Evidence map›Paper›PMID 21184614›Full record

ArticleChemical research in toxicology2011

Immediate consequences of cigarette smoking: rapid formation of polycyclic aromatic hydrocarbon diol epoxides.

Yan Zhong, Steven G Carmella, Pramod Upadhyaya, J Bradley Hochalter, Diane Rauch, Andrew Oliver, Joni Jensen, Dorothy Hatsukami, Jing Wang, Cheryl Zimmerman and 1 more

Abstract read
In one paragraph

Article in Chemical research in toxicology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 3 pooled it
3.4field-weighted citation impact, top 8% 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

25 citing papers in PubMed, 3 syntheses or guidelines pooled it, 55 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Trial
  5. Trial
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Biomarkers of exposure to new and emerging tobacco delivery products.American journal of physiology. Lung cellular and molecular physiology · 2017
    Review
  15. Article
  16. Biomarkers of Tobacco Exposure: Summary of an FDA-Sponsored Public Workshop.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2017
    Article
  17. Article
  18. Article
  19. Article
  20. 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

11 authors at 2 institutions in 2 countries.

Yan ZhongMasonic Cancer Center and Department of Pharmacology, University of Minnesota, MMC 806, 420 Delaware Street, SE, Minneapolis, Minnesota 55455, United States.
Steven G Carmella
Pramod Upadhyaya
J Bradley Hochalter
Diane Rauch
Andrew Oliver
Joni Jensen
Dorothy Hatsukami
Jing Wang
Cheryl Zimmerman
Stephen S Hecht
University of Minnesota · USPharmac · NZ

Funding

Women's CancerP30CA077598 · NCI · UNIVERSITY OF MINNESOTA TWIN CITIES · PI Douglas Yee · 1998 to 2026
$100.4M
Benzo(a) pyrene Metabolism: Phenotyping and GenotypingR01CA092025 · NCI · UNIVERSITY OF MINNESOTA TWIN CITIES · PI HECHT, STEPHEN S · 2001 to 2016
$5.0M
NCI NIH HHS CA-77598NCI NIH HHS CA-92025NCI NIH HHS P30 CA077598NCI NIH HHS R01 CA092025
6 · The paper itself

Abstract

Polycyclic aromatic hydrocarbons (PAH) are among the likely major causative agents for lung cancer in smokers. PAH require metabolic activation to exert their carcinogenic effects, and one important pathway proceeds through a three-step sequence resulting in the formation of diol epoxides, which react with DNA to produce adducts that can cause mutations and initiate the carcinogenic process. However, no previous published studies have examined this critical pathway in humans specifically exposed to PAH by inhalation of cigarette smoke. This study used a unique approach employing a stable isotope derivative of phenanthrene, the simplest PAH with a bay region, a feature closely associated with PAH carcinogenicity. Twelve subjects each smoked a cigarette to which [D(10)]phenanthrene had been added. Plasma was analyzed for [D(10)]r-1,t-2,3,c-4-tetrahydroxy-1,2,3,4-tetrahydrophenanthrene ([D(10)]PheT), the major end product of the diol epoxide metabolism pathway of phenanthrene. The analysis was performed by gas chromatography--negative ion chemical ionization--tandem mass spectrometry, using [(13)C(6)]PheT as internal standard. The results demonstrated that the three-step pathway resulting in the formation of diol epoxides, as monitored by [D(10)]PheT, occurred with remarkable rapidity. Levels of [D(10)]PheT in plasma of all subjects were maximal at the earliest time points examined, 15-30 min after smoking the cigarette containing [D(10)]phenanthrene, and decreased thereafter. These results demonstrate that the formation of a PAH diol epoxide occurs rapidly in smokers. Because PAH diol epoxides are mutagenic and carcinogenic, the results clearly demonstrate immediate negative health consequences of smoking, which should serve as a major warning to anyone contemplating initiating tobacco use.

Indexed as

Epoxy CompoundsHumansPhenanthrenesPolycyclic Aromatic HydrocarbonsSmokingEpoxy CompoundsPhenanthrenesPolycyclic Aromatic Hydrocarbonsr-1,t-2,3,c-4-tetrahydroxy-1,2,3,4-tetrahydrophenanthrene

Identifiers

PMID21184614
PMCPMC3042042
OpenAlexW2075177446

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.