Comparative effects of diesel exhaust and ambient particles on cardiovascular system.

摘要

Air pollution has been associated with cardiovascular diseases (CVD) by many epidemiology studies. However, the components of air pollution that are responsible for the CVD are unknown and the mechanisms underlying the associations need to be elucidated.;The objectives of this study were to investigate (1) whether sub-chronic inhalation of ambient particulate matter (PM), whole diesel exhaust (WDE), or diesel exhaust gases (DEG), leads to exacerbation of atherosclerosis, alteration of endothelial function, and pulmonary/systemic inflammation; (2) to what extent do WDE, and DEG, contribute to air pollution enhanced CVD; (3) whether there is interaction between DEG and ambient PM in inducing/enhancing cardiovascular effects.;ApoE-/- mice were exposed via inhalation for 5 h/d, 4 d/wk, for up to 5 months (mo) to 5 different exposure atmospheres, including: (1) filtered air (FA), (2) concentrated ambient fine particles PM2.5 (CAPs, av. conc. 105 mug/m 3), (3) WDE (with DEP conc. at 436 mug/m3), (4) DEG (equivalent to gas levels in WDE which contains 436 mug/m3 DEP), and (5) CAPs+DEG (PM: 113 mug/m3; Gas: equivalent to that in WDE at 436 mug/m3 DEP). After 3 mo and 5 mo of exposure, lung lavage fluid and blood sera were analyzed for inflammation, and atherosclerotic plaques were quantified using 3 methods: non-invasive serial ultrasound imaging, H&E histology stain, and en-face Sudan IV stain. Vascular functions were assessed after 5 mo of exposure.;The results of this study show that in the ApoE-/- mouse model for atherosclerosis: (1) Sub-chronic inhalation of CAPs, WDE and DEG all increased the serum VCAM-1 expression and enhanced the PE-induced vasoconstriction to a similar level; (2) For plaque exacerbation, the effects of CAPs > WDE >DEG = FA, indicating that PM (rather than gases), especially some components of the ambient PM (not present in WDE), were more responsible for the plaque development; (3) There were no interactions between CAPs and DEG on plaque exacerbation, vasomotor dysfunction, and pulmonary/systemic inflammation.