Cardiovascular mortality and long-term exposure to particulate air pollution - Epidemiological evidence of general pathophysiological pathways of disease

被引:1950
作者
Pope, CA
Burnett, RT
Thurston, GD
Thun, MJ
Calle, EE
Krewski, D
Godleski, JJ
机构
[1] Brigham Young Univ, Provo, UT 84602 USA
[2] Hlth Canada, Ottawa, ON K1A 0L2, Canada
[3] Univ Ottawa, Ottawa, ON, Canada
[4] NYU, Sch Med, Tuxedo Pk, NY USA
[5] Amer Canc Soc, Atlanta, GA 30329 USA
[6] Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA
关键词
mortality; pulmonary heart disease; cardiovascular diseases; smoking;
D O I
10.1161/01.CIR.0000108927.80044.7F
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Background - Epidemiologic studies have linked long-term exposure to fine particulate matter air pollution ( PM) to broad cause-of-death mortality. Associations with specific cardiopulmonary diseases might be useful in exploring potential mechanistic pathways linking exposure and mortality. Methods and Results - General pathophysiological pathways linking long-term PM exposure with mortality and expected patterns of PM mortality with specific causes of death were proposed a priori. Vital status, risk factor, and cause-of-death data, collected by the American Cancer Society as part of the Cancer Prevention II study, were linked with air pollution data from United States metropolitan areas. Cox Proportional Hazard regression models were used to estimate PM-mortality associations with specific causes of death. Long-term PM exposures were most strongly associated with mortality attributable to ischemic heart disease, dysrhythmias, heart failure, and cardiac arrest. For these cardiovascular causes of death, a 10-mug/m(3) elevation in fine PM was associated with 8% to 18% increases in mortality risk, with comparable or larger risks being observed for smokers relative to nonsmokers. Mortality attributable to respiratory disease had relatively weak associations. Conclusions - Fine particulate air pollution is a risk factor for cause-specific cardiovascular disease mortality via mechanisms that likely include pulmonary and systemic inflammation, accelerated atherosclerosis, and altered cardiac autonomic function. Although smoking is a much larger risk factor for cardiovascular disease mortality, exposure to fine PM imposes additional effects that seem to be at least additive to if not synergistic with smoking.
引用
收藏
页码:71 / 77
页数:7
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