European journal of preventive cardiology · 2026
Interaction Between Air Pollution and Genetic Predisposition to Blood Pressure and LDL-C on Cardiovascular Events.
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Dazard Jean-Eudes, Schumacher Fredrick, Chen Zhuo, Koyama Satoshi, Jiang Meijie, Ponnana Sai R, Zhang Tong, Sirasapalli Santosh K, Al-Kindi Sadeer G, Deo Salil V, Gao Xu, Gasparrini Antonio, Quint Jennifer, Natarajan Pradeep, Brook Robert D, Rajagopalan Sanjay
Аннотация
AIMS: Particulate matter ≤2.5μm (PM2.5) air pollution is a leading global environmental risk factor. We investigated the impact of PM2.5 on cardiovascular risk with lifetime genetic predisposition to low-density lipoprotein cholesterol (LDL-C) and systolic blood pressure (SBP).
METHODS: We conducted a Mendelian Randomization (MR) study of participants from the UK Biobank study (n = 412,446) over 13.85 years. Polygenic Risk Scores (PRS) for LDL-C and SBP were used as instrument variables to estimate association and causal effects with major adverse cardiovascular events (MACE). The interaction between exogenous PM2.5 exposure with individual or combined LDL-C, SBP PRS, and clinical phenotypes was assessed using adjusted survival regression, causal inference, and machine learning models.
RESULTS: A significant negative interaction was observed between PM2.5 and PRS on MACE incidence for both SBP and LDL-C. The association of 1-SD PRS increase for SBP (≈ 10 mm Hg) and LDL-C (≈38.6 mg/dl) with MACE was attenuated at higher PM2.5 levels (HR = 0.947, p = 0.039, HR = 0.943, p = 0.025, respectively). Analyses with phenotype showed a similar trend for SBP, further confirmed by causal effects interactions (HR = 0.9979, p < 0.001, HR = 0.9995, p = 0.093, respectively). Absolute risk analysis showed that predicted risk remained highest in the high-PRS groups across PM2.5 levels.
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. These findings support a gene-environment interaction between air pollution exposure and genetically proxied cardiovascular risk factors.
METHODS: We conducted a Mendelian Randomization (MR) study of participants from the UK Biobank study (n = 412,446) over 13.85 years. Polygenic Risk Scores (PRS) for LDL-C and SBP were used as instrument variables to estimate association and causal effects with major adverse cardiovascular events (MACE). The interaction between exogenous PM2.5 exposure with individual or combined LDL-C, SBP PRS, and clinical phenotypes was assessed using adjusted survival regression, causal inference, and machine learning models.
RESULTS: A significant negative interaction was observed between PM2.5 and PRS on MACE incidence for both SBP and LDL-C. The association of 1-SD PRS increase for SBP (≈ 10 mm Hg) and LDL-C (≈38.6 mg/dl) with MACE was attenuated at higher PM2.5 levels (HR = 0.947, p = 0.039, HR = 0.943, p = 0.025, respectively). Analyses with phenotype showed a similar trend for SBP, further confirmed by causal effects interactions (HR = 0.9979, p < 0.001, HR = 0.9995, p = 0.093, respectively). Absolute risk analysis showed that predicted risk remained highest in the high-PRS groups across PM2.5 levels.
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. These findings support a gene-environment interaction between air pollution exposure and genetically proxied cardiovascular risk factors.