Evidence map›Paper›PMID 27701119›Full record

ArticleToxicological sciences : an official journal of the Society of Toxicology2017

Molecular Impact of Electronic Cigarette Aerosol Exposure in Human Bronchial Epithelium.

Elizabeth Moses, Teresa Wang, Sean Corbett, George R Jackson, Eduard Drizik, Catalina Perdomo, Claudia Perdomo, Eric Kleerup, Daniel Brooks, George O'Connor and 4 more

Open access · bronzeAbstract readValidation Study
In one paragraph

Article in Toxicological sciences : an official journal of the Society of Toxicology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed, 2 pooled it
5.1field-weighted citation impact, top 5% 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

39 citing papers in PubMed, 2 syntheses or guidelines pooled it, 70 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Vaping and Lung Inflammation and Injury.Annual review of physiology · 2022
    Review
  15. Article
  16. The chemistry and toxicology of vaping.Pharmacology & therapeutics · 2021
    Review
  17. Recent updates on biomarkers of exposure and systemic toxicity in e-cigarette users and EVALI.American journal of physiology. Lung cellular and molecular physiology · 2021
    Review
  18. Review
  19. Reactive Oxygen Species, Mitochondrial Membrane Potential, and Cellular Membrane Potential Are Predictors of E-Liquid Induced Cellular Toxicity.Nicotine & tobacco research : official journal of the Society for Research on Nicotine and Tobacco · 2020
    Article
  20. Dose-Dependent Pulmonary Toxicity of Aerosolized Vitamin E Acetate.American journal of respiratory cell and molecular biology · 2020
    Article
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

14 authors at 3 institutions in 1 country.

Elizabeth MosesSection of Computational Biomedicine, Department of Medicine Boston University School of Medicine, Boston, Massachusetts 02118.
Teresa WangSection of Computational Biomedicine, Department of Medicine Boston University School of Medicine, Boston, Massachusetts 02118.
Sean CorbettSection of Computational Biomedicine, Department of Medicine Boston University School of Medicine, Boston, Massachusetts 02118.
George R JacksonMatTek Corporation, Ashland, Massachusetts 01721.
Eduard DrizikSection of Computational Biomedicine, Department of Medicine Boston University School of Medicine, Boston, Massachusetts 02118.
Catalina PerdomoSection of Computational Biomedicine, Department of Medicine Boston University School of Medicine, Boston, Massachusetts 02118.
Claudia PerdomoUniversity of California Los Angeles, Los Angeles, California 90095.
Eric KleerupUniversity of California Los Angeles, Los Angeles, California 90095.
Daniel BrooksDepartment of Epidemiology, Boston University School of Public Health, Boston, Massachusetts 02118.
George O'ConnorPulmonary Center, Boston University School of Medicine, Boston, Massachusetts 02118.
Steven DubinettUniversity of California Los Angeles, Los Angeles, California 90095.
Patrick HaydenMatTek Corporation, Ashland, Massachusetts 01721.
Marc E LenburgSection of Computational Biomedicine, Department of Medicine Boston University School of Medicine, Boston, Massachusetts 02118; mlenburg@bu.edu.
Avrum SpiraSection of Computational Biomedicine, Department of Medicine Boston University School of Medicine, Boston, Massachusetts 02118.
Boston University · USUniversity of California, Los Angeles · USMatTek Corporation (United States) · US

Funding

BIOLOGY OF THE LUNG--MULTIDISCIPLINARY PROGRAMT32HL007035 · NHLBI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI Darrell N. Kotton, JOSEPH P MIZGERD · 1985 to 2026
$24.3M
The UCLA - Boston University Lung Cancer Biomarker Development LaboratoryU01CA152751 · NCI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI DUBINETT, STEVEN M., ELASHOFF, DAVID · 2010 to 2015
$5.0M
NCI NIH HHS U01 CA152751NHLBI NIH HHS T32 HL007035
6 · The paper itself

Abstract

Little evidence is available regarding the physiological effects of exposure to electronic cigarette (ECIG) aerosol. We sought to determine the molecular impact of ECIG aerosol exposure in human bronchial epithelial cells (HBECs). Gene-expression profiling was conducted in primary grown at air liquid interface and exposed to 1 of 4 different ECIG aerosols, traditional tobacco cigarette (TCIG) smoke, or clean air. Findings were validated experimentally with quantitative polymerase chain reaction and a reactive oxygen species immunoassay. Using gene set enrichment analysis, signatures of in vitro ECIG exposure were compared with those generated from bronchial epithelial brushings of current TCIG smokers and former TCIG smokers currently using ECIGs. We found 546 genes differentially expressed across the ECIG, TCIG, and air-exposed groups of HBECs (ANOVA; FDR q < .05; fold change > 1.5). A subset of these changes were shared between TCIG- and ECIG-exposed HBECs. ECIG exposure induced genes involved in oxidative and xenobiotic stress pathways and increased a marker of reactive oxygen species production in a dose-dependent manner. ECIG exposure decreased expression of genes involved in cilia assembly and movement. Furthermore, gene-expression differences observed in vitro were concordant with differences observed in airway epithelium collected from ECIG users (q < .01). In summary, our data suggest that ECIG aerosol can induce gene-expression changes in bronchial airway epithelium in vitro, some of which are shared with TCIG smoke. These changes were generally less pronounced than the effects of TCIG exposure and were more pronounced in ECIG products containing nicotine than those without nicotine. Our data further suggest that the gene-expression alterations seen with the in vitro exposure system reflects the physiological effects experienced in vivo by ECIG users.

Indexed as

AerosolsElectronic Nicotine Delivery SystemsBronchiEpitheliumHumansReal-Time Polymerase Chain ReactionAerosolselectronic cigarette.gene expressionsmoketobacco

Identifiers

PMID27701119
PMCPMC5216655
OpenAlexW2529428100

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.