Maternal Environmental Tobacco Smoke Exposure Research Articles

Maternal environmental tobacco smoke exposure and adverse birth outcomes in Egypt: a cross sectional study

Maternal environmental tobacco smoke exposure and adverse birth outcomes in Egypt: a cross sectional study

The effects of maternal environmental tobacco smoke exposure on periodontal health and mother-infant bonding in relation to salivary cotinine level

Background: Environmental tobacco smoking is produced by active smokers burning the tip of a cigarette and breathed by nonsmokers and measured by cotinine level. It has the potential to raise the risk of periodontal disease. One of the most frequent chronic diseases in adults is periodontal disease. The lower maternal-fetal attachment has been found to predict smoking status in previous studies, but no research has examined whether maternal-fetal attachment predicts environmental tobacco smoking. This study assessed the effects of maternal environmental tobacco smoke exposure on periodontal health and mother-infant bonding concerning salivary cotinine levels. Materials and methods: This is a comparative cross-sectional study comparing environmental tobacco smoke on exposed and non-exposed mothers aged between 20-35 years with their infants aged up to one year who attended primary health care centers in rural areas of AL-Karkh sector/Baghdad. Along with the essential socio-demographic data, a secondhand smoke exposure scale and postpartum bonding questionnaire were employed. Collection of unstimulated saliva from mothers was done according to Navazesh and Kumer in 2008. After that, the clinical Assessment of gingival bleeding and periodontal pockets was performed by using Community Periodontal Index according to the world health organization in 1997. Results: Out of 150 subjects,67(44.66%) were exposed to environmental tobacco whereas the non-exposed mothers were composed of 83 (55.33%). The highest mean number of CPI0(healthy gingiva) and CPI1(gingival bleeding) were among the non-exposed mothers while the highest mean number of CPI2(dental calculus), CPI3 (shallow pocket 4-5mm) and CPI4(deep pocket 6mm or more) were among the exposed mothers. The mean value of cotinine level among the non-exposed mothers was lower than exposed mothers with significant results. A higher salivary cotinine level was linked to a lower maternal-fetal bonding score. Conclusions: Mother’s exposure to environmental tobacco smoke significantly negatively impacts periodontal disease. Furthermore, mothers who have a stronger sense of attachment and affiliation to their fetus have lower salivary cotinine concentrations than mothers who have a less sense of fetal attachment.

Association between maternal smoke exposure and congenital heart defects from a case–control study in China

There is a gap in knowledge how maternal exposure to environmental tobacco smoke (ETS) is associated with offspring congenital heart defects (CHDs). In this case–control study, we collected data on 749 fetuses with CHDs and 880 fetuses without any congenital anomalies to examine the association of maternal ETS with fetal CHDs and the potentially moderating effect by maternal hazardous and noxious substances (HNS), periconceptional folate intake and paternal smoking. Maternal exposure to ETS in first trimester was associated with increased risk of CHDs in a dose–response gradient, with the AORs (95% CI) were1.38 (1.00–1.92), 1.60 (1.07–2.41), and 4.94 (2.43–10.05) for ETS < 1 h/day, 1–2 h/day, and ≥ 2 h/day, respectively. With the doubly unexposed group as reference categories, AORs for maternal ETS exposure ≥ 2 h/day in the absence of folate intake, in the presence of HNS exposure or paternal smoking, were 7.21, 11.43, and 8.83, respectively. Significant additive interaction between ETS exposure and maternal folate intake on CHDs was detected. Maternal ETS exposure during first trimester may increase the risk of offspring CHDs in a dose–response shape, and such effect may be modified by maternal folate intake or other potential factors.

Critical window for the association between prenatal environmental tobacco smoke exposure and preterm birth

Although environmental tobacco smoke (ETS) exposure is considered to be a severe public health problem and a modifiable risk factor for preterm birth (PTB), we still lack a comprehensive understanding of the PTB risk associated with trimester-specific prenatal ETS exposure. This study aimed to examine the accumulation of risk across trimester ETS exposure and the critical window of the association between maternal ETS exposure during pregnancy and PTB. A total of 63,038 mother-child pairs were involved in the analysis of the 2017 survey of Longhua Child Cohort Study. Information about socio-demographic characteristics, prenatal ETS exposure, and birth outcomes were collected using a self-report questionnaire. A series of logistic regression models were employed to assess the associations between prenatal ETS exposure and PTB. We found that maternal ETS exposure during pregnancy significantly increased the risk of PTB and this association increased with both the average level of daily ETS exposure and the number of trimesters of ETS exposure. Moreover, mothers who were initially exposed to ETS in the 1st trimester of pregnancy had significant higher risk of PTB (OR = 1.34, 95% CI: 1.25–1.44). Furthermore, mothers exposed to ETS in the 1st trimester only (OR = 1.26, 95%CI: 1.04–1.50), in both 1st and 2nd trimester (OR = 1.35, 95%CI: 1.08–1.67) and throughout pregnancy (OR = 1.35, 95%CI: 1.24–1.46) experienced a significantly high risk of PTB. Prenatal maternal ETS exposure during only the 2nd trimester also resulted in a high risk of PTB with marginal significance (OR = 1.33, 95% CI:0.78–2.13). To conclude, the 1st and early 2nd trimester might be the critical window for prenatal ETS exposure causing PTB.

Maternal Smoking During Pregnancy Affects Adult Onset of Asthma in Offspring: A Follow Up From Birth to Age 46 Years

Previous evidence has revealed an effect of environmental tobacco smoke (ETS) exposure on the development of childhood asthma. However, few studies have investigated the link between prenatal ETS exposure and adult-onset asthma. Therefore, in this study, we aim to determine if an association exists between adult-onset asthma and prenatal ETS exposure. Genetic predisposition to the development of asthma was also examined in conjunction with prenatal ETS exposure.This study was comprised of mothers and their offspring who were included in the Northern Finland Birth Cohort in 1966, a total of 12053 births. Data were collected from 7148 subjects, and 5491 met the inclusion criteria. The final study population consisted of 5200 subjects.Analysis was conducted on maternal smoking status in the last 3 months of pregnancy, and asthma status was conducted at 31 and 46 years of age (n = 5200). Questionnaire data were collected from subjects at 31 and 46 years of age regarding history of asthma or wheeze to determine incident asthma between 31 and 46 years. Information regarding maternal smoking status was gathered at clinical visits via questionnaire at 6- and 7-months’ gestation. Association between the development of asthma and maternal smoking (1 or more cigarette/pipe per day) was analyzed via Pearson’s χ2 test. Maternal smoking and associated changes in forced expiratory volume in 1 second (FEV1) and the FEV1 to forced vital capacity ratio were examined by using linear regression. Binary logistic regression was used to evaluate the relationship between maternal smoking status, adult-onset asthma, and single-nucleotide polymorphisms (SNPs). Linear regression controlled for covariates including maternal education and parental asthma as well as offspring smoking status, education, ponderal index, parity, and Apgar score at first minute.Maternal smoking during the last 3 months of pregnancy was associated with an increased risk for the development of asthma in offspring between 31 and 46 years of age, and reduced offspring FEV1 to forced vital capacity ratio at 31 years of age. This association was more prominent in individuals with haplotype rs11702779-AA and with the subgroup that reported previous wheeze. No association was found between maternal smoking during the last 3 months of pregnancy and offspring FEV1 at 31 years.Gestational smoke exposure is associated with increased incidence of adult-onset asthma and reduced pulmonary function in adult offspring.The results of this study are consistent with previous research revealing an association between gestational maternal smoke exposure and the subsequent development of asthma in offspring. This reveals susceptibility of the developing airway to maternal ETS exposure and the importance of smoking cessation during pregnancy. A limitation of this study is the inability to distinguish the role of prenatal maternal smoke exposure from maternal smoking in the home during the postnatal period.

Urinary cotinine assessment of maternal smoking and environmental tobacco smoke exposure status and its associations with perinatal outcomes: a cross-sectional birth study

Tobacco consumption and environmental tobacco smoke (ETS) exposure remains an important public health concern. Pregnant women require particular attention as active and passive smoking during pregnancy are associated with multiple adverse perinatal outcomes. This study aimed to biochemically validate self-reported smoking and ETS exposure status among pregnant women, to more precisely ascertain its association with adverse perinatal outcomes. Data refers to 595 pregnant women who sought prenatal care in a public hospital in Porto, Portugal. A standard questionnaire on smoking and ETS-related variables was completed. Urinary cotinine (UC) concentrations were assessed by solid-phase competitive ELISA, in maternal urine samples collected on the day of delivery. The results showed that the optimal UC cut-off value to distinguish smokers from non-smokers and within non-smokers those who were exposed to ETS from those non-exposed in the third trimester of pregnancy was 74.1 ng/mL (sensitivity and specificity of 96.7% and 98.0%, respectively) and 1.6 ng/mL (sensitivity of 66.2% and specificity of 75.7%, respectively). The agreement between maternal self-reported and UC-based smoking status was very good (κ=0.919, p<0.001), but much lower for ETS exposure (κ=0.386, p<0.001). Maternal active smoking in the third trimester of pregnancy was associated with a significant decrease in birth weight, length and head circumference of 157.66 g (95% CI: −245.81, −69.52; p<0.001), 0.78 cm (95% CI: −1.22, −0.34; p=0.001) and 0.39 cm (95% CI: −0.70, −0.07; p=0.016), respectively. Maternal ETS exposure in the third trimester of pregnancy was associated with a non-significant increase in birth weight of 38.37 g (95% CI: −28.91, 105.64; p=0.263). Furthermore, maternal smoking cessation was associated with the increase of approximately 172 g in birth weight (95% CI: 50.00, 293.19). As such, there is an urgent need for increased public health awareness campaigns to encourage smoking cessation during pregnancy, in order to improve perinatal outcomes.

The association of in utero tobacco smoke exposure, quantified by serum cotinine, and Autism Spectrum Disorder.

Previous studies on in utero exposure to maternal environmental tobacco smoke (ETS) or maternal active smoking and Autism Spectrum Disorder (ASD) have not been entirely consistent, and no studies have examined in utero cotinine concentrations as an exposure classification method. We measured cotinine in stored second trimester maternal serum for 498 ASD cases and 499 controls born in California in 2011-2012. We also obtained self-reported maternal cigarette smoking during and immediately prior to pregnancy, as well as covariate data, from birth records. Using unconditional logistic regression, we found no association between log10 cotinine concentrations and odds for developing ASD among children of non-smokers (aOR: 0.93 [95% CI: 0.69, 1.25] per ng/ml), which represents exposure to ETS, though there may be a possible interaction with race. We found no association between cotinine-defined smoking (≥3.08 ng/ml vs. <3.08 ng/ml) (adjusted odds ratio [aOR]: 0.73 (95% confidence interval [95% CI]: 0.35, 1.54)) or self-reported smoking (aOR: 1.64 [95% CI: 0.65, 4.16]) and ASD. In one of the few studies of ETS and the first with measured cotinine, our results indicate no overall relationship between in utero exposure to tobacco smoke from maternal ETS exposure or active smoking, and development of ASD. LAY SUMMARY: This study found that women who smoke or are exposed to tobacco smoke during pregnancy are not more likely to have children with Autism Spectrum Disorder (ASD). This is the first ASD study to measure a chemical in the mother's blood during pregnancy to identify exposure to tobacco smoke.

Prenatal environmental tobacco smoke exposure alters children’s cognitive control circuitry: A preliminary study

Background and ObjectivesPrenatal exposure to environmental tobacco smoke (ETS) is associated with increased attention problems in children, however, the effects of such exposure on children’s brain structure and function have not been studied. Herein, we probed effects of prenatal ETS on children’s cognitive control circuitry and behavior. MethodsForty-one children (7–9 years) recruited from a prospective longitudinal birth cohort of non-smoking mothers completed structural and task-functional magnetic resonance imaging to evaluate effects of maternal ETS exposure, measured by maternal prenatal urinary cotinine. Attention problems and externalizing behaviors were measured by parent report on the Child Behavior Checklist. ResultsCompared to non-exposed children, exposed children had smaller left and right thalamic and inferior frontal gyrus (IFG) volumes, with large effect sizes (p-FDR < .05, Cohen’s D range from 0.79 to 1.07), and increased activation in IFG during the resolution of cognitive conflict measured with the Simon Spatial Incompatibility Task (38 voxels; peak t(25) = 5.25, p-FWE = .005). Reduced thalamic volume was associated with increased IFG activation and attention problems, reflecting poor cognitive control. Mediation analyses showed a trend toward left thalamic volume mediating the association between exposure and attention problems (p = .05). ConclusionsOur findings suggest that maternal ETS exposure during pregnancy has deleterious effects on the structure and function of cognitive control circuitry which in turn affects attentional capacity in school-age children. These findings are consistent with prior findings documenting the effects of active maternal smoking on chidlren’s neurodevleoment, pointing to the neurotixicity of nicotine regardless of exposure pathway.

Environmental tobacco smoke exposure during pregnancy has limited effect on infant birthweight and umbilical vein endothelial nitric oxide synthase

Women who smoke, deliver significantly smaller infants. These infants have reduced levels of the vasodilator endothelial nitric oxide synthase (eNOS) levels in the umbilical vessels, which may reduce fetal growth. Serum cotinine, the degradation product of nicotine, can be used to determine the level of tobacco exposure. Newborns of environmental smokers are suggested to be smaller and shorter in weight, length, and head circumference. eNOS levels have not yet been studied in these infants. We investigated the existence of a relation between maternal environmental tobacco smoke exposure, eNOS activity, concentration, and birthweight. We included 263 healthy singleton pregnancies categorized into three groups according to measured cotinine levels: 175 nonsmokers, 38 smokers, and 50 environmental smokers. Cotinine was quantified by mass spectrometry with a detection limit of .2ng/mL; eNOS activity and concentration were measured in endothelial cells (ECs) of the umbilical vein. Infants born to environmental smokers had similar weights to infants born to nonsmokers (47g heavier, P=.48). Cotinine concentrations were .06/.09/.12ng/mL (quartiles) in infants born to nonsmokers, .27/.37/.81ng/mL in infants born to women exposed to environmental tobacco smoke, and 43.0/63.8/108.1ng/mL in infants born to smokers. The eNOS concentration was 1.65±.92ng/106 ECs (mean±SD) in nonsmokers and 1.71±1.00ng/106 ECs in environmental smokers. The eNOS activity was 52.0±20.6pmol l-citrulline/min/106 ECs in nonsmokers and 48.7±19.8pmol l-citrulline/min/106 ECs in environmental smokers. Infants born to environmental smokers, as judged by umbilical serum cotinine levels close to .2ng/mL, are not associated with lower birthweight or reduced eNOS activity, or concentration in the fetal vascular bed.

Trends in Environmental Tobacco Smoke (ETS) Exposure and Preterm Birth: Use of Smoking Bans and Direct ETS Exposure Assessments in Study Designs.

For decades, many studies have linked maternal smoking to an increased risk of preterm birth. As a result, the scientific community has long hypothesized that exposure to environmental tobacco smoke (ETS), commonly referred to as second-hand smoke, is also associated with an increased risk of preterm birth. Multiple studies have examined this proposed association through different strategies and approaches. Recently, a small number of epidemiology studies have examined preterm birth trends before and after the implementation of antismoking legislation in various jurisdictions. We found that these studies have largely revealed a significant trend of decreasing population-level preterm birth rates after the implementation of smoking bans. However, most of the studies reviewed did not distinguish the impact of maternal smoking from ETS in their analyses, making it difficult to specifically evaluate the effects of smoking bans on ETS exposure. Other studies have taken the approach of directly measuring maternal ETS exposure and associations with preterm birth within particular study populations. In contrast to smoking ban studies, the latter group of studies had more inconclusive results. The use of a variety of exposure assessment methods ranging from different self-reporting techniques to biomarker measurements posed a challenge to compare studies. We evaluate current scientific literature for evidence of an association between maternal ETS exposure and risk of preterm birth. We also discuss the strengths and weaknesses of the different approaches to study this association as well as methods used for ETS exposure assessment. We propose that more studies, specifically, evaluating rates of preterm birth among nonsmoking women before and after smoking bans, are needed as well as using better ETS exposure assessments methods in studies measuring maternal ETS exposure.

Mediating role of maternal serum interleukin-1beta and tumor necrosis factor-alpha in the association between environmental tobacco smoke exposure in pregnancy and low birth weight at term

Objectives: To explore the mediation effects of maternal serum interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) on the association between environmental tobacco smoke (ETS) exposure during pregnancy and low birth weight (LBW) at term.Methods: ETS exposure, birth weight, blood sample and covariates were collected from 195 pregnant women delivered term LBW infants and 195 controls delivered normal birth weight infants in two Maternity and Child Hospitals in Guangdong, China. Maternal serum IL-1β and TNF-α were measured by flow cytometry. Logistic regression models and path analyses explored the mediation effects of maternal IL-1β and TNF-α on the association between ETS exposure and LBW.Results: LBW was significantly associated with maternal ETS exposure (OR = 2.14 (95% CI =1.06–4.32)). TNF-α and IL-1β were significantly associated with both LBW (OR = 1.87 (1.41–2.47) and OR = 1.53 (1.14–2.05)) and ETS (β = 0.32 (0.04–0.60) and β = 0.27 (0.05–0.49)). Traditional mediation analyses indicated the separate mediation effect of TNF-α and IL-1β was 32.2% and 24.6%, respectively. Path analysis revealed the combined mediation effects of TNF-α and IL-1β as 29.4% in the pathway from ETS exposure to LBW.Conclusions: Maternal serum IL-1β and TNF-α may play a mediating role in the association between maternal ETS exposure during pregnancy and term LBW.

The Impacts of Cord Blood Cotinine and Glutathione-S-Transferase Gene Polymorphisms on Birth Outcome

This study aimed to investigate the association between cord blood cotinine levels and birth outcome, and to determine whether fetal metabolic gene polymorphisms of glutathione-S-transferase (GST) modulate the effect of environmental tobacco smoke exposure during pregnancy. This study included 328 maternal and neonatal pairs. Maternal and cord blood cotinine levels were measured using high performance liquid chromatography. The GST T1 (GSTT1) and GST M1 (GSTM1) polymorphisms were examined using the polymerase chain reaction method. The birth outcomes included birth weight, length, and head circumference, and the risks of having low birth weight and being small for gestational age (SGA). Cord cotinine level had a dose-dependent impact on the reduction of birth weight, length, and head circumference in newborns. Elevation of cord blood cotinine concentration increased the rate of SGA and low birth weight. The neonates who had GSTT1 or GSTM1 polymorphism were associated with an increased risk of being SGA. A combination of the GSTT1 and GSTM1 null genotype exacerbated the effect of maternal environmental tobacco smoke exposure on SGA more than the presence of either genotype alone (odds ratio=8.90, 95% confidence interval=1.00-79.5). Cord blood cotinine adversely affects birth outcomes. GSTT1 and GSTM1 null genotype may modify the effect of cord blood cotinine on birth outcomes.

Influence of maternal environmental tobacco smoke exposure assessed by hair nicotine levels on birth weight.

While the perinatal outcomes of active maternal smoking are well documented, results of the effects of environmental tobacco smoke (ETS) exposure during pregnancy are inconsistent. We aimed to examine the effect of ETS exposure, assessed by maternal hair nicotine levels at 35th week of gestation, on birth weight and the risk of small for gestational age (SGA) and low birth weight (LBW). A total of 871 non-smoking healthy pregnant women were recruited by one Korean hospital between 1 October 2006 and 31 July 2007. Hair samples were collected and anthropometric questionnaires administered at 35th week of gestation. The primary outcome was birth weight and secondary outcomes were the risk of babies being SGA and LBW. Log-transformed hair nicotine concentrations were inversely related with birth weight after adjusting for confounding variables (β=-0.077, p=0.037). After stratifying hair nicotine levels by tertiles (T1, low [0.0-0.28 ng/mg]; T2, medium [0.29-0.62 ng/mg]; and T3, high [0.63-5.99 ng/mg]), the mean birth weight in each groups were 3,342 g (T1) 3,296 g (T2) and 3,290 g (T3), respectively. However the difference between groups was not statistically significant by analysis of co-variance (ANCOVA) adjusting for covariates (p=0.062). In logistic regression analysis, the risk of SGA was higher in the T3 (OR=1.59, 95%CI 1.05-2.42) than in the reference group (T1), after controlling for confounding variables. The risk of low birth weight (<2,500 g, LBW) was not significantly higher (OR=1.44, 95%CI 0.95-2.19), but the risk of babies being below 3,000g birth weight was increased in the T3 group (OR=1.53, 95%CI 1.00-2.36) compared with that in the T1 group. Maternal ETS exposure during pregnancy was inversely related with birth weight. The risk of SGA increased in the highest ETS exposure group compared with in the low exposure group. To prevent ETS exposure during pregnancy, more comprehensive tobacco control policies are needed.

Prenatal exposure to environmental tobacco smoke and language development in toddlers

Background: Maternal exposure to environmental tobacco smoke (ETS) associated with children’s neurobehavioral development has been reported. There is also a study indicating that maternal smoking during pregnancy can affect newborns’ speech processing ability. Language is a result of cognitive development; however, there is no study focus on the effects of maternal ETS exposure during pregnancy to toddlers’ language and communication development. Aims: The aim of this study is to examine the effect of prenatal exposure to ETS on the language development in toddlers. Methods: A total of 103 children from the Taiwan Birth Panel Study (TBPS) were followed up in northern Taiwan. We enrolled their mothers before delivery, interviewed them using a structured questionnaire, and collected umbilical cord blood. Umbilical cord cotinine, a blood indicator of prenatal ETS exposure, was analyzed by using HPLC-MS/MS. The Mandarin-Chinese Communicative Developmental Inventory (MCDI) for toddlers was used to assess these children’s language and communication development at 2 years of age. We examined the children’s language development between exposed and control groups by multiple linear and logistic regression models to control for potential confounders. Results: Maternal ETS exposure during pregnancy was negatively associated with language and communication development. The adverse effects to the exposed group was significantly showed on the total MCDI score (?=-71.04; p=0.0396), word produced part (?=-65.81; p=0.0433) and syntax complexity part (?=-4.91; p=0.146) in multiple linear regression models. Conclusions: Our results indicate that maternal ETS exposure was related to the adverse effects on early children’s language development. Further studies are needed to clarify the causal relationship between cord blood cotinine and children’s language development.

Active and passive maternal smoking during pregnancy and birth outcomes: the Kyushu Okinawa Maternal and Child Health Study

BackgroundIn Western countries, active maternal smoking during pregnancy is recognized as the most important preventable risk factor for adverse birth outcomes. However, the effect of passive maternal smoking is less clear and has not been extensively studied. In Japan, there has been only one epidemiological study which examined the effects of active smoking during early pregnancy on birth outcomes although the effects of passive smoking were not assessed.MethodsStudy subjects were 1565 mothers with singleton pregnancies and the babies born from these pregnancies. Data on active maternal smoking status in the first, second, and third trimesters and maternal environmental tobacco smoke (ETS) exposure at home and work were collected with self-administered questionnaires.ResultsCompared with children born to mothers who had never smoked during pregnancy, children born to mothers who had smoked throughout their pregnancy had a significantly increased risk of small-for-gestational-age (SGA) (adjusted odd ratio [OR] = 2.87; 95% confidence interval: 1.11 − 6.56). However, active maternal smoking only in the first trimester and active maternal smoking in the second and/or third trimesters but not throughout pregnancy were not significantly associated with SGA. With regard to the risk of preterm birth, the adjusted ORs for the above-mentioned three categories were not significant; however, the positive linear trend was significant (P for trend = 0.048). No significant association was found between active maternal smoking during pregnancy and the risk of low birth weight. There was a significant inverse relationship between active maternal smoking during pregnancy and birth weight; newborns of mothers who had smoked throughout pregnancy had an adjusted mean birth weight reduction of 169.6 g. When classifying babies by gender, a significant positive association between active maternal smoking throughout pregnancy and the risk of SGA was found only in male newborns, however, the interaction was not significant. Maternal ETS exposure at home or work was not significantly associated with any birth outcomes.ConclusionsThis is the first study in Japan to show that active maternal smoking throughout pregnancy, but not during the first trimester, is significantly associated with an increased risk of SGA and a decrease in birth weight. Thus, women who smoke should quit smoking as soon as possible after conception.

Mother's environmental tobacco smoke exposure during pregnancy and externalizing behavior problems in children

BackgroundWhile the impact of active maternal smoking during pregnancy on child health has been well investigated, the association between maternal passive smoking, or environmental tobacco smoke (ETS), or second-hand smoke, and behavioral development of offspring is less clear. This study examines the association between maternal ETS exposure during pregnancy and child behavior problems. MethodsCross-sectional data of 646 mother–child pairs from the Jintan China Cohort Study were used in the analyses. Mother's exposure to tobacco smoking at home, the workplace, and other places during pregnancy (for the determination of maternal ETS exposure) and children's behaviors (via Child Behavior Checklist) were assessed when the children were 5–6 years old. Logistic regression models were constructed to examine associations between maternal exposure to ETS during pregnancy and internalizing and externalizing behavior problems, adjusting for potential cofounders including child sex and parental characteristics. Results37% of mothers reported ETS during pregnancy. Children of mothers exposed to ETS during pregnancy had higher scores for externalizing and total behavior problems, with 25% of children whose mothers were exposed to ETS compared to 16% of children of unexposed mothers. After adjusting for potential confounders, ETS exposure was associated with a higher risk of externalizing behavior problems in offspring of exposed mothers (OR=2.08, 95% confidence interval [CI] 1.27–3.43). Analysis after multiple imputations and sensitivity analysis further verified the association, but no dose–response relationship was found. ETS exposure, however, was not associated with internalizing or total behavior problems. ConclusionThis study suggests that maternal ETS exposure during pregnancy may impact child behavioral development, particularly externalizing behaviors.

GSTM1 Modifies the Effect of Maternal Exposure to Environmental Tobacco Smoke on Neonatal Primitive Reflexes

The aim of this study was to examine whether infant metabolic gene polymorphisms modify the effect of maternal environmental tobacco smoke (ETS) on neonatal neurobehavior. We conducted a birth cohort study of 87 nonsmoking women who delivered single births of normal birth weight. We enrolled the women before delivery, interviewed them using a structured questionnaire, and collected umbilical cord blood. Umbilical cord cotinine, a blood indicator of prenatal ETS exposure, was analyzed. The Neonatal Neurobehavioral Examination-Chinese Version (NNE-C) was administrated within 5 days after delivery to examine neonatal neurobehavior. Four infant metabolic genes, CYP1A1 MspI, CYP1A1 Ile462Val, GSTT1, and GSTM1, were identified. Maternal ETS exposure during pregnancy was not related to neonatal neurobehavior when infant genetic polymorphisms were not considered. However, maternal ETS exposure did cause adverse effects in neonates with the absent type of GSTM1. Adverse effects were seen on the total NNE-C (β = -2.55; p = .02) and on primitive reflexes (β = -1.70; p = .004), especially in grasp reflexes (β = -.36; p = .011) and tonic neck reflexes (β = -.36; p = .049). In addition, there was a significant interaction between maternal ETS exposure and infant GSTM1 genotype on neonate grasp reflexes (p for interaction = .019). These data indicate that weaker responses in neonatal primitive reflexes in infants with the absent type GSTM1 were related to maternal ETS exposure during pregnancy.

CYP1A1 Modifies the Effect of Maternal Exposure to Environmental Tobacco Smoke on Child Behavior

Introduction: Maternal environmental tobacco smoke (ETS) has been identified as a key risk factor for problem behavior in children, but the role of genetic susceptibility is not clear. The purpose of this study was to examine the metabolic genetic modification effect of exposure to ETS in nonsmoking mothers on child behavior at 2 years of age. Methods: A prospective cohort study was conducted among 191 mothers who gave births between 2004 and 2005 and their infants in Taiwan. The mothers completed a questionnaire before delivery in which they provided information on exposure to ETS during pregnancy. Four metabolic genes, CYP1A1 MspI, CYP1A1 Ile462Val, GSTT1, and GSTM1 were isolated from both maternal and infant DNA samples. Children's behavior problems at 2 years of age were reported by their mothers using the Child Behavior Checklist/1.5-5. Multiple linear models were used to estimate the effects of ETS and genotype on child behavior. Results: Maternal ETS exposure was associated with the anxious score. The ETS-exposed group with both the CYP1A1 MspI and the CYP1A1 Ile462 Val variants had higher scores, as reflected in total CBCL score as well as scores on the internalizing scale and its emotional subdomain, the anxious scale, and the externalizing scale and its aggressive subdomain. Conclusions: Child behavioral problems may be associated with prenatal ETS exposure, and this effect may be modified by infant CYP1A1 MspI and CYP1A1 Ile462 Val genes.

GSTM1 Modify the Effect of Cord Blood Cotinine on Neurodevelopment at Three Days of Age

ISEE-0741 Background and Objective: Maternal exposure to environmental tobacco smoke (ETS) has been reported to be associated with children’s neurobehavioral development but there have been few studies investigating the genetic susceptibilities to maternal ETS exposure during pregnancy on children’s neurodevelopment. The potential health effects are still unclear. The aim of this study was to explore the modification effect of metabolic gene polymorphisms and cord blood cotinine levels on children’s neurodevelopment at three days of age. Methods: The study population was 117 mother-infant pairs who gave birth in Taiwan between August 2004 and January 2005 from Taiwan Birth Panel Study. We interviewed them using a structured questionnaire before delivery, collected umbilical cord blood at birth, and performed the Neonatal Neurobehavioral Examination–Chinese Version (NNE-C) after birth within three days. The NNE-C scale consisted of three parts: behavioral responses, tone and motor patterns, primitive reflexes, and each part contains nine items to test by trained physical therapists. The higher the score is, the poorer the child’s performance. The cotinine in cord blood was used as an indicator of environmental tobacco smoke and was analyzed by using HPLC-MS/MS. The detection limited of this method was 0.05 ng/mL. CYP1A1 MspI, CYP1A1 Ile462Val, GSTT1 and GSTM1 were identified from infant’s DNA. Multiple linear regression models were used to explore the effect of ETS exposure and gene interaction on early child neurodevelopment. Results: High cord blood cotinine exposure combined with a GSTM1 polymorphism was associated with a negative NNE-C score (b ± SE =−1.14 ± 0.47, P-value = 0.016) and a negative primitive reflexes score (b ± SE = −1.97 ± 0.87, P-value = 0.025). Conclusion: It can be concluded that the GSTM1 metabolic gene can modify the effect of maternal exposure to ETS on early child neurodevelopment.

CYP1A1 Ile462Val and GSTT1 modify the effect of cord blood cotinine on neurodevelopment at 2 years of age

Maternal exposure to environmental tobacco smoke (ETS) has been reported to be associated with children's neurobehavioral development but there was no studies investigating the genetic susceptibilities to maternal ETS exposure on children's neurodevelopment. The aim of the study was to explore the modification effect of metabolic gene polymorphisms to cord blood cotinine on children's neurodevelopment at the 2 years of age. This study is one investigation of the Taiwan Birth Panel Study and a total of 145 pregnant women and their neonates were recruited between April 2004 and January 2005. We interviewed them by a structured questionnaire after delivery and collected umbilical cord blood at birth. Cotinine in umbilical cord blood as an indicator of environmental tobacco smoke was analyzed by using HPLC–MS/MS and the detection limited of this method was 0.05 ng/mL. Four metabolic genes, CYP1A1 MspI, CYP1A1 Ile462Val, GSTT1 and GSTM1 were identified. The Comprehensive Developmental Inventory for Infants and Toddlers (CDIIT) was used for assessing children's neurodevelopment at the 2 years of age accompanying with the measurement of Home Observation for Measurement of the Environment scale. We used multiple linear regression models to estimate the effects of cord blood cotinine and gene modification. Cotinine levels were significantly negatively associated with developmental quotients (DQs) of the whole test, and cognitive, language, fine-motor and social subtests of the CDIIT. Lower cognitive and language DQs were found in exposed group with absent type of GSTT1. In addition, the lowest scores in fine-motor and whole test DQs were detected in exposed group with CYP1A1 Ile462Val variant type and GSTT1 absent type. It can be concluded that CYP1A1 Ile462Val and GSTT1 metabolic genes can modify the effect of cord blood cotinine on early child neurodevelopment especially for language and fine motor development.