Air Pollution and Cardiovascular InjuryEpidemiology, Toxicology, and Mechanisms
Boris Z. Simkhovich, MD, PhD*, ,
Michael T. Kleinman, PhD and
Robert A. Kloner, MD, PhD, FACC*,,*
* The Heart Institute, Good Samaritan Hospital, Los Angeles, California
Division of Cardiovascular Medicine, Keck School of Medicine, University of Southern California, Los Angeles, California
Department of Community and Environmental Medicine, University of California Irvine, Irvine, California.
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Figure 1 Pathophysiological Mechanisms of Lung- and Circulation-Mediated Cardiovascular Toxicity of Particulate Air Pollutants
Inhaled ambient air particles increase production of reactive oxygen species (ROS) in the airways and lung alveoli and stimulate local inflammatory reaction in the lungs. The ROS and pro-inflammatory cytokines released into the blood stream affect autonomic cardiac control (heart rate, heart rate variability, and cardiac contractility), blood pressure, vascular tone and reactivity, blood coagulability, and progression of atherosclerosis. Ultrafine particles may translocate into the circulation and induce oxidative stress and pro-inflammatory changes directly in the cardiac muscle and vasculature. Lung- and circulation-mediated and direct pathophysiological mechanisms exacerbate myocardial ischemia and increase cardiovascular mortality. CRP = C-reactive protein; IL = interleukin; TNF = tumor necrosis factor. Figure illustration by Rob Flewell.
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