Noise pollution has grown to be a major public health issue worldwide. We sought to profile serum metabolite expression changes related to occupational noise exposure by untargeted metabolomics, as well as to evaluate the potential roles of serum metabolites in occupational noise-associated arterial stiffness (AS). Our study involved 30 noise-exposed industrial personnel (Lipo group) and 30 noise-free controls (Blank group). The untargeted metabolomic analysis was performed by employing a UPLC-HRMS. The associations of occupational noise and significant differential metabolites (between Blank/Lipo groups) with AS were evaluated using multivariable-adjusted generalized linear models. We performed the least absolute shrinkage and selection operator regression analysis to further screen for AS's risk metabolites. We explored 177 metabolites across 21 categories significantly differentially expressed between Blank/Lipo groups, and these metabolites were enriched in 20 metabolic pathways. Moreover, 15 metabolites in 4 classes (including food, glycerophosphocholine, sphingomyelin [SM] and triacylglycerols [TAG]) were adversely associated with AS (all P < 0.05). Meanwhile, five metabolites (homostachydrine, phosphatidylcholine (PC) (32:1e), PC (38:6p), SM (d41:2) and TAG (45:1) have been proven to be useful predictors of AS prevalence. However, none of these 15 metabolites were found to have a mediating influence on occupational noise-induced AS. Our study reveals specific metabolic changes caused by occupational noise exposure, and several metabolites may have protective effects on AS. However, the roles of serum metabolites in noise-AS association remain to be validated in future studies.