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Background: A recent decline in the male:female (M:F) sex ratio may relate to pregnancy cigarette smoke exposure., Aim: To assess trends and cigarette exposure dose-response effects on the sex ratio., Subjects and Methods: A retrospective analysis was carried out of deliveries at the Liverpool Women's Hospital between 1998 and 2003, and of deliveries reported in community surveys from the same area in 1998 and 2006., Results: For the hospital sample, the M:F sex ratio was 1.14 if no parent smoked, and 0.77 when both parents smoked during the mother's pregnancy (p < 0.001). Heavy maternal smokers (>10 cigarettes per day) were more likely to deliver a female baby than light smokers (p < 0.001). Smoking was associated with increased likelihood of female birth controlling for birth year, socio-economic status, alcohol exposure, maternal haemoglobin and body mass index (adjusted OR: 1.41, 95% CI 1.12-1.92, p < 0.001). In the community sample controlling for socio-economic status the ratios were 1.13 (95% CI 1.03-1.24, p = 0.015) in 1998 and 1.31 (95% CI 1.16-1.48, p < 0.001) in 2006. Secular trends showed decreasing ratios in hospital and community samples for both smokers and non-smokers., Conclusion: Pregnancy cigarette smoking increased the proportion of female births with evidence for a dose-response association.

Background: Prenatal smoking exposure causes intrauterine fetal growth restriction (IUGR), although its effects on fetal proportionality are less clearly defined., Aim: The present study assessed fetal proportionality in babies with IUGR using maternal salivary cotinine to indicate maternal smoking exposure., Subjects and Methods: A case-control study at the Liverpool Women's Hospital, UK of babies with asymmetric and symmetric IUGR and non-growth restricted babies was carried out., Results: 270 white women including 90 IUGR cases and 180 controls were enrolled. Asymmetry presented in 52.2% of IUGR cases. Geometric mean maternal cotinine concentration was higher with asymmetric (p=0.002) than symmetric IUGR (p=0.07), when compared to controls. Maternal smoking exposure was independently associated with asymmetric IUGR (OR 2.4, 95% CI, 1.5-4.4, p

Background: Smoking is preventable factor for pregnancy outcomes such as low birth weight (LBW). In this study, we assessed the effects of smoking cessation in pregnancy period on the birth weight in Randomized Controlled Trial studies (RCTs). Methods: International databases of Pub Med, Scopus, and Web of Science, by the MeSH heading and/or additional terms, were searched to assess relevant studies in systematic possess. I2 statistics was used to assess of heterogeneity. Pooled effects size was obtained by random effects model. Meta-regression was used to explore of heterogeneity using Stata software version 12 (Stata Corp, College Station, TX). Results: A total 16 RCTs, 6192 women were enrolled to assess of smoking cessation in pregnancy period on the birth weight. Relative risk (RR) of not smoking at the end of pregnancy in intervention group was 2.47 (95% CI: 1.73-3.20). The odds ratio (OR) for effect of smoking cessation on LBW was 0.65 (95% CI: 0.42-0.88) and standardized mean difference (SMD) was significantly increased in the intervention group, 0.28 (95% CI: 0.05-0.50). Conclusions: Results of this study approve results of previous RCTs that smoking cessation in pregnancy is a good practical action to prevention of LBW in infants. [ABSTRACT FROM AUTHOR]

To assess the impact of parental asthma on risk of pre-term birth (PTB) and intrauterine growth restriction, and their subsequent association with childhood asthma. Three sequential cross-sectional surveys were conducted in 1993 (3,746), 1998 (1,964) and 2006 (1,074) in the same 15 schools among 5-11 year old children in Merseyside using the same respiratory health questionnaire completed by parents (sample size in brackets). Between 1993 and 2006, prevalence of PTB varied between 12.4 and 15.2 %, and of small for gestational age (SGA or growth restricted) babies between 2.1 and 4.6 %, and maternal asthma prevalence between 8.1 and 13.4 %. For the combined surveys mothers with asthma were more likely to have a PTB than non-asthmatic mothers (OR 1.39, 95 % CI 1.10-1.95, p < 0.001), and in the 2006 survey were more likely to have an SGA baby. 40.9 % of PTBs of asthmatic mothers developed doctor diagnosed asthma compared to 34.3 % for term babies (adjusted OR 1.65, 1.34-2.04, p < 0.001). The corresponding estimates for the symptom triad of cough, wheeze and breathlessness were 19.4 and 17.6 % (adjusted OR 1.78, 0.79-3.98). Conversely SGA babies were less likely to develop doctor diagnosed asthma (adjusted OR 0.49, 0.27-0.90, p < 0.021), or the symptom triad of cough, wheeze and breathlessness (adjusted OR 0.22, 0.05-0.97, p < 0.043), whether or not the mother was asthmatic. Maternal asthma is an independent risk factor for PTB which predisposes to childhood asthma. Intrauterine growth restriction was protective against childhood asthma. [ABSTRACT FROM AUTHOR]

Background: The combined dose response effects of pregnancy cigarette smoke exposure on childhood overweight, obesity and short stature have not been reported. Method: A community based cross-sectional survey of 3038 children aged 5–11 years from 15 primary schools in Merseyside, UK. Self-completed parental questionnaires were used for family characteristics, socio-economic status and parental smoking practices. Children were measured for height and weight and z-scores calculated for parental smoking categories. Results: Of 689 (34.0%) mothers who smoked during pregnancy 50.5% smoked ten or more cigarettes daily (heavy smokers). Children of maternal non-smokers had prevalence estimates for overweight, obesity and short stature of 25, 9.6 and 3.2%, respectively. Prevalence estimates were higher in children of mothers who were heavy smokers during pregnancy, 31.5% (P = 0.001), 15.6% (P < 0.001) and 5.5% (P = 0.001), respectively. Mean height for age z-scores was lower among heavy maternal (P < 0.001) and paternal smokers (P < 0.01) compared to non-smokers. Childhood overweight, obesity or short stature were all associated with heavy maternal smoking during pregnancy (all P < 0.001). Mean body mass index (BMI) z-scores were higher in boys of mothers who smoked (P = 0.043). The adjusted odds ratio for short stature in children of heavy maternal smokers was 2.76 (95% CI 1.21–6.33) and 4.28 (1.37–13.37) if both parents were heavy smokers. The adjusted OR for obesity in children of maternal smokers was 1.61(1.19–2.18). The population attributable risk for short stature was 8.8% (1.1–22.7) for heavy maternal smokers. Conclusion: A dose-response association was observed between pregnancy smoking exposure, short stature and obesity. [ABSTRACT FROM AUTHOR]

Abstract: Objectives: To determine the role of maternal CYP1A1, GSTT1, and GSTM1 metabolic gene polymorphisms in modulating the association between pregnancy smoking exposure and fetal growth restriction. Study design: A case-control study was conducted to investigate if the association of pregnancy smoking and birth outcome was modulated by maternal gene polymorphisms. A total of 90 mothers with an IUGR baby (cases) and 180 mothers without IUGR (controls) were enrolled. Results: Almost half of smokers who carried a CYP1A1 variant (51.3%), GSTT1 null (43.6%), or GSTM1 null genotypes (64.1%) delivered a baby with IUGR. Smokers with the variant CYP1A1 “aa” genotype had babies with lower mean birthweight than non-smokers with the same genotype (p =0.004). An interaction test showed increased prevalence of IUGR in smokers with the CYP1A1 (Aa/aa) variant (adjusted OR, 1.9; 95% CI, 1.4–5.5, p =0.01), or with the GSTT1 null (AOR, 1.5; 1.1–3.1, p =0.001), or GSTM1 null genotypes (AOR, 1.5; 1.2–3.7, p =0.001). Conclusions: Risk of fetal growth restriction in mothers who smoked during pregnancy was modulated by maternal metabolic gene polymorphisms. The genetic control of the conversion of toxic metabolites of tobacco smoke to less damaging substances is important for maternal and fetal health. [Copyright &y& Elsevier]

The role of salivary cotinine for monitoring maternal pregnancy smoking as an alternative to self-reported smoking exposure is not well established. This was a case-control study to assess the correlation between maternal self-reported pregnancy smoking exposure and postnatal salivary cotinine levels in 90 mothers with a baby with fetal growth restriction (cases) and 180 mothers with a normal birthweight for gestational age infant (controls) attending the Liverpool Women's Hospital for delivery between 2004 and 2005. Cases had increased exposure to cigarette smoke during pregnancy compared to controls. Using the salivary cotinine assay as the reference two-thirds of women, both cases and controls, correctly reported their smoking status during pregnancy. There are limitations with the accuracy of self-reported pregnancy smoking as an exposure indicator, especially in mothers delivering babies with Intrauterine fetal growth restriction (IUGR) who are also those most likely to smoke. In view of this there is a need to consider using salivary cotinine measurements In antenatal settings in order to facilitate monitoring of smoking exposure in pregnancy and for evaluation of deterrent interventions. [ABSTRACT FROM AUTHOR]

Cigarette smoking amongst pregnant adolescents is a preventable risk factor associated with low birthweight (<2500 g), preterm birth (<37 weeks) and infant mortality. The aim of this study was to compare birth outcomes of adolescents who smoke during pregnancy with those who do not and to construct their birthweight-for-gestational-age curves. Methods: A retrospective cohort analysis of 534 adolescents (≤19 years) and 8972 adults who delivered singleton births between 1998-2003 at the Liverpool Women's Hospital. Results: Adolescent pregnancy occurred in 5.6% of deliveries. Mean age of adolescents was 18.1 years (SD = 1.0) and 46.2% smoked during pregnancy including 83.5% light smokers (<10 cigarettes daily). Babies born to adolescent smokers were significantly lighter by 170g(P=0,005). The prevalence of low birthweight was almost double in adolescents who smoked (12.1% versus 6.8%, RR = 1.7; Cl = 1.0-3.0), and their mean Apgar scores at 5 rain were lower (<0.05). A higher prevalence of preterm birth (P < 0.05) and maternal anaemia (P < 0.01) occurred amongst adolescent smokers. Adolescents smoking >10 cigarettes daily had babies with larger birthweight reduction (P = 0.001). Conclusion: Almost half of all adolescents smoked during their pregnancy. Birthweight-for-gestationalage curves of smoking adolescents showed a marked fall-off in weight from 36 weeks of gestation, and at least 10% of adolescent smokers showed fetal growth restriction from before 32 weeks of gestation. [ABSTRACT FROM AUTHOR]