Adverse cardiovascular effects of air pollution

被引:570
|
作者
Mills, Nicholas L. [1 ]
Donaldson, Ken [2 ]
Hadoke, Paddy W.
Boon, Nicholas A. [1 ]
MacNee, William [2 ]
Cassee, Flemming R. [3 ]
Sandstrom, Thomas [4 ]
Blomberg, Anders [4 ]
Newby, David E. [1 ]
机构
[1] Univ Edinburgh, Ctr Cardiovasc Sci, Edinburgh EH16 4SU, Midlothian, Scotland
[2] Univ Edinburgh, ELEI Colt Lab, Edinburgh EH16 4SU, Midlothian, Scotland
[3] Natl Inst Publ Hlth & Environm, Dept Inhalat Toxicol, NL-3720 BA Bilthoven, Netherlands
[4] Umea Univ, Dept Resp Med & Allergy, S-90187 Umea, Sweden
来源
关键词
air pollution; atherothrombosis; endothelium; inflammation; risk; DIESEL-EXHAUST INHALATION; LONG-TERM EXPOSURE; ULTRAFINE PARTICLES; PARTICULATE MATTER; BLOOD-PRESSURE; ENDOTHELIAL DYSFUNCTION; PULMONARY INFLAMMATION; EPIDEMIOLOGIC EVIDENCE; HEART-DISEASE; MORTALITY;
D O I
10.1038/ncpcardio1399
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Air pollution is increasingly recognized as an important and modifiable determinant of cardiovascular disease in urban communities. Acute exposure has been linked to a range of adverse cardiovascular events including hospital admissions with angina, myocardial infarction, and heart failure. Long-term exposure increases an individual's lifetime risk of death from coronary heart disease. The main arbiter of these adverse health effects seems to be combustion-derived nanoparticles that incorporate reactive organic and transition metal components. Inhalation of this particulate matter leads to pulmonary inflammation with secondary systemic effects or, after translocation from the lung into the circulation, to direct toxic cardiovascular effects. Through the induction of cellular oxidative stress and proinflammatory pathways, particulate matter augments the development and progression of atherosclerosis via detrimental effects on platelets, vascular tissue, and the myocardium. These effects seem to underpin the atherothrombotic consequences of acute and chronic exposure to air pollution. An increased understanding of the mediators and mechanisms of these processes is necessary if we are to develop strategies to protect individuals at risk and reduce the effect of air pollution on cardiovascular disease.
引用
收藏
页码:36 / 44
页数:9
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