Ambient air pollution associated with increased risk of incident HF

Introduction and methods

Epidemiological studies have shown that short term to air pollution is associated with a greater risk of hospitalization for HF and mortality. It has also been shown that patients with HF are at increased risk of pollution-related hospitalization for ischemic heart disease and chronic obstructive pulmonary disorders [1-4]. However, whether a relation exists between long-term exposure to various air pollutants and incidence of HF remains unknown. It is also unknown whether genetic variations can modify the association between air pollution exposure and HF.

This prospective study introduced an air pollution score to assess the association between long-term joint exposure to a mixture of air pollutants including particulate matter (PM) with diameters ≤2.5 µm (PM2.5), ≤10 µm (PM10), between 2.5 and 10 µm (PM2.5–10), and nitrogen oxides (NO2, and NOx) with risk of incident HF. In addition, the association between air pollution score and genetic susceptibility with HF was explored.

A total of 432 530 participants from the UK Biobank [5] who had complete data for exposure to air pollution and no HF, AF or CHD at baseline were included in the analysis. A subgroup of 327 151 participants of European descent were included in the genetic analysis. The annual average concentrations of PM2.5, PM10, PM2.5–10, NO2, and NOx were estimated with a model from the European Study of Cohorts for Air Pollution Effects project [6,7]. Air pollution exposures of the participants were based on their residential addresses at baseline. An air pollution score was created by adding concentrations of PM2.5, PM10, PM2.5–10, NO2, and NOx, weighted by the multivariable-adjusted risk estimates on HF. A higher air pollution score indicated higher exposure to air pollution and participants were classified into five quintiles of the air pollution score. HR’s were adjusted for age, sex, race, UK Biobank assessment center, Townsend Deprivation index, alcohol consumption, smoking status, BMI, physical activity, healthy diet score, diabetes, hypertension, SBP, and DBP. A genetic risk score (GRS) for HF using 12 SNPs was based on a genome-wide association study [8]. Participants were classified intro three tertiles (low, intermediate and high genetic risk of HF). Median follow-up was of 10.1 years. The primary outcome was incident HF.

Main results

• PM2.5, PM10, NO2, and NOx were each significantly associated with increased risk of incident HF. Adjusted HRs for the risk of incident HF for a 10 µg/m^3 increase in PM2.5, PM10, NO2, and NOx were 1.85 ( 95%CI 1.34-2.55, P trend<0.001), 1.61 (95%CI 1.30-2.00, P trend<0.001), 1.10 (95%CI 1.04-1.15, P trend<0.001), and 1.04 (95%CI 1.02-1.06, P trend<0.001), respectively. PM2.5-10 was not significantly associated with incident HF.
• The newly introduced air pollution score was associated with increased risk of incident HF. Adjusted HRs for HF in Q2, Q3, Q4, and Q5, compared to Q1 as reference, were 1.16 (95%CI 1.05-1.28), 1.19 (95%CI 1.08-1.32), 1.21 (95%CI 1.09-1.35), and 1.31 (95%CI 1.17-1.48), respectively. P trend <0.001.
• HF GRS was significantly associated with risk of incident HF in a multivariable adjusted model (HR for HF: 2.65, 95%CI 1.99–3.53, P trend <0.001).
• There was no statistically significant interaction between the air pollution score and HF GRS with risk of incident HF. However, participants with high GRS and air pollution score in Q5 had a 46% greater risk of HF (HR 1.46, 95% CI 1.18-1.81) compared to participants with low GRS and air pollution score in Q1.

Conclusion

References

Find this article online at Eur Heart J.