Prevention & lipidsResearch article
Interaction between air pollution and genetic predisposition to blood pressure and low-density lipoprotein cholesterol on cardiovascular events
- Mendelian randomisation study
Authors' conclusion
Higher-genetic-risk groups for SBP and LDL-C carried the greatest absolute cardiovascular risk when exposed to air pollution, even though PM2.5 conferred lower relative risk, perhaps related to high baseline risk.
Study context
- Population
- UK Biobank participants
- Participants
- 412,446 participants
- Comparison
- Interaction between PM2.5 exposure and Polygenic Risk Scores (PRS) for low-density lipoprotein cholesterol (LDL-C) and systolic blood pressure (SBP) on major adverse cardiovascular events (MACE)
- Outcome
- MACE incidence (interaction between PM2.5 and PRS for SBP and LDL-C)
- Follow-up
- 13.85 years
Main finding
As reported in the abstract
Interaction of PM2.5 with PRS on MACE (association of 1-SD PRS increase with MACE at higher PM2.5)
- SBP PRS × PM2.5 · 1-SD PRS ≈ 10 mm Hg; attenuated at higher PM2.5
- HR 0.947; P = 0.039
- LDL-C PRS × PM2.5 · 1-SD PRS ≈38.6 mg/dl; attenuated at higher PM2.5
- HR 0.943; P = 0.025
Further findings
| Outcome | HR | P value |
|---|---|---|
| Causal effects interactions with phenotype (SBP, LDL-C) and PM2.5 — SBP × PM2.5 | 0.9979 | P < 0.001 |
| Causal effects interactions with phenotype (SBP, LDL-C) and PM2.5 — LDL-C × PM2.5 | 0.9995 | P = 0.093 |
Absolute risk
- Predicted risk remained highest in the high-PRS groups across PM2.5 levels
Original publication
Interaction between air pollution and genetic predisposition to blood pressure and low-density lipoprotein cholesterol on cardiovascular events. Eur J Prev Cardiol. Published 17 June 2026. doi:10.1093/eurjpc/zwag298
Summarised from the published abstract; every number is checked against it