Evidence map›Paper›PMID 30124840›Full record

ReviewEuropean heart journal2018

Effects of gaseous and solid constituents of air pollution on endothelial function.

Thomas Münzel, Tommaso Gori, Sadeer Al-Kindi, John Deanfield, Jos Lelieveld, Andreas Daiber, Sanjay Rajagopalan

Open access · hybridAbstract readReview
In one paragraph

Review in European heart journal, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 156 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
156citing papers in PubMed, 4 pooled it
15.5field-weighted citation impact, top 1% 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

156 citing papers in PubMed, 4 syntheses or guidelines pooled it, 378 citations in OpenAlex.

  1. Association between PMBMC public health · 2026
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96 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 6 institutions in 3 countries.

Thomas MünzelCenter for Cardiology, Cardiology I, Angiology and Intensive Care Medicine, University Medical Center of the Johannes Gutenberg University, Langenbeckstrasse 1, Mainz, Germany.
Tommaso GoriCenter for Cardiology, Cardiology I, Angiology and Intensive Care Medicine, University Medical Center of the Johannes Gutenberg University, Langenbeckstrasse 1, Mainz, Germany.
Sadeer Al-KindiDivision of Cardiovascular Medicine, Harrington Heart and Vascular Institute, Case Western Reserve School of Medicine, 11100 Euclid Ave, Cleveland, OH, USA.
John DeanfieldUCL Institute of Cardiovascular Science, 170 Tottenham Court Road, London, UK.
Jos LelieveldAtmospheric Chemistry Department, Max Planck Institute for Chemistry, Hahn-Meitner-Weg 1, Mainz, Germany.
Andreas DaiberCenter for Cardiology, Cardiology I, Angiology and Intensive Care Medicine, University Medical Center of the Johannes Gutenberg University, Langenbeckstrasse 1, Mainz, Germany.
Sanjay RajagopalanDivision of Cardiovascular Medicine, Harrington Heart and Vascular Institute, Case Western Reserve School of Medicine, 11100 Euclid Ave, Cleveland, OH, USA.
Case Western Reserve University · USGerman Centre for Cardiovascular Research · DEJohannes Gutenberg University Mainz · DEMax Planck Institute for Chemistry · DEUniversity College London · GBUniversity Medical Center of the Johannes Gutenberg University Mainz · DE

Funding

Air Pollution and Hypertension: Vascular MechanismsR01ES015146 · NIEHS · UNIVERSITY OF MARYLAND BALTIMORE · PI RAJAGOPALAN, SANJAY · 2007 to 2018
$4.5M
NIEHS NIH HHS R01 ES015146
6 · The paper itself

Abstract

Ambient air pollution is a leading cause of non-communicable disease globally. The largest proportion of deaths and morbidity due to air pollution is now known to be due to cardiovascular disorders. Several particulate and gaseous air pollutants can trigger acute events (e.g. myocardial infarction, stroke, heart failure). While the mechanisms by which air pollutants cause cardiovascular events is undergoing continual refinement, the preponderant evidence support rapid effects of a diversity of pollutants including all particulate pollutants (e.g. course, fine, ultrafine particles) and gaseous pollutants such as ozone, on vascular function. Indeed alterations in endothelial function seem to be critically important in transducing signals and eventually promoting cardiovascular disorders such as hypertension, diabetes, and atherosclerosis. Here, we provide an updated overview of the impact of particulate and gaseous pollutants on endothelial function from human and animal studies. The evidence for causal mechanistic pathways from both animal and human studies that support various hypothesized general pathways and their individual and collective impact on vascular function is highlighted. We also discuss current gaps in knowledge and evidence from trials evaluating the impact of personal-level strategies to reduce exposure to fine particulate matter (PM2.5) and impact on vascular function, given the current lack of definitive randomized evidence using hard endpoints. We conclude by an exhortation for formal inclusion of air pollution as a major risk factor in societal guidelines and provision of formal recommendations to prevent adverse cardiovascular effects attributable to air pollution.

Indexed as

Air PollutantsAir PollutionAnimalsCardiovascular DiseasesEndothelium, VascularEnvironmental ExposureGreenhouse GasesHumansOxidative StressParticulate MatterRisk FactorsAir PollutantsGreenhouse GasesParticulate Matter

Identifiers

PMID30124840
PMCPMC6174028
OpenAlexW2887797512

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.