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

Research output: Contribution to journalArticle

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.

Original languageEnglish (US)
Article number2468
JournalInternational journal of environmental research and public health
Volume16
Issue number14
DOIs
StatePublished - Jul 2 2019

Fingerprint

Aryl Hydrocarbon Receptors
Cytochrome P-450 CYP1A1
Aerosols
Tobacco Products
Carcinogens
Tobacco
Smoke
7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide
Benzo(a)pyrene
Keratinocytes
Hydrolysis
Cell Line
Messenger RNA
pyrene
Electronic Cigarettes
Proteins

All Science Journal Classification (ASJC) codes

  • Public Health, Environmental and Occupational Health
  • Health, Toxicology and Mutagenesis

Cite this

@article{c1da89130af14c28b8c2a50434eabe35,
title = "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",
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.",
author = "Sun, {Yuan Wan} and Wieslawa Kosinska and Guttenplan, {Joseph B.}",
year = "2019",
month = "7",
day = "2",
doi = "10.3390/ijerph16142468",
language = "English (US)",
volume = "16",
journal = "International Journal of Environmental Research and Public Health",
issn = "1661-7827",
publisher = "Multidisciplinary Digital Publishing Institute (MDPI)",
number = "14",

}

TY - JOUR

T1 - 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

AU - Sun, Yuan Wan

AU - Kosinska, Wieslawa

AU - Guttenplan, Joseph B.

PY - 2019/7/2

Y1 - 2019/7/2

N2 - 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.

AB - 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.

UR - http://www.scopus.com/inward/record.url?scp=85070377907&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85070377907&partnerID=8YFLogxK

U2 - 10.3390/ijerph16142468

DO - 10.3390/ijerph16142468

M3 - Article

C2 - 31373329

AN - SCOPUS:85070377907

VL - 16

JO - International Journal of Environmental Research and Public Health

JF - International Journal of Environmental Research and Public Health

SN - 1661-7827

IS - 14

M1 - 2468

ER -