Biomarkers of exposure and effect as indicators of potential carcinogenic risk arising from in vivo metabolism of ethylene to ethylene oxide

Carcinogenesis. 2000 Sep;21(9):1661-9. doi: 10.1093/carcin/21.9.1661.

Abstract

The purposes of the present study were: (i) to investigate the potential use of several biomarkers as quantitative indicators of the in vivo conversion of ethylene (ET) to ethylene oxide (EO); (ii) to produce molecular dosimetry data that might improve assessment of human risk from exogenous ET exposures. Groups (n = 7/group) of male F344 rats and B6C3F1 mice were exposed by inhalation to 0 and 3000 p. p.m. ET for 1, 2 or 4 weeks (6 h/day, 5 days/week) or to 0, 40, 1000 and 3000 p.p.m. ET for 4 weeks. N:-(2-hydroxyethyl)valine (HEV), N:7-(2-hydroxyethyl) guanine (N7-HEG) and HPRT: mutant frequencies were assessed as potential biomarkers for determining the molecular dose of EO resulting from exogenous ET exposures of rats and mice, compared with background biomarker values. N7-HEG was quantified by gas chromatography coupled with high resolution mass spectrometry (GC-HRMS), HEV was determined by Edman degradation and GC-HRMS and HPRT: mutant frequencies were measured by the T cell cloning assay. N7-HEG accumulated in DNA with repeated exposure of rodents to 3000 p.p.m. ET, reaching steady-state concentrations around 1 week of exposure in most tissues evaluated (brain, liver, lung and spleen). The dose-response curves for N7-HEG and HEV were supralinear in exposed rats and mice, indicating that metabolic activation of ET was saturated at exposures >/=1000 p.p.m. ET. Exposures of mice and rats to 200 p.p.m. EO for 4 weeks (as positive treatment controls) led to significant increases in HPRT: mutant frequencies over background in splenic T cells from exposed rats and mice, however, no significant mutagenic response was observed in the HPRT: gene of ET-exposed animals. Comparisons between the biomarker data for both unexposed and ET-exposed animals, the dose-response curves for the same biomarkers in EO-exposed rats and mice and the results of the rodent carcinogenicity studies of ET and EO suggest that too little EO arises from exogenous ET exposure to produce a significant mutagenic response or a carcinogenic response under standard bioassay conditions.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Biomarkers / analysis
  • Biotransformation
  • Carcinogens / pharmacokinetics
  • Carcinogens / toxicity
  • DNA / drug effects
  • DNA / metabolism
  • DNA Damage
  • Dose-Response Relationship, Drug
  • Ethylene Oxide / metabolism*
  • Ethylene Oxide / pharmacokinetics
  • Ethylene Oxide / toxicity*
  • Ethylenes / pharmacokinetics*
  • Ethylenes / toxicity*
  • Guanine / analogs & derivatives*
  • Guanine / biosynthesis
  • Hemoglobins / metabolism
  • Hypoxanthine Phosphoribosyltransferase / genetics
  • Inhalation Exposure
  • Male
  • Mice
  • Mice, Inbred Strains
  • Mutation
  • Rats
  • Rats, Inbred F344
  • T-Lymphocytes / enzymology
  • Valine / analogs & derivatives*
  • Valine / biosynthesis

Substances

  • Biomarkers
  • Carcinogens
  • Ethylenes
  • Hemoglobins
  • 2-hydroxyethylvaline
  • N(7)-hydroxyethylguanine
  • Guanine
  • DNA
  • ethylene
  • Hypoxanthine Phosphoribosyltransferase
  • Valine
  • Ethylene Oxide