© 2001 by Oxford University Press
Journal of the National Cancer Institute, Vol. 93, No. 8, 645-647,
April 18, 2001
© 2001 Oxford University Press
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Maternal Genetic Effects on Neonatal Susceptibility to Oxidative Damage From Environmental Tobacco Smoke
Affiliations of authors: Y.-C. Hong (Department of Occupational and Environmental Medicine), M.-W. Im (Department of Obstetrics and Gynecology), K.-H. Lee (Department of Preventive Medicine), Inha University College of Medicine, Inchon, Korea; H. Kim, Department of Preventive Medicine, College of Medicine, Chungbuk National University, Cheongju, Korea; B.-H. Woo, Department of Obstetrics and Gynecology, Ewha Women's University College of Medicine, Seoul, Korea; D. C. Christiani, Department of Environmental Health, Harvard School of Public Health, Boston, MA.
Correspondence to: Yun-Chul Hong, M.D., Ph.D., Department of Occupational and Environmental Medicine, Inha University College of Medicine, 7206, 3-Ga Shinheung-Dong, Jung-Gu, Inchon, 400103, South Korea (e-mail: ychong@inha.ac.kr).
Molecular epidemiologic studies (1,2) have demonstrated an association between environmental pollutants and in utero developmental damage. Among the environmental pollutants to which developing fetuses are reported to be vulnerable is environmental tobacco smoke (ETS) (3). ETS is a complex mixture of volatiles and particulate matter comprising numerous compounds, including polycyclic aromatic hydrocarbons (PAHs), which cause oxidative damage (4). Maternal ETS exposure has been found to be an important risk factor for reduced birth weight, small-for-gestational age, and premature delivery (58). Recently, biologic monitoring methods for the measurement of PAH exposure and the resulting oxidative injury have been used to evaluate the effects of environmental pollutant exposure (9,10). Sensitive biologic markers allow a more accurate quantification of PAH exposure levels and early biologic effects than external
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