Cardiovascular Effects of Long-Term Exposure to Air Pollution: A Population-Based Study With 900 845 Person-Years of Follow-up

Abstract

Background: Studies have shown that long-term exposure to air pollution such as fine particulate matter (≤2.5 μm in aerodynamic diameter [PM_2.5]) increases the risk of all-cause and cardiovascular mortality. To date, however, there are limited data on the impact of air pollution on specific cardiovascular diseases. This study aimed to evaluate cardiovascular effects of long-term exposure to air pollution among residents of Seoul, Korea.

Methods and results: Healthy participants with no previous history of cardiovascular disease were evaluated between 2007 and 2013. Exposure to air pollutants was estimated by linking the location of outdoor monitors to the ZIP code of each participant's residence. Crude and adjusted analyses were performed using Cox regression models to evaluate the risk for composite cardiovascular events including cardiovascular mortality, acute myocardial infarction, congestive heart failure, and stroke. A total of 136 094 participants were followed for a median of 7.0 years (900 845 person-years). The risk of major cardiovascular events increased with higher mean concentrations of PM_2.5 in a linear relationship, with a hazard ratio of 1.36 (95% confidence interval, 1.29-1.43) per 1 μg/m³ PM_2.5. Other pollutants including PM_2.5-10 of CO, SO₂, and NO₂, but not O₃, were significantly associated with increased risk of cardiovascular events. The burden from air pollution was comparable to that from hypertension and diabetes mellitus.

Conclusions: This large-scale population-based study demonstrated that long-term exposure to air pollution including PM_2.5 increases the risk of major cardiovascular disease and mortality. Air pollution should be considered an important modifiable environmental cardiovascular risk factor.

Keywords: air pollution; cardiovascular disease risk factors; epidemiology; particulate matter.

Figure 1

The concentrations of PM _2.5 in Seoul, 2007–2013. (A) Maps of average PM _2.5 concentrations, and (B) yearly concentrations of PM _2.5 at each monitor. PM_2.5 indicates fine particulate matter ≤2.5 μm in aerodynamic diameter.

Figure 2

Relationship between long exposure to PM _2.5, PM _2.5–10, CO, SO ₂, and NO ₂ and composite cardiovascular events. Cox regression model for cardiovascular risk in response to PM _2.5 exposure was smoothed using penalized spline methods with 3 df. The y‐axis represents the log hazard ratio (solid line). CO indicates carbon monoxide; NO₂, nitrogen dioxide: O₃, ozone; PM_2.5, fine particulate matter ≤2.5 μm in aerodynamic diameter; PM_2.5–10 indicates fine particulate matter ≤2.5 to 10 μm in aerodynamic diameter; SO₂, sulfur dioxide.

Figure 3

Kaplan–Meier survival curves for composite cardiovascular events in response to long‐term exposure to ambient PM _2.5. PM_2.5 indicates fine particulate matter ≤2.5 μm in aerodynamic diameter.

Figure 4

Subgroup analysis for cardiovascular risk of long‐term exposure to PM _2.5. The x‐axis represents hazard ratios with 95% confidence intervals. Int P denotes interaction P value; PM_2.5 indicates fine particulate matter ≤2.5 μm in aerodynamic diameter.