Adverse cardiovascular effects of air pollution.
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.
Mills
Nicholas L
NL
Centre for Cardiovascular Science, University of Edinburgh, UK. nick.mills@ed.ac.uk
Donaldson
Ken
K
Hadoke
Paddy W
PW
Boon
Nicholas A
NA
MacNee
William
W
Cassee
Flemming R
FR
Sandström
Thomas
T
Blomberg
Anders
A
Newby
David E
DE
D000397:Air Pollution / Q000009:adverse effects*; D001145:Arrhythmias, Cardiac / Q000209:etiology / Q000378:metabolism; D050197:Atherosclerosis / Q000209:etiology / Q000378:metabolism; D001792:Blood Platelets / Q000378:metabolism; D001808:Blood Vessels / Q000378:metabolism; D002318:Cardiovascular Diseases / Q000209:etiology* / Q000378:metabolism / Q000517:prevention & control; D006801:Humans; D007249:Inflammation / Q000209:etiology / Q000378:metabolism; D018836:Inflammation Mediators / Q000378:metabolism*; D019570:Inhalation Exposure; D008168:Lung / Q000378:metabolism; D008171:Lung Diseases / Q000209:etiology / Q000378:metabolism; D009206:Myocardium / Q000378:metabolism; D018384:Oxidative Stress; D052638:Particulate Matter / Q000009:adverse effects*; D017382:Reactive Oxygen Species / Q000378:metabolism*; D012307:Risk Factors; D013927:Thrombosis / Q000209:etiology / Q000378:metabolism
D018836:Inflammation Mediators; D052638:Particulate Matter; D017382:Reactive Oxygen Species