Serum metabolome perturbation in relation to noise exposure: Exploring the potential role of serum metabolites in noise-induced arterial stiffness.

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.

Association of noise exposure, plasma microRNAs with metabolic syndrome and its components among Chinese adults.

AIMS: We aimed to evaluate the association of occupational noise with metabolic syndrome (MetS) and its components, and to assess the potential role of miRNAs in occupational noise-associated MetS. METHODS: A total of 854 participants were enrolled in our study. Cumulative noise exposure (CNE) was estimated in conjunction with workplace noise test records and research participants' employment histories. Logistic regression models adjusted for potential confounders were used to assess the association of CNE and miRNAs with MetS and its components. RESULTS: We observed linear positive dose-response associations between occupational noise exposure and the prevalence of MetS (OR: 1.031; 95 % CI: 1.008, 1.055). And linear and nonlinear relationship were also found for the association of occupational noise exposure with high blood pressure (OR: 1.024; 95 % CI: 1.007, 1.041) and reduced high-density lipoprotein (OR: 1.051; 95 % CI: 1.031, 1.072), respectively. MiR-200a-3p, miR-92a-3p and miR-21-5p were inversely associated with CNE, or the prevalence of MetS and its components (all P < 0.05). However, we did not find any statistically significant mediation effect of miRNAs in the associations of CNE with MetS. Furthermore, the prevalence of bilateral hearing loss in high-frequency increased (OR: 1.036; 95 % CI: 1.008, 1.067) with CNE level rising, and participants with bilateral hearing loss in high-frequency had a significantly higher risk of MetS (OR: 1.727; 95 % CI: 1.048, 2.819). CONCLUSION: Our study suggests that occupational noise exposure is associated with MetS and its components, and the role of miRNAs in noise-induced increasing MetS risk needs to be confirmed in future studies.