title: Relationship between ambient air pollution and DNA damage in Polish mothers and newborns.
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 MI (GSTM1) and cytochrome P4501A1 (CYP1A1) Msp 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 (p < or = 0.05). Maternal smoking (active and passive) significantly increased maternal (p < or = 0.01) but not newborn adduct levels. Neither CYP1A1 Msp nor GSTM1 polymorphisms was associated with maternal adducts. However, adducts were significantly higher in newborns heterozygous or homozygous for the CYP1A1 Msp 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 Mspl polymorphism.
authors.affiliation: Columbia University School of Public Health, New York, New York, USA.
authors.forename: R M
authors.initials: RM
authors.lastname: Whyatt
authors.forename: R M
authors.initials: RM
authors.lastname: Santella
authors.forename: W
authors.initials: W
authors.lastname: Jedrychowski
authors.forename: S J
authors.initials: SJ
authors.lastname: Garte
authors.forename: D A
authors.initials: DA
authors.lastname: Bell
authors.forename: R
authors.initials: R
authors.lastname: Ottman
authors.forename: A
authors.initials: A
authors.lastname: Gladek-Yarborough
authors.forename: G
authors.initials: G
authors.lastname: Cosma
authors.forename: T L
authors.initials: TL
authors.lastname: Young
authors.forename: T B
authors.initials: TB
authors.lastname: Cooper
authors.forename: M C
authors.initials: MC
authors.lastname: Randall
authors.forename: D K
authors.initials: DK
authors.lastname: Manchester
authors.forename: F P
authors.initials: FP
authors.lastname: Perera
mesh_terms: D000328:Adult; D000393:Air Pollutants / Q000009:adverse effects* / Q000032:analysis; D015415:Biomarkers / Q000097:blood; D019363:Cytochrome P-450 CYP1A1 / Q000235:genetics; D018736:DNA Adducts / Q000097:blood; D004249:DNA Damage; D004781:Environmental Exposure / Q000009:adverse effects* / Q000032:analysis / Q000145:classification; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D005838:Genotype; D005982:Glutathione Transferase / Q000235:genetics; D006801:Humans; D007231:Infant, Newborn; D016014:Linear Models; D016555:Matched-Pair Analysis; D018811:Maternal Exposure / Q000009:adverse effects; D011044:Poland; D011084:Polycyclic Aromatic Hydrocarbons / Q000032:analysis; D016133:Polymerase Chain Reaction; D012150:Polymorphism, Restriction Fragment Length; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D012189:Retrospective Studies; D012907:Smoking / Q000009:adverse effects; D014504:Urban Health
chemical_list: D000393:Air Pollutants; D015415:Biomarkers; D018736:DNA Adducts; D011084:Polycyclic Aromatic Hydrocarbons; D019363:Cytochrome P-450 CYP1A1; D005982:Glutathione Transferase