[Estimation of passive smoking during pregnancy by cotinine measurement and its effect on fetal growth].
ABSTRACT Maternal cigarette smoking has been associated with some complications of pregnancy, including low birth weight and increased morbidity. Recently, it has been reported that maternal passive smoking also affects the fetal environment and causes fetal growth disturbance. In this study, we aimed to investigate the effects of maternal passive smoking on pregnant women and their fetuses by measuring cotinine concentrations in maternal urine and umbilical cord blood. The results were as follows: 1) Among 259 pregnant women, 17 cases (6.6%) were active smokers. The women who were not aware of passive smoking at all, were only 39 cases (15.1%). More than 80% of the pregnant women smoked either passively or actively each day. 2) Cotinine concentrations in both maternal urine and umbilical cord blood increased with the increase in passive smoking. Those in maternal serum, however, did not correlate with the increase in passive smoking. 3) The relative birth weight (R.B.W.) of the newborn infants delivered by the mothers whose cotinine concentration was more than 9.0ng/ml (This value represented the mean +1.5SD of the cotinine concentration in the urine from the mother who did not passively or actively smoke) was significantly lower than that of the mothers whose cotinine concentration was less than 9.0ng/ml. It is concluded that the measurement of the cotinine concentration in maternal urine or umbilical cord blood is very useful in estimating the effects of passive smoking on pregnant women. And passive smoking as well as active smoking also has a harmful effect on the fetal growth mechanism.
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ABSTRACT: Evidence shows that fetuses and infants are more affected than adults by a variety of environmental toxicants because of differential exposure, physiologic immaturity, and a longer lifetime over which disease initiated in early life can develop. In this article we review data on the effects of in utero exposure to common environmental contaminants, including polycyclic aromatic hydrocarbons (PAH), particulate matter and environmental tobacco smoke (ETS). We then summarize results from our molecular epidemiologic study to assess risks from in utero exposures to ambient air pollution and ETS. This research study, conducted in Poland, used biomarkers to measure the internal and bioeffective dose of toxicants and individual susceptibility factors. The study included 160 mothers and 160 newborns. Ambient air pollution was significantly associated (p= 0.05) with the amount of PAH bound to DNA (PAH-DNA adducts) in both maternal and infant cord white blood cells (WBC). Newborns with elevated PAH-DNA adducts (greater than the median) had significantly decreased birth weight (p= 0.05), birth length (p= 0.02), and head circumference (p= 0.0005) compared to the newborns with lower adducts (n= 135). Maternal and infant cotinine levels were increased by active and passive cigarette smoke exposure of the mother (p= 0.01). An inverse correlation was seen between newborn plasma cotinine (nanograms per milliliter) and birth weight (p= 0.0001) and length (p= 0.003). Adducts were elevated in placental tissue and WBC of newborns who were heterozygous or homozygous for the cytochrome P4501A1 MspI restriction fragment length polymorphism (RFLP) compared to newborns without the RFLP. Levels of PAH-DNA and cotinine were higher in newborns than mothers. These results document that there is significant transplacental transfer of PAH and ETS constituents from mother to fetus; that PAH-DNA adduct levels in maternal and newborn WBC were increased with environmental exposure to PAH from ambient pollution; and that the fetus is more sensitive to genetic damage than the mother. The study also provided the first molecular evidence that transplacental PAH exposure to the fetus is compromising fetal development. If confirmed, these findings could have significant public health implications since a number of studies have found that reduction of head circumference at birth correlates with lower intelligence quotient as well as poorer cognitive functioning and school performance in childhood.Environmental Health Perspectives 07/1999; 107 Suppl 3:451-60. · 7.26 Impact Factor
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ABSTRACT: Polycyclic aromatic hydrocarbons (PAHs) such as benzo[a]pyrene (BaP) are widespread air contaminants released by transportation vehicles, power generation, and other combustion sources. Experimental evidence indicates that the developing fetus is more susceptible than the adult to carcinogenic effects of PAHs, although laboratory studies in rodents suggest that the dose to fetal tissues is an order of magnitude lower than that to maternal tissues. To assess fetal versus adult susceptibility to PAHs and environmental tobacco smoke (ETS), we compared carcinogen-DNA adducts (a biomarker associated with increased cancer risk) and cotinine (a biomarker of tobacco smoke exposure) in paired blood samples collected from mothers and newborns in New York City. We enrolled 265 nonsmoker African-American and Latina mother-newborn pairs in New York City between 1997 and 2001 (estimated average ambient air BaP concentrations < 0.5 ng/m3). Despite the estimated 10-fold lower fetal dose, mean levels of BaP-DNA adducts as determined by high-performance liquid chromatography-fluorescence were comparable in paired New York City newborn and maternal samples (0.24 adducts per 10(8) nucleotides, 45% of newborns with detectable adducts vs. 0.22 per 10(8) nucleotides, 41% of mothers with detectable adducts). However, by the Wilcoxon signed-rank test, the levels in newborns were higher (p = 0.02). Mean cotinine was higher in newborns than in mothers (1.7 ng/mL, 47% detectable vs. 1.28 ng/mL, 44% detectable). Consistent with our prior study in a Caucasian Polish population, these results indicate increased susceptibility of the fetus to DNA damage and reduced ability to clear ETS constituents. The findings have implications for risk assessment, given the need to protect children as a sensitive subset of the population.Environmental Health Perspectives 08/2004; 112(10):1133-6. · 7.26 Impact Factor
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ABSTRACT: Young children and the developing fetus may be more susceptible to effects of environmental toxicants than adults due to differential exposure patterns and developmental immaturities. Biologic markers offer the potential of quantitative dosimeters of biologic dose and/or indices of biologic effect associated with fetal/childhood exposures. They can facilitate evaluation of interindividual variability in response and the magnitude of age-related susceptibilities. Thus far, biologic markers have not been widely used in developmental epidemiology of environmental exposures. Research by our group and others has seen elevations in biologic markers in samples from children and fetal tissue associated with a spectrum of environmental exposures, including tobacco smoke (active and passive), ambient pollution, and dietary contaminants. Studies also suggest that biologic markers can provide powerful dosimeters for investigating reproductive effects. Validation of biologic markers offering the greatest promise for developmental epidemiology is needed.Environmental Health Perspectives 10/1995; 103 Suppl 6:105-10. · 7.26 Impact Factor