Scientific Reports (Jun 2025)

Effect modification by cardiovascular and metabolic disease onset on long-term PM2.5 exposure and mortality: a nationwide cohort study

  • Hyemin Jang,
  • Jinah Park,
  • Eun Soo Lee,
  • Dongmug Kang,
  • Jeongmin Moon,
  • Insung Song,
  • Seoyeong Ahn,
  • Ayoung Kim,
  • Cinoo Kang,
  • Jieun Oh,
  • Dohoon Kwon,
  • Jieun Min,
  • Ejin Kim,
  • Michelle L. Bell,
  • Ho Kim,
  • Whanhee Lee

DOI
https://doi.org/10.1038/s41598-025-04498-z
Journal volume & issue
Vol. 15, no. 1
pp. 1 – 14

Abstract

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Abstract Cardiovascular and metabolic diseases–specifically myocardial infarction, congestive heart failure, cerebrovascular disease, peripheral vascular disease, renal disease, and liver disease–are major public health concerns worldwide. However, studies examining how these diseases modify the relationship between long-term PM2.5 exposure and mortality remain scarce. Using a Cox regression model with a population-representative cohort from South Korea, we estimated the modifying effects of six major cardiovascular and metabolic diseases on PM2.5-mortality association in two cohorts: (1) individuals without underlying diseases (NoUD) and (2) those with only hypertension and/or diabetes (HTN/DM). The interaction between PM2.5 and each disease onset was used to estimate effect modification, with results presented as relative hazard ratios (RHRs) per 10 µg/m3 increase in PM2.5. Among 183,834 subjects, non-accidental deaths occurred in 18.0% of the NoUD (N = 134,584) and 25.7% of the HTN/DM (N = 49,250). In the NoUD cohort, renal disease (RHR: 1.58; 95% CI: 1.27–1.97), myocardial infarction (1.41; 1.15–1.73), and liver disease (1.40; 1.25–1.57) significantly modified the effect of PM2.5 on mortality. In the HTN/DM cohort, renal disease (1.74; 1.43–2.12), myocardial infarction (1.62; 1.29–2.05), and cerebrovascular disease (1.32; 1.17–1.51) showed higher RHRs. Our findings highlight the importance of consistent and preemptive care for renal disease and myocardial infarction and provide evidence for target-specific interventions to reduce the risk of PM2.5 on mortality.

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