Maternal Cotinine Research Articles

Evaluation of past smoking of mothers and DNA methylation in cord blood of infants

Background: Maternal smoking is related to multiple adverse health outcomes in children. We previously reported an association between maternal smoking during pregnancy and differential DNA methylation in newborn cord bloods for CpG sites (CpGs) in genes involved in the aryl hydrocarbon receptor signaling pathway and key developmental processes. However, it remains unclear whether these modifications to the infant epigenome reflect in utero exposures only or the inheritance of epigenetic marks from the mother. Aims: We evaluated the association between maternal smoking before or during pregnancy and DNA methylation for 21 CpGs previously identified as differentially methylated in response to maternal smoking in 1,047 newborn cord bloods from the Norwegian Mother and Child Cohort Study (MoBa). Methods: Maternal self-report of smoking as well as maternal plasma cotinine measured during pregnancy were used to distinguish mothers into four groups (never smokers, former smokers, smokers who smoked during pregnancy but quit by 18 weeks, and active smokers throughout pregnancy). The association between smoking and methylation was assessed using linear regression. Results: Having a mother who formerly smoked was not associated with differential methylation in cord blood for any of the 21 CpGs (at FDR of 0.05). Quitting during pregnancy was also not significantly associated with differential methylation (at FDR of 0.05) although methylation differences were larger than those for former smokers compared to never smokers. Only active smoking throughout pregnancy was statistically significantly associated with differential methylation (at FDR of 0.05). Conclusions: Differential methylation in newborn cord blood at the 21 CpGs that we previously found to be related to maternal smoking in pregnancy was only observed where mothers smoked during pregnancy. These findings suggest that DNA methylation at these locations in the infant epigenome reflects in utero exposure rather than epigenetic inheritance of smoking-related modifications in the mother.

Prenatal Glucocorticoids and Maternal Smoking During Pregnancy Independently Program Adult Nicotine Dependence in Daughters: A 40-Year Prospective Study

Maternal smoking during pregnancy (MSDP) is an independent risk factor for offspring nicotine dependence (ND), but mechanisms remain unknown. We investigated prenatal glucocorticoid (cortisol) and androgen (testosterone) associations with offspring ND over 40 years and the possibility that prenatal glucocorticoids and androgens would mediate links between MSDP and offspring ND. Participants were 1086 mother-adult offspring pairs (59% female) from the New England Family Study, a 40-year longitudinal follow-up of the Collaborative Perinatal Project. MSDP was assessed prospectively at each prenatal visit. Maternal cortisol, testosterone, and cotinine (nicotine metabolite) were assayed from third trimester maternal sera. Offspring lifetime ND was assessed via structured interview. Significant bivariate associations emerged for: 1) MSDP/cotinine and lifetime ND; and 2) maternal cortisol and lifetime ND, for daughters only. In multivariate models, maternal cortisol and MSDP/cotinine remained significantly and independently associated with increased odds of lifetime ND of daughters. However, cortisol did not mediate the MSDP-lifetime ND relation. No associations emerged between maternal testosterone and offspring ND. Results provide the first evidence in support of prenatal glucocorticoid programming of adult ND over 40 years in daughters only. Our study highlights two independent prenatal pathways leading to increased risk for ND in daughters: elevated prenatal glucocorticoids and MSDP/nicotine exposure. Daughter-specific effects of glucocorticoid and MSDP programming over 40 years highlight the breadth and persistence of sexually dimorphic programming effects in humans. Results do not support androgen programming of offspring ND.

Maternal and cord blood miR-223 expression associates with prenatal tobacco smoke exposure and low regulatory T-cell numbers

There is evidence that microRNAs (miRNAs) are sensitive to environmental stressors, including tobacco smoke. On the other hand, miRNAs are involved in immune regulation, such as regulatory T (Treg) cell differentiation. The aim of the present study was to investigate the association between prenatal tobacco smoke exposure, miRNAs, and Treg cell numbers. Within a prospective mother-child study (Lifestyle and Environmental Factors and Their Influence on Newborns Allergy Risk), we analyzed the expression of miR-155 and miR-223 together with Treg cell numbers in maternal blood during pregnancy, as well as in cord blood (n = 441). Tobacco smoke exposure was assessed based on questionnaire answers and maternal urine cotinine levels. Additionally, the concentration of smoking-related volatile organic compounds was measured in dwellings of study participants. Both maternal and cord blood miR-223 expressions were positively correlated with maternal urine cotinine levels. An association was also found between maternal miR-223 expression and indoor concentrations of benzene and toluene. High miR-223 expression was associated with lower Treg cell numbers in maternal and cord blood. Furthermore, children with lower Treg cell numbers at birth had a higher risk of atopic dermatitis during the first 3 years of life. The concentration of the toluene metabolite S-benzylmercapturic acid in maternal urine was associated with decreased cord blood, but not maternal blood, miR-155 expression. A relationship between miR-155 expression and Treg cell numbers was not found. For the first time, we show that maternal tobacco smoke exposure during pregnancy correlates with the level of miRNA-223 expression in blood, with an effect on children's cord blood Treg cell numbers and subsequent allergy risk.

Association of Maternal Smoking With Child Cotinine Levels

Introduction:Our aim was to understand the strength of association between parental smoking and child environmental tobacco smoke (ETS) exposure in order to inform the development of future tobacco control policies. ETS was measured using child cotinine levels below the active smoking threshold. Methods:Participants were drawn from the Avon Longitudinal Study of Parents and Children and included 3,128 participants at age 7 years and 1,868 participants at age 15 years. The primary outcome was cotinine levels of nonsmoking children, to investigate the relationship between maternal smoking and child cotinine levels. The secondary outcome was cotinine levels of all individuals to investigate the relationship between child smoking and child cotinine levels. Maternal and child smoking behavior was assessed by self-report questionnaire. We adjusted for several sociodemographic variables.Results:We found an association between maternal smoking and child cotinine at age 7 years (mean cotinine = 1.16ng/ml serum, ratio of geometric means = 3.94, 95% CI = 2.86–5.42) and at age 15 years (mean cotinine = 0.94ng/ml serum, ratio of geometric means = 5.26, 95% CI = 3.06–9.03), after adjustment for potential confounders. Conclusions:The magnitude of this association for children whose mothers were heavy smokers was comparable with the quantity of half the levels of cotinine observed among children who were irregular (i.e., nonweekly) active smokers, and it was greater than five times higher than that seen in nonsmoking children whose mothers didn’t smoke. This provides further evidence for the importance of public health interventions to reduce smoking exposure in the home.

Persistent Snoring in Preschool Children: Predictors and Behavioral and Developmental Correlates

To clarify whether persistent snoring in 2- to 3-year-olds is associated with behavioral and cognitive development, and to identify predictors of transient and persistent snoring. Two hundred forty-nine mother/child pairs participated in a prospective birth cohort study. Based upon parental report of loud snoring ≥ 2 times weekly at 2 and 3 years of age, children were designated as nonsnorers, transient snorers (snored at 2 or 3 years of age, but not both), or persistent snorers (snored at both ages). We compared groups by using validated measures of behavioral and cognitive functioning. Potential predictors of snoring included child race and gender, socioeconomic status (parent education and income), birth weight, prenatal tobacco exposure (maternal serum cotinine), childhood tobacco exposure (serum cotinine), history and duration of breast milk feeding, and body mass relative to norms. In multivariable analyses, persistent snorers had significantly higher reported overall behavior problems, particularly hyperactivity, depression, and inattention. Nonsnorers had significantly stronger cognitive development than transient and persistent snorers in unadjusted analyses, but not after demographic adjustment. The strongest predictors of the presence and persistence of snoring were lower socioeconomic status and the absence or shorter duration of breast milk feeding. Secondary analyses suggested that race may modify the association of childhood tobacco smoke exposure and snoring. Persistent, loud snoring was associated with higher rates of problem behaviors. These results support routine screening and tracking of snoring, especially in children from low socioeconomic backgrounds; referral for follow-up care of persistent snoring in young children; and encouragement and facilitation of infant breastfeeding.

450K Epigenome-Wide Scan Identifies Differential DNA Methylation in Newborns Related to Maternal Smoking during Pregnancy

Background: Epigenetic modifications, such as DNA methylation, due to in utero exposures may play a critical role in early programming for childhood and adult illness. Maternal smoking is a major risk factor for multiple adverse health outcomes in children, but the underlying mechanisms are unclear.Objective: We investigated epigenome-wide methylation in cord blood of newborns in relation to maternal smoking during pregnancy.Methods: We examined maternal plasma cotinine (an objective biomarker of smoking) measured during pregnancy in relation to DNA methylation at 473,844 CpG sites (CpGs) in 1,062 newborn cord blood samples from the Norwegian Mother and Child Cohort Study (MoBa) using the Infinium HumanMethylation450 BeadChip (450K).Results: We found differential DNA methylation at epigenome-wide statistical significance (p-value < 1.06 × 10–7) for 26 CpGs mapped to 10 genes. We replicated findings for CpGs in AHRR, CYP1A1, and GFI1 at strict Bonferroni-corrected statistical significance in a U.S. birth cohort. AHRR and CYP1A1 play a key role in the aryl hydrocarbon receptor signaling pathway, which mediates the detoxification of the components of tobacco smoke. GFI1 is involved in diverse developmental processes but has not previously been implicated in responses to tobacco smoke.Conclusions: We identified a set of genes with methylation changes present at birth in children whose mothers smoked during pregnancy. This is the first study of differential methylation across the genome in relation to maternal smoking during pregnancy using the 450K platform. Our findings implicate epigenetic mechanisms in the pathogenesis of the adverse health outcomes associated with this important in utero exposure.

The impact of intrauterine tobacco exposure on the cerebral mass of the neonate based on the measurement of head circumference

The objective of the study was to assess cerebral mass, based on head circumference measurements in neonates exposed to tobacco smoke in utero, and to determine the relative proportions of the cerebral and body mass. The study included 147 neonates born in the period 2003–2004 at the Princess Anna Mazowiecka University Hospital and admitted to the Neonatal and Intensive Care Department of the Medical University in Warsaw. Subjects were divided into three groups on the basis of maternal status as active, passive, or nonsmokers determined by maternal urinary cotinine concentration and a questionnaire. Neonates whose mothers were active smokers throughout the whole period of pregnancy had a lower head circumference and in consequence a lower cerebral mass significantly more frequently when compared with those whose mothers were nonsmokers, P= 0.002. (Median difference in cerebral mass was 48.27 g.) The risk of lower cerebral mass was 3.9 (1.4–10.8, CI 95%) in the group of neonates whose mothers actively smoked cigarettes during pregnancy. A negative correlation was seen between cerebral mass and maternal urinary cotinine concentration (correlation coefficient r=−23, P= 0.006). The ratio of the cerebral to body mass was similar for neonates in all three groups. Active smoking during pregnancy had a negative effect on the cerebral mass of the neonate, however no such effect was observed in neonates whose mothers were passive smokers. The deficiency in cerebral mass increased with greater smoking intensity. Active smoking by the mother during pregnancy inhibits the growth of the brain as well as that of the body mass of the neonate.

Effect of Passive Smoking Using Maternal and Neonatal Salivary Cotinine Measurements

In Japan, the rate of passive smoking among pregnant women is 52.7%, and smokers are usually their husbands (80.8%). Fetal environmental tobacco smoke has been measured using cotinine levels in maternal and neonatal hair, urine, or umbilical cord blood. However, using saliva from neonates immediately after birth has not been explored among noninvasive methods. The aims of this study were to (a) determine the relationship between fathers' smoking status during pregnancy and neonatal and maternal salivary cotinine immediately after delivery and (b) evaluate the potential use of salivary cotinine measurements immediately after birth to determine the exposure of the neonates to passive smoke. A cross-sectional survey design was used. The participants were 34 pairs of nonsmoking mothers and their neonates who had visited for a health check-up at a general hospital in Tokyo. Saliva samples were collected from mothers and their neonates within 24 hours of delivery. All samples were analyzed using an enzyme-linked immunosorbent assay. Information about maternal age, neonate's birth weight, and smoking status of the father were obtained by interview and questionnaire. Salivary cotinine levels in neonates and mothers with indoor-smoking fathers were significantly higher compared with those in neonates and mothers with nonsmoking and outdoor-smoking fathers. A very strong positive correlation was observed between neonatal and maternal cotinine levels. Smoking indoors by the father affected the mother and neonate. Salivary cotinine measurement is a feasible method to evaluate passive exposure of neonates to tobacco smoke.

Comparison of Biomarkers and Parent Report of Tobacco Exposure to Predict Wheeze

To identify the optimal measure of active and passive prenatal tobacco exposure to predict wheeze in early life. We conducted a birth cohort study of 398 mother-infant dyads enrolled during the second trimester of pregnancy and followed through age 2 years. We measured tobacco exposure with maternal report, serum cotinine level, and meconium cotinine level. We assessed wheeze with parent report every 6 months. We used a repeated measures logistic regression model. Of 367 children with respiratory data, 26% percent had parent reported active or passive prenatal maternal tobacco exposure, but cotinine was detected in 61% of mothers during pregnancy. Compared with children of mothers in the fifth percentile of tobacco exposure, children of mothers in the 95th percentile had increased odds of wheeze when exposure was measured with maternal serum cotinine level (adjusted OR, 2.6; 95% CI, 1.3-5.2; P < .006) versus meconium cotinine level (adjusted OR, 2.0; 95% CI, 1.0-4.0; P = .04) and total parent-reported exposure (adjusted OR, 1.7; 95% CI, 1.1-2.7; P = .01). Serum cotinine, a biomarker of tobacco exposure, was more strongly associated with wheeze than parent-reported exposure. Studies that rely on parent report of prenatal tobacco exposure may underestimate risk of wheeze.

Hair Biomarkers as Measures of Maternal Tobacco Smoke Exposure and Predictors of Fetal Growth

Most biomarker studies of the effects of maternal smoking on fetal growth have been based on a single blood or urinary cotinine value, which is inadequate in capturing maternal tobacco exposure over the entire pregnancy. We used hair biomarkers to compare the associations of maternal self-reported smoking, hair nicotine, and hair cotinine with birth weight for gestational age (BW for GA) among active and passive smokers during pregnancy. We collected maternal hair in the immediate postpartum period and measured nicotine and cotinine concentrations averaged over the pregnancy in 444 term controls drawn from 5,337 participants in a multicenter nested case-control study of preterm birth. BW for GA Z-score and small for gestational age (SGA) were based on Canadian population-based standards. The addition of hair nicotine to multiple linear regression models containing self-reported active smoking, hair cotinine, or both explained significantly more variance in the BW for GA Z-score (p = .01, .03 and .04, respectively). Similarly, women with hair nicotine, but not cotinine, at or above the median value had a significant increase in the risk of SGA birth (odds ratio: 3.07, 95% CI: 1.25-7.52). No significant association was observed between maternal passive smoking and BW for GA based on hair biomarkers. Hair nicotine is a better predictor of reductions in BW for GA than either hair cotinine or self-report. Our negative results for passive smoking suggest that previously reported small but significant effects may be explained by misclassification of active smokers as passive smokers based on self-report.

Prenatal Exposure to Smoking in a Mother-infant Study in South Taiwan

PP-31-129 Background/Aims: The purpose of this study is to evaluate the effect of smoking exposure on fetus since first trimester till birth. Methods: This is a prospective study from June 2008 to September 2009. This study was conducted in the Department of Obstetrics, Dong-Kong Hospital. Two hundred seventy-six pregnant women were enrolled. A questionnaire was administered to assess smoking exposure. Urine was collected for measurement of cotinine. Association of maternal smoking exposure and birth outcome was analyzed. Results: The prevalence of maternal smoking, their husbands' smoking, and smoking in their family (husband excluded) was 7.6%, 59.4%, and 47.5% separately. After adjusting maternal age, the incidence of low-birth-weight babies in active smoking women was borderline significantly higher than that in nonsmoking women without exposure to smoking environment (AOR = 7.1; 95% CI: 0.86–61.61; P = 0.07). Newborn chest circumference was 33.0 ± 1.5 cm in the group with maternal urine cotinine ≥120 μg/g creatinine, and 32.7 ± 2.7 cm in the group with maternal urine cotinine <120 μg/g creatinine. There was a significant difference of newborn chest circumference in 2 groups (P < 0.0001). On postnatal day 3, the mean newborn bilirubin level in the group with maternal urine cotinine3 120 μg/g creatinine was significantly lower than that in the group with maternal urine cotinine <120 μg/g creatinine (P < 0.001). Conclusion: Maternal smoking exposure is associated with low birth weight, great chest circumference, and low newborn bilirubin in this series.

Measuring prenatal secondhand smoke exposure in mother–baby couplets

Pregnant women often underreport their smoking status and extent of secondhand smoke (SHS) exposure. Biomarker confirmation is the recommended method to assess smoking behaviors and SHS exposure in both mothers and infants. The primary aims are to (a) examine the relationship between smoking behaviors and SHS exposure in mother-baby couplets using maternal and infant hair nicotine and maternal urine cotinine analyses and (b) determine whether there is an association between maternal and infant hair nicotine samples obtained shortly after birth. A cross-sectional study with a multiethnic sample of 210 mother-baby couplets assessing SHS exposure. The level of maternal hair nicotine (MHN) was significantly different among three groups: nonsmoking, nonsmoking/passive exposed, and smoking (p < .0001), with nonsmoking and nonexposed women having the lowest level. Urine cotinine was strongly associated with self-reported smoking status (rho = .88; p < .0001). Maternal and infant hair nicotine were correlated, although MHN correlated more strongly with smoking status (rho = .46, p < .0001) than infant hair nicotine (rho = .39, p < .0001). MHN was a more precise biomarker of prenatal SHS exposure than infant hair nicotine; mothers' urine cotinine was strongly correlated with self-reported smoking status.

Newborns’ cord blood plasma cotinine concentrations are similar to that of their delivering smoking mothers

Background In utero exposure to constituents of tobacco smoke has perinatal and postnatal health consequences. Umbilical cord plasma cotinine levels have been shown to correlate with self-reported daily number of cigarettes at the end of pregnancy, but the exact relationship between maternal and newborn plasma cotinine (and nicotine) is unknown. Methods Concentrations of cotinine, nicotine's main metabolite, were determined in venous blood of delivering mothers and in arterial umbilical cord blood of their newborns at birth. Data from eighteen mother–newborn dyads were analyzed. Results The mothers smoked 95.1 (SD = 96, range 10–420) cigarettes the week preceding delivery. Their mean plasma cotinine concentration at delivery was 106 ng/mL (SD = 53, range 17–245) and the newborns’ mean umbilical cord plasma cotinine was 88.2 ng/mL (SD = 53, range 10–198, p <0.001). The difference can be explained by the elimination time of around 6 h which occurred between sampling in mothers and in umbilical cord blood. Arterial umbilical cord blood plasma cotinine was highly associated with that of the smoking mothers: y = 0.79 x + 0.97, Rsq = 0.95, p < 0.001. Conclusions Maternal and newborn plasma cotinine concentrations are strongly associated. There is probably no placental barrier for plasma cotinine between pregnant mothers and their newborns. Lack of a placental barrier for cotinine (and probably nicotine) can partially explain smoking related perinatal disorders.

Low-level prenatal exposure to nicotine and infant neurobehavior

Objective To examine the association between prenatal exposure to nicotine from tobacco smoke and infant neurobehavior using tobacco biomarkers and a sensitive and comprehensive measure of infant neurobehavior. Study design Participants were 318 infants (206 White, 95 Black, 17 Other) and their mothers. Prenatal tobacco smoke exposure was measured twice during pregnancy and once at delivery using maternal serum cotinine. Infant neurobehavior was assessed with the NICU Network Neurobehavioral Scale at approximately 5 weeks after birth. Results Prenatal tobacco smoke exposure was significantly associated with infant neurobehavior after controlling for important covariates, but the specific behaviors associated with exposure varied by race. In White infants, higher cotinine was associated with increased arousal ( p = .030) and excitability ( p = .034), and decreased self-regulation ( p = .010). In contrast, among Black infants, higher cotinine was associated with decreased arousal ( p = .001), excitability ( p = .021), and special handling required to complete the assessment ( p = .003), and increased self-regulation ( p = .021) and hypotonicity ( p = .016). In secondary analyses, we found racial differences in the effects of postnatal exposure to second hand smoke and low-level prenatal exposure. Conclusions Low-level prenatal tobacco smoke exposure is associated with infant neurobehavior at 5 weeks of age, but the specific effects differ by race. These effects may reflect racial differences in nicotine metabolism that are similar to differences reported in adult and child studies of tobacco.

PAHs: Choi et al. Respond

PAHs: Choi et al. Respond

Maternal smoking during pregnancy and testicular cancer in the sons: A nested case–control study and a meta-analysis

Some large ecological studies have noted a significant association of testicular cancer (TC) with maternal smoking during pregnancy, while several more controlled studies have been negative. It has been difficult to obtain reliable data on exposure because of the long lag time to cancer diagnosis. We performed a case–control study nested within Finnish, Swedish and Icelandic maternity cohorts exploiting early pregnancy serum samples to evaluate the role of maternal smoking in the risk of TC in the offspring. After reviewing the literature, we also performed a meta-analysis of published studies. For each index mother of the TC patient, three to nine matched control mothers with a cancer-free son born at the same time as the TC case were identified within each cohort. First trimester sera were retrieved from the 70 index mothers and 519 control mothers and were tested for cotinine level by a novel HPLC–MS–MS method developed. No statistically significant association between maternal cotinine level and risk of TC in the offspring was found (OR 0.68; 95% CI 0.35, 1.34). This is the first study based on individual exposure measurements. Its results agree with our meta-analysis of seven previous epidemiological studies (total number of 2149 cases, 2762 controls) using indirect exposure assessment (OR 1.0; 95% CI 0.88, 1.12).

Maternal Smoking during Pregnancy and Newborn Neurobehavior: Effects at 10 to 27 Days

To examine effects of maternal smoking during pregnancy on newborn neurobehavior at 10 to 27 days. Participants were 56 healthy infants (28 smoking-exposed, 28 unexposed) matched on maternal social class, age, and alcohol use. Maternal smoking during pregnancy was determined by maternal interview and maternal saliva cotinine. Postnatal smoke exposure was quantified by infant saliva cotinine. Infant neurobehavior was assessed through the NICU Network Neurobehavioral Scale. Smoking-exposed infants showed greater need for handling and worse self-regulation (P < .05) and trended toward greater excitability and arousal (P < .10) relative to matched, unexposed infants (all moderate effect sizes). In contrast to prior studies of days 0 to 5, no effects of smoking-exposure on signs of stress/abstinence or muscle tone emerged. In stratified, adjusted analyses, only effects on need for handling remained significant (P < .05, large effect size). Effects of maternal smoking during pregnancy at 10 to 27 days are subtle and consistent with increased need for external intervention and poorer self-regulation. Along with parenting deficits, these effects may represent early precursors for long-term adverse outcomes from maternal smoking during pregnancy. That signs of abstinence shown in prior studies of 0- to 5-day-old newborns did not emerge in older newborns provides further evidence for the possibility of a withdrawal process in exposed infants.

Effect of gestational smoke exposure on atopic dermatitis in the offspring

The adverse impact of smoking on respiratory diseases and birth outcomes in children is well-known. However, the influence of smoke exposure including environmental tobacco smoke (ETS) and maternal smoking during pregnancy on atopic dermatitis (AD) is not clear. The purpose of this study was to evaluate the effect of gestational smoke exposure on the development of AD in the offspring on the basis of the maternal and cord blood cotinine. We recruited 261 mother and newborn pairs in 2004. Cord blood and information on perinatal factors of children were gathered at birth. At 2 yr of age, information about development of AD and environmental exposures were collected. We compared AD with non-AD children for the concentration of cotinine in cord and maternal blood measured by high performance liquid chromatography-mass spectrometry. Multiple logistic regressions were performed to estimate the relationship of cotinine levels and AD. About 150 mother and child pairs completed the follow-up study and specimen collection with 38 (25.3%) children developing AD. Two (1.3%) out of 150 mothers smoked during pregnancy, while 38 (25.3%) mothers reported having ETS exposure. Cotinine levels in cord blood and maternal blood were highly correlated (r = 0.71, p < 0.001). The risk of AD was found to increase with maternal and cord blood cotinine levels in a dose-response manner (p for trend = 0.01). Children exposed to high levels (>75th percentile) had a significantly increased risk of AD. Smoke exposure during pregnancy might increase the risk of AD in children. Avoidance of prenatal smoke exposure may be warranted for early prevention.

Maternal exposure to environmental tobacco smoke, GSTM1/T1 polymorphisms and oxidative stress

Environmental tobacco smoking (ETS) is known to be associated with adverse pregnancy outcomes. The purpose of this study was to investigate the relationship between maternal exposure to ETS and oxidative stress for neonates, as well as the effect of maternal genetic polymorphisms, glutathione- S-transferase M1 (GSTM1) and GSTT1, on this relationship. We used the radioimmunoassay to measure the urinary concentration of cotinine in 266 pregnant women who denied smoking cigarettes during pregnancy and in their singleton babies. In addition, the urinary concentration of malondialdehyde (MDA) and 8-hydroxy-2-deoxyguanosine (8-OH-dG) were assessed using high-performance liquid chromatography and enzyme-linked immunosorbent assay, respectively. We also extracted DNA from whole blood obtained from the mothers and then conducted polymerase chain reaction on the samples to determine the GSTM1 and GSTT1 genotypes. The maternal cotinine concentration was found to be significantly associated with the fetal cotinine concentration, particularly for mothers whose urine cotinine concentrations were above 120 μg/g cr ( p < 0.01). The fetal urine cotinine concentration was also found to be significantly associated with the fetal urine MDA concentration ( p < 0.01). When the null type maternal GSTM1 or the wild type GSTT1 was present, the maternal oxidative stress level increased significantly as the maternal continine concentration increased (MDA: p < 0.01; 8-OH-dG: p < 0.01). No significant relationships were found between maternal cotinine and fetal oxidative stress markers, however, the fetal MDA levels increased significantly as fetal cotinine levels increased. These results suggest that the maternal exposure to ETS affects the fetal urine cotinine concentration and induces production of maternal oxidative stress. In addition, maternal genetic polymorphisms of GSTM1 and GSTT1 may modify the oxidative stress by maternal exposure to ETS.

Prenatal exposure to passive smoking and duration of breastfeeding in nonsmoking women: Krakow inner city prospective cohort study

The relationship between tobacco smoking in pregnancy and breastfeeding is of public health importance. The present birth cohort study provided the opportunity to investigate whether the negative relationship between passive smoking measured by the cotinine concentrations in maternal blood at delivery and breastfeeding in postpartum could also be confirmed in nonsmoking mothers. The study sample included 441 healthy pregnant women who were recruited in the first and second trimester of pregnancy. Enrollment included only nonsmoking women of the age of 18-35 years with singleton pregnancies, without illicit drug use and free from chronic diseases. After delivery, breastfeeding duration was defined using the answers recorded in the interviews with mothers conducted every 3 months. An infant was considered to be fully breastfed when breast milk was the only source of nourishment. Any breastfeeding was defined as an infant's being fully breastfed or receiving both breast milk and formula, with or without solids. In the statistical analysis only total duration of breastfeeding up to 6 months was considered for both forms of breastfeeding. Subjects were categorized into environmental tobacco smoke (ETS) exposure groups according to maternal blood cotinine level at delivery or self-reported exposure to ETS during pregnancy. The adjusted relative risk of discontinuation of any breastfeeding after infant's first 6 months was more than two times higher (OR = 2.42; 95% CI: 1.42-4.14) in women whose blood cotinine level at delivery was above 75th percentile of cotinine distribution (>0.15 ng/mL); the corresponding risk of discontinuation of full breastfeeding was OR = 1.71; 95% CI: 1.03-2.82. Estimated relative risk of discontinuation of any breastfeeding based on self-reported ETS was also significant but much less marked; the corresponding risk of discontinuation of full breastfeeding was insignificant. The results obtained support the hypothesis that ETS may affect breastfeeding duration and support the avoidance of passive smoking as a necessary additional measure for breastfeeding promotion.