Metabolic Profiling Reveals PM2.5- and PM10-Induced Vitamin and Oxidative Stress Pathway Alterations Associated with...

Particulate matter (PM) is a global air pollutant causing respiratory pathology and systemic effects through bloodstream distribution, including placental transfer that potentially disrupts fetal development. Zebrafish, with rapid development and 82% orthology to human genes, provide an excellent model for studying the developing embryo. This study investigated the effects of PM2.5 and PM10 at 500 and 1000 μg/mL during embryogenesis (4-50 h postfertilization). PM2.5 exposure uniquely caused a 22 h hatching delay, suggesting developmental disruption. Untargeted metabolomics via LC-MS/MS was employed to investigate underlying mechanisms. Principal component analysis revealed distinct clustering by concentration (PC1, PC2) and particle size (PC1, PC3). Volcano plot analysis identified more altered metabolites (>2-fold change, p < 0.05) in PM2.5 versus PM10 at both concentrations. Pathway analysis demonstrated PM2.5 significantly disrupted pantothenate/CoA, retinol, and riboflavin metabolism, indicating these pathways mediate PM2.5-induced effects on embryonic development. At 1000 μg/mL, riboflavin significantly decreased in PM2.5 versus PM10 groups. Glutathione metabolism showed differential responses: reduced glutathione was depleted in PM2.5 but increased in PM10-exposed embryos, suggesting particle size-dependent oxidative stress responses. These findings demonstrate PM2.5 more potently disrupts embryonic metabolic pathways than PM10, potentially informing prevention strategies, including vitamin supplementation for PM-related developmental abnormalities.