HPRT Mutation Frequencies in Benzene-Exposed Oil Refinery Workers During an Eleven-Year-Long Follow-Up Study

Jenö Major, Mátyás G. Jakab and Anna Tompa

Department of Cytogenetics and Molecular Toxicology, National Institute of Chemical Safety, József Fodor National Center for Public Health

Corresponding author: Dr. Jenö Major
    Department of Cytogenetics and Molecular Toxicology,
    National Institute of Chemical Safety, József Fodor National Center for Public Health
    P.O. Box 36
    H-1450 Budapest, Hungary
    Telephone: (+36) 1476 1111
    Fax number: (+36) 1476 1227
    E-mail: okbi@elender.hu

CEJOEM 2000, Vol.6. No.4.:288-299

Key words:
Alcohol, benzene, genotoxicity, HPRT, lymphocytes, risk assessment, smoking

Abbreviations:

ALAT = (serum) alanine aminotransferase
ASAT = (serum) aspartate aminotransferase
GGT = (serum) gamma glutamyl transferase
HPRT = hypoxanthine-guanine phosphoribosyl transferase
LI = labelling index
MC = maximum concentration
MF = mutation frequency

PBL = peripheral blood lymphocyte
PHA = phytohaemagglutinin-P
SCN = ferric-thiocyanate
SE = standard error
TG = 6-thioguanine
VF = variant frequency
.

Abstract:
Mutation (MF) and variant frequencies (VF) of the hypoxanthine-guanine-phosphoribosyl transferase (HPRT) loci of peripheral blood lymphocytes (PBL) of 43 occupationally benzene-exposed, 30-40-year-old workers with increased chromosome aberration frequencies were investigated by autoradiography in an eleven-year-long follow-up study in order to assess the (cancer) risk of the donors. Data were compared to those of 87 age-matched industrial controls collected during the study. Life style confounding factors as current smoking and drinking habits were also considered. Serum or urine SCN levels followed the decrease in the rate of smokers during the follow-up, however, the decrease in the rate of drinkers was not reflected in the rate of the subjects with increased liver enzyme (ALAT, ASAT and/or GGT) activity. Ambient air benzene concentrations were measured with gas chromatography by the company's occupational safety services. Average peak benzene concentrations in the ambient air samples were over the maximum concentration limits in each year except 1996 and 2000. Compared to the controls, the values of the labelling indices in PBLs of the exposed donors were decreased indicating a reduced response to lectine stimulation in the genotoxicologically compromised cells. In the years 1992-1993 the mean HPRT VFs of the exposed workers were significantly higher than those of the controls, but not in the previous or subsequent years. The distribution of the individual VFs also indicated exposure-related increases in the years 1991-1993. Drinking habits as a life-style-confounding factor actually influenced VF. However, smoking had no apparent influence on VF. The obtained data indicate that occupational benzene exposures at the measured levels can increase the mutation frequencies in the cells of the exposed workers.

Received: 30 November 2000
Accepted: 11 December 2000

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