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Environmental Noise and Cardiovascular Risk: A Causal Inference Study.

Hua Xiao1, Lei Sun1, Xiu Qin1

  • 1School of Public Health, Guangdong Pharmaceutical University, Guangzhou, China.

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|May 5, 2026
PubMed
Summary
This summary is machine-generated.

Environmental noise exposure alters DNA methylation (DNAm), causally linking it to cardiovascular diseases (CVDs) and risk factors. This study reveals specific DNAm sites influencing heart health through Mendelian randomization analysis.

Keywords:
Cardiovascular diseaseDNA methylationEpigeneticsMendelian randomizationNoise

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Area of Science:

  • Environmental epigenetics
  • Cardiovascular epidemiology
  • Genetic epidemiology

Background:

  • Environmental noise is an emerging risk factor for cardiovascular disease (CVD).
  • DNA methylation (DNAm) alterations may mediate the relationship between environmental exposures and disease.
  • Causal links between noise-induced DNAm and CVD remain underexplored.

Purpose of the Study:

  • To investigate the causal association between noise-related DNAm alterations and CVDs.
  • To examine the role of DNAm in mediating the impact of environmental noise on cardiovascular risk factors.

Main Methods:

  • Two-sample Mendelian randomization (MR) analysis using publicly available GWAS and EWAS data.
  • Identified 13 noise-associated DNAm sites as exposures.
  • Utilized genetic instruments (methylation quantitative trait loci) for 6 CVDs and 6 risk factors.

Main Results:

  • 11 out of 13 noise-related DNAm sites showed significant associations with at least one CVD outcome.
  • Specific sites (cg13402217, cg16218477) were linked to increased CVD risk, while cg19270309 showed protective effects.
  • Sensitivity analyses confirmed the robustness of the findings.

Conclusions:

  • Provides novel causal evidence for DNAm alterations mediating the effects of environmental noise on CVDs.
  • Highlights specific DNAm sites as potential mechanistic links between noise exposure and cardiovascular health.
  • Supports the role of epigenetics in environmental disease etiology.