Prenatal nicotine exposure alters pulmonary function in newborn rhesus monkeys

Epidemiological studies have shown that offspring of women who smoke during pregnancy have abnormal lung function and associated higher incidences of lower respiratory disorders. The recent identification of nicotinic acetylcholine receptors (nAChR) in fetal lung suggests that the direct interaction between nicotine and nAChR in fetal lung may underlie the postnatal pulmonary abnormalities seen in such infants. This hypothesis was tested in monkeys to determine if maternal nicotine exposure would produce changes in lung mechanics in newborn monkeys similar to those observed in human infants whose mothers smoked during pregnancy. Timed pregnant rhesus monkeys were infused with either nicotine (1.5 mg/kg/d, n = 7) or saline (n = 7) using subcutaneous osmotic pumps from Day 26 to 160 of gestation. On Day 160 of pregnancy (term = 165 d), fetuses were delivered by C-section, and the following day were subjected to pulmonary function testing. After testing, animals were sacrificed, and lungs weighed and fixed. Lung weight and fixed lung volume decreased (16% and 14%, respectively) significantly following in utero nicotine exposure. Peak tidal expiratory flow, FEV(0.2), mean mid-expiratory flow, forced expiratory volume at peak expiratory flow (FEV(PEF)), and FEV(PEF)/FVC% were significantly lower in newborns exposed to nicotine during gestation. Absolute and specific pulmonary resistance increased significantly whereas absolute and specific dynamic compliance remained unchanged in prenatally nicotine-treated pups. These changes in pulmonary function are strikingly similar to the changes observed in offspring of human smokers. This suggests that the interaction of nicotine with nAChR in developing lung is responsible for the altered pulmonary mechanics observed in human infants whose mothers smoked during pregnancy.     

Similar associations of parental prenatal smoking suggest child blood pressure is not influenced by intrauterine effects

Maternal smoking in pregnancy may be associated with higher offspring blood pressure; however, results of previous studies have been inconsistent and included varying confounder adjustments. We studied the association between maternal smoking in pregnancy and offspring blood pressure at 7 years in the Avon Longitudinal Study of Parents and Children, accounting for important social and environmental confounders and using partner smoking to investigate intrauterine effects. Analysis was carried out in 6509 children with maternal smoking data and 7149 children with partner smoking data. In models adjusting for child age and sex, modest differences in systolic blood pressure were observed between children of mothers who did and did not smoke during pregnancy (beta=0.64 mm Hg; 95% CI: 0.09 to 1.20; P=0.02). Adjusting for all of the confounders attenuated this difference toward the null (beta=0.05 mm Hg; 95% CI: -0.59 to 0.68; P=0.9), mostly because of adjustment for breastfeeding, maternal education, and family social class. Associations were similar between maternal and partner smoking with offspring systolic blood pressure (for partner smoking: beta=0.62 mm Hg; 95% CI: 0.17 to 1.07; P=0.07 minimally adjusted and beta=0.26 mm Hg; 95% CI: -0.36 to 0.87; P=0.4 fully adjusted), providing further evidence that differences in child blood pressure observed in minimally adjusted models are not because of a biological influence of maternal smoking on the intrauterine environment.     

The effect of parental smoking on lung function and development during infancy

While the adverse effects of parental smoking on respiratory health during childhood are well recognized, its potential impact on early lung development is less clear. This review summarizes current evidence on the effect of parental smoking on lung function during infancy. It is difficult to separate the effects of pre- and postnatal exposure, since the majority of mothers who smoke in pregnancy (currently around 30% worldwide) continue to do so thereafter. Nevertheless, measurements undertaken prior to any postnatal exposure have consistently demonstrated significant changes in tidal flow patterns in infants whose mothers smoked in pregnancy. While there is, as yet, no convincing evidence from studies in human infants that smoking during pregnancy is associated with increased airway responsiveness at birth, many studies have demonstrated a reduction in forced expiratory flows (on average by 20%) in infants exposed to parental smoking. While maternal smoking during pregnancy remains the most significant source of such exposure and is likely to be responsible for diminished airway function in early life, continuing postnatal tobacco smoke exposure will increase the risk of respiratory infections, the combination of both being responsible for the two- to fourfold increased risk of wheezing illnesses observed during the first year of life in infants whose parents smoke. These findings emphasize the need to keep infants in a smoke-free environment both before and after birth, not least because of growing awareness that airway function in later life is largely determined by that during foetal development and early infancy.     

The effect of maternal smoking during pregnancy on early infant lung function.

We studied the effect of prenatal maternal cigarette smoking on the pulmonary function (PF) of 80 healthy infants tested shortly after birth (mean, 4.2 +/- 1.9 wk). Mothers' prenatal smoking was measured by: (1) questionnaire reports at each prenatal visit of the number of cigarettes smoked per day, and (2) urine cotinine concentrations (corrected for creatinine) obtained at each visit. Infant PF was assessed by partial expiratory flow-volume curves and helium-dilution measurement of FRC. Forced expiratory flow rates were significantly lower in infants born to smoking mothers, both when unadjusted and after controlling for infant size, age, sex, and passive exposure to environmental tobacco smoke (ETS) between birth and the time of PF testing. Flow at functional residual capacity (VFRC) in infants born to smoking mothers was lower than that found in infants whose mothers did not smoke during pregnancy (74.3 +/- 15.9 versus 150.4 +/- 8.9 ml/s; p = 0.0007). Differences remained significant when flow was corrected for lung size (VFRC/FRC: 0.87 +/- 0.26 versus 1.77 +/- 0.12 s-1; p = 0.013). No differences in pulmonary function were evident among infants exposed and unexposed to ETS in the home after stratifying by prenatal exposure status. We conclude that maternal smoking during pregnancy is associated with significant reductions in forced expiratory flow rates in young infants. The results suggest that maternal smoking during pregnancy may impair in utero airway development and/or alter lung elastic properties. We speculate that these effects of maternal prenatal smoking on early levels of forced expiratory flow may be an important factor predisposing infants to the occurrence of wheezing illness later in childhood.     

Parental smoking and risk of coeliac disease in offspring

OBJECTIVE: In adults, smoking seems to give protection against coeliac disease (CD). But, only one study has thus far investigated the association between maternal smoking during pregnancy and risk of CD in offspring. However, that study did not adjust for duration of exclusive breastfeeding, or look at passive smoking after birth. MATERIAL AND METHODS: The current study was part of a prospective cohort study of infants born between 1 October 1997 and 1 October 1999 (the ABIS study; All Babies in Southeast Sweden). Data on smoking and exclusive breastfeeding were obtained through questionnaires distributed at infant birth and at 1 year of age. Coeliac disease was confirmed through small-bowel biopsy. Subgroup analyses were carried out according to maternal body mass index. RESULTS: Nine out of 53 (17%) children with CD as opposed to 1699 out of 15,344 (11.1%) non-coeliac children had mothers who had smoked during pregnancy (p = 0.172). Mothers who had smoked during pregnancy were hence not at increased risk of having a child with CD (OR = 1.64; 95% CI OR =0.80-3.37). Adjusting for duration of exclusive breastfeeding and the sex of infants in some 9585 children with data on exclusive breastfeeding lowered the OR for CD in mothers who smoked (adjusted OR (AOR) =0.89; 95% CI AOR = 0.27-2.93; p =0.843). Parents who smoked during the child's first year of life were not at increased risk of having an offspring with CD (OR = 1.94; 95% CI AOR =0.69-5.47; p =0. 203). CONCLUSIONS: No association was found between CD and parental smoking habits during pregnancy or during the child's first year of life. However, further studies with larger numbers of coeliac children are needed.     

Effect of smoking on neonatal and maternal serum and breast milk leptin levels

Maternal smoking is considered to be a risk factor for low birth weight. It is hypothesized that alteration in leptin concentration may be associated with reduced fetal growth. In this study, we assess the effect of smoking during pregnancy on maternal and neonatal serum leptin concentrations, and also on breast milk leptin levels. When the infants were brought to routine physical examination at 7 days old, blood samples and breast milk specimens were taken for leptin measurement from mothers who smoked during pregnancy and their newborns. Nonsmoking mothers and their infants were recruited randomly over the same period as a control group. Maternal age, number of pregnancy, weight of the mothers, birth weight, and gestational age of the infants were similar in both groups (p > 0.05). There was no significant difference between groups in maternal serum and breast milk leptin levels (p = 0.14 and p = 0.96, respectively). However, serum leptin levels were found significantly lower in neonates born to smoking mothers compared with infants born to nonsmoking mothers (p = 0.02). Our findings suggest that maternal smoking dose not have an effect on maternal serum and breast milk leptin levels but decreases neonatal serum leptin concentration independent of birth weight.     

Does hypertensive disorder of pregnancy predict offspring blood pressure at 21 years? Evidence from a birth cohort study

Although few studies found that the offspring of women who experienced preeclampsia have higher blood pressure (BP) at childhood and adolescence, no study has observed whether this association exists for adult offspring. To examine whether maternal hypertensive disorder of pregnancy (HDP) predicts adult offspring BP. We followed a sub-sample of 2608 mother-offspring pairs for 21 years from an original cohort of 7223 singleton infants whose mothers gave birth in Brisbane, Australia between 1981 and 1983. HDP was defined as diastolic BP (DBP) over 90?mm?Hg on at least two occasions beyond 20 weeks gestation associated with proteinuria and/or excessive fluid retention. Adult offspring's systolic BP (SBP) and DBP were measured at 21 years. Multivariable regressions were used to examine the independent associations of HDP with offspring BP. Unadjusted regression analysis showed that offspring of women who experienced HDP have 3.46?mm?Hg greater SBP and 3.02?mm?Hg greater DBP at 21 years. This association remained consistent after adjusting for potential confounding and mediating factors including offspring gender, age, percentile birth weight for gestation, placenta weight and body mass index (BMI) at 21 year, maternal age, education, racial origin, and smoking during pregnancy and their pre-pregnancy BMI. Findings of this study suggest that maternal HDP predicts adult offspring BP.     

Smoking cessation or reduction in pregnancy treatment methods: a meta-evaluation of the impact of dissemination

Active and passive exposure to tobacco smoke during pregnancy and infancy is the most serious and preventable cause of adverse maternal, fetal, and infant outcomes in the United States. The multiple risks of tobacco exposure to mothers and infants are definitive, and the clinical and economic benefits of cessation have been documented. This article provides a synopsis of the state of the science and art in this specialized area and reviews the evidence for validity of patient assessment methods and the effectiveness of smoking cessation/reduction treatments for pregnant women. A synthesis of 4 topics is presented: (1) the validity of patient reports of smoking status and recent trends during pregnancy and postpartum; (2) definition of "Best Practice" smoking cessation methods for pregnant women; (3) the effect of dissemination of effective clinical practice methods among the 800,000+ pregnant US smokers each year; and (4) the evidence for the cost-benefit of improved maternal and infant outcomes from cessation.     

Maternal Smoking and Environmental Tobacco Smoke Exposure and the Risk of Allergic Diseases in Japanese Infants: The Osaka Maternal and Child Health Study

Purpose. It remains controversial whether environmental tobacco smoke increases the risk of allergic diseases. The present prospective cohort study examined whether in utero exposure to maternal smoking and postnatal exposure to environmental tobacco smoke were associated with the development of wheeze, asthma, and atopic eczema in Japanese infants. Methods. Study subjects included 763 infants. Data were obtained through the use of questionnaires completed by the mother during pregnancy and at 2 to 9 and 16 to 24 months postdelivery. Information regarding maternal smoking during pregnancy and postnatal exposure to environmental tobacco smoke was collected at 2 to 9 months postdelivery, and information on allergic symptoms was collected when the infant was between 16 to 24 months of age. Cases were defined according to criteria of the International Study of Asthma and Allergies in Childhood for wheeze and atopic eczema. Additionally, doctor-diagnosed asthma and atopic eczema were identified. Adjustment was made for maternal age, family income, maternal and paternal education, parental history of asthma, atopic eczema, allergic rhinitis, indoor domestic pets, baby's older siblings, baby's sex, birth weight, and time of surveys. Results. The cumulative incidence of wheeze, atopic eczema, doctor-diagnosed asthma, and doctor-diagnosed atopic eczema was 22.1%, 18.6%, 4.3%, and 9.0%, respectively. Maternal smoking during pregnancy was not related to the risk of wheeze, whereas postnatal maternal smoking in the same room as the child increased the risk of wheeze. No significant association was observed between perinatal tobacco smoke exposure and the development of asthma and atopic eczema. Conclusions. Our findings suggest that postnatal maternal smoking might be associated with an increased risk of wheeze in Japanese infants.     

Exposure to second-hand smoke and reproductive outcomes depending on maternal asthma

Tobacco consumption and exposure to second-hand smoke (SHS) are associated with reduced birth weight. One issue that has not been clarified previously is that of the potential higher risk of this outcome in mothers with asthma. We assessed the role of prenatal maternal tobacco use and SHS on reproductive outcomes and assessed the interaction with maternal history of asthma. Data was collected from the INMA study, a maternal birth cohort selected from the general population established in Spain in 2002. We measured cotinine at the 32nd week of pregnancy in 2,219 females. Diagnosed maternal asthma was self-reported during pregnancy. 35% of mothers reported not being exposed to smoking or SHS during pregnancy. Active smoking (i.e. self-reported or cotinine >50 ng·mL(-1)) was related to a 134 g decrease in birth weight and a relative risk of 1.8 for small for gestational age and fetal growth restriction. These results were not modified by maternal asthma. Maternal asthma had a similar frequency in all exposure groups. Non SHS-exposed females had the lowest prevalence of asthma. SHS (i.e. cotinine 20-50 ng·mL(-1)) decreased birth weight by 32 g among those without maternal asthma, but these differences were not statistically significant (95% CI -88.76-24.76). Maternal asthma did not promote these effects. Maternal history of asthma did not modify the effects of smoking on reproductive outcomes in a cohort sampled from the general population.     

Maternal exposure to smoking and infant's wheeze and asthma: Japan Environment and Children's Study

BackgroundEvidence regarding independent effects of maternal smoking in different time frames of pregnancy and maternal exposure to secondhand smoke on the development of wheeze/asthma in her offspring is limited. We aimed to investigate the effect of maternal exposure to tobacco smoke on wheeze/asthma development at 1 year of age in her offspring using data from the nationwide birth cohort study in Japan.MethodsPregnant women who lived in the 15 designated regional centers throughout Japan were recruited. We obtained information about maternal smoking or secondhand smoke status and wheeze/asthma development in the offspring from a self-administered questionnaire.ResultsWe analyzed 90,210 singleton births. Current maternal smoking during pregnancy increased the risks of wheeze/asthma in the offspring compared with no maternal smoking (wheeze: 1–10 cigarettes/day: adjusted odds ratio (aOR) 1.436, 95% CI 1.270–1.624; ≧11 cigarettes/day: aOR 1.669, 95% CI 1.341–2.078; asthma: 1–10 cigarettes/day: aOR 1.389, 95% CI 1.087–1.774; ≧11 cigarettes/day: aOR 1.565, 95% CI 1.045–2.344). Daily maternal exposure to secondhand smoke during pregnancy also increased the risks of wheeze/asthma in her offspring compared with no secondhand smoke exposure (wheeze: aOR 1.166, 95% CI 1.083–1.256; asthma: aOR 1.258, 95% CI 1.075–1.473). The combination of current maternal smoking during pregnancy and maternal history of allergy increased the risks of wheeze/asthma in her offspring (wheeze: aOR 2.007, 95% CI 1.739–2.317; asthma: aOR 1.995, 95% CI 1.528–2.605).ConclusionsWe found that current maternal smoking and maternal secondhand smoke exposure during pregnancy increased the risks of wheeze and asthma in her offspring.     

Perinatal smoking exposure and risk of asthma in the first three years of life: A prospective prebirth cohort study

BackgroundThere is limited evidence on the association between prenatal smoking exposure and the risk of asthma in children. The aim of this prebirth cohort study was to investigate the association between prenatal and postnatal tobacco smoke exposure and the risk of asthma in Japanese children.MethodsStudy subjects were 1304 mother–child pairs. Information on the variables under study was obtained using repeated questionnaires that were completed by mothers, first prior to delivery, then shortly after birth and subsequently around 4, 12, 24, and 36 months after delivery. Ever asthma was defined as a maternal report of physician-diagnosed asthma at any time since birth. Current asthma was defined as the use of asthma medication at the time of the sixth survey.ResultsLogistic regression models revealed that maternal active smoking, either before pregnancy or during pregnancy, was not associated with the risk of ever asthma or current asthma. Further, no association was observed between postnatally living with at least one household smoker and the risk of asthma. Among children whose mothers are never smokers, maternal second-hand smoke (SHS) exposure at work and/or at home during pregnancy increased the risk of ever asthma and current asthma in children; adjusted odds ratio (95% confidence intervals) for ever asthma and current asthma were 2.41 (1.13–5.05) and 4.82 (1.68–13.43), respectively.ConclusionsOur findings suggest that maternal SHS exposure during pregnancy might be associated with an increased risk of ever asthma and current asthma in young children whose mothers have never smoked.     

Two Generations of Maternal Alcohol Consumption in Mice: Effect on Pregnancy Outcome

This study investigated whether female offspring of alcohol-treated mothers are, themselves, more or less susceptible than control offspring to the deleterious effects of alcohol on the outcome of their own pregnancy. One group of pregnant C57BL mice was fed a liquid diet containing 25% ethanol-derived calories (EDC) and another group was pair-fed an isocaloric (0% EDC) control diet. A third group was fed lab chow ad libitum (LC). The female offspring resulting from those matings were subsequently mated upon reaching 90 days of age. These pregnant mice were then separated into three prenatal treatments (25% EDC, 0% EDC, and LC). On gestation-day 19, second generation fetuses were removed by cesarean section, weighed, and sexed. Results indicated that number of implants, live births, and percent prenatal mortality did not differ between groups. However, fetal weight was lower in groups prenatally exposed to ethanol than in controls, regardless of the prenatal history of the mothers, themselves. More importantly, the data suggest that offspring of alcohol-treated mothers who do not consume alcohol themselves during their own pregnancy may still have a tendency to have offspring of lower birth weight. On the other hand, if mothers prenatally exposed to alcohol do consume alcohol during their own pregnancy, the impact of fetal weight suppression is even greater than expected for in utero alcohol exposure alone. These effects may be due to the fact that mothers who were prenatally exposed to alcohol weighed less than controls at the time of becoming pregnant.(ABSTRACT TRUNCATED AT 250 WORDS)     

Salivary cotinine levels in children presenting with wheezing to an emergency department

We set out to evaluate salivary cotinine concentrations to judge tobacco smoke exposure among infants and children, and to examine the results in relation to age and wheezing. This was a case-control study of wheezing children (n = 165) and children without respiratory tract symptoms (n = 106) who were enrolled in the Pediatric Emergency Department at the University of Virginia. The age range of both wheezing and control patients was 2 months to 16 years. Questionnaires were combined with cotinine assays in saliva to evaluate exposure to environmental tobacco smoke (ETS) for each child. The prevalence of exposure to one or more smokers at home was high (68%); and 43% of the children enrolled were exposed to ETS from their mothers. According to the questionnaires, and after adjusting for age and race, a wheezing child in this study was more likely than a control to be exposed to at least one smoker at home (odds ratio = 1.9; 95% CI = 1.1-3.4). However, the odds of exposure to ETS from smoking mothers did not differ significantly between wheezing and control patients, and no significant association was found between the presence of wheezing and salivary cotinine levels. Among children exposed to ETS at home, cotinine levels were significantly higher in saliva from those under the age of two years, and from toddlers aged 2 and 3 years, compared to values from children over age 4 years. Moreover, the number of smokers in the home strongly influenced cotinine levels from children under age 4 years. In addition, higher cotinine levels were observed in saliva from children under age 2 years who were exposed to ETS from their mothers. Cotinine levels were similar and significantly correlated in paired samples of saliva and serum from children under 4 years of age (n = 54), (r = 0.92, P < 0.001). Based on information gathered from questionnaires, the results indicate that wheezing children were more likely than controls to be exposed to ETS at home. However, significant differences in ETS exposure between wheezing and control groups with respect to maternal smoke exposure or comparisons of salivary cotinine levels were not apparent. It was clear that determinations of salivary cotinine for monitoring the prevalence and intensity of household smoke exposure in this study were most valuable during the first 4 years of life.     

Trial of an intervention to reduce passive smoking in infancy

We tested a health education intervention program to reduce passive smoking in infancy. The aim was to develop an instrument for study of tobacco smoke exposure and childhood respiratory illness. One hundred and eighty-four women who had smoked during pregnancy were allocated by month of delivery to an intervention group, to a minimal contact group, or to a follow-up only comparison group. Exposure to smoke was assessed 3 months later by questionnaire and by measurement of cotinine in samples of maternal and infant urine. There was a reduction in maternal smoking associated with contact with research staff, but this was not statistically significant. There were no differences between the groups in the exposure of infants to tobacco smoke. Reasons for this finding may include the timing of the intervention, the heterogeneity of the target group, and the manner in which information was presented on health risks caused by parental smoking.     

The influence of maternal body mass index,maternal diabetes mellitus,and maternal smoking during pregnancy on the risk of childhood‐onset type 1 diabetes mellitus in the offspring: Systematic review and meta‐analysis of observational studies

There is emerging evidence that events occurring before and shortly after birth may be important in determining the risk of childhood‐onset type 1 diabetes mellitus (T1DM). We aimed to summarize and synthesize the associations between maternal body mass index (BMI), maternal diabetes mellitus (DM), and maternal smoking during pregnancy and the risk of childhood‐onset T1DM in the offspring by performing a systematic review and meta‐analysis of observational studies. A random effects model was used to generate the summary risk estimates. The PubMed and Web of Science databases were searched to identify relevant observational studies. Twenty one observational studies were included in the present meta‐analysis. Compared with offspring of mothers with normal weight, offspring of women with overweight or obesity were at an increased risk of developing childhood‐onset T1DM (overweight: relative risk [RR] 1.09, 95% confidence interval [CI], 1.03‐1.15; obesity: RR 1.25, 95% CI, 1.16‐1.34; per 5 kg m^?2 increase in BMI: RR 1.10, 95% CI, 1.06‐1.13). No association was found for maternal underweight (RR 0.92, 95% CI, 0.75‐1.13). Maternal DM was associated with an increased risk of childhood‐onset T1DM (RR 3.26, 95% CI, 2.84‐3.74). Regarding the type of maternal DM, the greatest risk of T1DM in the offspring appeared to be conferred by maternal T1DM (RR 4.46, 95% CI, 2.89‐6.89), followed by maternal gestational diabetes mellitus (RR 1.66, 95% CI, 1.16‐2.36), and lastly by maternal type 2 diabetes mellitus (RR 1.11, 95% CI, 0.69‐1.80). Additional analysis of studies comparing maternal versus paternal T1DM within the same population revealed that offspring of fathers with T1DM had a 1.5 times higher risk of developing childhood‐onset T1DM than offspring of mothers with T1DM (RR 9.58, 95% CI, 6.33‐14.48 vs. RR 6.24, 95% CI, 5.52‐7.07). Furthermore, a reduced risk of childhood‐onset T1DM was observed in infants born to mothers who smoked during pregnancy compared with infants born to mothers who did not smoke during pregnancy (RR 0.79, 95% CI, 0.71‐0.87). In summary, our findings add further evidence that early‐life events or environmental factors may play a role in modulating infants' risk of developing T1DM later in life.     

Parental smoking and risk of coeliac disease in offspring

Objective. In adults, smoking seems to give protection against coeliac disease (CD). But, only one study has thus far investigated the association between maternal smoking during pregnancy and risk of CD in offspring. However, that study did not adjust for duration of exclusive breastfeeding, or look at passive smoking after birth. Material and methods. The current study was part of a prospective cohort study of infants born between 1 October 1997 and 1 October 1999 (the ABIS study; All Babies in Southeast Sweden). Data on smoking and exclusive breastfeeding were obtained through questionnaires distributed at infant birth and at 1 year of age. Coeliac disease was confirmed through small-bowel biopsy. Subgroup analyses were carried out according to maternal body mass index. Results. Nine out of 53 (17%) children with CD as opposed to 1699 out of 15,344 (11.1%) non-coeliac children had mothers who had smoked during pregnancy (p=0.172). Mothers who had smoked during pregnancy were hence not at increased risk of having a child with CD (OR=1.64; 95% CI OR=0.80–3.37). Adjusting for duration of exclusive breastfeeding and the sex of infants in some 9585 children with data on exclusive breastfeeding lowered the OR for CD in mothers who smoked (adjusted OR (AOR)=0.89; 95% CI AOR=0.27–2.93; p=0.843). Parents who smoked during the child's first year of life were not at increased risk of having an offspring with CD (OR=1.94; 95% CI AOR=0.69–5.47; p=0. 203). Conclusions. No association was found between CD and parental smoking habits during pregnancy or during the child's first year of life. However, further studies with larger numbers of coeliac children are needed.     

Etiologic correlates in a study of congenital heart disease in 56,109 births

From a prospective study of 56,109 total births some incidence factors and etiologic correlates for congenital heart disease have been identified. The risk of congenital heart disease in infants with Down's syndrome was found to be 1:3, for the offspring of mothers with congenital heart disease 1:20, for the offspring of diabetic mothers 1:39, and for twin infants 1:61. Data from the offspring of mothers with congenital heart disease and from offspring who are twins or siblings of twins suggest that there may be a relatively large element of inheritance in the etiology of pulmonary stenosis. The risk of a great vessel abnormality for offspring of diabetic mothers is reaffirmed. The role of maternal age in the production of congenital heart disease in the offspring is assessed, and several correlates of transposition of the great vessels are identified. Preliminary data are presented on the association of maternal viral infection with congenital heart disease in the offspring.     

Tobacco smoke exposure, wheeze, and atopy

We investigated the effect of in utero and postnatal environmental tobacco smoke (ETS) exposure on respiratory symptoms and atopy in the first 3 years of life in children at high risk of allergic disease (both parents atopic). Three hundred and sixty-nine children were followed from birth and reviewed at ages 1 and 3 years (respiratory questionnaire, skin testing). Parental smoking questionnaires were administered, and plasma cotinine in cord and peripheral blood (at age 1 year) was measured (capillary column gas-liquid chromatography). Wheezing starting in the first year of life was significantly more common in children of smoking mothers (54.2% vs. 39.5%, P = 0.017), but not wheezing starting after age 1 year (10.8% vs. 10.9%, smoking and nonsmoking mothers, P = 0.99). Detectable cord cotinine was not associated with wheeze. More frequent wheeze in infancy was significantly more common in those with detectable 1-year cotinine (e.g., wheeze without colds, 17.8% vs. 5.6%, P = 0.02; wheeze most days, 6.5% vs. 0%, P = 0.04). ETS exposure was not associated with atopy. In the multivariate regression analysis, maternal smoking during pregnancy and/or in the first year of life remained associated with wheeze in the first year of life (odds ratio, 1.88; 95% confidence interval, 1.14-3.12; P = 0.01). ETS exposure in "high-risk" infants increases the risk of wheezing starting in the first year of life, but not after age 1 year. However, ETS exposure has little or no effect on the development of atopy. Measurement of plasma cotinine was no more useful than tobacco exposure assessment by questionnaire in our cohort.     

Pre- and postnatal parental smoking and wheeze in infancy: cross cultural differences. Avon Study of Parents and Children (ALSPAC) Study Team, European Longitudinal Study of Pregnancy and Childhood (ELSPAC) Co-ordinating Centre.

In longitudinal cohort studies, the relationships between prenatal and postnatal tobacco smoke exposure and infant wheezing illnesses were compared in two geographically defined populations in Avon, UK and Brno and Znojmo in the South Moravian Region of the Czech Republic. Pregnant females living in defined regions and with expected dates of delivery between defined dates were recruited. Females completed self-report questionnaires during pregnancy and when their infant was 6 months old. For this analysis, responses to questions about smoking during pregnancy, environmental tobacco smoke (ETS) exposure and reported wheezing illnesses of infants at 6 months after birth were used. Odds ratios for wheeze in relation to the smoking variables were calculated with adjustment for potential confounding effects. The prevalence of smoking during pregnancy was higher in Avon (17.5%) than the Czech Republic (7.1%). Exposure of infants to ETS during the first 6 months after birth was also reported to be higher in Avon (35.5%) than the Czech Republic (9.7%). The prevalence of reported wheezing by 6 months of age was 21.4% in Avon and 10.3% in Brno and Znojmo. In Avon, there was a significant relationship between infant wheeze and maternal smoking during pregnancy (odds ratio (95% confidence interval) 1.30 (1.09-1.56), p=0.004) but not with environmental exposure after birth (1.11 (0.98-1.25)). In contrast, in Brno and Znojmo in the Czech Republic, there was a significant relationship between infant wheeze and ETS exposure (1.66 (1.17-2.36), p=0.04) but not with maternal smoking during pregnancy (0.99 (0.64-1.55)). This study demonstrated an apparent difference in the associations between prenatal and postnatal tobacco smoke exposure and infant wheezing illnesses in two populations with different smoking prevalence. The relationships were independent of a number of potential confounding variables that have been associated with infant wheezing. Possible explanations of these observations include dose-related effects of prenatal and postnatal tobacco smoke exposure of infants.