Particulate air pollution induces progression of atherosclerosis

Abstract

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

Particulate matter air pollution exposure promotes recruitment of monocytes into atherosclerotic plaques

“…We recently demonstrated (45) that chronic exposure to PM 10 causes downstream vascular effects that result in progression of atherosclerosis, and this has recently been confirmed in human studies (25). PM 10 exposure also induces phenotypic changes in plaques characteristic of plaque vulnerability and instability (45).…”

“…The EHC-93 suspension was sonicated before instillation to ensure even distribution and prevent aggregation of the particles. The rabbits were anesthetized with 5% isoflurane, and 1 ml of normal saline or PM 10 (5 mg EHC-93 mixed with 1 ml saline) was instilled twice a week for 4 wk, as previously described (29,45). One milliliter of blood was collected with 22-gauge needles into Vacutainers containing ethylenediaminetetraacetic acid (EDTA) from the central ear artery twice before instillation for baseline measurements, 0.5, 1, 2, 4, 8, 12, and 24 h after the initial instillation to observe acute effects, and subsequently once weekly to determine the chronic effects on monocyte adhesion molecule expression.…”

Ultrastructural changes in atherosclerotic plaques following the instillation of airborne particulate matter into the lungs of rabbits

“…Suwa et al (26) provided light microscopic evidence that PM 10 exposure leads to increased plaque size, lipid deposition and inflammatory cell recruitment into atherosclerotic plaques in Watanabe heritable hyperlipidemic (WHHL) rabbits. Sun et al (27,28) used an apolipoprotein E knockout (ApoE -/-) mouse model to show that long-term exposure to low concentrations of PM 2.5 (particles smaller than 2.5 µm in diameter) altered vasomotor tone, and increased tissue-factor expression, vascular inflammation and atherosclerotic burden in these animals.…”

“…The model used to test the hypothesis of the present study has been established in the James Hogg iCAPTURE Research Centre, Providence Heart + Lung Institute (Vancouver, British Columbia), and is well characterized with regard to both the local and the systemic response (20,26,32,36,37). Briefly, the experimental rabbits (n=8) were lightly anesthetized with 5% halo thane while 5 mg of EHC-93, suspended in 1 mL of sterile saline, was deposited just above the larynx using a blunt curved needle twice per week for four weeks.…”

“…Our laboratory has previously shown that when particles are deposited in the lung using this instillation protocol, a rapid release of polymorphonuclear leukocytes (26) and monocytes (20) into the circulation from the bone marrow is induced. Furthermore, this response is proportional to the amount of particulate matter phagocytosed by alveolar macrophages (20).…”