Vaccination News Home Page

http://cebp.aacrjournals.org/cgi/content/abstract/11/10/1134

Full Text of this Article Reprint (PDF) Version of this Article Similar articles found in: CEBP Online Search Medline for articles by: Perera, F. || O’Neill, J. P. Alert me when: new articles cite this article   Download to Citation Manager

Cancer Epidemiology Biomarkers & Prevention Vol. 11, 1134-1137, October 2002
© 2002 American Association for Cancer Research
 

In Utero DNA Damage from Environmental Pollution Is Associated with Somatic Gene Mutation in Newborns¹

Frederica Perera², Karl Hemminki, Wieslaw Jedrychowski, Robin Whyatt, Ulka Campbell, Yanzhi Hsu, Regina Santella, Richard Albertini and James P. O’Neill

Columbia University School of Public Health, New York, New York 10032 [F. P., R. W., U. C., Y. H., R. S.]; College of Medicine, Jagiellonian University, Krakow 31-034, Poland [K. H., W. J.]; and University of Vermont Genetics Laboratory, Burlington, Vermont 05405 [J. P. O.]

Transplacental exposure to carcinogenic air pollutants from the combustion of fossil fuels is a growing health concern, given evidence of the heightened susceptibility of the fetus. These mutagenic/carcinogenic pollutants include aromatic compounds such as polycyclic aromatic hydrocarbons that bind to DNA, forming chemical-DNA adducts. We have investigated the genotoxic effects of transplacental exposure in humans by analyzing aromatic-DNA adducts and the frequency of gene mutations at the hypoxanthine-guanine phosphoribosyltransferase (HPRT) locus in umbilical cord and maternal blood samples. Here we show, in a cross-sectional study of 67 mothers and 64 newborns from the Krakow Region of Poland, that aromatic-DNA adducts measured by ³²P-postlabeling are positively associated with HPRT mutant frequency in the newborns (ß = 0.56, P = 0.03) after controlling for exposure to tobacco smoke, diet, and socioeconomic status. In contrast to the fetus, HPRT mutations and DNA adducts do not reflect similar exposure periods in the mother, and the maternal biomarkers were not correlated. Adducts were higher in the newborn than the mother, indicating differential susceptibility of the fetus to DNA damage; but HPRT mutation frequency was 4-fold lower, consistent with the long lifetime of the biomarker. These results provide the first demonstration of a molecular link between somatic mutation in the newborn and transplacental exposure to common air pollutants, a finding that is relevant to cancer risk assessment.

Copyright © 2002 by the American Association for Cancer Research.

Vaccination News Home Page

ALL INFORMATION, DATA, AND MATERIAL CONTAINED, PRESENTED, OR PROVIDED HERE IS FOR GENERAL INFORMATION PURPOSES ONLY AND IS NOT TO BE CONSTRUED AS REFLECTING THE KNOWLEDGE OR OPINIONS OF THE PUBLISHER, AND IS NOT TO BE CONSTRUED OR INTENDED AS PROVIDING MEDICAL OR LEGAL ADVICE.  THE DECISION WHETHER OR NOT TO VACCINATE IS AN IMPORTANT AND COMPLEX ISSUE AND SHOULD BE MADE BY YOU, AND YOU ALONE, IN CONSULTATION WITH YOUR HEALTH CARE PROVIDER.