Evidence map›Paper›PMID 31373329›Full record

ArticleInternational journal of environmental research and public health2019

E-cigarette Aerosol Condensate Enhances Metabolism of Benzo(a)pyrene to Genotoxic Products, and Induces CYP1A1 and CYP1B1, Likely by Activation of the Aryl Hydrocarbon Receptor.

Yuan-Wan Sun, Wieslawa Kosinska, Joseph B Guttenplan

Open access · goldAbstract read
In one paragraph

Article in International journal of environmental research and public health, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.9field-weighted citation impact, top 31% 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

15 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. E-Cigarette effects on oral health: A molecular perspective.Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association · 2025
    Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. Review
  10. E-Cigarette Toxicology.Annual review of pharmacology and toxicology · 2022
    Review
  11. Article
  12. Electronic Cigarettes and Oral Health.Journal of dental research · 2021
    Article
  13. Review
  14. Review
  15. 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

3 authors at 2 institutions in 1 country.

Yuan-Wan SunDepartment of Biochemistry and Molecular Biology, Pennsylvania State University, Hershey, PA 17033, USA.
Wieslawa KosinskaDepartment of Basic Science, New York University College of Dentistry, New York, NY 10010, USA.
Joseph B GuttenplanDepartment of Basic Science, New York University College of Dentistry, New York, NY 10010, USA. jbg1@nyu.edu.
New York University · USPenn State Milton S. Hershey Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

E-cigarette aerosol contains lower levels of most known carcinogens than tobacco smoke, but many users of e-cigarettes are also smokers, and these individuals may be vulnerable to possible promoting and/or cocarcinogenic effects of e-cigarettes. We investigated the possibility that a condensate of e-cigarette aerosol (EAC) enhances the metabolism of the tobacco carcinogen, benzo(a)pyrene (BaP), to genotoxic products in a human oral keratinocyte cell line. Cells were pretreated with EAC from two popular e-cigs and then with BaP. Metabolism to its ultimate carcinogenic metabolite, anti-7,8-dihydroxy-9,10-epoxy-7,8,9,10-tetrahydro B[a]P (BPDE), was assayed by measuring isomers of its spontaneous hydrolysis products, BaP tetrols. The pretreatment of cells with EAC enhanced the rate of BaP tetrol formation several fold. Pretreatment with the e-liquid resulted in a smaller enhancement. The treatment of cells with EAC induced CYP1A1/1B1 mRNA and protein. The enhancement of BaP tetrol formation was inhibited by the aryl hydrocarbon receptor (AhR) inhibitor, α-napthoflavone, indicating EAC likely induces CYP1A1/1B1 and enhances BaP metabolism by activating the AhR. To our knowledge, this is first report demonstrating that e-cigarettes can potentiate the genotoxic effects of a tobacco smoke carcinogen.

Indexed as

AerosolsBasic Helix-Loop-Helix ProteinsBenzo(a)pyreneCarcinogensCell Line, TumorCytochrome P-450 CYP1A1Cytochrome P-450 CYP1B1Electronic Nicotine Delivery SystemsHumansMutagensReceptors, Aryl HydrocarbonSmokeAerosolsAHR protein, humanBasic Helix-Loop-Helix ProteinsBenzo(a)pyreneCarcinogensCYP1A1 protein, humanCYP1B1 protein, humanCytochrome P-450 CYP1A1Cytochrome P-450 CYP1B1MutagensReceptors, Aryl HydrocarbonSmokeaerosolaryl hydrocarbon receptorbenzo(a)pyreneCYP1A1CYP1B1E-cigarette

Identifiers

PMID31373329
PMCPMC6678103
OpenAlexW2957915547

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.