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Combined cytotoxicity of polystyrene nanoplastics and phthalate esters on human lung epithelial A549 cells and its mechanism
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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.
Awareness of risks posed by widespread presence of nanoplastics (NPs) and bioavailability and potential to interact with organic pollutants has been increasing. Inhalation is one of the more important pathways of exposure of humans to NPs. In this study, combined toxicity of concentrations of polystyrene NPs and various phthalate esters (PAEs), some of the most common plasticizers, including dibutyl phthalate (DBP) and di-(2-ethyl hexyl) phthalate (DEHP) on human lung epithelial A549 cells were investigated. When co-exposed, 20 μg NPs/mL increased viabilities of cells exposed to either DBP or DEHP and the modulation of toxic potency of DEHP was greater than that of DBP, while the 200 μg NPs/mL resulted in lesser viability of cells. PAEs sorbed to NPs decreased free phase concentrations (C) of PAEs, which resulted in a corresponding lesser bioavailability and joint toxicity at the lesser concentration of NPs. The opposite effect was observed at the greater concentration of NPs, which may result from the dominated role of NPs in the combined toxicity. Furthermore, our data showed that oxidative stress and inflammatory reactions were mechanisms for combined cytotoxicities of PAEs and NPs on A549 cells. Results of this study emphasized the combined toxic effects and mechanisms on human lung cells, which are helpful for assessing the risk of the co-exposure of NPs and organic contaminants in humans.
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Combined toxicity evaluation of polystyrene nanoplastics and Nano-ZnO of distinctive morphology on human lung epithelial cells
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Researchers tested how polystyrene nanoplastics combined with zinc oxide nanoparticles affect human lung cells, finding that the two pollutants interact differently depending on their shapes and concentrations. Zinc oxide primarily damaged cell membranes while nanoplastics mainly triggered oxidative stress and cell death, and their combined effects varied from additive to counteracting. This study is important because people are likely exposed to both nanoplastics and metal particles in polluted air, and understanding their combined effects is key to assessing real-world health risks.
Unveiling the Pulmonary Toxicity of Polystyrene Nanoplastics: A Hierarchical Oxidative Stress Mechanism Driving Acute–Subacute Lung Injury
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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.
In vitro evaluation of nanoplastics using human lung epithelial cells, microarray analysis and co-culture model
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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 nanoplastics mediate oxidative stress, senescence, and apoptosis in a human alveolar epithelial cell line
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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.
Short-Term Cellular Responses to Sub-100 nm PMMA and Polystyrene-Based Copolymer Nanoplastics in Human Embryonic Lung Fibroblasts: Cytotoxicity and Redox-Associated Markers
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Scientists exposed human lung cells to tiny plastic particles, the kind you might inhale from air pollution, and found that different plastic types affected cell stress and damage responses differently, with one formulation causing harm at much lower amounts than others. This early lab study suggests not all nanoplastics are equally risky, but more research is needed before we understand real-world health effects.
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