Whyatt R M, Santella R M, Jedrychowski W, Garte S J, Bell D A, Ottman R, Gladek-Yarborough A, Cosma G, Young T L, Cooper T B, Randall M C, Manchester D K, Perera F P
Columbia University School of Public Health, New York, New York, USA.
Environ Health Perspect. 1998 Jun;106 Suppl 3(Suppl 3):821-6. doi: 10.1289/ehp.98106821.
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.
波兰的工业化地区具有高环境污染的特点，包括工业和家庭取暖燃煤产生的多环芳烃（PAHs）。在实验生物测定中，某些PAHs是经胎盘致癌物和发育毒物。生物标志物有助于评估环境PAHs对发育中婴儿的影响。我们测量了母亲和脐带血白细胞中与DNA结合的PAHs量（PAH-DNA加合物）。该队列由来自波兰克拉科夫的70名母亲和新生儿组成，克拉科夫是一个空气污染程度较高的工业化城市。我们还研究了先前与肺癌风险相关的基因型，特别是谷胱甘肽S-转移酶MI（GSTM1）和细胞色素P4501A1（CYP1A1）Msp限制性片段长度多态性（RFLP）对加合物水平的调节作用。在未离家工作的受试者中，母亲和新生儿的加合物水平与女性居住地的环境污染呈剂量相关增加（p≤0.05）。母亲吸烟（主动和被动）显著增加了母亲的加合物水平（p≤0.01），但未增加新生儿的加合物水平。CYP1A1 Msp和GSTM1多态性均与母亲的加合物无关。然而，与没有RFLP的新生儿相比，具有CYP1A1 Msp RFLP杂合或纯合的新生儿的加合物显著更高（p = 0.04）。结果表明，环境空气污染会增加母亲和新生儿中PAH诱导的DNA损伤。在胎儿中，这种损伤似乎因CYP1A1 Mspl多态性而增强。
