New aspects in the biomonitoring of occupational exposure to styrene

被引:17
作者
Vodicka, P
Stetina, R
Koskinen, M
Soucek, P
Vodicková, L
Hlavác, P
Kuricová, M
Necasová, R
Hemminki, K
机构
[1] Acad Sci Czech Republ, Inst Expt Med, Prague 14220 4, Czech Republic
[2] Purkyne Mil Med Acad, Dept Toxicol, Hradec Kralove, Czech Republic
[3] Orion Pharma, Dept Pharmacokinet Preclin & Clin R&D, Espoo, Finland
[4] Natl Inst Publ Hlth, Prague, Czech Republic
[5] Reg Hyg Stn, Usti Orlici, Czech Republic
[6] Inst Prevent & Clin Med, Bratislava, Slovakia
[7] Karolinska Inst, Novum, Dept Biosci, Ctr Nutr & Toxicol, Huddinge, Sweden
关键词
styrene; biological monitoring; DNA adducts; haemoglobin adducts; chromosomal aberrations; HPRT mutation frequency;
D O I
10.1007/s00420-002-0357-x
中图分类号
R1 [预防医学、卫生学];
学科分类号
1004 ; 120402 ;
摘要
Objective: Based on our previous studies we analysed DNA and haemoglobin adducts, single-strand breaks in DNA, chromosomal aberrations and HPRT mutant frequencies in styrene-exposed workers, in relation to employment time, with respect to markers of individual susceptibility. In our study the risk assessment of genotoxic styrene in occupationally exposed humans is reviewed in the light of adaptation and/or population selection. Various styrene-induced DNA adducts (representing important integral measures of DNA damage) are discussed as potential powerful biomarkers of styrene exposure, with respect to DNA repair. Methods: The complexity of followed markers required multiple methodological approaches, including modified P-32-post-labelling assay, PCR-based methods for genotyping, cytogenetic analysis, T-cell cloning assay, comet assay and tests for DNA repair capacity, and statistical tests. Results: Haemoglobin and DNA adducts, single-strand breaks in DNA, chromosomal aberrations and mutant frequencies at the HPRT gene were assessed with respect to the duration of exposure. No apparent accumulation of these biomarkers was found to be dependent on the years of employment, suggesting that adaptive processes play a role in chronically exposed workers. Statistically significant differences between the exposed and control individuals were found for the deduced epoxide hydrolase activity (P=0.041) and the frequency of heterozygous Ala/Val genotype in GSTP1, exon 5 (P=0.025). Significantly increased DNA repair capacity was found in styrene-exposed laminators compared with control individuals. Conclusions: In the light of present knowledge well-designed population studies on styrene genotoxicity are needed. Such studies should cover important areas of individual susceptibility (metabolising and repair enzymes, distributions of genetic polymorphisms) and possible role of adaptation, as well as the crucial role of DNA repair. Additionally, genotoxic effects of in-vivo formed 3,4-styrene oxide should be also addressed.
引用
收藏
页码:S75 / S85
页数:11
相关论文
共 46 条
[1]  
Alapetite C, 1999, INT J CANCER, V83, P83, DOI 10.1002/(SICI)1097-0215(19990924)83:1<83::AID-IJC16>3.3.CO
[2]  
2-#
[3]  
[Anonymous], 1987, AIR QUAL GUID EUR
[4]  
Bolognesi C, 1997, CANCER EPIDEM BIOMAR, V6, P249
[5]   Is human exposure to styrene a cause of cytogenetic damage? A re-analysis of the available evidence [J].
Bonassi, S ;
Montanaro, F ;
Ceppi, M ;
Abbondandolo, A .
BIOMARKERS, 1996, 1 (04) :217-225
[6]   BIOMARKERS IN STYRENE-EXPOSED BOATBUILDERS [J].
BRENNER, DD ;
JEFFREY, AM ;
LATRIANO, L ;
WAZNEH, L ;
WARBURTON, D ;
TOOR, M ;
PERO, RW ;
ANDREWS, LR ;
WALLES, S ;
PERERA, FP .
MUTATION RESEARCH, 1991, 261 (03) :225-236
[7]  
Collins Andrew R., 1998, Molecular Aspects of Medicine, V19, P359, DOI 10.1016/S0098-2997(99)00003-5
[8]   Oxidative damage to DNA: Do we have a reliable biomarker? [J].
Collins, AR ;
Dusinska, M ;
Gedik, CM ;
Stetina, R .
ENVIRONMENTAL HEALTH PERSPECTIVES, 1996, 104 :465-469
[9]   A PHYSIOLOGICAL PHARMACOKINETIC MODEL FOR STYRENE AND STYRENE-7,8-OXIDE IN MOUSE, RAT AND MAN [J].
CSANADY, GA ;
MENDRALA, AL ;
NOLAN, RJ ;
FILSER, JG .
ARCHIVES OF TOXICOLOGY, 1994, 68 (03) :143-157
[10]   UV-enhanced reactivation of a UV-damaged reporter gene suggests transcription-coupled repair is UV-inducible in human cells [J].
Francis, MA ;
Rainbow, AJ .
CARCINOGENESIS, 1999, 20 (01) :19-26