Epidemiologic studies have shown an association between exposure to ambient particulate air pollution less than 10 µm in diameter(PM₁₀) and increased cardiovascular morbidity and mortality. We have previously shown that PM₁₀ exposure causes progression of atherosclerosis in coronary arteries. We postulate that the recruitment of monocytes from the circulation into atherosclerotic lesions is a key step in this PM₁₀-induced acceleration of atherosclerosis. The study objective was to quantify the recruitment of circulating monocytes into vessel walls and the progression of atherosclerotic plaques induced by exposure to PM₁₀. Female Watanabe Heritable Hyperlipidemic rabbits, that naturally develop systemic atherosclerosis, were exposed to PM₁₀(EHC-93) or vehicle by intratracheal instillation twice a week for four weeks. Monocytes, labeled with 5’bromo-2’-deoxyuridine(BrdU) in donors, were transfused to recipient rabbits as whole blood and the recruitment of BrdU-labeled cells into vessel walls and plaques in recipients were measured using quantitative histological methodology. Exposure to PM₁₀ caused progression of atherosclerotic lesions in thoracic and abdominal aorta. It also decreased circulating monocyte counts, decreased circulating monocytes expressing high levels of CD31(PECAM-1) and CD49d(VLA-4 chain) and increased expression of CD54(ICAM-1) and CD106(VCAM-1) in plaques. Exposure to PM₁₀ increased the number of BrdU-labeled monocytes adherent to endothelium over plaques and increase the migration of BrdU-labeled monocytes into plaques and smooth muscle underneath plaques. We conclude that exposure to ambient air pollution particles promotes the recruitment of circulating monocytes into atherosclerotic plaques and speculate that this is a critically important step in the PM₁₀-induced progression of atherosclerosis.