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Maternal Smoking (maternal + smoking)
Selected AbstractsEffects of maternal smoking in pregnancy on prenatal brain development.EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 3 2007The Generation R Study Abstract Nicotine, as has been shown in animal studies, is a neuroteratogen, even in concentrations that do not cause growth retardation. In humans, there is only indirect evidence for negative influences of nicotine on brain development from studies on the association between maternal smoking in pregnancy and behavioural and cognitive development in the offspring. We investigated the associations of maternal smoking in pregnancy with foetal head growth characteristics in 7042 pregnant women. This study was embedded in the Generation R Study, a population-based prospective cohort study from foetal life until adulthood. Maternal smoking was assessed by questionnaires in early, mid- and late pregnancy. Head circumference, biparietal diameter, transcerebellar diameter and atrial width of lateral ventricles were repeatedly measured by ultrasound. When mothers continued to smoke during pregnancy, foetal head circumference showed a growth reduction of 0.13 mm [95% confidence interval (CI): ,0.18, ,0.09] per week compared to foetuses of mothers who never smoked during pregnancy. Biparietal diameter of foetuses with smoking mothers grew 0.04 mm (95% CI: ,0.05, ,0.02) less per week than that of foetuses of nonsmoking mothers. Atrial width of lateral ventricle was 0.12 mm (95% CI: ,0.22, ,0.02) smaller and transcerebellar diameter was 0.08 mm (95% CI: ,0.15, ,0.00) smaller if mothers smoked, but growth per week of these characteristics was not affected by maternal smoking in pregnancy. In conclusion, continuing to smoke during pregnancy leads to reduced growth of the foetal head. Further research should focus on the causal pathway from prenatal cigarette exposure via brain development to behavioural and cognitive functions. [source] Hypoplasia of the arcuate nucleus and maternal smoking during pregnancy in sudden unexplained perinatal and infant deathNEUROPATHOLOGY, Issue 4 2004Anna Maria Lavezzi Maternal smoking during pregnancy is the most important risk factor for sudden perinatal and infant death in more industrialized countries. The frequent observation of hypoplasia of the arcuate nucleus in the brainstem of these victims prompted the verification of whether maternal cigarette smoking could be related to defective development of this nucleus during intrauterine life, by affecting the expression of specific genes involved in its developmental process. In serial sections of the brainstem of 54 cases of sudden and unexplained fetal and infant deaths (13 stillbirths, 7 neonatal deaths and 34 sudden infant death syndrome (SIDS) victims), morphological and morphometrical analysis was used to observe the different structural alterations of the arcuate nucleus (bilateral hypoplasia, monolateral hypoplasia, partial hypoplasia, delayed neuronal maturation and decreased neuronal density) detected in 24 cases (44%). Correlating this finding with smoking in pregnancy, a significantly increased incidence of cytoarchitectural alterations of the arcuate nucleus was found in stillborns and SIDS victims with smoker mothers compared to victims with non-smoker mothers. Moreover, the observation of a wide range of developing morphological defects of the arcuate nucleus related to maternal smoking led to the hypothesis that the constituents of the gas phase in cigarette smoke could directly affect the expression of genes involved in the development of this nucleus, such as the homeobox En-2 gene. [source] Maternal smoking during pregnancy: a comparison between concurrent and retrospective self-reportsPAEDIATRIC & PERINATAL EPIDEMIOLOGY, Issue 2 2008Ann Post Summary Retrospective reports of smoking in pregnancy are of importance for clinical or scientific purposes. Careful analyses of stability and accuracy of recalled behaviour are, therefore, needed. In 1998, the mothers of 2369 pre-teens born in Sweden retrospectively reported their smoking behaviour during the first trimester of the index pregnancy. We matched these reports with those recorded by midwives at the beginning of the index pregnancy, using information from the Swedish Medical Birth Registry. Using this registry as gold standard, the sensitivity and specificity of the retrospective reports containing any smoking were 83.9% and 92.8% respectively, but the sensitivity was low for daily smoking, 56.0%. Of the 222 discordant reports, 19.0% were due to mothers recalling daily smoking which was not reported at the time of pregnancy, and 42% were due to failure to recall smoking reported at the time of pregnancy, while the remaining 39% retrospectively reported occasional smoking, whereas they were registered as non-daily smokers when pregnant. Retrospective recall of pregnancy smoking is fairly stable over time. [source] Interactions between fetal HLA-DQ alleles and maternal smoking influence birthweightPAEDIATRIC & PERINATAL EPIDEMIOLOGY, Issue 5 2006G. Malcolm Taylor Summary Maternal smoking during pregnancy inhibits fetal growth, and is a major cause of childhood and adult morbidity, including increased risks of cardiovascular disease and diabetes. However, the use of birthweight as a proxy for future smoking-related morbidity is hindered by its wide variability, suggesting a role for other birthweight-modifying factors. We report here, for the first time, that interactions between specific fetal HLA-DQA1 and DQB1 alleles and maternal smoking can influence birthweight. We compared mean birthweights of a series of term, HLA-DQ typed white UK newborns (n = 552) whose mothers had either smoked (n = 211) or not smoked (n = 341) during pregnancy. Maternal smoking during pregnancy resulted in an average birthweight reduction of 244 g, but the combined effects of maternal smoking and fetal DQA1*0101 or DQB1*0501 alleles resulted in a 230 and 240 g further reduction in mean birthweight, respectively, resulting from interactions between smoking and these DQ types. Other fetal DQ allele-specific interactions with maternal smoking are suggested by a ,protective' effect on smoking-associated birthweight reduction in newborns typing for DQA1*0201 and DQB1*0201. Our results suggest biological interactions between maternal cigarette smoking during pregnancy and specific fetal DQ alleles that affect fetal growth. The precise nature of these interactions merits further investigation, as knowledge of fetal HLA-DQ type may be useful in refining risk estimates of severe fetal growth restriction because of maternal smoking during pregnancy. [source] Hypospadias and maternal exposures to cigarette smokePAEDIATRIC & PERINATAL EPIDEMIOLOGY, Issue 6 2005Suzan L. Carmichael Summary The few previous studies of hypospadias and smoking have suggested either no association or a reduced risk. This study, which uses data from the National Birth Defects Prevention Study, a multi-state, population-based case,control study, includes data on males born with severe hypospadias (i.e. the urethra opens at the penile shaft, scrotum or perineum) from 1997 to 2000. Non-malformed, liveborn male controls were selected randomly from birth certificates or from birth hospitals. Maternal interviews were completed by telephone with 453 case mothers and 1267 control mothers. Maternal smoking was not associated with hypospadias risk. For example, during the third month of pregnancy, smoking < 0.5 pack/day had an odds ratio (OR) of 1.1 [95% CI 0.6, 1.9]; 0.5 pack/day, 0.6 [0.4, 1.1]; and ,,1 pack/day, 0.8 [0.4, 1.6]. Exposure to any secondhand smoke at home during the third month of pregnancy showed an OR of 0.6 [95% CI 0.4, 1.0], and exposure at work or school, an OR of 0.7 [0.5, 1.1]. Similar risks were observed for other months during the periconceptional period, and adjustment for several potential confounders did not substantially alter results. This analysis does not confirm a recent report suggesting that maternal smoking is associated with a reduced risk of having offspring with hypospadias. [source] Atopy among schoolchildren in northern and southern Sweden in relation to pet ownership and early life eventsPEDIATRIC ALLERGY AND IMMUNOLOGY, Issue 1 2001L. Bråbäck Studies have suggested a higher prevalence of asthma and allergies in northern, as compared to southern, Scandinavia. The aim of this study was to evaluate regional differences in atopy in relation to pet ownership and certain early life events among schoolchildren (n = 2108) aged 10,11 years from Linköping in southern Sweden and Östersund in northern Sweden. The parents completed a questionnaire, comprising questions on home environment, heredity, socio-economic conditions, and the core questions on symptoms from the International Study of Asthma and Allergies in Childhood. The children were skin-prick tested to eight common inhalant allergens. Information on maternal smoking habits, gestational age, and anthropometric measures were obtained from the Swedish Medical Birth Registry. The prevalence of atopic symptoms and sensitization to pollen were similar in Östersund and in Linköping. A higher prevalence of sensitization to animal dander among children in Östersund could be linked to a higher occurrence of pets in the community. Current cat ownership was related to less sensitivity to cat allergen but only in children with an atopic heredity. Ponderal index > 30 kg/m3 was related to an increased risk of atopic sensitization, both in Linköping (adjusted odds ratio 2.1; 95% confidence interval 1.1,4.0) and in Östersund (adjusted odds ratio 2.0; 95% confidence interval 1.1,3.5). Maternal smoking during pregnancy was related to an increased risk of atopic sensitization among children in Linköping, whereas current smoking was associated with a decreased risk of sensitization in Östersund. In conclusion, we demonstrated that a high occurrence of pets in the community was associated with sensitization, whereas atopic symptoms were essentially unaffected. This study has also suggested an association between body size at birth and atopic sensitization at 10,11 years of age. [source] Fetal macrosomia and pregnancy outcomesAUSTRALIAN AND NEW ZEALAND JOURNAL OF OBSTETRICS AND GYNAECOLOGY, Issue 5 2009Hong JU Background:, Pregnancies with a macrosomic fetus comprise a subgroup of high-risk pregnancies. There is uncertainty in the clinical management and outcomes of such pregnancies. Aim:, We sought to examine clinical management and maternal and fetal outcomes in pregnancies with macrosomic infants at Royal Brisbane and Women's Hospital (RBWH). Methods:, Data from 276 macrosomic births (weighing , 4500 g) and 294 controls (weighing 3250,3750 g) delivered during 2002,2004 at RBWH were collected from the hospital database. Univariate and logistic regression analyses were performed for maternal risk factors and maternal and neonatal outcomes that were associated with fetal macrosomia. Results:, Macrosomia was more than two times likely in women with body mass index (BMI) of > 30 kg/m2 (odds ratio (OR) 2.41, 95% confidence interval (CI) 1.26,4.61) and in male infant sex (OR 2.05, 95% CI 1.35,3.12), and four times more likely in gestation of > 40 weeks (OR 3.93, 95% CI 1.99,7.74). Maternal smoking reduced the risk of fetal macrosomia (OR 0.27, 95% CI 0.14,0.51). Macrosomia was associated with nearly two times higher risk of emergency caesarean section (OR 1.75, 95% CI 1.02,2.97) and maternal hospital stay of > 3 days (OR 1.66, 95% CI 1.11,2.50), and four times higher risk of shoulder dystocia (OR 4.08, 95% CI 1.62,10.29). Macrosomic infants were twice as likely to have resuscitation (OR 2.21, 95% CI 1.46,3.34) and intensive care nursery admission (OR 1.89, 95% CI 1.03,3.46). Conclusion:, Macrosomia was associated with an increased risk of adverse maternal and neonatal health outcomes. Optimal management strategies of macrosomic pregnancies need evaluation. [source] Maternal smoking during pregnancy predicts nicotine disorder (dependence or withdrawal) in young adults , a birth cohort studyAUSTRALIAN AND NEW ZEALAND JOURNAL OF PUBLIC HEALTH, Issue 4 2009Frances V. O'Callaghan Abstract Objective: To investigate whether maternal smoking during pregnancy predicts offspring nicotine disorder (dependence or withdrawal) at 21 years. Method: Participants comprised a prospective birth cohort involving 7,223 singleton children whose mothers were enrolled between 1981 and 1983 at the first antenatal visit to the Mater Mothers' Hospital, Brisbane, Queensland. The present sub-cohort consisted of 2,571 youth who completed the Composite International Diagnostic Interview-computerised version (CIDI-Auto) that assesses nicotine dependence and withdrawal according to DSM-IV diagnostic criteria at the 21-year follow-up. Results: 12.8% of offspring met criteria for nicotine dependence and 8.5% met criteria for withdrawal. 16.6% met criteria for either dependence or withdrawal. Smoking during pregnancy resulted in offspring being more likely to have dependence or withdrawal at 21 years than offspring of mothers who never smoked (age adjusted odds ratio 1.53 (95% CI: 1.19-1.96). Conclusions: Findings emphasise the long-term adverse effects of maternal smoking during pregnancy, including nicotine dependence in young adult offspring. Implications: Public health approaches should strengthen arguments for mothers to cease smoking during pregnancy in view of the long-term health implications for offspring, and reinforce measures to help smokers among pregnant women and women of childbearing age to stop. [source] Maternal smoking and the risk for clubfoot in infants,BIRTH DEFECTS RESEARCH, Issue 2 2008Kathryn C. Dickinson Abstract BACKGROUND: Clubfoot is one of the most common major birth defects, with a prevalence of approximately 1 per 1,000 live births. The etiology of clubfoot is complex and not well understood, and yet, few epidemiologic studies of risk factors have been conducted. Maternal smoking has been suggested as a possible risk factor. The purpose of this population-based, case-control study was to examine the association between maternal smoking and clubfoot. METHODS: Data from the North Carolina Birth Defects Monitoring Program matched to North Carolina birth certificates and health services data were used in the analysis of 443 cases of clubfoot and 4,492 randomly sampled controls for the years 1999,2003. Smoking data were ascertained from the birth certificates, and the reliability of the data was assessed by comparing them with reported smoking from the North Carolina Pregnancy Risk Assessment Monitoring System. Multiple logistic regression was used to calculate crude and adjusted ORs and 95% CIs for smoking and clubfoot. RESULTS: The crude OR for maternal smoking during pregnancy and clubfoot was 1.49 (95% CI: 1.15, 1.92). Controlling for maternal age, race/ethnicity, infant's sex, and timing of prenatal care initiation did not appreciably change the results (adjusted OR 1.40; 95% CI: 1.07, 1.83). CONCLUSIONS: This study is consistent with the hypothesis that smoking during pregnancy is associated with a slightly increased risk of an infant being born with clubfoot. Further research is needed to confirm this association, and to identify potential genetic factors that may modify the magnitude of the risk. Birth Defects Research (Part A) 2008. © 2007 Wiley-Liss, Inc. [source] Orofacial clefts and spina bifida: N -Acetyltransferase phenotype, maternal smoking, and medication useBIRTH DEFECTS RESEARCH, Issue 5 2002Iris A.L.M. Van Rooij Background Orofacial clefts and spina bifida are midline defects with a multifactorial etiology. Maternal smoking and medication use periconceptionally have been studied as risk factors for these malformations. The biotransformation enzyme N -acetyltransferase 2 (NAT2), plays a part in the inactivation of toxic compounds in cigarette smoke and medication. We investigated maternal NAT2 phenotype and the interaction with smoking and medication use periconceptionally on orofacial cleft and spina bifida risk in offspring. Methods In this case-control study of 45 mothers of orofacial cleft children, 39 mothers of spina bifida children and 73 control mothers, NAT2 acetylator status was determined by measuring urinary caffeine metabolites. Results Slow NAT2 acetylators showed no increased risk for orofacial cleft (OR = 1.0, 95% CI: 0.4,2.3) or spina bifida offspring (OR = 0.7, 95% CI: 0.3,1.7) compared to fast NAT2 acetylators. More mothers with orofacial cleft and spina bifida offspring smoked cigarettes (36% and 23% respectively) and used medication periconceptionally (38% and 44% respectively) compared to control mothers (smoking:18%, medication use:19%). No interaction between maternal NAT2 acetylator status and smoking or medication use was observed for orofacial cleft and spina bifida risk. Conclusions Maternal smoking and medication use is associated with orofacial cleft risk as well as medication use is with spina bifida. The maternal NAT2 acetylator status, however, was not associated with an increased risk for orofacial cleft or spina bifida offspring, nor in combination with periconceptional smoking or medication use. Teratology 66:260,266, 2002. © 2002 Wiley-Liss, Inc. [source] Incidence of and risk factors for neonatal morbidity after active perinatal care: extremely preterm infants study in Sweden (EXPRESS)ACTA PAEDIATRICA, Issue 7 2010The EXPRESS Group Abstract Aims:, The aim of this study was to determine the incidence of neonatal morbidity in extremely preterm infants and to identify associated risk factors. Methods:, Population based study of infants born before 27 gestational weeks and admitted for neonatal intensive care in Sweden during 2004,2007. Results:, Of 638 admitted infants, 141 died. Among these, life support was withdrawn in 55 infants because of anticipation of poor long-term outcome. Of 497 surviving infants, 10% developed severe intraventricular haemorrhage (IVH), 5.7% cystic periventricular leucomalacia (cPVL), 41% septicaemia and 5.8% necrotizing enterocolitis (NEC); 61% had patent ductus arteriosus (PDA) and 34% developed retinopathy of prematurity (ROP) stage ,3. Eighty-five per cent needed mechanical ventilation and 25% developed severe bronchopulmonary dysplasia (BPD). Forty-seven per cent survived to one year of age without any severe IVH, cPVL, severe ROP, severe BPD or NEC. Tocolysis increased and prolonged mechanical ventilation decreased the chances of survival without these morbidities. Maternal smoking and higher gestational duration were associated with lower risk of severe ROP, whereas PDA and poor growth increased this risk. Conclusion:, Half of the infants surviving extremely preterm birth suffered from severe neonatal morbidities. Studies on how to reduce these morbidities and on the long-term health of survivors are warranted. [source] Prenatal and postnatal parental smoking and acute otitis media in early childhoodACTA PAEDIATRICA, Issue 1 2010SE Håberg Abstract Aim:, To explore the associations between acute otitis media in early childhood and prenatal and postnatal tobacco smoke exposure. Methods:, Subjects were 32 077 children born between 2000 and 2005 in the Norwegian Mother and Child Study with questionnaire data on tobacco smoke exposure and acute otitis media up to 18 months of age. Multivariate regression models were used to obtain adjusted relative risks for acute otitis media. Results:, Acute otitis media was slightly more common in children exposed to parental smoking. The incidence from 0 to 6 months was 4.7% in unexposed children and 6.0% in children exposed both prenatally and postnatally. After adjusting for postnatal exposure and covariates, the relative risk for acute otitis media 0,6 months when exposed to maternal smoking in pregnancy was 1.34, 95% confidence interval: 1.06,1.69. Maternal smoking in pregnancy was associated with acute otitis media up to 12 months of age. Compared with non-exposed children, there was a slightly increased risk of recurrent acute otitis media for children exposed both prenatally and postnatally with a relative risk of 1.24, 95% confidence interval: 1.01,1.52. Conclusion:, Even in a cohort with relatively low exposure levels of parental smoking, maternal smoking in pregnancy was associated with an increased risk of acute otitis media in early childhood. [source] The epidemiology of attention-deficit/hyperactivity disorder (ADHD): A public health viewDEVELOPMENTAL DISABILITIES RESEARCH REVIEW, Issue 3 2002Andrew S. Rowland Abstract Attention-deficit/hyperactivity disorder (ADHD) is the most common neurodevelopmental disorder of childhood. However, basic information about how the prevalence of ADHD varies by race/ethnicity, sex, age, and socio-economic status remains poorly described. One reason is that difficulties in the diagnosis of ADHD have translated into difficulties developing an adequate case definition for epidemiologic studies. Diagnosis depends heavily on parent and teacher reports; no laboratory tests reliably predict ADHD. Prevalence estimates of ADHD are sensitive to who is asked what, and how information is combined. Consequently, recent systematic reviews report ADHD prevalence estimates as wide as 2%,18%. The diagnosis of ADHD is complicated by the frequent occurrence of comorbid conditions such as learning disability, conduct disorder, and anxiety disorder. Symptoms of these conditions may also mimic ADHD. Nevertheless, we suggest that developing an adequate epidemiologic case definition based on current diagnostic criteria is possible and is a prerequisite for further developing the epidemiology of ADHD. The etiology of ADHD is not known but recent studies suggest both a strong genetic link as well as environmental factors such as history of preterm delivery and perhaps, maternal smoking during pregnancy. Children and teenagers with ADHD use health and mental health services more often than their peers and engage in more health threatening behaviors such as smoking, and alcohol and substance abuse. Better methods are needed for monitoring the prevalence and understanding the public health implications of ADHD. Stimulant medication is the treatment of choice for treating ADHD but psychosocial interventions may also be warranted if comordid disorders are present. The treatment of ADHD is controversial because of the high prevalence of medication treatment. Epidemiologic studies could clarify whether the patterns of ADHD diagnosis and treatment in community settings is appropriate. Population-based epidemiologic studies may shed important new light on how we understand ADHD, its natural history, its treatment and its consequences. MRDD Research Reviews 2002;8:162,170. © 2002 Wiley-Liss, Inc. [source] Effects of maternal smoking in pregnancy on prenatal brain development.EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 3 2007The Generation R Study Abstract Nicotine, as has been shown in animal studies, is a neuroteratogen, even in concentrations that do not cause growth retardation. In humans, there is only indirect evidence for negative influences of nicotine on brain development from studies on the association between maternal smoking in pregnancy and behavioural and cognitive development in the offspring. We investigated the associations of maternal smoking in pregnancy with foetal head growth characteristics in 7042 pregnant women. This study was embedded in the Generation R Study, a population-based prospective cohort study from foetal life until adulthood. Maternal smoking was assessed by questionnaires in early, mid- and late pregnancy. Head circumference, biparietal diameter, transcerebellar diameter and atrial width of lateral ventricles were repeatedly measured by ultrasound. When mothers continued to smoke during pregnancy, foetal head circumference showed a growth reduction of 0.13 mm [95% confidence interval (CI): ,0.18, ,0.09] per week compared to foetuses of mothers who never smoked during pregnancy. Biparietal diameter of foetuses with smoking mothers grew 0.04 mm (95% CI: ,0.05, ,0.02) less per week than that of foetuses of nonsmoking mothers. Atrial width of lateral ventricle was 0.12 mm (95% CI: ,0.22, ,0.02) smaller and transcerebellar diameter was 0.08 mm (95% CI: ,0.15, ,0.00) smaller if mothers smoked, but growth per week of these characteristics was not affected by maternal smoking in pregnancy. In conclusion, continuing to smoke during pregnancy leads to reduced growth of the foetal head. Further research should focus on the causal pathway from prenatal cigarette exposure via brain development to behavioural and cognitive functions. [source] Neonatal health care costs related to smoking during pregnancyHEALTH ECONOMICS, Issue 3 2002E. Kathleen Adams Abstract Research objective: Much of the work on estimating health care costs attributable to smoking has failed to capture the effects and related costs of smoking during pregnancy. The goal of this study is to use data on smoking behavior, birth outcomes and resource utilization to estimate neonatal costs attributable to maternal smoking during pregnancy. Study design: We use 1995 data from the Center for Disease Control's (CDC) Pregnancy Risk Assessment Monitoring System (PRAMS) database. The PRAMS collects representative samples of births from 13 states (Alabama, Alaska, California, Florida, Georgia, Indiana, Maine, Michigan, New York (excluding New York City), Oklahoma, South Carolina, Washington, and West Virginia), and the District of Columbia. The 1995 PRAMS sample is approximately 25 000. Multivariate analysis is used to estimate the relationship of smoking to probability of admission to an NICU and, separately, the length of stay for those admitted or not admitted to an NICU. Neonatal costs are predicted for infants ,as is' and ,as if' their mother did not smoke. The difference between these constitutes smoking attributable neonatal costs; this divided by total neonatal costs constitutes the smoking attributable fraction (SAF). We use data from the MarketScanÔ database of the MedStatÔ Corporation to attach average dollar amounts to NICU and non-NICU nursery nights and data from the 1997 birth certificates to extrapolate the SAFs and attributable expenses to all states. Principal findings: The analysis showed that maternal smoking increased the relative risk of admission to an NICU by almost 20%. For infants admitted to the NICU, maternal smoking increased length of stay while for non- NICU infants it appeared to lower it. Over all births, however, smoking increased infant length of stay by 1.1%. NICU infants cost $2496 per night while in the NICU and $1796 while in a regular nursery compared to only $748 for non-NICU infants. The combination of the increased NICU use, longer stays and higher costs result in a positive smoking attributable fraction (SAF) for neonatal costs. The SAF across all states is 2.2%. Across the states, the SAF varied from a low of 1.3% in Texas to a high of 4.6% in Indiana. Conclusions: These results further confirm the adverse effects of smoking. Among mothers who smoke, smoking adds over $700 in neonatal costs. The smoking attributable neonatal costs in the US represent almost $367 million in 1996 dollars; these costs vary from less than a million in smaller states to over $35 million in California. These costs are highly preventable since the adverse effects of maternal smoking occur in the short-run and can be avoided by even a temporary cessation of maternal smoking. These cost estimates can be used by managed care plans, state and local public health officials and others to evaluate alternative smoking cessation programs. Copyright © 2002 John Wiley & Sons, Ltd. [source] Estimating treatment effects in randomized clinical trials with non-compliance: the impact of maternal smoking on birthweightHEALTH ECONOMICS, Issue 5 2001Barton H. Hamilton Abstract This paper assesses the causal impact of late-term (8th month) maternal smoking on birthweight using data from a randomized clinical trial, in which some women were encouraged not to smoke, while others were not. The estimation of treatment effects in this case is made difficult as a result of the presence of non-compliers, women who would not change their smoking status, regardless of the receipt of encouragement. Because these women are not at risk of changing treatment status, treatment effect distributions may be difficult to construct for them. Consequently, the paper focuses on obtaining the distribution of treatment impacts for the sub-set of compliers found in the data. Because compliance status is not observed for all subjects in the sample, a Bayesian finite mixture model is estimated that recovers the treatment effect parameters of interest. The complier average treatment effect implies that smokers give birth to infants weighing 348 g less than those of non-smokers, on average, although the 95% posterior density interval contains zero. The treatment effect is stronger for women who were moderate smokers prior to pregnancy, implying a birthweight difference of 430 g. However, the model predicts that only about 22% of the women in the sample were at risk of changing their smoking behaviour in response to encouragement to quit. Copyright © 2001 John Wiley & Sons, Ltd. [source] Interrelations between maternal smoking during pregnancy, birth weight and sociodemographic factors in the prediction of early cognitive abilitiesINFANT AND CHILD DEVELOPMENT, Issue 6 2006S. C. J. Huijbregts Abstract Maternal prenatal smoking, birth weight and sociodemographic factors were investigated in relation to cognitive abilities of 1544 children (aged 3.5 years) participating in the Québec Longitudinal Study of Children's Development. The Peabody Picture Vocabulary Test (PPVT) was used to assess verbal ability, the Wechsler Preschool and Primary Scale of Intelligence-Revised (WPPSI-R) block design test to assess visuospatial ability, and the Visually Cued Recall (VCR) task to assess short-term memory. Prenatal smoking was related to performance on the WPPSI-R, the PPVT, and the VCR, although it did not independently predict any cognitive ability after maternal education was taken into account. Birth weight was a more robust predictor of all outcome measures and independently predicted VCR-performance. Birth weight interacted significantly with family income and maternal education in predicting visuospatial ability, indicating a greater influence of birth weight under relatively poor socio-economic conditions. Parenting and family functioning mediated associations between maternal education/family income and cognitive task performance under different birth weight conditions, although there were indications for stronger effects under relatively low birth weight. We conclude that investigations of moderating and mediating effects can provide insights into which children are most at risk of cognitive impairment and might benefit most from interventions. Copyright © 2006 John Wiley & Sons, Ltd. [source] Prevalence and determinants of cytomegalovirus infection in pre-school childrenJOURNAL OF PAEDIATRICS AND CHILD HEALTH, Issue 5 2009Timothy P O'Brien Aim: The aim of this study is to measure the seroprevalence of cytomegalovirus (CMV) infection in 3.5-year-old children, and identify the determinants of seropositivity. Methods: A total of 1714 children were enrolled at birth. Approximately half were small for gestational age and half were appropriate for gestational age. Information on the children was collected at birth, 1 year and 3.5 years. At 3.5 years blood was collected and tested for CMV-specific immunoglobulin by an enzyme-linked immunosorbent assay in 530 children. Results: The weighted seroprevalence of CMV was 32.8% (95% confidence interval (CI) 27.4,38.1%). The seroprevalence of CMV varied markedly by ethnicity (European: 26.5% (95% CI 20.9,32.2%); Maori: 68.0% (44.0,92.0%); Pacific: 74.5% (56.3,92.6%); Indian: 50.0% (20.2,79.8%); Chinese: 47.2% (10.8,83.5%); Other: 21.9% (0.0,52.7%); P < 0.001). Socio-economic factors, number of siblings, day care centres attendance, maternal smoking, breastfeeding and other factors examined were not related to CMV seropositivity. Conclusions: The seroprevalence of CMV in New Zealand pre-school children is similar to that reported from other developed countries. The finding of marked ethnic differences is unexplained by socio-economic factors, or other factors that were examined. [source] Infant care practices associated with sudden infant death syndrome: Findings from the Pacific Islands Families studyJOURNAL OF PAEDIATRICS AND CHILD HEALTH, Issue 5 2007Philip J Schluter Aim: To report infant care practice prevalence for known modifiable sudden infant death syndrome (SIDS) risk factors among a generally disadvantaged yet low-SIDS rate population of mothers with Pacific infants. Methods: The Pacific Islands Families study follows a cohort of Pacific infants born at a large tertiary hospital in South Auckland, between 15 March and 17 December 2000. Maternal self-report of infant care practices was undertaken at interview 6 weeks post-partum. Results: Overall, 1376 mothers self-reported upon their care practices for infants with median age of 7 weeks. Current maternal smoking was reported by 29%. Of infants: 50% were fully breastfed; 1% were placed prone to sleep; 50% usually bed-shared with their mother and 12% usually bed-shared with a mother who smoked; and 94% usually and 1% occasionally slept in the same room as their mother. Except for room sharing (P = 0.09), there were significant differences in these practices between the three major Pacific Island ethnic subgroups (all P < 0.001). Conclusion: Adoption of bed-sharing and room-sharing practices appears to be saving Pacific infants' lives, even though the New Zealand Cot Death Association has discouraged bed-sharing and not actively promoted room sharing. Mothers need to receive adequate information antenatally about the risks and benefits of room-sharing, bed-sharing and safe-sleeping practices and environments should they decide or have no option but to bed-share. [source] Risk factors for small-for-gestational-age babies: The Auckland Birthweight Collaborative StudyJOURNAL OF PAEDIATRICS AND CHILD HEALTH, Issue 4 2001JMD Thompson Objective: This case-control study determined whether internationally recognized risk factors for small-for-gestational-age (SGA) term babies were applicable in New Zealand. Methodology: All babies were born at 37 or more completed weeks of gestation in one of three hospitals in Auckland. Cases weighed less than the sex specific 10th percentile for gestational age at birth, and controls (appropriate-for-gestational-age (AGA)) were a random selection of heavier babies. Information was collected by maternal interview and from obstetric databases. Results: Information from 1714 completed interviews (844 SGA and 870 AGA) was available for analysis. Computerized obstetric records were available for 1691 of the 1701 women who consented to such access. In a multivariate analysis allowing for sex, gestational age at birth, social class and other potential confounders, mothers who smoked had a significantly increased risk of an SGA baby (adjusted OR 2.41; 95% CI 1.78,;3.28), as did primiparous mothers (adjusted OR 1.34; 95% CI 1.03,;1.73), mothers of Indian ethnicity (adjusted OR 3.22; 95% CI 1.95,;5.30), women with pre-eclamptic toxaemia (adjusted OR 2.42; 95% CI 1.08,;5.40) and those with pre-existing hypertension toxaemia (adjusted OR 5.49; 95% CI 1.81,;16.71). Mothers of SGA infants were shorter (P < 0.001) and reported lower prepregnancy body weights (P < 0.001) than mothers of AGA infants. The population attributable fraction for smoking suggests that up to 18% of SGA infants born in the ABC Study could be related to maternal smoking. Conclusions: Risk factors associated with SGA births in other countries are also important in New Zealand. Smoking in pregnancy is an important and potentially modifiable behaviour, and efforts to decrease the number of women who smoke during pregnancy should be encouraged. [source] Perinatal risk factors and coeliac disease in children and young adults: a record linkage studyALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 2 2009S. E. ROBERTS Summary Background, Little is known about perinatal risk factors and coeliac disease. Aim, To investigate the relationship between perinatal risk factors and subsequent coeliac disease among offspring. Methods, Record linked abstracts of birth registrations, maternity, in-patient and day case records in a defined population of southern England. Results, Using univariate analysis, coeliac disease in the child was associated with maternal coeliac disease (odds ratio = 20.6; 95% CI = 5.04,84.0; based on two cases in both mother and child) and with social class, year of birth, maternal smoking and parity. Multivariate analysis confirmed an increased risk of coeliac disease of 3.79 (95% CI = 1.85,7.79) for classes IV and V compared with I and II, an increased risk of 1.92 (1.06,3.49) for births during 1975,1979 compared with 1970,1974 and an increased risk of 1.80 (1.05,3.09) for ,subsequent' compared with ,first' births. Smoking during pregnancy was no longer associated with coeliac disease. Because numbers were small, maternal coeliac disease was excluded from the multivariate anaylsis. Conclusions, This study shows increased risks of coeliac disease for manual social classes, births during the late 1970s and ,subsequent' births. Overall, perinatal risk factors seem to have a limited role in the aetiology of coeliac disease in children and young adults. [source] Maternal smoking increases risk of allergic sensitization and wheezing only in children with allergic predisposition: longitudinal analysis from birth to 10 yearsALLERGY, Issue 3 2009T. Keil Background:, The role of passive smoking for allergies and asthma in children above the age of 3 years remains unclear and possible interactive effects with parental allergies have not been formally evaluated in long-term studies. To examine the interaction of passive smoking and an allergic predisposition regarding allergic sensitization, allergic airway symptoms and respiratory infections during the first 10 years of life. Methods:, In a prospective multicenter birth cohort study with 1314 recruited children in Germany, we assessed serum immunoglobulin E against common allergens at seven time points, and parental smoking and respiratory symptoms annually by using questionnaires. Longitudinal analyses were performed using generalized estimating equation models (stratified by parental allergy status). Results:, During the first 10 years, 18% of the children were exposed to regular maternal smoking since pregnancy, 43% to irregular maternal or only paternal smoking. Among children with two allergic parents, a mother who smoked regularly significantly increased the odds for allergic sensitization (adjusted OR 4.8, 95% CI 1.3,18.2) and wheezing (adjusted OR 5.7, 95% CI 1.7,19.0) in her child compared with children who were never exposed. For those with only one allergic parent, the odds were doubled and also statistically significant, whereas in children without allergic parents maternal smoking had no effects. There was no association of maternal smoking with allergic rhinitis or respiratory infections. Conclusions:, Our results suggest that regular maternal smoking is a strong risk factor for allergic sensitization and asthma symptoms during the first 10 years of life, but only in children with allergic parents. [source] Hypoplasia of the arcuate nucleus and maternal smoking during pregnancy in sudden unexplained perinatal and infant deathNEUROPATHOLOGY, Issue 4 2004Anna Maria Lavezzi Maternal smoking during pregnancy is the most important risk factor for sudden perinatal and infant death in more industrialized countries. The frequent observation of hypoplasia of the arcuate nucleus in the brainstem of these victims prompted the verification of whether maternal cigarette smoking could be related to defective development of this nucleus during intrauterine life, by affecting the expression of specific genes involved in its developmental process. In serial sections of the brainstem of 54 cases of sudden and unexplained fetal and infant deaths (13 stillbirths, 7 neonatal deaths and 34 sudden infant death syndrome (SIDS) victims), morphological and morphometrical analysis was used to observe the different structural alterations of the arcuate nucleus (bilateral hypoplasia, monolateral hypoplasia, partial hypoplasia, delayed neuronal maturation and decreased neuronal density) detected in 24 cases (44%). Correlating this finding with smoking in pregnancy, a significantly increased incidence of cytoarchitectural alterations of the arcuate nucleus was found in stillborns and SIDS victims with smoker mothers compared to victims with non-smoker mothers. Moreover, the observation of a wide range of developing morphological defects of the arcuate nucleus related to maternal smoking led to the hypothesis that the constituents of the gas phase in cigarette smoke could directly affect the expression of genes involved in the development of this nucleus, such as the homeobox En-2 gene. [source] Prenatal polychlorinated biphenyl exposures in eastern Slovakia modify effects of social factors on birthweightPAEDIATRIC & PERINATAL EPIDEMIOLOGY, Issue 3 2008Dean Sonneborn Summary Polychlorinated biphenyls (PCB) were widely used for industrial purposes and consumer products, but because of their toxicity, production was banned by most industrialised countries in the late 1970s. In eastern Slovakia, they were produced until 1985. During 2002,04, a birth cohort of mothers (n = 1057) residing in two Slovak districts was enrolled at delivery, and their specimens and information were collected after birth. Congeners of PCBs were measured in maternal serum by high-resolution gas chromatography with electron capture detection. In this study, we used multiple linear regression to examine the effects of prenatal PCB exposure on birthweight adjusted for gestational age, controlling for inter-pregnancy interval, and maternal smoking, age, education, ethnicity, pre-pregnancy body mass index and height. The association between total maternal serum PCB levels and birthweight was not statistically significant. However, an interaction model indicated that maternal PCB concentrations were associated with lower birthweight in Romani boys. Based on the fitted regression model, the predicted birthweight of Romani boys at the 90th percentile of maternal PCBs (12.8 ng/mL) was 133 g lower than the predicted birthweight at the 10th percentile of maternal PCBs (1.6 ng/mL). This is a similar magnitude of effect to that observed for maternal smoking and birthweight. These results suggest that higher levels of PCBs in maternal blood sera may inhibit growth in boys, particularly in those already affected by social factors related to ethnicity. This study is consistent with previous findings that boys are more susceptible than girls to growth restriction induced by in utero organochlorine exposures, and further indicates that high PCBs may magnify the influence of social disadvantage in this vulnerable group of boys. [source] Active and passive maternal smoking during pregnancy and the risks of low birthweight and preterm birth: the Generation R StudyPAEDIATRIC & PERINATAL EPIDEMIOLOGY, Issue 2 2008Vincent W. V. Jaddoe Summary The objective of this study was to examine the associations between active and passive smoking in different periods of pregnancy and changing smoking habits during pregnancy, with low birthweight and preterm birth. The study was embedded in the Generation R Study, a population-based prospective cohort study from early fetal life onwards in Rotterdam, The Netherlands. Active and passive smoking were assessed by questionnaires in early, mid- and late pregnancy. Analyses were based on 7098 pregnant women and their children. Active smoking until pregnancy was ascertained and was not associated with low birthweight and preterm birth. Continued active smoking after pregnancy was also recorded and was associated with low birthweight (adjusted odds ratio 1.75 [95% CI 1.20, 2.56]) and preterm birth (adjusted odds ratio 1.36 [95% CI 1.04, 1.78]). The strongest associations were found for active maternal smoking in late pregnancy. Passive maternal smoking in late pregnancy was associated with continuously measured birthweight (P for trend <0.001). For all active smoking categories in early pregnancy, quitting smoking was associated with a higher birthweight than continuing to smoke. Tendencies towards smaller non-significant beneficial effects on mean birthweight were found for reducing the number of cigarettes without quitting completely. This study shows that active and passive smoking in late pregnancy are associated with adverse effects on weight and gestational age at birth. Smoking in early pregnancy only, seems not to affect fetal growth adversely. Health care strategies for pregnant women should be aimed at quitting smoking completely rather than reducing the number of cigarettes. [source] Interactions between fetal HLA-DQ alleles and maternal smoking influence birthweightPAEDIATRIC & PERINATAL EPIDEMIOLOGY, Issue 5 2006G. Malcolm Taylor Summary Maternal smoking during pregnancy inhibits fetal growth, and is a major cause of childhood and adult morbidity, including increased risks of cardiovascular disease and diabetes. However, the use of birthweight as a proxy for future smoking-related morbidity is hindered by its wide variability, suggesting a role for other birthweight-modifying factors. We report here, for the first time, that interactions between specific fetal HLA-DQA1 and DQB1 alleles and maternal smoking can influence birthweight. We compared mean birthweights of a series of term, HLA-DQ typed white UK newborns (n = 552) whose mothers had either smoked (n = 211) or not smoked (n = 341) during pregnancy. Maternal smoking during pregnancy resulted in an average birthweight reduction of 244 g, but the combined effects of maternal smoking and fetal DQA1*0101 or DQB1*0501 alleles resulted in a 230 and 240 g further reduction in mean birthweight, respectively, resulting from interactions between smoking and these DQ types. Other fetal DQ allele-specific interactions with maternal smoking are suggested by a ,protective' effect on smoking-associated birthweight reduction in newborns typing for DQA1*0201 and DQB1*0201. Our results suggest biological interactions between maternal cigarette smoking during pregnancy and specific fetal DQ alleles that affect fetal growth. The precise nature of these interactions merits further investigation, as knowledge of fetal HLA-DQ type may be useful in refining risk estimates of severe fetal growth restriction because of maternal smoking during pregnancy. [source] Hypospadias and maternal exposures to cigarette smokePAEDIATRIC & PERINATAL EPIDEMIOLOGY, Issue 6 2005Suzan L. Carmichael Summary The few previous studies of hypospadias and smoking have suggested either no association or a reduced risk. This study, which uses data from the National Birth Defects Prevention Study, a multi-state, population-based case,control study, includes data on males born with severe hypospadias (i.e. the urethra opens at the penile shaft, scrotum or perineum) from 1997 to 2000. Non-malformed, liveborn male controls were selected randomly from birth certificates or from birth hospitals. Maternal interviews were completed by telephone with 453 case mothers and 1267 control mothers. Maternal smoking was not associated with hypospadias risk. For example, during the third month of pregnancy, smoking < 0.5 pack/day had an odds ratio (OR) of 1.1 [95% CI 0.6, 1.9]; 0.5 pack/day, 0.6 [0.4, 1.1]; and ,,1 pack/day, 0.8 [0.4, 1.6]. Exposure to any secondhand smoke at home during the third month of pregnancy showed an OR of 0.6 [95% CI 0.4, 1.0], and exposure at work or school, an OR of 0.7 [0.5, 1.1]. Similar risks were observed for other months during the periconceptional period, and adjustment for several potential confounders did not substantially alter results. This analysis does not confirm a recent report suggesting that maternal smoking is associated with a reduced risk of having offspring with hypospadias. [source] A dose-response relationship between maternal smoking during late pregnancy and adult intelligence in male offspringPAEDIATRIC & PERINATAL EPIDEMIOLOGY, Issue 1 2005Erik Lykke Mortensen Summary An association between maternal smoking during pregnancy and cognitive and behavioural development has been observed in several studies, but potential effects of maternal smoking on offspring adult intelligence have not been investigated. The objective of the present study was to investigate a potential association between maternal smoking during pregnancy and offspring intelligence in young adulthood. Adult intelligence was assessed at the mean age of 18.7 years by a military draft board intelligence test (Børge Priens Prøve) for 3044 singleton males from the Copenhagen Perinatal Cohort with information regarding maternal smoking during the third trimester coded into five categories (about 50% of the mothers were smokers). The following potential confounders were included as covariates in multivariable analyses: parental social status and education, single mother status, mother's height and age, number of pregnancies, and gestational age. In separate analyses, birthweight and length were also included as covariates. Maternal cigarette smoking during the third trimester, adjusted for the seven covariates, showed a negative association with offspring adult intelligence (P = 0.0001). The mean difference between the no-smoking and the heaviest smoking category amounted to 0.41 standard deviation, corresponding to an IQ difference of 6.2 points [95% confidence interval 0.14, 0.68]. The association remained significant when further adjusted for birthweight and length (P = 0.007). Both unadjusted and adjusted means suggested a dose-response relationship between maternal smoking during pregnancy and offspring adult intelligence. When subjects with missing data were excluded, essentially the same results were obtained in the reduced sample (n = 1829). These results suggest that smoking during pregnancy may have long-term negative consequences on offspring adult intelligence. [source] Does maternal smoking during pregnancy cause childhood overweight?PAEDIATRIC & PERINATAL EPIDEMIOLOGY, Issue 2 2003Marius Widerøe Summary The objective of this study was to examine a possible association between maternal smoking in pregnancy and childhood overweight. From a population-based cohort of 5722 women from Trondheim, Bergen (Norway) and Uppsala (Sweden) enrolled in early pregnancy during 1986,92, a random sample of 482 women was selected for participation. They were followed up throughout pregnancy, and their children from birth until 5 years of age. Data on maternal smoking and diet, socio-economic determinants and breast feeding were recorded prospectively. During pregnancy and childhood, anthropometric measures were also recorded. Maternal smoking status was based on reported number of cigarettes smoked in week 17 of pregnancy. Child overweight was defined by body mass index (BMI) and sum of skinfold thickness (SFT) , 85th percentile at 5 years of age. Children of mothers who smoked in pregnancy had increased risk of overweight at 5 years of age (RR 2.5, 95% CI 1.5, 4.2 for BMI; and RR 1.8, 95% CI 1.1, 3.0 for SFT). Adjusting for maternal diet, breast feeding, maternal obesity and socio-economic status did not suggest confounding. However, adjustment for birthweight increased the observed risk. A linear increase in BMI and SFT was observed with increasing number of cigarettes smoked. In conclusion, smoking during pregnancy may be a risk factor for development of childhood overweight. This study may support the hypothesis of ,fetal origin of adult disease', but the risk of overweight associated with smoking during pregnancy was independent of intrauterine growth retardation, and may thus be attributed to specific effects of cigarette smoke. [source] Maternal, paternal and environmental tobacco smoking and breast feedingPAEDIATRIC & PERINATAL EPIDEMIOLOGY, Issue 3 2002Gabriel M. Leung Summary The effects of environmental tobacco smoke (ETS) on breast-feeding patterns are poorly understood, while those of parental smoking on breast-feeding initiation vs. duration have not been clearly delineated. We conducted a prospective, population-based birth cohort study to examine the independent effects of maternal, paternal and ETS on breast-feeding initiation and duration. A total of 6747 Hong Kong Chinese infants were recruited and followed up in 1997,8. We obtained detailed household smoking history and recorded breast-feeding patterns in three follow-up interviews over 9 months. We found that both maternal and paternal smoking were associated with not initiating breast feeding (odds ratio [OR] for ever maternal smoking = 2.51, 95% confidence interval [CI] = 1.63, 3.86; OR for ever paternal smoking = 1.22, 95% CI = 1.08, 1.39). Exposure to ETS in utero and post partum were also related to not starting breast feeding (ORETS in utero = 1.10, 95% CI = 0.99,1.24; ORETS post partum = 1.21, 95% CI = 1.08, 1.36). These effects, however, did not persist for breast-feeding duration of , 4 months. Cox proportional hazards modelling confirmed the lack of association between any form of smoking and breast-feeding duration. Our findings suggest that smoking of any kind, during or after pregnancy, is a strong risk indicator for not initiating breast feeding. Smoking as a risk indicator for underlying socio-economic, demographic and psychosocial factors is probably responsible for most of the observed adverse effects, although we cannot rule out direct contributions from pathophysiological mechanisms. Public health strategies directed at these underlying factors should be vigorously pursued to reduce the adverse effects of tobacco on breast feeding and infant health in general. [source] | |||||||||||||||||||||||||||||||