Vascular and Cardiac Impairments in Rats Inhaling Ozone and Diesel Exhaust Particles

Background: Mechanisms of cardiovascular injuries from exposure to gas and particulate air pollutants are unknown. Objecitve: We sought to determine whether episodic exposure of rats to ozone or diesel exhause particles (DEP) causes differential cardiovascular impairments that are exacerbated by ozo...

Full description

Saved in:

Bibliographic Details
Published in:	Environmental health perspectives Vol. 119; no. 3; pp. 312 - 318
Main Authors:	Kodavanti, Urmila P., Thomas, Ronald, Ledbetter, Allen D., Schladweiler, Mette C., Shannahan, Jonathan H., Wallenborn, J. Grace, Lund, Amie K., Campen, Matthew J., Butler, Elizabeth O., Gottipolu, Reddy R., Nyska, Abraham, Richards, Judy E., Andrews, Deborah, Jaskot, Richard H., McKee, John, Kotha, Sainath R., Patel, Rishi B., Parinandi, Narasimham L.
Format:	Journal Article
Language:	English
Published:	Research Triangle Park, NC National Institute of Environmental Health Sciences 01-03-2011 US Department of Health and Human Services
Subjects:	Air Air Pollutants - toxicity Air pollution Anger Animals Aorta Biological and medical sciences Biological markers Biomarkers - metabolism Cardiovascular System - drug effects Chemical hazards Diesel Diesel exhaust Diesel fuels Diesel motor exhaust gas Environment. Living conditions Environmental pollutants toxicology Fatty acids Health aspects Heart diseases Impairment Inflammation - chemically induced Inflammation - metabolism Inhibitors Lipids Lungs Male Medical sciences Messenger RNA Oxidative Stress - drug effects Ozone Ozone - toxicity Particulate Matter - toxicity Proteins Public health. Hygiene Public health. Hygiene-occupational medicine Rats Rats, Inbred WKY Risk factors Thrombosis - chemically induced Thrombosis - metabolism Toxicology Vasoconstriction - drug effects Vehicle Emissions - toxicity United States Japan, Honshu, Kyoto Prefect., Kyoto Heart Rat Toxicity Rodentia Diesel engine Ozone cardiovascular LOX-1 vascular Inhalation Particle Vertebrata Mammalia Health and environment diesel exhaust particles Animal Blood vessel Aorta Air pollution Exhaust gas Circulatory system Public health
Online Access:	Get full text
Tags:	Add Tag No Tags, Be the first to tag this record!

Description
Summary:	Background: Mechanisms of cardiovascular injuries from exposure to gas and particulate air pollutants are unknown. Objecitve: We sought to determine whether episodic exposure of rats to ozone or diesel exhause particles (DEP) causes differential cardiovascular impairments that are exacerbated by ozone plus DEP. Methods and results: Male Wistar Kyoto rats (10-12 weeks of age) were exposed air, ozone (0.4 ppm), DEP (2.1 mg/m³), or ozone (0.38 ppm) + DEP (2.2 mg/m³) for 5 hr/day, 1 day/week for 16 weeks, or to air, ozone (0.15 or 1.0 ppm), or DEP (1.9 mg/m³) 5 hr/day for 2 days. At the end of each exposure period, we examined pulmonary and cardiovascular biomarkers of injury. In the 16-week study, we observed mild pulmonary pathology in the ozone, DEP, and ozone + DEP exposure groups, a slight decrease in circulating lymphocytes in the ozone and DEP groups, and decreased platelets in the DEP group. After 16 weeks of exposure, mRNA biomarkers of oxidative strees (hymeoxygenase-1), thrombosis (tissure factor, plasminogen activator inhibitor-1, tissue plasminogen activator, and von Willebrand factor), vasoconstriction (endothelin-1, endothelin receptors A and B, endothelial NO synthase) and proteolysis [matrix metalloprotease (MMP)-2, MMP-3, and tissue inhibitor of matrix metalloprotease-2] were increased by DEP and/or ozone in the aorta, but not in the heart. Aortic LOX-1 (lectin-like oxidized low-density lipoprotein receptor-1) mRNA and protein increased after ozone exposure, and LOX-1 protein increased after exposure to ozone + DEP. RAGE (receptor for advanced glycation end products) mRNA increased in the ozone + DEP group. Exposure to ozone or DEP depleted cardic mitochondrial phospholipid fatty acids (DEP > ozone). The combined effect of ozone and DEP exposure was less pronounced than exposure to either pollutant alone. Exposure to ozone or DEP for 2 days (acute) caused mild changes in the aorta. Conclusions: In animals exposed to ozone or DEP alone for 16 weeks, we observed elevated biomarkers of vascular impairments in the aorta, with the loss of phospholipid fatty acids in myocardial mitochondria. We conclude that there is a possible role of oxidized lipids and protein through LOX-1 and/or RAGE signalling.
Bibliography:	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 Current address: Department of Zoology, Shri Venkateshwara University, Tirupati, India. A.K.L. is employed by Lovelace Respiratory Research Institute. The authors declare they have no actual or potential competing financial interests.
ISSN:	0091-6765 1552-9924
DOI:	10.1289/ehp.1002386