Abnormal DNA repair activities in lymphocytes of workers exposed to 1,3-butadiene

L. M. Hallberg, W. E. Bechtold, J. Grady, M. S. Legator, W. W. Au

Research output: Contribution to journalArticle

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Abstract

Exposure to high concentrations of butadiene has been shown to cause cancer among exposed workers. We have conducted a biomarker study to elucidate whether current butadiene exposure conditions are hazardous to workers. Twenty-four workers exposed consistently to butadiene were matched with 19 co-workers who had much less contact with butadiene and who served as our controls. In the standard cytogenetic assay, there was no difference in chromosome aberration frequencies between the exposed and control groups. In the challenge assay, the exposed group shows a consistent, but non-significant, increase in chromosome aberrations indicating some abnormality in DNA repair response. The observed dicentric frequency in the challenge assay (indicative of abnormal repair of damaged chromosomes) is significantly correlated with a butadiene metabolite, 1,2-dihydroxy-4-(N-acetylcysteinyl)butane, in urine (r = 0.52; p = 0.04). Furthermore, cigarette smokers had consistently abnormal repair response compared with non-smokers for both the control and exposed groups. A small subset of the studied workers were evaluated for toxicant-induced DNA repair deficiency using an independent cat-host cell reactivation (CAT-HCR) assay. When cigarette smokers and non-smokers were combined in our analysis, we observed that the exposed group (n = 9) had a significant reduction of DNA repair activities (p = 0.009) compared with the control group (n = 6). Cigarette smoking contributed significantly to the effect as exposed smokers (n = 4) had a significant reduction in DNA repair activities (p = 0.04) compared with exposed non-smokers. The results from the two independently conducted assays support each other and confirm the previously reported abnormal DNA repair response in another group of butadiene workers, In conclusion, our data indicates that exposure to environmental toxicants, such as butadiene, can cause DNA repair defects. Therefore, the current butadiene exposure conditions are still hazardous to workers. However, our data indicates that butadiene is not a potent genotoxic agent. Furthermore, the butadiene-induced effect is significantly enhanced by the cigarette smoking habit.

Original languageEnglish (US)
Pages (from-to)213-221
Number of pages9
JournalMutation Research - DNA Repair
Volume383
Issue number3
DOIs
StatePublished - May 1 1997

Fingerprint

Lymphocytes
DNA Repair
Repair
DNA
Assays
Tobacco Products
Chromosomes
Aberrations
Chromosome Aberrations
Control Groups
Smoking
1,3-butadiene
DNA Repair-Deficiency Disorders
Environmental Exposure
Biomarkers
Metabolites
Cytogenetics
Habits
Cats
Urine

Keywords

  • Butadiene
  • Chromosome aberration
  • DNA repair defect
  • Host cell reactivation assay
  • Population monitoring

ASJC Scopus subject areas

  • Toxicology
  • Genetics
  • Molecular Biology

Cite this

Abnormal DNA repair activities in lymphocytes of workers exposed to 1,3-butadiene. / Hallberg, L. M.; Bechtold, W. E.; Grady, J.; Legator, M. S.; Au, W. W.

In: Mutation Research - DNA Repair, Vol. 383, No. 3, 01.05.1997, p. 213-221.

Research output: Contribution to journalArticle

Hallberg, L. M. ; Bechtold, W. E. ; Grady, J. ; Legator, M. S. ; Au, W. W. / Abnormal DNA repair activities in lymphocytes of workers exposed to 1,3-butadiene. In: Mutation Research - DNA Repair. 1997 ; Vol. 383, No. 3. pp. 213-221.
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