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Vascular and Cardiac Impairments in Rats Inhaling Ozone and Diesel Exhaust Particles
Citation:
KODAVANTI, U. P., R. THOMAS, A. Lund, M. SCHLADWEILER, M. J. Campen, G. Wallenborn, R. R. Gottipolu, A. D. LEDBETTER, J. E. RICHARDS, A. Nyska, D. L. ANDREWS, J. MCKEE, R. H. JASKOT, S. Kotha, R. B. Patel, E. O. Butler, AND N. L. Parinandi. Vascular and Cardiac Impairments in Rats Inhaling Ozone and Diesel Exhaust Particles. ENVIRONMENTAL HEALTH PERSPECTIVES. National Institute of Environmental Health Sciences (NIEHS), Research Triangle Park, NC, 119(3):312-318, (2011).
Impact/Purpose:
This research shows that subchronic, episodic ozone and diesel exhaust inhalation causes vascular and cardiac molecular alterations which are progressive over time. This paper also proposes a new mechanism by which pollutants might induce vascular toxicity.
Description:
Background -Mechanisms of cardiovascular injuries from exposure to gas and particulate air pollutants are unknown. Objective -We hypothesized that episodic exposure of rats to ozone or diesel exhaust particles (DEP) will cause differential cardiovascular impairments, which will be exacerbated by ozone+DEP. Methods and Results -Male Wistar Kyoto rats (10-12 wk) were exposed to air, ozone (OAppm), bulk DEP (2.1mg/m3) or ozone (0.38ppm)+DEP (2.2mg/m3), 5h/d, 1 d/wk for 16 wks, or to air, ozone (0.51 or 1.0ppm), or DEP (1.9mg/m3) , 5h/d for 2 days. Pulmonary and cardiovascular biomarkers of injury were examined. Mild to minimal pulmonary inflammation and pathology occurred following acute or 16-wk exposure to DEP and ozone. Biomarkers of oxidative stress (HO-1), inflammation (MIP-2), thrombosis (TF, PAI-1, tPA, and vWf), vasoconstriction (ET-1, ET receptor A and B, eNOS) and proteolysis (MMP-2, MMP-3, MMP-9 and TIMP-2) were variably upregulated in the aorta but not in lung or heart in16-wk study. Aortic LOX-1 protein was increased by ozone and ozone+DEP with a trend of increase in mRNA. RAGE mRNA was slightly increased by ozone+DEP. Exposure to either ozone or DEP depleted cardiac mitochondrial phospholipid fatty acids. The combined effects of ozone+DEP were less pronounced than either pollutant alone. Acute exposures caused relatively mild changes in the aorta. Conclusions -Subchronic episodic exposures to ozone or DEP alone elevated biomarkers of vascular impairments in the aorta together with the loss of phospholipid fatty acids in the myocardial mitochondria. A possible role of the oxidized lipids through LOX-1 signaling is postulated.
