PM_2.5 air pollution and cause-specific cardiovascular disease mortality

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 (PM_2.5) exposure which now occur in the USA and elsewhere. Methods: We investigated the relationship of ambient PM_2.5 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. PM_2.5 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 PM_2.5 (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 PM_2.5 exposure <8 μg/m³ (referent), risks for CVD were increased in relation to PM_2.5 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 PM_2.5 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 PM_2.5 (12 μg/m³), indicating the need for continued improvements in air pollution abatement for CVD prevention.