The DOI matches its Crossref record; 51 of the 51 references it cites were found in a registry or an index.
Pulmonary ozone exposure induces vascular dysfunction, mitochondrial damage, and atherogenesis
Open accessAbstract
More than 100 million people in the United States live in areas that exceed current ozone air quality standards. In addition to its known pulmonary effects, environmental ozone exposures have been associated with increased hospital admissions related to cardiovascular events, but to date, no studies have elucidated the potential molecular mechanisms that may account for exposure-related vascular impacts. Because of the known pulmonary redox and immune biology stemming from ozone exposure, we hypothesized that ozone inhalation would initiate oxidant stress, mitochondrial damage, and dysfunction within the vasculature. Accordingly, these factors were quantified in mice consequent to a cyclic, intermittent pattern of ozone or filtered air control exposure. Ozone significantly modulated vascular tone regulation and increased oxidant stress and mitochondrial DNA damage (mtDNA), which was accompanied by significantly decreased vascular endothelial nitric oxide synthase protein and indices of nitric oxide production. To examine influences on atherosclerotic lesion formation, apoE-/- mice were exposed as above, and aortic plaques were quantified. Exposure resulted in significantly increased atherogenesis compared with filtered air controls. Vascular mitochondrial damage was additionally quantified in ozone- and filtered air-exposed infant macaque monkeys. These studies revealed that ozone increased vascular mtDNA damage in nonhuman primates in a fashion consistent with known atherosclerotic lesion susceptibility in humans. Consequently, inhaled ozone, in the absence of other environmental toxicants, promotes increased vascular dysfunction, oxidative stress, mitochondrial damage, and atherogenesis.
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“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 [60]
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Cited by
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Ozone pollution: A Major health hazard worldwide
Zhang, J. (., Wei, Y., & Fang, Z. (2019) · Frontiers in Immunology · doi:10.3389/fimmu.2019.02518 · Cited by 828
Oxidative stress and air pollution exposure
Lodovici, M., & Bigagli, E. (2011) · Journal of Toxicology · doi:10.1155/2011/487074 · Cited by 720
The effects of ozone on human health
Nuvolone, D., Petri, D., & Voller, F. (2018) · Environmental Science and Pollution Research · doi:10.1007/s11356-017-9239-3 · Cited by 619
Integration of cellular bioenergetics with mitochondrial quality control and autophagy
Hill, B. G., Benavides, G. A., Lancaster, J. R., Ballinger, S. W., Dell’Italia, L., Zhang, J., & Darley-Usmar, V. M. (2012) · Biological Chemistry · doi:10.1515/hsz-2012-0198 · Cited by 495
Oxidative stress pathways of air pollution mediated toxicity: Recent insights
Gangwar, R. S., Bevan, G. H., Palanivel, R., Das, L. M., & Rajagopalan, S. (2020) · Redox Biology · doi:10.1016/j.redox.2020.101545 · Cited by 428
Metadata
- Authors
- Chuang, G. C., Yang, Z., Westbrook, D. G., Pompilius, M., Ballinger, C. A., White, C. R., Krzywanski, D. M., Postlethwait, E. M., & Ballinger, S. W.
- Affiliations
- University of Alabama at Birmingham (US)
- ORCID
- Venue
- American Journal of Physiology-Lung Cellular and Molecular Physiology
- Publisher
- American Physiological Society
- Published
- 2009-08
- Volume
- 297
- Issue
- 2
- Pages
- L209-L216
- ISSN
- 1040-0605 (ISSN-L)
- 1522-1504
- PMC
- PMC2742788
- OpenAlex
- W2016752913
- Cited by
- 145
- References
- 51
- Citations by year
- 2026: 4 · 2025: 5 · 2024: 7 · 2023: 4 · 2022: 9 · 2021: 12 · 2020: 11 · 2019: 6 · 2018: 4 · 2017: 13 · 2016: 3 · 2015: 14 · 2014: 5 · 2013: 14 · 2012: 8
- FWCI
- 8.05
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- American Journal of Physiology-Lung Cellular and Molecular Physiology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Heart, Lung, and Blood Institute (HL 77419, HL-054696, R01HL054696, R01HL077419)
- National Institute of Diabetes and Digestive and Kidney Diseases (DK079626)
- National Institute of Environmental Health Sciences (P01-ES11617, ES11172, R01ES011172, P01ES011617)
- Topics
- Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Air Quality and Health Impacts
- Health Sciences › Medicine › Physiology (medical) › Nitric Oxide and Endothelin Effects
- Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
- Keywords
- ozone inhalation, vascular dysfunction, mitochondrial DNA damage, oxidative stress, atherogenesis, endothelial nitric oxide synthase, nitric oxide production, vascular tone regulation, aortic plaque, ApoE-deficient mice, air pollution health effects, cardiovascular risk
- MeSH terms
- Superoxide Dismutase 2, Air Pollutants, Animals, Aorta, Blood Pressure, DNA Damage, DNA, Mitochondrial, Heart Rate, Lung Diseases, Macaca mulatta, Male, Mice, Inbred C57BL, Mitochondria, Nitrates, Nitric Oxide, Nitrites, Ozone, Superoxide Dismutase, Tyrosine, Oxidants, Oxidative Stress, Mitochondrial Diseases, Atherosclerosis, Mice, Nitric Oxide Synthase Type III
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