Chronic obstructive pulmonary disease (COPD) is a risk factor for development of cardiovascular events, independent of smoking. The mechanisms are unclear, but systemic inflammation associated with COPD may contribute to this cardiovascular risk. Similar to cigarette smoking, exposure to particulate air pollution is associated with an increase in the mortality and morbidity from respiratory and cardiovascular diseases. The exposure of humans to high levels of ambient particles stimulates the bone marrow and the release of neutrophils, band cells, and monocytes into the circulation. This bone marrow simulation is associated with increased levels of circulating interleukin-1beta and interleukin-6, similar to cigarette smoking. In animals, exposure to particulate matter accelerates the transit of neutrophils and monocytes in bone marrow and expands the leukocyte pool size. This systemic inflammatory response to particle inhalation causes endothelial activation and upregulation adhesion molecules that are critically important in leukocyte recruitment into atherosclerotic plaques. Exposure to particles also causes disease progression and destabilization of atherosclerotic plaques in rabbits that develop atherosclerosis naturally. We suspect, therefore, that the systemic inflammatory responses described activate vascular endothelium and cause progression and instability of atherosclerotic plaques. We speculate that this mechanism may contribute to the cardiovascular morbidity and mortality associated with COPD.