The Frequency of Premature Chromosome Condensation in Peripheral Blood Lymphocytes of 400 Control and Occupationally Exposed Human Donors

Jenõ Major, Mátyás G. Jakab, and Anna Tompa

National Institute of Chemical Safety, Department of Human Genotoxicology, Budapest, Hungary(1)
Corresponding author: Jenõ Major,

National Institute of Chemical Safety,
Department of Human Genotoxicology
H-1450 Budapest, P.O. Box 36, Hungary,
Tel: (+36) 1 215-7890
Fax: (+36) 1 215-2904

CEJOEM 1998, Vol.4. No.2.:146-154

Chromosome aberrations, genotoxicology monitoring, risk assessment

ACN = acrylonitrile, MC = permitted maximum concentration;
AML = acute myeloid leukaemia; PAH = polycyclic aromatic hydrocarbons;
BrdU = 5-Bromo-2-deoxyuridine; PBL = peripheral blood lymphocyte;
CA = chromosome aberration; PCB = polychlorinated biphenyls;
DMF = dimethyl-formamide; PCC = premature chromosome condensation;
ECD = early centromere division; SA = satellite association;
ETO = ethylene oxide; SE = standard error. 

Premature chromosome condensation (PCC) has importance among others in Down’s syndrome and ataxia teleangiectasia, and in human neoplastic diseases. PCC can be induced by environmental chemical and physical genotoxic agents, as well as it can be used in the investigation of chromosome aberration formation during the cell cycle, and as a biological dosimeter for ionising irradiation. The published data suggest a significance of PCC in risk assessment. In order to investigate the significance of PCC in (cancer) risk assessment, we studied the chemical exposure-induced PCC frequencies in 400 Hungarian subjects including 188 control donors and 212 subjects occupationally exposed to different genotoxic chemicals, such as acrylonitrile (ACN) and/or dimethylformamide (DMF), benzene, cytostatic drugs, ethylene oxide (ETO), mixed exposure in rubber industry, mixed organic solvents including CCl4, hot oil mist, bitumen, and polychlorinated biphenyls (PCB). Mitotic chromosomes were prepared by the standard methods and 100 metaphases per donor were scored. PCC data were compared with the obtained structural and numeric chromosome aberration frequencies. Here we present preliminary, chemical exposure-induced PCC frequency data. In the 101 controls nobody, while in the 87 industrial controls only 1 donor (0,01 %) had PCC. No PCC was found in oil mist exposure and among Adriamycin synthesisers. Similarly, no significant PCC increases were observed with benzene and polychlorinated biphenyl and mixed exposures, as well as in Adriamycin fermentators or hospital nurses exposed to ethylene oxide. Increased (P<0.05) PCC frequencies were observed in the following exposed groups: mixed industrial solvents (including aromatic solvents and CCl4), bitumen (PAH), acrylonitrile and dimethyl-formamide, and hospital nurses with cytostatic drugs. The results suggest that certain occupational exposures can increase the PCC frequency in human PBLs. The investigation of the significance of PCC in cancer risk assessment needs further studies which are in progress. 

Received: 13 March 1998
Accepted: 07 May 1998 
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Posted: 15 November 1998