Evidence map›Paper›PMID 27303906›Full record

ReviewAnnals of the New York Academy of Sciences2016

Chlorine-induced cardiopulmonary injury.

Matthew Carlisle, Adam Lam, Erik R Svendsen, Saurabh Aggarwal, Sadis Matalon

Open access · greenAbstract readReview
In one paragraph

Review in Annals of the New York Academy of Sciences, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
3.6field-weighted citation impact, top 7% 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

31 citing papers in PubMed, 45 citations in OpenAlex.

  1. A human airway-on-a-chip microphysiological system for modeling chlorine gas toxicity.Toxicological sciences : an official journal of the Society of Toxicology · 2026
    Article
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  9. Countermeasures against Pulmonary Threat Agents.The Journal of pharmacology and experimental therapeutics · 2024
    Review
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  15. Article
  16. Review
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  19. Review
  20. Hyaluronan and halogen-induced airway hyperresponsiveness and lung injury.Annals of the New York Academy of Sciences · 2020
    Review
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

5 authors at 2 institutions in 1 country.

Matthew CarlisleDepartment of Anesthesiology and Perioperative Medicine, University of Alabama at Birmingham, Birmingham, Alabama.
Adam LamDepartment of Anesthesiology and Perioperative Medicine, University of Alabama at Birmingham, Birmingham, Alabama.
Erik R SvendsenDepartment of Public Health Sciences, Medical University of South Carolina, Charleston, South Carolina.
Saurabh AggarwalDepartment of Anesthesiology and Perioperative Medicine, University of Alabama at Birmingham, Birmingham, Alabama.
Sadis MatalonDepartment of Anesthesiology and Perioperative Medicine, University of Alabama at Birmingham, Birmingham, Alabama.
University of Alabama at Birmingham · USMedical University of South Carolina · US

Funding

Bromine Inhalation Induced Lung Injury: Novel Mechanisms and Treatment StrategiesU01ES026458 · NIEHS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI MATALON, SADIS · 2015 to 2019
$3.9M
Long-Term Lung Health After Exposure to Chlorine GasR01ES015532 · NIEHS · UNIVERSITY OF SOUTH CAROLINA AT COLUMBIA · PI SVENDSEN, ERIK ROBERT · 2010 to 2014
$2.7M
Central Role of Heme Oxygenase in Reversing Bromine Morbidity and MortalityR21ES025423 · NIEHS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI AGARWAL, ANUPAM, MATALON, SADIS · 2014 to 2015
$771k
Mitochondrial Bioenergetic Dysfunction and Chlorine ToxicityR21ES024027 · NIEHS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI DARLEY-USMAR, VICTOR M, MATALON, SADIS · 2013 to 2014
$735k
Mechanisms and countermeasures of halogen-induced injury to pregnant miceR21ES026829 · NIEHS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI JILLING, TAMAS SANDOR, MATALON, SADIS · 2015 to 2015
$351k
NIEHS NIH HHS R01 ES015532NIEHS NIH HHS R21 ES024027NIEHS NIH HHS R21 ES025423NIEHS NIH HHS R21 ES026829NIEHS NIH HHS U01 ES026458
6 · The paper itself

Abstract

Chlorine (Cl2 ) is utilized worldwide for a diverse range of industrial applications, including pulp bleaching, sanitation, and pharmaceutical development. Though Cl2 has widespread use, little is known regarding the mechanisms of toxicity associated with Cl2 exposure, which occurs during industrial accidents or acts of terrorism. Previous instances of Cl2 exposure have led to reported episodes of respiratory distress that result in high morbidity and mortality. Furthermore, studies suggest that acute Cl2 exposure also results in systemic vascular injury and subsequent myocardial contractile dysfunction. Here, we review both lung and cardiac pathology associated with acute Cl2 inhalation and discuss recently published data that suggest that mitochondrial dysfunction underlies the pathogenesis of Cl2 -induced toxicity. Last, we discuss our findings that suggest that upregulation of autophagy protects against Cl2 -induced lung inflammation and can be a potential therapeutic target for ameliorating the toxic effects of Cl2 exposure.

Indexed as

AnimalsChlorineEnvironmental ExposureHeart InjuriesHumansLung InjuryMitochondriaPublic HealthChlorineautophagycardiac injurychlorinelung injurymitochondrial dysfunction

Identifiers

PMID27303906
PMCPMC4940235
OpenAlexW2421826484

What OpenQuestion holds

Textmetadata
LicenceTDM
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.