Vascular and cardiac impairments in rats inhaling ozone and diesel exhaust particles
Open accessAbstract
BACKGROUND: Mechanisms of cardiovascular injuries from exposure to gas and particulate air pollutants are unknown. OBJECTIVE: We sought to determine whether episodic exposure of rats to ozone or diesel exhaust 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 to air, ozone (0.4 ppm), DEP (2.1 mg/m(3)), or ozone (0.38 ppm) + DEP (2.2 mg/m(3)) for 5 hr/day, 1 day/week for 16 weeks, or to air, ozone (0.51 or 1.0 ppm), or DEP (1.9 mg/m(3)) for 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 stress (hemeoxygenase-1), thrombosis (tissue 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 cardiac 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 signaling.
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Animal studies with high ozone exposures have generated more consistent findings on cardiovascular effects of ozone through altering vascular tone, mRNA for genes encoding thrombogenic factors, and atherogenesis.
“In contrast, animal studies with high ozone exposures have generated more consistent findings on cardiovascular effects of ozone through altering vascular tone (60–62), mRNA for genes encoding thrombogenic factors (63), and atherogenesis (60).”
From Ozone pollution: A Major health hazard worldwide (2019) · cites this paper as [63]
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Ozone pollution: A Major health hazard worldwide
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- Authors
- Kodavanti, U. P., Thomas, R., Ledbetter, A. D., Schladweiler, M. C., Shannahan, J. H., Wallenborn, J. G., Lund, A. K., Campen, M. J., Butler, E. O., Gottipolu, R. R., Nyska, A., Richards, J. E., Andrews, D., Jaskot, R. H., McKee, J., Kotha, S. R., Patel, R. B., & Parinandi, N. L.
- Affiliations
- Environmental Protection Agency (US)
- Curriculum in Toxicology and
- University of North Carolina at Chapel Hill (US)
- Lovelace Respiratory Research Institute (US)
- University of New Mexico (US)
- The Ohio State University Wexner Medical Center (US)
- Tel Aviv University (IL)
- Research Core Units, National Health and Environmental Effects Research Laboratory, Office of Research and Development, U.S. Environmental Protection Agency, Research Triangle Park, North Carolina, USA
- Corresponding author
- Kodavanti, Urmila P.
- ORCID
- Venue
- Environmental Health Perspectives
- Publisher
- American Chemical Society (ACS)
- Published
- 2010-10-27
- Volume
- 119
- Issue
- 3
- Pages
- 312-318
- ISSN
- 0091-6765 (ISSN-L)
- 1552-9924
- PMC
- PMC3059992
- OpenAlex
- W2005048980
- Cited by
- 119
- References
- 41
- Citations by year
- 2026: 4 · 2025: 8 · 2024: 5 · 2023: 6 · 2022: 3 · 2021: 9 · 2020: 5 · 2019: 8 · 2018: 8 · 2017: 7 · 2016: 9 · 2015: 10 · 2014: 10 · 2013: 11 · 2012: 11
- FWCI
- 6.60
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- public-domain
- creativecommons.org/licenses/by/4.0/ (vor, 2620 d)
- Locations
- Environmental Health Perspectives (publishedVersion, public-domain)
- PubMed Central (publishedVersion, public-domain)
- PubMed (publishedVersion)
- Carolina Digital Repository (University of North Carolina at Chapel Hill) (submittedVersion)
- UNC Libraries
- Funders
- U.S. Environmental Protection Agency
- National Institute of Environmental Health Sciences (R00ES016586, R01ES014639)
- Topics
- Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Air Quality and Health Impacts
- Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
- Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Indoor Air Quality and Microbial Exposure
- Keywords
- ozone, diesel exhaust particles, cardiovascular damage, air pollution, oxidative stress, heme oxygenase-1, thrombosis, vasoconstriction, LOX-1, RAGE, aorta, lung injury, oxidative stress biomarkers, particulate matter, acute exposure, long-term exposure, rats, combined pollutant exposure
- MeSH terms
- Air Pollutants, Animals, Vehicle Emissions, Cardiovascular System, Inflammation, Male, Ozone, Rats, Inbred WKY, Thrombosis, Vasoconstriction, Biomarkers, Oxidative Stress, Rats, Particulate Matter
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