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PM2.5 air pollution and cause-specific cardiovascular disease mortality

569

Citations

38

References

2019

Year

TLDR

Ambient air pollution is a modifiable risk factor for cardiovascular disease, but the magnitude of risk at lower fine particulate matter (PM2.5) levels remains uncertain. The study estimated PM2.5 exposure with a hybrid land‑use regression model and used multivariate Cox regression on 565,477 participants over 7.5 million person‑years to evaluate cause‑specific cardiovascular mortality. A 10 μg/m³ increase in PM2.5 was associated with a 16 % rise in ischemic heart disease mortality and a 14 % rise in stroke mortality, with risks increasing across exposure brackets and persisting even below the current US standard of 12 μg/m³, highlighting the need for further air‑pollution abatement.

Abstract

Abstract Background Ambient air pollution is a modifiable risk factor for cardiovascular disease, yet uncertainty remains about the size of risks at lower levels of fine particulate matter (PM2.5) exposure which now occur in the USA and elsewhere. Methods We investigated the relationship of ambient PM2.5 exposure with cause-specific cardiovascular disease mortality in 565 477 men and women, aged 50 to 71 years, from the National Institutes of Health-AARP Diet and Health Study. During 7.5 x 106 person-years of follow up, 41 286 cardiovascular disease deaths, including 23 328 ischaemic heart disease (IHD) and 5894 stroke deaths, were ascertained using the National Death Index. PM2.5 was estimated using a hybrid land use regression (LUR) geostatistical model. Multivariate Cox regression models were used to estimate relative risks (RRs) and 95% confidence intervals (CI). Results Each increase of 10 μg/m3 PM2.5 (overall range, 2.9–28.0 μg/m3) was associated, in fully adjusted models, with a 16% increase in mortality from ischaemic heart disease [hazard ratio (HR) 1.16; 95% CI 1.09-1.22] and a 14% increase in mortality from stroke (HR 1.14; CI 1.02-1.27). Compared with PM2.5 exposure <8 μg/m3 (referent), risks for CVD were increased in relation to PM2.5 exposures in the range of 8–12 μg/m3 (CVD: HR 1.04; 95% CI 1.00-1.08), in the range 12–20 μg/m3 (CVD: HR 1.08; 95% CI 1.03-1.13) and in the range 20+ μg/m3 (CVD: HR 1.19; 95% CI 1.10-1.28). Results were robust to alternative approaches to PM2.5 exposure assessment and statistical analysis. Conclusions Long-term exposure to fine particulate air pollution is associated with ischaemic heart disease and stroke mortality, with excess risks occurring in the range of and below the present US long-term standard for ambient exposure to PM2.5 (12 µg/m3), indicating the need for continued improvements in air pollution abatement for CVD prevention.

References

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