Journal
EUROPEAN HEART JOURNAL
Volume 42, Issue 16, Pages 1582-1591Publisher
OXFORD UNIV PRESS
DOI: 10.1093/eurheartj/ehaa1031
Keywords
Air pollution; Heart failure; Joint association; Cohort
Categories
Funding
- National Heart, Lung, and Blood Institute [HL071981, HL034594, HL126024]
- National Institute of Diabetes and Digestive and Kidney Diseases [DK115679, DK091718, DK100383, DK078616]
- Fogarty International Center [TW010790]
- American Heart Association Scientist Development Award [0730094N]
- National Institute of General Medical Sciences [P20GM109036]
- China Scholarship Council [201906010346]
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The study found that long-term exposure to various ambient air pollutants is associated with an increased risk of incident heart failure, and the air pollution score is positively correlated with the risk of developing heart failure in a dose-response manner, which is also influenced by genetic susceptibility.
Aims Little is known about the relation between the long-term joint exposure to various ambient air pollutants and the incidence of heart failure (HF). We aimed to assess the joint association of various air pollutants with HF risk and examine the modification effect of the genetic susceptibility. Methods and results This study included 432 530 participants free of HF, atrial fibrillation, or coronary heart disease in the UK Biobank study. All participants were enrolled from 2006 to 2010 and followed up to 2018. The information on particulate matter (PM) with diameters <= 2.5 mu m (PM2.5), <= 10 mu m (PM10), and between 2.5 and 10 mu m (PM2.5-10) as well as nitrogen oxides (NO2 and NOx) was collected. We newly proposed an air pollution score to assess the joint exposure to the five air pollutants through summing each pollutant concentration weighted by the regression coefficients with HF from single-pollutant models. We also calculated the weighted genetic risk score of HF. During a median of 10.1 years (4 346 642 person-years) of follow-up, we documented 4201 incident HF. The hazard ratios (HRs) [95% confidence interval (CI)] of HF for a 10 mu g/m(3) increase in PM2.5, PM10, PM2.5-10, NO2, and NOx were 1.85 (1.34-2.55), 1.61 (1.30-2.00), 1.13 (0.80-1.59), 1.10 (1.04-1.15), and 1.04 (1.02-1.06), respectively. We found that the air pollution score was associated with an increased risk of incident HF in a dose-response fashion. The HRs (95% CI) of HF were 1.16 (1.05-1.28), 1.19 (1.08-1.32), 1.21 (1.09-1.35), and 1.31 (1.17-1.48) in higher quintile groups compared with the lowest quintile of the air pollution score (P trend <0.001). In addition, we observed that the elevated risk of HF associated with a higher air pollution score was strengthened by the genetic susceptibility to HF. Conclusion Our results indicate that the long-term joint exposure to various air pollutants including PM2.5, PM10, PM2.5-10, NO2, and NOx is associated with an elevated risk of incident HF in an additive manner. Our findings highlight the importance to comprehensively assess various air pollutants in relation to the HF risk. [GRAPHICS] .
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