by respirable micro and nano polystyrene particles in the pathogenesis of pulmonary diseases
Researchers exposed human lung and immune cells to polystyrene micro and nanoparticles and found they triggered a type of inflammation that does not require infection, called sterile inflammation. Aged (oxidized) particles and those that interacted with immune cells were especially potent at activating inflammatory pathways including the NLRP3 inflammasome. This suggests that breathing in airborne microplastics could cause chronic lung inflammation over time.
Intratracheal Administration of Polystyrene Micro(nano)plastics with a Mixed Particle Size Promote Pulmonary Fibrosis in Rats by Activating TGF-β1 Signaling and Destabilizing Mitochondrial Dynamics and Mitophagy in a Dose- and Time-Dependent Manner.
SD rats exposed to mixed polystyrene micro(nano)plastics via intratracheal administration at escalating doses over time developed pulmonary fibrosis and mitochondrial dysfunction, with severity linked to dose. The findings demonstrated a clear biological pathway connecting inhaled microplastic exposure to lung injury.
Repeated inhalation exposure to polystyrene nanoplastics induced sustained pulmonary injury and fibrosis in mice.
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.