Particulate air pollution induces progression of atherosclerosis
Tatsushi Suwa, MD, PhD*,
James C. Hogg, MD, PhD*,
Kevin B. Quinlan, BSc*,
Akira Ohgami, MD, PhD*,
Renaud Vincent, PhD and
Stephan F. van Eeden, MD, PhD*,*
* McDonald Research Laboratory and iCAPTURE Centre, University of British Columbia, St. Paul’s Hospital, Vancouver, British Columbia, Canada
Environmental Health Directorate, Health Canada, Ottawa, Ontario, Canada
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Figure 1 Photomicrograph of formalin-fixed, paraffin-embedded rabbit lung tissue stained with hematoxylin-eosin. An alveolar macrophage containing particulate matter <10 µm (>5% of the cytoplasmic surface area) (arrow). Bar = 10 µm.
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Figure 2 The circulating polymorphonuclear leukocyte (PMN) band cell counts (A) and accumulative number of 5"-bromo-2"-deoxyuridine (BrdU)-labeled PMNs from the bone marrow mitotic pool (weakly stained cells, G1 cells) in the circulation (B). (A) The circulating PMN band cell counts increased during the second and third weeks of exposure (day 15: p < 0.01; day 18: p < 0.05). Rabbits were exposed to particulate matter <10 µm (PM10) for four weeks (solid circles; n = 10) or saline (control; open circles; n = 6). Data are presented as the mean value ± SE. *p < 0.01 and p < 0.05, compared with control group. (B) Exposure to PM10 increased the size of the marrow mitotic pool. Rabbits were exposed to PM10 for four weeks (solid circles; n = 10) or saline (control; open circles; n = 6). Data are presented as the mean value ± SE. *p < 0.05, compared with control group.
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Figure 3 Photomicrographs of formalin-fixed, paraffin-embedded rabbit coronary artery tissue stained with Movat’s pentachrome, showing type I to V lesions. The bars represent 100 µm (A–C) or 200 µm (D, E). The type I lesion (A) showed intimal thickening, with an increase in the number of intimal macrophages, as well as isolated, small groups of foam cells. The type II lesion showed layers of foam cells and lipids within intimal smooth muscle cells (B). The type III lesion showed extracellular lipid pools (C), and the type IV lesion showed a larger, more confluent and disruptive core of extracellular lipids (D). The type V lesion showed thick layers of fibrous connective tissue, in addition to the lipid core (E).
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Figure 4 (A) The vol/vol of atherosclerotic lesions in the left main coronary artery (LMCA) and right coronary artery (RCA). The particulate matter <10 µm (PM10)-exposed group had a higher vol/vol of atherosclerotic lesions in the LMCA and RCA, as compared with the control group. Data are presented as the mean value ± SE. *p < 0.05, compared with control group. (B) The correlation between the percentage of alveolar macrophages that phagocytosed particles and the vol/vol of atherosclerotic lesions in the LMCA and RCA (r = 0.53, p < 0.05). Results were from rabbits exposed to PM10 for four weeks (solid circles; n = 10) or saline (control; open circles; n = 6).
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Figure 5 The volume fraction (vol/vol) of 5"-bromo-2"-deoxyuridine (BrdU)-positive atherosclerotic nuclei in the vessel, corrected for the amount of atherosclerotic (AS) lesions. The particulate matter <10 µm (PM10) group showed a higher vol/vol of BrdU-positive atherosclerotic nuclei in the coronary arteries and aorta. *p < 0.01 and p < 0.05, compared with control group.
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