Fant 10273 publikasjoner. Viser side 142 av 411:
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Organ-specific in vitro models for prediction of hazard assessment of nanomaterials
Organ-specific multicellular in vitro models are used to mimic the lung-blood-brain axis, and to assess the nanomaterials (NMs) safety in humans. We employed a triculture lung model, a whole-blood model, an astrocytes-neurons coculture to examine health outcomes by three cerium dioxide (CeO2) NMs and silver (Ag) nanowires. Endpoints included cytotoxicity, gene expression, genotoxicity, inflammatory markers at the air–liquid interface (ALI), complement activation, and secondary toxicity in astrocytes-neurons coculture. Post-exposure, CeO2–3.5 nm high-dose decreased cell viability, no DNA damage was detected. At epithelial-macrophages interface, CeO2–50 nm upregulated surfactant protein A (SPA), cell surface death receptor (FAS), and heme oxygenase-1 (HMOX1), whereas CeO2–3.5 nm downregulated SPA. Ag-nanowires upregulated HMOX1, macrophage inflammatory protein-1β (MIP-1β), granulocyte colony-stimulator factor (G-CSF), chemokine C-X-C-motif ligand 1 (CXCL1). At endothelial side, CeO2–50 nm and − 3.5 nm, and Ag-nanowires upregulated HMOX1. In whole-blood model, CeO2–3.5 nm high-dose reduced terminal complement complex (TCC) proteins, while CeO2–50 nm and Ag-nanowires increased them. Nanomaterials activated CD11b+ on granulocytes and monocytes. Ag-nanowires conditioned-medium (CM) on astrocytes-neurons coculture, decreased cell viability. CeO2–50 nm CM upregulated IL1β, NFκB, and HMOX1. Overall, CeO₂–3.5 nm exhibits lung toxicity; CeO₂–50 nm CM triggers inflammatory response and Ag-nanowires CM may induce cytotoxicity in brain cells.
2026
2000
2011
An optimized low volume sampler was developed to determine both gas- and particle bound concentrations of short and medium-chain chlorinated paraffins (S/MCCPs). Background contamination was limited by the sampler design, providing method quantification limits (MQLs) at least two orders of magnitude lower than other studies within the gas (MQL: 500 pg (ΣSCCPs), 1.86 ng (ΣMCCPs)) and particle (MQL: 500 pg (ΣSCCPs), 1.72 ng (ΣMCCPs) phases. Good repeatability was observed between parallel indoor measurements (RSD ≤ 9.3% (gas), RSD ≤ 14% (particle)) with no breakthrough/saturation observed after a week of continuous sampling. For indoor air sampling, SCCPs were dominant within the gas phase (17 ± 4.9 ng/m3) compared to MCCPs (2.7 ± 0.8 ng/m3) while the opposite was observed in the particle bound fraction (0.28 ± 0.11 ng/m3 (ΣSCCPs) vs. 2.7 ± 1.0 ng/m3 (ΣMCCPs)). Only SCCPs in the gas phase could be detected reliably during outdoor sampling and were considerably lower compared to indoor concentrations (0.27 ± 0.10 ng/m3). Separation of the gas and particle bound phase was found to be crucial in applying the appropriate response factors for quantification based on the deconvoluted S/MCCP sample profile, thus avoiding over- (gas phase) or underestimation (particle phase) of reported concentrations. Very short chain chlorinated paraffins (vSCCPs, C5-C9) were also detected at equal or higher abundance compared to SCCP congener groups (C10-C13) congener groups, indicating an additional human indoor inhalation risk.
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