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1 St. Paul's Hospital, James Hogg iCAPTURE Centre for Cardiovascular and Pulmonary Research, University of British Columbia, Vancouver, British Columbia, Canada
2 Environmental Health Directorate, Health Canada, Ottawa, Ontario, Canada
* To whom correspondence should be addressed. E-mail: svaneeden{at}mrl.ubc.ca.
Exposure to air pollution (PM10) causes a systemic inflammatory response that includes stimulation of the bone marrow (BM) and progression of atherosclerosis. Monocytes are known to play a key role in atherogenesis by migration into subendothelial lesions where they appear foam cells. The present study was designed to quantify the BM monocyte response in Watanabe heritable hyperlipidemic (WHHL) rabbits following PM10 exposure. WHHL rabbits were given twice weekly intrapharyngeal instillations of 5mg of PM10 for 4 weeks to a total of 40mg and compared to control WHHL or New Zealand White (NZW) rabbits. The thymidine analog, 5'-bromo-2'-deoxyuridine (BrdU) was used to label dividing cells in the BM and a monoclonal antibody to identify monocytes in peripheral blood. The transit time of monocytes through the BM was faster in WHHL than in NZW rabbits (30.4 ± 1.9 hours vs. 35.2 ± 0.9 hours, WHHL vs. NZW; P<0.05). PM10 instillation exposure increased circulating band cell counts (day 15: 17.4 ± 3.9 vs. 5.2 ± 2.7 x107/L, PM10 vs. control; P<0.05), caused rapid release of monocytes from the BM, and further shortened their transit time through the BM to 23.2 ± 1.6 hours (P<0.05). The percentage of alveolar macrophages containing particles in the lung correlated with the BM transit time of monocytes (r2 = 0.45, P<0.05). We conclude that atherosclerosis increases the release of monocytes from the BM and PM10 exposure accelerates this process in relation to the amount of particles phagocytosed by alveolar macrophages.
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