Macrophage-Mediated Pulmonary Inflammatory Response and Underlying Mechanisms Induced by Lithium Cobalt Oxide Nanoparticles
Lithium cobalt oxide (LCO) nanoparticles (NPs), generated during the lifecycle of LCO batteries via mechanical wear, pose respiratory health risks. This study systematically assessed LCO NPs' physicochemical properties, ion release, and immunotoxicity using multi-scale models. LCO NPs exhibited irregular morphology, layered crystal structure, good dispersion, and negative surface charge. Cobalt ion release was minimal: 1.03% in deionized water and 0.11% in cell culture medium. In vitro, LCO NPs significantly induced reactive oxygen species (ROS) production and secretion of pro-inflammatory cytokines (IL-6, IL-1β, TNF-α) in macrophages, promoting M1 polarization. In vivo, intranasal exposure caused dose-dependent pulmonary accumulation, alveolar destruction, inflammatory cell infiltration, and elevated cytokines in bronchoalveolar lavage fluid (BALF). Transcriptomic analysis revealed significant enrichment of NF-κB, JAK-STAT, and Toll-like receptor signaling pathways, implicating these in macrophage activation and inflammation amplification. This multi-level study elucidates LCO NPs' immunotoxicity mechanisms, providing a scientific basis for environmental health risk assessment and management of lithium-ion battery materials.