Long-term PM2.5 component exposure, genetic susceptibility, and myocardial infarction risk
Authors' conclusion
Chronic PM2.5 component exposure was linked to an increased MI risk, and genetic susceptibility may modify these associations.
Study context
- Population
- Participants free of CVD at baseline9,327 developed myocardial infarction (MI)
- Participants
- 452,693 participants
- Exposure
- Per IQR increase in long-term PM2.5 component exposure
- Outcome
- Incident MI (all-cause mortality as competing event)
- Follow-up
- Median 11.75 years
Methodological detailsFine-Gray competing risk regression, quantile-based g-computation, polygenic risk score
- Fine-Gray competing risk regression
- Quantile-based g-computation
- Polygenic risk score
Main finding
As reported in the abstract
MI risk per IQR increase in PM2.5 component
Hazard ratio (95% CI)
Black carbon
1.171(1.141–1.202)
Ammonium
1.356(1.332–1.381)
Nitrate
1.073(1.048–1.100)
Sulphate
1.232(1.210–1.254)
Per IQR increase, as printed
Observational data: associations, not effects.
Further findings
Combined effects of PM2.5 components (quantile-based g-computation)
- Sulphate contributed most to the combined effects of PM2.5 components
Genetic susceptibility (polygenic risk score) × PM2.5 components
- Significant additive interactions and joint effects between genetic susceptibility and each PM2.5 component on MI risk
Original publication
Long-term PM2.5 component exposure, genetic susceptibility, and myocardial infarction risk. Eur J Prev Cardiol. Published 30 July 2025. doi:10.
Summarised from the published abstract; every number is checked against it