Evidence map›Paper›PMID 19395667›Full record

ArticleAmerican journal of physiology. Lung cellular and molecular physiology2009

Pulmonary ozone exposure induces vascular dysfunction, mitochondrial damage, and atherogenesis.

Gin C Chuang, Zhen Yang, David G Westbrook, Melissa Pompilius, Carol A Ballinger, C Roger White, David M Krzywanski, Edward M Postlethwait, Scott W Ballinger

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Lung cellular and molecular physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
74citing papers in PubMed, 2 pooled it
8.0field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

74 citing papers in PubMed, 2 syntheses or guidelines pooled it, 135 citations in OpenAlex.

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14 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 1 institution in 1 country.

Gin C ChuangDepartment of Pathology, University of Alabama at Birmingham, USA.
Zhen Yang
David G Westbrook
Melissa Pompilius
Carol A Ballinger
C Roger White
David M Krzywanski
Edward M Postlethwait
Scott W Ballinger
University of Alabama at Birmingham · US

Funding

Project 4 - Dosimetry Modeling and Interspecies ExtrapolationP01ES011617 · NIEHS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI POSTLETHWAIT, EDWARD M · 2003 to 2010
$11.5M
UAB Diabetes Research and Training CenterP60DK079626 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI GARVEY, W TIMOTHY · 2008 to 2012
$8.4M
Gestational cigarette smoke exposure increases adult CVDR01HL077419 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI BALLINGER, SCOTT W. · 2004 to 2008
$1.7M
SURFACE LINING LAYER DEPENDENT OXIDANT LUNG INJURYR01HL054696 · NHLBI · UNIVERSITY OF TEXAS MEDICAL BR GALVESTON · PI POSTLETHWAIT, EDWARD M · 1996 to 2006
$1.4M
Mitochondrial integrity and function in atherogenesisR01ES011172 · NIEHS · UNIVERSITY OF TEXAS MEDICAL BR GALVESTON · PI BALLINGER, SCOTT W · 2001 to 2005
$1.1M
NHLBI NIH HHS HL-054696NHLBI NIH HHS HL-77419NHLBI NIH HHS R01 HL054696NHLBI NIH HHS R01 HL077419NIDDK NIH HHS DK-079626NIEHS NIH HHS ES-11172NIEHS NIH HHS P01 ES011617NIEHS NIH HHS P01-ES-11617NIEHS NIH HHS R01 ES011172
6 · The paper itself

Abstract

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.

Indexed as

Air PollutantsAnimalsAortaAtherosclerosisBlood PressureDNA DamageDNA, MitochondrialHeart RateLung DiseasesMacaca mulattaMaleMiceMice, Inbred C57BLMitochondriaMitochondrial DiseasesNitrates3-nitrotyrosineAir PollutantsDNA, MitochondrialNitratesNitric OxideNitric Oxide Synthase Type IIINitritesNos3 protein, mouseOxidantsOzoneSuperoxide DismutaseSuperoxide Dismutase 2Tyrosine

Identifiers

PMID19395667
PMCPMC2742788
OpenAlexW2016752913

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.