Evidence map›Paper›PMID 22138703›Full record

ArticleEnvironmental health perspectives2012

Overt and latent cardiac effects of ozone inhalation in rats: evidence for autonomic modulation and increased myocardial vulnerability.

Aimen K Farraj, Mehdi S Hazari, Darrell W Winsett, Anthony Kulukulualani, Alex P Carll, Najwa Haykal-Coates, Christina M Lamb, Edwin Lappi, Dock Terrell, Wayne E Cascio and 1 more

Open access · diamondAbstract read
In one paragraph

Article in Environmental health perspectives, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 2 pooled it
2.1field-weighted citation impact, top 16% 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

20 citing papers in PubMed, 2 syntheses or guidelines pooled it, 43 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Article
  5. Mild allergic airways responses to an environmental mixture increase cardiovascular risk in rats.Toxicological sciences : an official journal of the Society of Toxicology · 2023
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  20. Inhaled matters of the heart.Cardiovascular regenerative medicine
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors at 2 institutions in 1 country.

Aimen K FarrajEnvironmental Public Health Division, National Health and Environmental Effects Research Laboratory, U.S. Environmental Protection Agency, Research Triangle Park, North Carolina 27711, USA. farraj.aimen@epa.gov
Mehdi S Hazari
Darrell W Winsett
Anthony Kulukulualani
Alex P Carll
Najwa Haykal-Coates
Christina M Lamb
Edwin Lappi
Dock Terrell
Wayne E Cascio
Daniel L Costa
Environmental Protection Agency · USUniversity of North Carolina at Chapel Hill · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundOzone (O₃) is a well-documented respiratory oxidant, but increasing epidemiological evidence points to extrapulmonary effects, including positive associations between ambient O₃ concentrations and cardiovascular morbidity and mortality.

objectiveWith preliminary reports linking O₃ exposure with changes in heart rate (HR), we investigated the hypothesis that a single inhalation exposure to O₃ will cause concentration-dependent autonomic modulation of cardiac function in rats.

methodsRats implanted with telemeters to monitor HR and cardiac electrophysiology [electrocardiography (ECG)] were exposed once by whole-body inhalation for 4 hr to 0.2 or 0.8 ppm O₃ or filtered air. A separate cohort was tested for vulnerability to aconitine-induced arrhythmia 24 hr after exposure.

resultsExposure to 0.8 ppm O₃ caused bradycardia, PR prolongation, ST depression, and substantial increases in atrial premature beats, sinoatrial block, and atrioventricular block, accompanied by concurrent increases in several HR variability parameters that were suggestive of increased parasympathetic tone. Low-O₃ exposure failed to elicit any overt changes in autonomic tone, heart rhythm, or ECG. However, both 0.2 and 0.8 ppm O₃ increased sensitivity to aconitine-induced arrhythmia formation, suggesting a latent O₃-induced alteration in myocardial excitability.

conclusionsO₃ exposure causes several alterations in cardiac electrophysiology that are likely mediated by modulation of autonomic input to the heart. Moreover, exposure to low O₃ concentrations may cause subclinical effects that manifest only when triggered by a stressor, suggesting that the adverse health effects of ambient levels of air pollutants may be insidious and potentially underestimated.

Indexed as

Heart RateInhalation ExposureAconitineAnimalsArrhythmias, CardiacAutonomic AgentsCohort StudiesDose-Response Relationship, DrugElectrocardiographyHeartMaleOxidants, PhotochemicalOzoneRatsRats, Inbred SHRTelemetryAconitineAutonomic AgentsOxidants, PhotochemicalOzone

Identifiers

PMID22138703
PMCPMC3295357
OpenAlexW2029752625

What OpenQuestion holds

Textmetadata
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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.