We sought to determine the effect of exposure to air pollution particulate matter <10 μm (PM₁₀) on the progression of atherosclerosis in rabbits.

Epidemiologic studies have associated exposure to ambient PM₁₀with increased cardiovascular morbidity and mortality. We have previously shown that PM₁₀exposure induces a systemic inflammatory response that includes marrow stimulation, and we hypothesized that this response accelerates atherosclerosis.

Watanabe heritable hyperlipidemic rabbits were exposed to PM₁₀(n = 10) or vehicle (n = 6) for four weeks, and bone marrow stimulation was measured. Quantitative histologic methods were used to determine the morphologic features of the atherosclerotic lesions.

Exposure to PM₁₀caused an increase in circulating polymorphonuclear leukocytes (PMN) band cell counts (day 15: 24.6 ± 3.0 vs. 11.5 ± 2.7 × 10⁷/l [PM₁₀vs. vehicle], p < 0.01) and an increase in the size of the bone marrow mitotic pool of PMNs. Exposure to PM₁₀also caused progression of atherosclerotic lesions toward a more advanced phenotype. The volume fraction (vol/vol) of the coronary atherosclerotic lesions was increased by PM₁₀exposure (33.3 ± 4.6% vs. 19.5 ± 3.1% [PM₁₀vs. vehicle], p < 0.05). The vol/vol of atherosclerotic lesions correlated with the number of alveolar macrophages that phagocytosed PM₁₀(coronary arteries: r = 0.53, p < 0.05; aorta: r = 0.51, p < 0.05). Exposure to PM₁₀also caused an increase in plaque cell turnover and extracellular lipid pools in coronary and aortic lesions, as well as in the total amount of lipids in aortic lesions.

Progression of atherosclerosis and increased vulnerability to plaque rupture may underlie the relationship between particulate air pollution and excess cardiovascular death.