Maternal Smoking In Pregnancy Research Articles

Smoking during pregnancy and its effect on placental weight: a Mendelian randomization study

BackgroundThe causal relationship between maternal smoking in pregnancy and reduced offspring birth weight is well established and is likely due to impaired placental function. However, observational studies have given conflicting results on the association between smoking and placental weight. We aimed to estimate the causal effect of newly pregnant mothers quitting smoking on their placental weight at the time of delivery.MethodsWe used one-sample Mendelian randomization, drawing data from the Avon Longitudinal Study of Parents and Children (ALSPAC) (N = 690 to 804) and the Norwegian Mother, Father and Child Cohort Study (MoBa) (N = 4267 to 4606). The sample size depends on the smoking definition used for different analyses. The analysis was performed in pre-pregnancy smokers only, due to the specific role of the single-nucleotide polymorphism (SNP) rs1051730 (CHRNA5 – CHRNA3 – CHRNB4) in affecting smoking cessation but not initiation.ResultsFixed effect meta-analysis showed a 182 g [95%CI: 29,335] higher placental weight for pre-pregnancy smoking mothers who continued smoking at the beginning of pregnancy, compared with those who stopped smoking. Using the number of cigarettes smoked per day in the first trimester as the exposure, the causal effect on placental weight was 11 g [95%CI: 1,21] per cigarette per day. Similarly, smoking at the end of pregnancy was causally associated with higher placental weight. Using the residuals of birth weight regressed on placental weight as the outcome, we showed evidence of lower offspring birth weight relative to the placental weight, both for continuing smoking at the start of pregnancy as well as continuing smoking throughout pregnancy (change in z-score birth weight adjusted for z-score placental weight: -0.8 [95%CI: -1.6,-0.1]).ConclusionOur results suggest that continued smoking during pregnancy causes higher placental weights.

Placental pathology and neonatal morbidity: exploring the impact of gestational age at birth

AimTo evaluate placental pathology in term and post-term births, investigate differences in clinical characteristics, and assess the risk of adverse neonatal outcome.MethodsThis prospective observational study included 315 singleton births with gestational age (GA) > 36 weeks + 6 days meeting the local criteria for referral to placental histopathologic examination. We applied the Amsterdam criteria to classify the placentas. Births were categorized according to GA; early-term (37 weeks + 0 days to 38 weeks + 6 days), term (39 weeks + 0 days to 40 weeks + 6 days), late-term (41 weeks + 0 days to 41 weeks + 6 days), and post-term births (≥ 42 weeks + 0 days). The groups were compared regarding placental pathology findings and clinical characteristics. Adverse neonatal outcomes were defined as 5-minute Apgar score < 7, umbilical cord artery pH < 7.0, admission to the neonatal intensive care unit or intrauterine death. A composite adverse outcome included one or more adverse outcomes. The associations between placental pathology, adverse neonatal outcomes, maternal and pregnancy characteristics were evaluated by logistic regression analysis.ResultsLate-term and post-term births exhibited significantly higher rates of histologic chorioamnionitis (HCA), fetal inflammatory response, clinical chorioamnionitis (CCA) and transfer to neonatal intensive care unit (NICU) compared to early-term and term births. HCA and maternal smoking in pregnancy were associated with adverse outcomes in an adjusted analysis. Nulliparity, CCA, emergency section and increasing GA were all significantly associated with HCA.ConclusionsHCA was more prevalent in late and post-term births and was the only factor, along with maternal smoking, that was associated with adverse neonatal outcomes. Since nulliparity, CCA and GA beyond term are associated with HCA, this should alert the clinician and elicit continuous intrapartum monitoring for timely intervention.

Intergenerational transmission of tobacco smoking: The role of the child’s behavioral difficulties. Data from the Danish National Birth cohort (DNBC)

AimsThis study explores the role of offspring behavioral difficulties in the intergeneration transmission of tobacco smoking. MethodsThis longitudinal cohort study is based on children born in Denmark in 1996–2003 participating in the Danish National Birth Cohort (DNBC), followed-up until 18years of age. We included mother-child pairs with complete data regarding the exposure (4 trajectories of maternal daily smoking quantity during pregnancy: low, intermediate/stable, intermediate/decreasing and high), outcome (offspring daily smoking status at 18 years) and mediator (offspring symptoms of hyperactivity-inattention at 11 years), that is 24,588 mother-child pairs. ResultsIn our study population, during pregnancy respectively 86.2%, 6.80%, 4.08% and 2.97% mothers belonged to the low, intermediate/stable, intermediate/decreasing and high smoking trajectory groups. After controlling for covariates using propensity scores, the direct effect of maternal smoking in pregnancy on offspring smoking in adolescence was statistically significant, especially when the mother belonged to the intermediate/stable smoking trajectory group (ORIPW = 2.09, 95% CI: 1.70 – 2.61) or to the high smoking trajectory group (ORIPW = 2.08, 95% CI: 1.52 – 3.11) compared to the low smoking trajectory group. None of the indirect effects of maternal smoking in pregnancy were statistically significant, and neither were the proportions mediated. ConclusionMaternal pregnancy smoking seems to have an influence on offspring smoking in early adulthood, which does not appear to be mediated by offspring behavioral difficulties. Women should be strongly encouraged to quit smoking in pregnancy to reduce both short and long-term health risks among their offspring.

A prediction model for classifying maternal pregnancy smoking using California state birth certificate information.

Systematically recorded smoking data are not always available in vital statistics records, and even when available it can underestimate true smoking rates. To develop a prediction model for maternal tobacco smoking in late pregnancy based on birth certificate information using a combination of self- or provider-reported smoking and biomarkers (smoking metabolites) in neonatal blood spots as the alloyed gold standard. We designed a case-control study where childhood cancer cases were identified from the California Cancer Registry and controls were from the California birth rolls between 1983 and 2011 who were cancer-free by the age of six. In this analysis, we included 894 control participants and performed high-resolution metabolomics analyses in their neonatal dried blood spots, where we extracted cotinine [mass-to-charge ratio (m/z) = 177.1023] and hydroxycotinine (m/z = 193.0973). Potential predictors of smoking were selected from California birth certificates. Logistic regression with stepwise backward selection was used to build a prediction model. Model performance was evaluated in a training sample, a bootstrapped sample, and an external validation sample. Out of seven predictor variables entered into the logistic model, five were selected by the stepwise procedure: maternal race/ethnicity, maternal education, child's birth year, parity, and child's birth weight. We calculated an overall discrimination accuracy of 0.72 and an area under the receiver operating characteristic curve (AUC) of 0.81 (95% confidence interval [CI] 0.77, 0.84) in the training set. Similar accuracies were achieved in the internal (AUC 0.81, 95% CI 0.77, 0.84) and external (AUC 0.69, 95% CI 0.64, 0.74) validation sets. This easy-to-apply model may benefit future birth registry-based studies when there is missing maternal smoking information; however, some smoking status misclassification remains a concern when only variables from the birth certificate are used to predict maternal smoking.

Cotinine concentrations in maternal serum and amniotic fluid during pregnancy and risk of testicular germ cell cancer in the offspring: A prospective nested case-control study.

Maternal smoking in pregnancy may increase the risk of testicular germ cell cancer (TGCC) in offspring, but current evidence remains inconclusive. We performed a nested case-control study using cotinine measurements in maternal serum and amniotic fluid as a biomarker for tobacco exposure during pregnancy. A total of 654 males with maternal serum (n = 359, ncases/controls = 71/288) and/or amniotic fluid (n = 295, ncases/controls = 66/229) samples were included. Data on TGCC diagnoses and relevant covariates were derived from nationwide Danish health registries. Cotinine was quantified by liquid chromatography tandem mass spectrometry. An adapted cox regression model estimated the risk of TGCC considering active and inactive tobacco use defined according to cotinine concentrations of <, ≥15 ng/ml. Overall, the concentrations of cotinine were comparable in maternal serum and amniotic fluid (medianserum/amniotic fluid : 2.1/2.6 ng/ml). A strong statistically significant correlation was detected in 14 paired samples (Spearman rho: 0.85). Based on maternal serum cotinine concentrations, exposure to active tobacco use was not associated with risk of TGCC in offspring (HR 0.88, 95% CI 0.51; 1.52). Similarly, based on amniotic fluid cotinine concentrations, exposure to active tobacco use was not associated with risk of TGCC (HR 1.11, 95% CI 0.64; 1.95). However, different risks were observed for seminomas and nonseminomas in both matrices, but none were statistically significant. Our findings did not provide convincing evidence supporting that exposure to tobacco during pregnancy is associated with TGCC.

Polymorphisms in Glutathione S-Transferase (GST) Genes Modify the Effect of Exposure to Maternal Smoking Metabolites in Pregnancy and Offspring DNA Methylation.

Maternal smoking in pregnancy (MSP) affects the offspring's DNA methylation (DNAm). There is a lack of knowledge regarding individual differences in susceptibility to exposure to MSP. Glutathione S-transferase (GST) genes are involved in protection against harmful oxidants such as those found in cigarette smoke. This study aimed to test whether polymorphisms in GST genes influence the effect of MSP on offspring DNAm. Using data from the Isle of Wight birth cohort, we assessed the association of MSP and offspring DNAm in 493 mother-child dyads (251 male, 242 female) with the effect-modifying role of GST gene polymorphism (at rs506008, rs574344, rs12736389, rs3768490, rs1537234, and rs1695). MSP was assessed by levels of nicotine and its downstream metabolites (cotinine, norcotinine, and hydroxycotinine) in maternal sera. In males, associations of hydroxycotinine with DNAm at cg18473733, cg25949550, cg11647108, and cg01952185 and norcotinine with DNAm at cg09935388 were modified by GST gene polymorphisms (p-values < 0.05). In females, associations of hydroxycotinine with DNAm at cg12160087 and norcotinine with DNAm at cg18473733 were modified by GST gene polymorphisms (p-values < 0.05). Our study emphasizes the role of genetic polymorphism in GST genes in DNAm's susceptibility to MSP.

Association of Maternal Cigarette Smoking with Neonatal Death: A Population-Based Cohort Study

Introduction: Maternal pregnancy smoking has adverse perinatal outcomes and the relationship between maternal smoking and neonatal death has not been fully elucidated. We aimed to examine the risk of neonatal death in relation to maternal smoking and to quantify potential mediators of these associations. Methods: We did a population-based cohort study using Period Linked Birth-Infant Death data from 2016 to 2019 in the US National Vital Statistics System. The exposure was maternal smoking status. The main outcome was neonatal death. Association between maternal smoking and neonatal death was estimated through logistic regression. Mediation analysis was performed to assess the extent to which the association between maternal smoking and neonatal death was mediated by neonatal complications. Results: The final sample consisted of 14,717,020 mothers with live singleton births. The overall neonatal mortality rate was 2.2 per 1,000 live births. Maternal pregnancy smoking was associated with an increased risk of neonatal death {adjusted odds ratio (aOR, 1.33 [95% CI, 1.28–1.38]; p < 0.001)}, while smoking cessation during the whole pregnancy showed a comparable risk of neonatal death with nonsmokers (aOR, 1.06 [95% CI, 0.99–1.14]; p = 0.116). Mediation analysis indicated that the association between pregnancy smoking and neonatal death might be mainly mediated by preterm birth and low Apgar score at 5 min. Conclusions: Maternal pregnancy smoking, regardless of pregnancy trimester and intensity, was associated with increased risk of neonatal death. Efforts are needed for policymakers to promote smoking cessation before pregnancy, and professional perinatal care should be provided for those who smoked during pregnancy.

Maternal smoking in pregnancy and blood pressure during childhood and adolescence: a meta-analysis

Arterial hypertension during childhood or adolescence is rising, and smoking during pregnancy may constitute a modifiable risk factor. This study aims to evaluate the effect of maternal smoking during pregnancy on diastolic (DBP) and systolic blood pressure (SBP) in childhood and adolescence. A bibliographic search was conducted in PubMed, Embase, and CENTRAL databases in March 2022. Meta-analysis was performed with the difference in mean-adjusted SBP/DBP of children and adolescents aged 3–17 years, according to maternal smoking/non-smoking in pregnancy. A random effects model was applied; a leave-one-out analysis and meta-analysis by subgroups were performed. A modified Newcastle–Ottawa scale was used to assess the quality of the studies. Evidence levels were rated using the GRADE system. Fifteen studies were included in the meta-analysis; all of them evaluated the mean-adjusted SBP difference in children or adolescents (N = 73,448), and 6 also that of DBP (N = 31,459). Results showed that maternal smoking during pregnancy significantly increased SBP (β = 0.31 mmHg 95% CI 0.14–0.49). A greater increase in mean-adjusted SBP was observed in those studies that completed the recruitment before 1990, were conducted in non-European countries, used standard mercury or manual sphygmomanometry, adjusted for birth weight, and were in the lowest quality subgroup. No significant association was found for DBP. The GRADE level of evidence was low for SBP and very low for DBP.Conclusion: Smoking in pregnancy might increase SBP in childhood and adolescence. Due to the low level of evidence, solid inferences cannot be drawn about the clinical relevance of these findings. What is Known:• AHT is the leading cause of premature death among adults worldwide.• Deleterious effects derived from SHS exposure on children's health have been documented since early 1970. To date, there are contradictory results about the effects of prenatal SHS exposure on children’s BP.What is New:• Smoking in pregnancy may increase SBP during childhood and adolescence.• Maternal smoking during pregnancy could have greater influence on their offspring's SBP than on DBP.

Maternal Tobacco Smoking During Pregnancy and Children's Emotional and Behavioral Trajectories: The EDEN Mother-Child Birth Cohort Study.

The nature of the relationship between maternal tobacco smoking during pregnancy and the occurrence of children's behavioral problems is still a matter of controversy. We tested this association using data collected among a sample of pregnant women and their offspring followed up from birth to early adolescence (age 12 years), accounting for multiple parent, child, and family characteristics. Data come from 1424 mother-child pairs participating in the Étude des Déterminants pré et post-natals précoces du développement psychomoteur et de la santé de l'ENfant mother-child cohort in France. Using repeated measures (3, 5.5, 8, and 11.5 years) of the mother-reported Strengths and Difficulties Questionnaire, we estimated trajectories of children's emotional and behavioral difficulties. Two aspects of maternal smoking were studied: The timing (nonsmoker, smoking during the periconceptional period, or throughout pregnancy) and the level of use (cigarettes/day) during the first trimester of pregnancy. Robust Poisson regression models controlled for confounding factors including maternal mental health and socioeconomic characteristics using propensity scores with the overlap weighting technique. Contrary to bivariate analyses, in propensity score-controlled regression models, maternal smoking throughout pregnancy was no longer significantly associated with offspring emotional or behavioral difficulties. Maternal heavy smoking (≥10 cigarettes/day) remained significantly associated with intermediate levels of conduct problems (RR 1.25, 95% CI 1.19 to 1.31). The association between maternal smoking in pregnancy and offspring's emotional and behavioral difficulties appears to be largely explained by women's other characteristics. However, maternal heavy smoking appears to be related to offspring behavioral difficulties beyond the role of confounding characteristics. The relationship between maternal smoking during pregnancy (in two modalities: Timing and level of smoking) and behavioral difficulties in children is still a matter of debate. While the relationship between any maternal tobacco use and offspring behavioral difficulties appears to be largely explained by confounding factors, heavy maternal smoking in the first trimester of pregnancy seems to be associated with offspring behavioral difficulties beyond the socioeconomic and mental health characteristics transmitted across generations.

The effects of modifiable maternal pregnancy exposures on offspring molar-incisor hypomineralisation: A negative control study.

Explore associations between modifiable maternal pregnancy exposures: pre-pregnancy body mass index (BMI), pregnancy smoking and alcohol consumption with offspring molar-incisor hypomineralisation (MIH) and use negative control analyses to explore for the presence of confounding. Using data from a prospective UK birth cohort, Avon Longitudinal Study of Parents and Children, we performed logistic regression to explore confounder adjusted associations between maternal pre-pregnancy BMI and smoking and alcohol consumption during pregnancy with MIH. We compared these with negative control exposure (paternal BMI, smoking and alcohol) and outcome (offspring dental trauma) analyses. 5,536 mother/offspring pairs were included (297 (5.4%) MIH cases). We found a weak, positive association between maternal mean BMI and offspring MIH (Odds Ratio (OR) per 1-kg/m2 difference in BMI: 1.04, 95% confidence interval (CI): 1.00, 1.08). Results of subsequent analyses suggested this effect was non-linear and being driven by women in the highest BMI quintile (OR for women in the highest BMI quintile versus the lowest: 1.61 95%CI: 1.02, 2.60). Negative control analyses showed no evidence of an association between paternal BMI and offspring MIH (OR: 0.94, 95%CI: 0.89,1.00) and maternal BMI and offspring dental trauma (OR: 0.99, 95%CI: 0.96, 1.02). There was no clear evidence of an association for maternal smoking (OR: 0.76, 95%CI: 0.46,1.22) or alcohol consumption (OR: 0.79, 95%CI: 0.56, 1.21) with offspring MIH with results imprecisely estimated. We found a possible intrauterine effect for high maternal pre-pregnancy BMI on offspring MIH, but no robust evidence of an intrauterine effect for maternal pregnancy smoking or alcohol consumption. A key limitation includes possible misclassification of MIH. Replication of these results is warranted.

Smoking during pregnancy and children’s emotional and behavioural trajectories

Abstract Background The nature of the relationship between maternal tobacco smoking during pregnancy and the occurrence of children's behavioural problems is still a matter of controversy. We tested this association using data collected among a sample of children followed from pregnancy to early adolescence (age 11.5 years), accounting for multiple parents’, children's and family characteristics. Methods Data come from 1424 mother-child pairs participating in the EDEN mother-child cohort set up in France. Using repeated measures (3, 5.5, 8 and 11.5 years) of the mother-reported Strengths and Difficulties Questionnaire, we estimated trajectories of children's emotional and behavioural difficulties. Two aspects of maternal smoking were studied: the timing and the level of use (cigarettes/day) during the first trimester of pregnancy. Multinomial regression models controlled for confounding factors including maternal mental health and socioeconomic characteristics using propensity scores with the overlap weighting technique. Results Contrary to bivariate analyses, in propensity score-controlled regression models, maternal smoking throughout pregnancy was no longer significantly associated with offspring emotional or behavioural difficulties. Maternal heavy smoking (≥10cigarettes/day) remained significantly associated with intermediate levels of overall emotional and behavioural difficulties (OR 1.64, 95%CI 1.04-2.58) and conduct problems (OR 3.05 95%CI 1.22-7.61), as well as with high levels of conduct problems symptoms (OR 2.82 95%CI 0.88-9.06) - although the latter did not reach statistical significance. Conclusions The association between maternal smoking in pregnancy and offspring emotional and behavioural difficulties appears to be largely explained by women's other characteristics. However, maternal heavy smoking appears to be related to offspring behavioural difficulties beyond the role of confounding characteristics. Key messages • The association between maternal smoking in pregnancy and offspring emotional and behavioural difficulties seem largely explained by the family's socio-demographic and behavioural characteristics. • Maternal heavy smoking appears to be related to offspring behavioural difficulties beyond the role of confounding characteristics.

Identification of families in need of support: Correlates of adverse childhood experiences in the right@home sustained nurse home visiting program.

Little is known about the efficacy of pregnancy screening tools using non-sensitive sociodemographic questions to identify the possible presence of as yet undiagnosed disease in individuals and later adverse childhood events disclosure. The study aims were to: 1) record the prevalence of risk disclosed by families during receipt of a sustained nurse home visiting program; and 2) explore patterns of relationships between the disclosed risks for their child having adverse experiences and the antenatal screening tool, which used non-sensitive demographic questions. Retrospective, observational study. Data about the participants in the intervention arm of the Australian right@home trial, which is scaffolded on the Maternal Early Childhood Sustained Home-visiting model, collected between 2013 and 2017 were used. Screening data from the 10-item antenatal survey of non-sensitive demographic risk factors and disclosed risks recorded by the nurse in audited case files during the subsequent 2 year intervention were examined (n = 348). Prevalence of disclosed risks for their child having adverse experiences were analysed in 2019 using multiple response frequencies. Phi correlations were conducted to test associations between screening factors and disclosed risks. Among the 348 intervention participants whose files were audited, 300 were noted by nurses to have disclosed risks during the intervention, with an average of four disclosures. The most prevalent maternal disclosures were depression or anxiety (57.8%). Mental health issues were the most prevalent partner and family disclosures. Screening tool questions on maternal smoking in pregnancy, not living with another adult, poverty and self-reporting anxious mood were significantly associated with a number of disclosed risks for their child having adverse experiences. These findings suggest that a non-sensitive sociodemographic screening tool may help to identify families at higher risk for adverse childhood experiences for whom support from a sustained nurse home visiting program may be beneficial.

Mediators of socioeconomic inequalities in preterm birth: a systematic review

BackgroundRates of preterm birth are substantial with significant inequalities. Understanding the role of risk factors on the pathway from maternal socioeconomic status (SES) to preterm birth can help inform interventions and policy. This study therefore aimed to identify mediators of the relationship between maternal SES and preterm birth, assess the strength of evidence, and evaluate the quality of methods used to assess mediation.MethodsUsing Scopus, Medline OVID, “Medline In Process & Other Non-Indexed Citation”, PsycINFO, and Social Science Citation Index (via Web of Science), search terms combined variations on mediation, socioeconomic status, and preterm birth. Citation and advanced Google searches supplemented this. Inclusion criteria guided screening and selection of observational studies Jan-2000 to July-2020. The metric extracted was the proportion of socioeconomic inequality in preterm birth explained by each mediator (e.g. ‘proportion eliminated’). Included studies were narratively synthesised.ResultsOf 22 studies included, over one-half used cohort design. Most studies had potential measurement bias for mediators, and only two studies fully adjusted for key confounders. Eighteen studies found significant socioeconomic inequalities in preterm birth. Studies assessed six groups of potential mediators: maternal smoking; maternal mental health; maternal physical health (including body mass index (BMI)); maternal lifestyle (including alcohol consumption); healthcare; and working and environmental conditions. There was high confidence of smoking during pregnancy (most frequently examined mediator) and maternal physical health mediating inequalities in preterm birth. Significant residual inequalities frequently remained. Difference-of-coefficients between models was the most common mediation analysis approach, only six studies assessed exposure-mediator interaction, and only two considered causal assumptions.ConclusionsThe substantial socioeconomic inequalities in preterm birth are only partly explained by six groups of mediators that have been studied, particularly maternal smoking in pregnancy. There is, however, a large residual direct effect of SES evident in most studies. Despite the mediation analysis approaches used limiting our ability to make causal inference, these findings highlight potential ways of intervening to reduce such inequalities. A focus on modifiable socioeconomic determinants, such as reducing poverty and educational inequality, is probably necessary to address inequalities in preterm birth, alongside action on mediating pathways.

Identification and Characterization of Influential Factors in Susceptibility to Attention Deficit Hyperactivity Disorder Among Preschool-Aged Children.

Attention deficit hyperactivity disorder (ADHD) is the most common childhood-onset neurodevelopmental disorder. Currently, increasing amounts of attention have been focused on the epidemiologic profiling of ADHD in children, viewed as a continuously distributed risk dimension throughout the whole lifespan. This study aimed to identify and characterize potential influential factors susceptible to ADHD-related symptoms among preschool-aged children. A comprehensive questionnaire was self-designed for both children and their parents or guardians and was distributed to 30 kindergartens from Beijing and Hebei, collecting potential influential factors in susceptibility to ADHD. ADHD was assessed by the Conner’s Abbreviated Symptom Questionnaire (C-ASQ), and 7,938 children were analyzed. Least absolute shrinkage and selection operator (LASSO) regression and hierarchical degree of adjustment were used to control possible covariates. Five factors, namely, children’s secondhand smoking exposure, breastfeeding duration, sleep mode, maternal pregnancy smoking exposure, and parental self-rating for patience, were identified to be independently and significantly associated with ADHD susceptibility. Meanwhile, dose–response relationships were observed between breastfeeding duration, parental self-rating for patience, and ADHD-related symptoms. Finally, a nomogram model was created for predicting ADHD susceptibility based on significant and conventional attributes under each criterion.

Maternal smoking status during pregnancy and low birth weight in offspring: systematic review and meta-analysis of 55 cohort studies published from 1986 to 2020.

Maternal smoking during pregnancy may be associated with low birth weight (LBW) in offspring and global risk estimates have not been summarized previously. We aimed to systematically explore evidence regarding maternal smoking and the LBW risk in offspring globally and examine possible causes of heterogeneity across relevant studies. Comprehensive search of PubMed, Ovid Embase, Ovid Medline (R), and Web of science from inception until October 2021 was carried out. A random-effects meta-analysis was used to estimate the pooled odds ratio (OR) and corresponding 95% confidence interval (CI). Restricted cubic spline analysis with three knots was used to further examine the dose-response relationship. Literature searches yielded 4940 articles, of which 53 met inclusion criteria (comprising 55 independent studies). Maternal smoking during pregnancy was significantly associated with the risk of LBW in offspring (OR = 1.89, 95% CI = 1.80-1.98). Furthermore, an obvious dose-response relationship between the amount of cigarettes daily smoked in pregnancy and the risk of LBW in offspring was observed. The results of subgroup analyses indicated that the risk of maternal smoking on LBW was larger in more recently conducted studies (P = 0.020) and longer period of active smoking during pregnancy (P = 0.002). No evidence of publication bias was found. In summary, maternal smoking in pregnancy was significantly associated with a higher risk of LBW in offspring on a global scale. The risk of maternal smoking on infant LBW seems to be increasing over time, and was higher with longer smoking duration throughout pregnancy and more cigarettes smoked daily.

Maternal smoking during pregnancy and asthma during the first year of life: a comparative study between smokers and nonsmoker mothers.

We investigated the relationship between maternal smoking in pregnancy and health care problems in the offspring during the first year of life, particularly asthma. A cohort of 648 consecutive infants born at term and alive at Hospital de Sagunto (Valencia, Spain) over one year period was followed for 12 months. Clinical data of the infants were prospectively collected from the database of ambulatory medical records (ABUCASIS) of the Valencia health system. Smoking during pregnancy was recorded in 164 (25.3%) mothers. During the first year of life, asthma was diagnosed in 101 infants, with an incidence of 15.7%. The diagnoses of asthma (25.6% vs. 12.3%; P < 0.0001) and bronchiolitis (44.5% vs. 28.6%; P = 0.0002) during the first year of life were more common among infants in the smoking group. The probability of developing asthma during the first year of life was two-fold higher for the male gender and 2.5 times higher when mothers smoked while pregnant. Up to 52% of asthma cases could have been avoided in infants born to smoking mothers if they did not smoke during pregnancy. Infants in the smoking group showed a lower weight and length at birth than infants in the nonsmoking group differences almost disappeared at 6 months and 12 months. Asthma during the first year of life showed a clear relationship with maternal smoking in pregnancy. Pregnant women should be advised of the significant perinatal risk for respiratory diseases associated with tobacco use.

Ancestral smoking and developmental outcomes: a review of publications from a population birth cohort†.

The adverse effects on the child of maternal smoking in pregnancy is well-recognized, but little research has been carried out on the possible non-genetic effects of ancestral smoking prior to the pregnancy including parental initiation of cigarette smoking in their own childhoods or a grandmother smoking during pregnancy. Here, we summarize the studies that have been published mainly using data from the Avon Longitudinal Study of Parents and Children. We demonstrate evidence that ancestral smoking prior to or during pregnancy can often be beneficial for offspring health and both ancestor- and sex-specific. More specifically, we report evidence of (i) adverse effects of the father starting to smoke pre-puberty on his son’s development; (ii) beneficial effects on the grandson if his maternal grandmother had smoked in pregnancy; and (iii) mainly adverse effects on the granddaughter when the paternal grandmother had smoked in pregnancy. The ancestor- and sex-specificity of these results are consistent with earlier studies reporting associations of health and mortality with ancestral food supply in their parents’ and grandparents’ pre-pubertal childhoods.

Identifying preventable risk factors for hospitalised asthma in young Aboriginal children: a whole-population cohort study

BackgroundAustralia has one of the highest rates of asthma worldwide. Indigenous children have a particularly high burden of risk determinants for asthma, yet little is known about the asthma risk...

Effect of Maternal Prepregnancy/Early-Pregnancy Body Mass Index and Pregnancy Smoking and Alcohol on Congenital Heart Diseases: A Parental Negative Control Study.

BackgroundCongenital heart diseases (CHDs) are the most common congenital anomaly. The causes of CHDs are largely unknown. Higher prenatal body mass index (BMI), smoking, and alcohol consumption are associated with increased risk of CHDs. Whether these are causal is unclear.Methods and ResultsSeven European birth cohorts, including 232 390 offspring (2469 CHD cases [1.1%]), were included. We applied negative exposure paternal control analyses to explore the intrauterine effects of maternal BMI, smoking, and alcohol consumption during pregnancy, on offspring CHDs and CHD severity. We used logistic regression, adjusting for confounders and the other parent's exposure and combined estimates using a fixed‐effects meta‐analysis. In adjusted analyses, maternal overweight (odds ratio [OR], 1.15 [95% CI, 1.01–1.31]) and obesity (OR, 1.12 [95% CI, 0.93–1.36]), compared with normal weight, were associated with higher odds of CHD, but there was no clear evidence of a linear increase in odds across the whole BMI distribution. Associations of paternal overweight, obesity, and mean BMI were similar to the maternal associations. Maternal pregnancy smoking was associated with higher odds of CHD (OR, 1.11 [95% CI, 0.97–1.25]) but paternal smoking was not (OR, 0.96 [95% CI, 0.85–1.07]). The positive association with maternal smoking appeared to be driven by nonsevere CHD cases (OR, 1.22 [95% CI, 1.04–1.44]). Associations with maternal moderate/heavy pregnancy alcohol consumption were imprecisely estimated (OR, 1.16 [95% CI, 0.52–2.58]) and similar to those for paternal consumption.ConclusionsWe found evidence of an intrauterine effect for maternal smoking on offspring CHDs, but no evidence for higher maternal BMI or alcohol consumption. Our findings provide further support for the importance of smoking cessation during pregnancy.

Abstract P201: Early Life Exposure To Environmental Tobacco Smoke And Cardiometabolic Diseases In Middle Age: A 4-decade Follow-up Study Of The Collaborative Perinatal Project

Introduction: Environmental tobacco smoke (ETS) is a major source of indoor air pollution and has been associated with cardiovascular diseases (CVD) risks. There is little research on the associations of ETS exposure in early life with CVD risks in later life. Hypothesis: We hypothesized that ETS exposures in the uterus, childhood, and teenage increase midlife CVD risks. Methods: For 1,623 offspring born in 1959-1966 at two sites from the Collaborative Perinatal Project, we defined intrauterine ETS exposure in each trimester if the mother smoked (1-19 or ≥20 cigs/day). ETS exposure in each year from birth to 18 years was quantified by total daily-average hours of parents smoking weighted by daily packs from a questionnaire at the adult follow-up (mean age: 39 years). Ever diagnoses of diabetes (cumulative incidence: 3.0%), heart diseases (1.5%), hypertension (17.3%), and high cholesterol (25.3%) until adult follow-up were reported. Cardiometabolic diseases (CMD, cumulative incidence: 35.4%) were defined as any diagnosis. We estimated odds ratio (OR) for CMD by ETS exposures in each trimester adjusting for prenatal factors (maternal SES, pre-pregnancy BMI, parity, newborn sex); additionally adjusted for maternal smoking in pregnancy, birth weight, and gestational age for ETS exposure from birth to 18 years. We also stratified the analyses by adult smoking status. Results: Exposure to ≥20 cigs/day in the 1 st (OR: 1.52, 95% CI: 1.02-2.26) and 2 nd (OR: 1.50, 95% CI: 1.01-2.24) trimester was significantly associated with hypertension compared to none exposure, and the associations were stronger in adult offspring who were smokers. Among the 70% of participants who reported childhood ETS exposure, the average exposure was 8.5 smoker-hours/day and 10.5 smoker-hour*packs/day (HP/Day), with a declining trend from birth to 18 years. ETS exposure (per SD increment) in early life from birth to 18 years, separately or cumulatively (OR=1.24, 95% CI: 1.07-1.43), was associated with higher odds of adult hypertension. ETS exposure in teenage (11-18 years, OR=1.26, 95% CI: 1.05-1.50), but not in childhood (birth to 10 years, OR=1.18, 95% CI: 0.96-1.45), was associated with higher odds of a combination of adult heart disease and diabetes, which was more striking in adult non-smokers than smokers. Odds of adult CMD increased by 13% (95% CI: 1%-28%) for each SD (about 10 HP/Day) increment in ETS in the whole childhood and by 16% (95% CI: 3%-30%) in teenage. The results for smoker-hours/day were similar to those for smoker-hour*packs/day. Conclusions: Intrauterine exposure to maternal smoking and ETS exposures (time and total amount) from birth to 18 years increase the risk of adult hypertension. ETS exposure in early life may also increase the risk of adult cardiometabolic diseases. Teenage may be a sensitive window for elevated risk of adult heart diseases and diabetes associated with ETS exposure.