ArticleNoise & health
Systemic Inflammation as a Mediator of the Association Between Occupational Noise Exposure and Depression Risk: A Population-Based Study.
Article in Noise & health. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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6 authors.
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Abstract
objectiveTo examine the biological pathways underlying occupational noise-induced depression by assessing the association between noise duration and depression and the mediating role of systemic inflammation.
methodsWe analyzed cross-sectional data from 17,712 US adults in the National Health and Nutrition Examination Survey. Occupational noise exposure duration (no exposure for >15 years), depression risk (9-item Patient Health Questionnaire ≥ 10), and systemic inflammation (systemic inflammation response index [SIRI]) were assessed. Weighted multivariable logistic regression estimated noise-depression associations across three sequential models: crude, confounder-adjusted, and mediator-adjusted (log-transformed SIRI [lnSIRI]). Mediation (bootstrapping), subgroup, and sensitivity analyses were performed, with sensitivity analysis adjusting for nonoccupational noise, occupational type, and other inflammatory biomarkers.
resultsEach ordinal increase in noise exposure duration predicted a 9.0% higher depression risk (odds ratios = 1.090, P = 0.005) after covariate adjustment, demonstrating a dose-response effect. The association persisted across most subgroups but was attenuated among divorced/widowed individuals (Pinteraction = 0.027). lnSIRI mediated 4.0% of the total effect of occupational noise (B = 0.008, 95% CI = 0.003-0.014). Associations remained robust in all sensitivity analyses adjusting for nonoccupational noise, occupational type, and other inflammatory biomarkers.
conclusionThese findings establish occupational noise as a modifiable neuroimmunological risk factor. Integrated workplace interventions targeting acoustic stress and inflammatory pathways may mitigate depression risk.
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