Biological Pathway for PM Damage Similar to Cigarette Smoking
This review article explores potential mechanisms of vascular disease induced by lung inflammation.
Ambient particles and inhaled cigarette smoke are processed by alveolar macrophages and lung epithelial cells. These cells produce proinflammatory mediators such as cytokines that promote a local inflammatory response in the lung that are thought to contribute to the exacerbation of Chronic Obstructive Pulmonary Disease (COPD) and asthma and promote lung infection. These inflammatory mediators may also translocate into the circulation and induce a systemic inflammatory response. This response can include stimulation of the marrow to release leukocytes and platelets, activation of proteins such as C-reactive protein and fibroinogen that may increase coagulability, and activation of the vascular endothelium, the layer of cells that line the blood vessels and are in direct contact with the blood.
Together, researchers surmise, these effects could cause progression and instability of atherosclerotic plaques, precipitating or aggravating cardiovascular events.
van Eeden SF, Yeung A, Quinlam K, and Hogg JC. Systemic Response to Ambient Particulate Matter: Relevance to Chronic Obstructive Pulmonary Disease. Proc Am Thorac Soc 2005; 2:61-67.
For a copy of the abstract click here.
