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J Am Coll Cardiol, 2008; 52:719-726, doi:10.1016/j.jacc.2008.05.029 (Published online 13 August 2008).
© 2008 by the American College of Cardiology Foundation
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STATE-OF-THE-ART PAPER

Air Pollution and Cardiovascular Injury

Epidemiology, Toxicology, and Mechanisms

Boris Z. Simkhovich, MD, PhD*,{dagger}, Michael T. Kleinman, PhD{ddagger} and Robert A. Kloner, MD, PhD, FACC*,{dagger},*

* The Heart Institute, Good Samaritan Hospital, Los Angeles, California
{dagger} Division of Cardiovascular Medicine, Keck School of Medicine, University of Southern California, Los Angeles, California
{ddagger} Department of Community and Environmental Medicine, University of California Irvine, Irvine, California.

Manuscript received January 14, 2008; revised manuscript received May 14, 2008, accepted May 19, 2008.

* Reprint requests and correspondence: Dr. Robert A. Kloner, The Heart Institute, Good Samaritan Hospital, 1225 Wilshire Boulevard, Los Angeles, California 90017 (Email: rkloner{at}goodsam.org).

Recent epidemiologic studies show that increased levels of air pollutants are positively associated with cardiovascular morbidity and mortality. Inhalation of air pollutants affects heart rate, heart rate variability, blood pressure, vascular tone, blood coagulability, and the progression of atherosclerosis. Several categories within the general population (i.e., people with pre-existing cardiovascular disease and diabetic and elderly individuals) are considered to be more susceptible to air pollution–mediated cardiovascular effects. Major mechanisms of inhalation-mediated cardiovascular toxicity include activation of pro-inflammatory pathways and generation of reactive oxygen species. Although most studies focus on the influence of systemic effects, recent studies indicate that ultrafine particles may be translocated into the circulation and directly transported to the vasculature and heart where they can induce cardiac arrhythmias and decrease cardiac contractility and coronary flow.

Key Words: air pollution • cardiovascular effects • mechanisms

Abbreviations and Acronyms
  AD = aerodynamic diameter
  CAP = concentrated ambient particle
  HR = heart rate
  HRV = heart rate variability
  MI = myocardial infarction
  PM = particulate matter
  PM10 = coarse particle(s) (diameter ≤10 µm)
  PM2.5 = fine particle(s) (diameter <2.5 µm)
  ROS = reactive oxygen species
  UAP = urban air particle
  UFP = ultrafine particle (diameter <0.1 µm)






 
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