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Main Title Comparison of DNA Adduct Levels in Human Placenta from Polychlorinated Biphenyl Exposed Women and Smokers in Which CYP 1A1 Levels Are Similarly Elevated.
Author Gallagher, J. E. ; Everson, R. B. ; Lewtas, J. ; George, M. ; Lucier, G. W. ;
CORP Author Health Effects Research Lab., Research Triangle Park, NC. Genetic Toxicology Div. ;Environmental Health Research and Testing, Inc., Research Triangle Park, NC. ;National Inst. of Environmental Health Sciences, Research Triangle Park, NC.
Publisher cAug 94
Year Published 1994
Report Number EPA/600/J-94/520;
Stock Number PB95-148821
Additional Subjects DNA adducts ; Polychlorobiphenyl compounds ; Smoking ; Placenta ; Mutagens ; Humans ; Females ; Enzyme activation ; Metabolic activation ; Tobacco ; Reprints ; Cytochrome P450 1A1 ; Polychlorodibenzofurans
Library Call Number Additional Info Location Last
NTIS  PB95-148821 Some EPA libraries have a fiche copy filed under the call number shown. 07/26/2022
Collation 12p
Cigarette smoking is associated with high elevations in levels of both cytochrome P450 1A1 (CYP 1A1) and DNA adducts in human placenta. The identity of the smoking related adducts is not known. The DNA adducts identified in placenta of smokers could result from chemicals present in cigarette smoke, substances formed by CYP 1A1 metabolic activation of endogenous compounds, non-cigarette related exposures, or a combination of these processes. Exposure to contaminated rice oil containing large doses of polychlorinated biphenyls (PCBs) and polychlorinated dibenzofurans (PCDFs) also resulted in massive elevation of CTP 1A1 in human placenta but formation of DNA adducts from this exposure has not previously been reported. Using (32)P-postlabeling techniques that readily detect DNA adducts in placental tissue from smokers, we found no evidence of DNA adducts among specimens obtained from PCB/PCDF exposed individuals. These data suggest that CYP 1A1 induction does not induce DNA adducts detectable by this approach, and that smoking related adducts are not a consequence of CYP 1A1 induction mediated activation of endogenous compounds or xenobiotics other than cigarette smoke.