Carcinogenesis Advance Access originally published online on September 30, 2004
Carcinogenesis 2005 26(1):93-101; doi:10.1093/carcin/bgh294
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Carcinogenesis vol.26 no.1 © Oxford University Press 2005; all rights reserved.
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Interactions between CYP1A1 polymorphisms and exposure to environmental tobacco smoke in the modulation of lymphocyte bulky DNA adducts and chromosomal aberrations
National Hellenic Research Foundation, Institute of Biological Research and Biotechnology, 48 Vas Constantinou Avenue, Athens 116 35, Greece, 1 Laboratory of Genetic Ecotoxicology, Institute of Experimental Medicine of the Academy of Sciences of the Czech Republic and Health Institute of Hygiene of Central Bohemia, Videnska 1083, 142 20 Prague 4, Czech Republic, 2 Division of Genetics, Cell and Developmental Biology, Department of Biology, University of Patras, 26100 Patras, Greece, 3 Laboratory of Hygiene and Epidemiology, University of Athens Medical School, 115 27 Athens, Greece and 4 Department of Environmental and Occupational Medicine, University of Aarhus, Building 180, DK-8000 Aarhus C, Denmark
5 To whom correspondence should be addressed Email: panosg{at}eie.gr
CYP1A1 plays an important role in the metabolic activation of polycyclic aromatic hydrocarbons (PAH), carcinogenic components of air pollution. The influence of CYP1A1 genotype (*2A, *2B and *4) on the levels of lymphocyte bulky DNA adducts and the frequency of cells with aberrant chromosomes was assessed in 194 non-smoking subjects in whom recent exposure to environmental tobacco smoke (ETS) and airborne particulate-associated PAH were measured during two consecutive seasons (winter and summer). While CYP1A1*4 had no consistent effect on either biomarker of genetic damage, the levels of both biomarkers responded in a parallel fashion to changes in exposure/CYP1A1*2A genotype combinations during both seasons. Specifically, the levels of both biomarkers were increased in carriers of at least one CYP1A1*2A allele, as compared with CYP1A1*1 homozygotes, in subjects with ETS exposures >0.8 h/day during the previous 4 days and mean personal exposure to benzo[a]pyrene <0.9 ng/m3 during the previous 24 h (all P < 0.05). Outside these exposure limits the differential effect in CYP1A1*2A variants was lost. Although the numbers of subjects with the CYP1A1*2B polymorphism was small, the same trend appeared to be followed in this case. These effects are interpreted as resulting from differential induction of CYP1A1 expression in CYP1A1*2A and CYP1A1*2A/*2B carriers by components of ETS-polluted air at levels of exposure readily suffered by large segments of the general population and suggest that subjects with these genotypes may have increased susceptibility to the genotoxic effects of ETS.
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