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Robin M. Whyatt,¹ Regina M. Santella,¹ Wieslaw Jedrychowski,² Seymour J. Garte,³ Douglas A. Bell,⁴ Ruth Ottman,⁵ Alicja Gladek-Yarborough,¹ Greg Cosma,⁶ Tie-Lan Young,¹ Thomas B. Cooper,⁵ Mary C. Randall,¹ David K. Manchester,⁷ and Frederica P. Perera¹

¹Columbia University School of Public Health, New York, New York
²College of Medicine, Jagiellonian University, Krakow, Poland
³New York University Medical Center, New York, New York
⁴National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina
⁵New York State Psychiatric Institute, New York, New York
⁶Colorado State University, Fort Collins, Colorado
⁷University of Colorado, Denver, Colorado

Abstract

Industrialized regions in Poland are characterized by high ambient pollution, including polycyclic aromatic hydrocarbons (PAHs) from coal burning for industry and home heating. In experimental bioassays, certain PAHs are transplacental carcinogens and developmental toxicants. Biologic markers can facilitate evaluation of effects of environmental PAHs on the developing infant. We measured the amount of PAHs bound to DNA (PAH-DNA adducts) in maternal and umbilical white blood cells. The cohort consisted of 70 mothers and newborns from Krakow, Poland, an industrialized city with elevated air pollution. Modulation of adduct levels by genotypes previously linked to risk of lung cancer, specifically glutathione S-transferase M1 (GSTM1) and cytochrome P4501A1 (CYP1A1) MspI restriction fragment length polymorphism (RFLP) , was also investigated. There was a dose-related increase in maternal and newborn adduct levels with ambient pollution at the women's place of residence among subjects who were not employed away from home (p0.05) . Maternal smoking (active and passive) significantly increased maternal (p0.01) but not newborn adduct levels. Neither CYP1A1 MspI nor GSTM1 polymorphisms was associated with maternal adducts. However, adducts were significantly higher in newborns heterozygous or homozygous for the CYP1A1 MspI RFLP compared to newborns without the RFLP (p=0.04) . Results indicate that PAH-induced DNA damage in mothers and newborns is increased by ambient air pollution. In the fetus, this damage appears to be enhanced by the CYP1A1 MspI polymorphism. -- Environ Health Perspect 106(Suppl 3) :821-826 (1998) .

http://ehpnet1.niehs.nih.gov/docs/1998/Suppl-3/821-826whyatt/abstract.html

Key words: PAH-DNA adducts, air pollution, cigarette smoking, CYP1A1 MspI RFLP, GSTM1, newborns, Poland