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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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