Cardiovascular effects associated with air pollution: potential mechanisms and methods of testing.
A recent series of epidemiologic reports have shown associations between fine particulate matter (PM) levels and increased cardiovascular morbidity and mortality. Elevated PM levels have been linked with cardiac events, including serious ventricular arrhythmias and myocardial infarction. A workshop brought together epidemiologists, cardiologists, and toxicologists from academia, government, and industry to examine plausible mechanisms that could be responsible for such effects, and to consider the armamentarium of noninvasive tests available to examine these relationships. Possible mechanisms considered by the participants include: (a) effects on the autonomic nervous system; (b) alterations on ion channel function in myocardial cells; (c) ischemic responses in the myocardium; and (d) inflammatory responses triggering endothelial dysfunction, atherosclerosis, and thrombosis. A large number of tests were identified to assess specific mechanistic pathways underlying the cardiovascular effects of air pollution and include: (a) autonomic control of the cardiovascular system assessed primarily by heart-rate variability; (b) myocardial substrate and vulnerability assessed by the electrocardiogram and estimations of ejection fraction and wall motion abnormalities in imaging studies; and (c) endothelial function, atherosclerosis, and thrombosis assessed by clotting parameters, cytokines, lipid profiles, and forearm blood flow. A variety of approaches ranging from molecular and genetic investigations to human clinical studies were recommended to further investigate the important epidemiologic associations.
Utell
Mark J
MJ
Department of Medicine, University of Rochester Medical Center, Pulmonary Division, Box 692, Rochester, NY, USA. mark_utell@urmc.rochester.edu
Frampton
Mark W
MW
Zareba
Wojciech
W
Devlin
Robert B
RB
Cascio
Wayne E
WE
D000393:Air Pollutants / Q000009:adverse effects*; D001341:Autonomic Nervous System / Q000503:physiopathology; D002318:Cardiovascular Diseases / Q000139:chemically induced* / Q000175:diagnosis* / Q000503:physiopathology; D002986:Clinical Trials as Topic / Q000379:methods; D004562:Electrocardiography; D004730:Endothelium, Vascular / Q000503:physiopathology; D006801:Humans; D007249:Inflammation / Q000139:chemically induced / Q000503:physiopathology; D007473:Ion Channels / Q000187:drug effects / Q000503:physiopathology; D017202:Myocardial Ischemia / Q000139:chemically induced / Q000175:diagnosis / Q000503:physiopathology; D010316:Particle Size; D012107:Research Design; D012307:Risk Factors
D000393:Air Pollutants; D007473:Ion Channels