Objective While studies of the effects of prenatal smoking on child psychopathology have found positive relationships, most studies (1) failed to control for a range of correlates of maternal smoking that could affect children’s behavior; (2) have been conducted with school-age rather than younger children, so it is not clear when such problems emerge; and (3) have not examined the effects on internalizing problems. Method This study examined the effects of prenatal smoke exposure on behaviors associated with externalizing and internalizing behavior problems and negative temperament in a diverse community sample of 679 4-year-olds. Results After controlling for correlates that include socioeconomic status, life stress, family conflict, maternal depression, maternal scaffolding skills, mother–child attachment, child negative affect and effortful control, smoking during pregnancy was no longer associated with child behavior or emotional problems. Conclusions Future studies need to control for a wide range of covariates of maternal smoking.
adjustment; mental health; parenting; risk; smoking
Prenatal tobacco exposure is a risk factor for the development of externalizing behaviors and is associated with several adverse health outcomes. Because pregnancy smoking is a complex behavior with both daily fluctuations and changes over the course of pregnancy, quantifying tobacco exposure is a significant challenge. To better measure the degree of tobacco exposure, costly biological specimens and repeated self-report measures of smoking typically are collected throughout pregnancy. With such designs, there are multiple, and substantially correlated, indices that can be integrated via new statistical methods to identify patterns of prenatal exposure.
A multiple-imputation-based fuzzy clustering technique was designed to characterize topography of prenatal exposure. This method leveraged all repeatedly measured maternal smoking variables in our sample data, including (a) cigarette brand; (b) Fagerstrom nicotine dependence item scores; (c) self-reported smoking; and (d) cotinine level in maternal urine and infant meconium samples. Identified exposure groups then were confirmed using a suite of clustering validation indices based on multiple imputed datasets. The classifications were validated against irritable reactivity in the first month of life and birth weight of 361 neonates (Male_n = 185; Female_n = 176; Gestational Age_Mean = 39 weeks).
This proposed approach identified three exposure groups, non-exposed, lighter-tobacco-exposed, and heavier-tobacco-exposed based on high-dimensional attributes. Unlike cutoff score derived groups, these groupings reflect complex smoking behavior and individual variation of nicotine metabolism across pregnancy. The identified groups predicted differences in birth weight and in the pattern of change in neonatal irritable reactivity, as well as resulted in increased predictive power. Multiple-imputation based fuzzy clustering appears to be a useful method to categorize patterns of exposure and their impact on outcomes.
Prenatal tobacco exposure; fuzzy clustering; multiple imputation; exposure pattern; irritable reactivity
Studies on adverse childhood health and development outcomes associated with parental smoking have shown inconsistent results. Using a cohort of Belarusian children, we examined differences in cognition, behaviors, growth, adiposity, and blood pressure at 6.5 years according to prenatal and postnatal exposure to parental smoking.
Using cluster-adjusted multivariable regression, effects of exposure to prenatal smoking were examined by comparing (1) children whose mothers smoked during pregnancy with those of mothers who smoked neither during nor after pregnancy and (2) children whose mothers smoked during and after pregnancy with those whose mothers smoked after pregnancy only; effects of postnatal smoking were examined by comparing (1) children whose mothers smoked after pregnancy only with those of mothers who smoked neither during nor after pregnancy and (2) children whose fathers smoked with those whose fathers did not smoke among children of non-smoking mothers after adjusting for a wide range of socioeconomic and family characteristics.
After adjusting for confounders, children exposed vs unexposed to prenatal maternal smoking had no differences in mean IQ, teacher-rated behavioral problems, adiposity, or blood pressure. Children exposed to maternal postnatal smoking had slightly increased behavioral problems [0.9, 95% CI: 0.6, 1.2 for total difficulties], higher body mass index [0.2, 95% CI: 0.1, 0.3], greater total skinfold thickness [0.4, 95% CI: 0.04, 0.71], and higher odds of overweight or obesity [1.4, 95% CI; 1.1, 1.7]. Similar magnitudes of association were observed with postnatal paternal smoking.
No adverse cognitive, behavioral and developmental outcomes were associated with exposure to maternal prenatal smoking. Observed associations with postnatal smoking of both parents may reflect residual confounding by genetic and family environmental factors.
A large body of documented evidence shows that smoking during pregnancy is harmful to both the mother and fetus. Prenatal exposure to nicotine in various forms alters neurologic development in experimental animals and may increase the risk for neurologic conditions in humans. There is a direct association between maternal smoking and SIDS; however the connection with depression, attention disorders, learning and behavior problems, and nicotine addiction in humans is not straightforward. Nicotine’s action on the production and function of neurotransmitters makes it a prime suspect in the pathology of these diseases. Nicotine accentuates neurotransmitter function in adults but desensitizes these functions in prenatally exposed infants and children. This desensitization causes an abnormal response throughout the lifespan. Furthermore, nicotine use in the adolescent and adult can alleviate some of the symptoms caused by these neurotransmitter problems, but it also increases the risk for nicotine addiction. Although nicotine replacement drugs are allowed for pregnant women, there is no clear indication that they improve outcomes during pregnancy, and they may add to the damage to the developing neurologic system. Understanding the effects of nicotine exposure is important in providing safe care for pregnant women, children and families and for developing appropriate smoking cessation programs during pregnancy.
Nicotine; Smoking; Pregnancy; SIDS; ADHD
Maternal smoking during pregnancy is associated with increased risk of childhood overweight body mass index (BMI). Less is known about the association between prenatal secondhand tobacco smoke (SHS) exposure and childhood BMI. We followed 292 mother-child dyads from early pregnancy to 3 years of age. Prenatal tobacco smoke exposure during pregnancy was quantified using self-report and serum cotinine biomarkers. We used linear mixed models to estimate the association between tobacco smoke exposure and BMI at birth, 4 weeks, and 1, 2, and 3 years. During pregnancy, 15% of women reported SHS exposure and 12% reported active smoking, but 51% of women had cotinine levels consistent with SHS exposure and 10% had cotinine concentrations indicative of active smoking. After adjustment for confounders, children born to active smokers had higher BMI at 2 and 3 years of age (self-report or serum cotinine), compared to unexposed children. Children born to women with prenatal serum cotinine concentrations indicative of SHS exposure had higher BMI at 2 (Mean Difference [MD]:0.3; 95% confidence interval [CI]:−0.1, 0.7) and 3 (MD:0.4; [0, 0.8]) years compared to unexposed children. Using self-reported prenatal exposure resulted in non-differential exposure misclassification of SHS exposures that attenuated the association between SHS exposure and BMI compared to serum cotinine concentrations. These findings suggest active and secondhand prenatal tobacco smoke exposure may be related to an important public health problem in childhood and later life. In addition, accurate quantification of prenatal secondhand tobacco smoke exposures is essential to obtaining valid estimates.
Body Mass Index; Children; Cotinine; Growth; Prenatal; Tobacco Smoke
There is much evidence to suggest that risk for common clinical disorders begins in foetal life. Exposure to environmental risk factors however is often not random. Many commonly used indices of prenatal adversity (e.g. maternal gestational stress, gestational diabetes, smoking in pregnancy) are influenced by maternal genes and genetically influenced maternal behaviour. As mother provides the baby with both genes and prenatal environment, associations between prenatal risk factors and offspring disease maybe attributable to true prenatal risk effects or to the "confounding" effects of genetic liability that are shared by mother and offspring. Cross-fostering designs, including those that involve embryo transfer have proved useful in animal studies. However disentangling these effects in humans poses significant problems for traditional genetic epidemiological research designs.
We present a novel research strategy aimed at disentangling maternally provided pre-natal environmental and inherited genetic effects. Families of children aged 5 to 9 years born by assisted reproductive technologies, specifically homologous IVF, sperm donation, egg donation, embryo donation and gestational surrogacy were contacted through fertility clinics and mailed a package of questionnaires on health and mental health related risk factors and outcomes. Further data were obtained from antenatal records.
To date 741 families from 18 fertility clinics have participated. The degree of association between maternally provided prenatal risk factor and child outcome in the group of families where the woman undergoing pregnancy and offspring are genetically related (homologous IVF, sperm donation) is compared to association in the group where offspring are genetically unrelated to the woman who undergoes the pregnancy (egg donation, embryo donation, surrogacy). These comparisons can be then examined to infer the extent to which prenatal effects are genetically and environmentally mediated.
A study based on children born by IVF treatment and who differ in genetic relatedness to the woman undergoing the pregnancy is feasible. The present report outlines a novel experimental method that permits disaggregation of maternally provided inherited genetic and post-implantation prenatal effects.
The influence of community context on the effectiveness of evidence-based maternal and child home visitation programs following implementation is poorly understood. This study compared prenatal smoking cessation between home visitation program recipients and local-area comparison women across 24 implementation sites within one state, while also estimating the independent effect of community smoking norms on smoking cessation behavior.
Retrospective cohort design using propensity score matching of Nurse-Family Partnership (NFP) clients and local-area matched comparison women who smoked cigarettes in the first trimester of pregnancy. Birth certificate data were used to classify smoking status. The main outcome measure was smoking cessation in the third trimester of pregnancy. Multivariable logistic regression analysis examined, over two time periods, the association of NFP exposure and the association of baseline county prenatal smoking rate on prenatal smoking cessation.
The association of NFP participation and prenatal smoking cessation was stronger in a later implementation period (35.5% for NFP clients vs. 27.5% for comparison women, p < 0.001) than in an earlier implementation period (28.4% vs. 25.8%, p = 0.114). Cessation was also negatively associated with county prenatal smoking rate, controlling for NFP program effect, (OR = 0.84 per 5 percentage point change in county smoking rate, p = 0.002).
Following a statewide implementation, program recipients of NFP demonstrated increased smoking cessation compared to comparison women, with a stronger program effect in later years. The significant association of county smoking rate with cessation suggests that community behavioral norms may present a challenge for evidence-based programs as models are translated into diverse communities.
Home visitation; Community context; Implementation; Evaluation; Smoking cessation
There is some debate whether smoking during pregnancy causes or is only a risk factor for negative academic outcomes and increased risk of psychopathology in offspring. This study evaluated whether maternal smoking cessation would reduce the risk of adverse outcomes in school-aged children.
Women completed an online survey that included items about child scholastic performance and the Child Behavior Checklist (CBCL). Mothers were divided based on pre-pregnancy and pregnancy smoking status into: 1) Nonsmokers (N=320); 2) Women that smoked in the three months preceding and throughout pregnancy (Smokers, N=83); and 3) Smoking before, but not during pregnancy (Quitters, N=72).
The Smokers and Quitters groups each had lower education and incomes compared to Nonsmokers but were indistinguishable from each other on these measures. The offspring of Smokers were more likely (p<.05) to be behind their peers on standardized tests in math (27.8%) relative to both Nonsmokers (17.4%) and Quitters (13.0%) with similar findings for reading. Smokers reported more behavioral problems by their children in several areas including Hyperactivity and Impulsivity, Social problems, and Externalizing problems including Aggression and Rule-Breaking. Further, the children of Quitters had significantly fewer Attention and Externalizing problems than Smokers. These outcomes were observed even after accounting for the variance attributable to maternal education and several other potential confounds.
Together, these findings indicate that smoking cessation is associated with reduced risk of having children with academic and neuropsychological difficulties. These outcomes are discussed within the framework that nicotine may be a neurobehavioral teratogen.
aggression; attention; math; nicotine; psychopathology; prenatal
Prenatal exposure to secondhand smoke (SHS) is responsible for adverse perinatal outcomes, including preterm birth. Smoking in the home is the primary source of exposure to women during pregnancy. Hair nicotine analysis of mothers and infants was used to describe the relationship between prenatal SHS exposure and number of household smokers. Maternal hair nicotine was strongly correlated with number of household smokers, and a more sensitive measure of household smoking than infant hair. Home smoking bans and focused public media campaigns on the harmful effects of SHS exposure are necessary prevention strategies to avoid adverse perinatal outcomes.
Pregnancy; secondhand smoke; biomarker; preterm birth; nicotine
In Western countries, active maternal smoking during pregnancy is recognized as the most important preventable risk factor for adverse birth outcomes. However, the effect of passive maternal smoking is less clear and has not been extensively studied. In Japan, there has been only one epidemiological study which examined the effects of active smoking during early pregnancy on birth outcomes although the effects of passive smoking were not assessed.
Study subjects were 1565 mothers with singleton pregnancies and the babies born from these pregnancies. Data on active maternal smoking status in the first, second, and third trimesters and maternal environmental tobacco smoke (ETS) exposure at home and work were collected with self-administered questionnaires.
Compared with children born to mothers who had never smoked during pregnancy, children born to mothers who had smoked throughout their pregnancy had a significantly increased risk of small-for-gestational-age (SGA) (adjusted odd ratio [OR] = 2.87; 95% confidence interval: 1.11 − 6.56). However, active maternal smoking only in the first trimester and active maternal smoking in the second and/or third trimesters but not throughout pregnancy were not significantly associated with SGA. With regard to the risk of preterm birth, the adjusted ORs for the above-mentioned three categories were not significant; however, the positive linear trend was significant (P for trend = 0.048). No significant association was found between active maternal smoking during pregnancy and the risk of low birth weight. There was a significant inverse relationship between active maternal smoking during pregnancy and birth weight; newborns of mothers who had smoked throughout pregnancy had an adjusted mean birth weight reduction of 169.6 g. When classifying babies by gender, a significant positive association between active maternal smoking throughout pregnancy and the risk of SGA was found only in male newborns, however, the interaction was not significant. Maternal ETS exposure at home or work was not significantly associated with any birth outcomes.
This is the first study in Japan to show that active maternal smoking throughout pregnancy, but not during the first trimester, is significantly associated with an increased risk of SGA and a decrease in birth weight. Thus, women who smoke should quit smoking as soon as possible after conception.
In this prospective study, teenager mothers (mean age = 16; range = 12–18; 70% African American) were interviewed about their tobacco use during pregnancy. When their children were ten, mothers reported on their child’s behavior and the children completed a neuropsychological battery. We examined the association between prenatal cigarette smoke exposure (PCSE) and offspring neurobehavioral outcomes on data from the ten-year phase (n = 336). Multivariate regression analyses were conducted to test if PCSE predicted neurobehavioral outcomes, adjusting for demographic characteristics, maternal psychological characteristics, prenatal exposure to other substances, and exposure to environmental tobacco smoke. Independent effects of PCSE were found. Exposed offspring had more delinquent, aggressive and externalizing behaviors (CBCL). They were more active (Routh, EAS, SNAP) and impulsive (SNAP), and had more problems with peers (SNAP). On the Stroop test, deficits were observed in both baseline response processing measures and on the more complex interference task that requires both selective attention and response inhibition. The significant effects of PCSE on neurobehavioral outcomes were found for exposure to as few as 10 cigarettes per day. These results are consistent with results from an earlier assessment when the children were age 6, demonstrating that the effects of prenatal tobacco exposure can be identified early and are consistent through middle childhood.
prenatal smoking; neurobehavioral; teenage mothers; children
Although research has documented factors associated with maternal smoking, we need a more in-depth understanding of the risk factors associated with changes in smoking behaviors during the postpartum period. We investigate smoking patterns during pregnancy and 1 year postpartum as a function of relevant psychosocial factors. We use data on 3,522 postpartum mothers from the Fragile Families and Child Wellbeing Study to analyze the predictors of smoking among mothers who did not smoke during pregnancy but smoked at 1 year postpartum, mothers who smoked both during pregnancy and postpartum, and mothers who did not smoke during either period. Our covariates are grouped into four categories of risk factors for smoking: socioeconomic status, health care, life course and health, and partner and social support. Postpartum mothers in our sample were more likely to smoke throughout or after their pregnancies if they had only a high school education or less, had a household income three or more times below the poverty line, had public or no health insurance, breastfed for less than 5 months, were not married to the infant’s father, if the infant’s father currently smoked, and if they attended religious services less than once a week. Mental health problems were consistently associated with an increased risk of constant and postpartum smoking relative to non-smoking. Psychosocial factors play a role in postpartum smoking, but they have a stronger effect in predicting smoking that persists throughout pregnancy and the first year postpartum.
Postpartum; Pregnancy; Smoking; Psychosocial; Unmarried; Hispanic; Fragile Families
Maternal smoking during pregnancy is associated with fetal growth retardation. We examined whether a common genetic variant at chromosome 15q25 (rs1051730), which is known to be involved in nicotine metabolism, modifies the associations of maternal smoking with fetal growth characteristics.
This study was performed in 3,563 European mothers participating in a population-based prospective cohort study from early pregnancy onwards. Smoking was assessed by postal questionnaires and fetal growth characteristics were measured by ultrasound examinations in each trimester of pregnancy.
Among mothers who did not smoke during pregnancy (82.9%), maternal rs1051730 was not consistently associated with any fetal growth characteristic. Among mothers who continued smoking during pregnancy (17.1%), maternal rs1051730 was not associated with head circumference. The T-allele of maternal rs1051730 was associated with a smaller second and third trimester fetal femur length [differences −0.23 mm (95%CI −0.45 to −0.00) and −0.41 mm (95%CI −0.69 to −0.13), respectively] and a smaller birth length [difference −2.61 mm (95%CI −5.32 to 0.11)]. The maternal T-allele of rs1051730 was associated with a lower third trimester estimated fetal weight [difference −33 grams (95%CI −55 to −10)], and tended to be associated with birth weight [difference −38 grams (95%CI −89 to 13)]. This association persisted after adjustment for smoking quantity.
Our results suggest that maternal rs1051730 genotype modifies the associations of maternal smoking during pregnancy with impaired fetal growth in length and weight. These results should be considered as hypothesis generating and indicate the need for large-scale genome wide association studies focusing on gene – fetal smoke exposure interactions.
Maternal experience of childhood maltreatment and maternal antenatal depression are both associated with offspring childhood maltreatment and offspring adjustment problems. We have investigated the relative impact of maternal childhood maltreatment and exposure to depression in utero on offspring maltreatment and psychopathology.
The sample included 125 families from the South London Child Development Study. A prospective longitudinal design was used. Data on maternal childhood maltreatment, maternal antenatal depression (36 weeks of pregnancy), offspring childhood maltreatment (age 11 years) and offspring adolescent antisocial behaviour and depression (ages 11 and 16 years) were obtained from parents and offspring through clinical interview.
Mothers who experienced childhood maltreatment were significantly more likely to be depressed during pregnancy [odds ratio (OR) 10.00]. Offspring of mothers who experienced only childhood maltreatment or only antenatal depression were no more at risk of being maltreated or having psychopathology; however, offspring of mothers who experienced both maternal childhood maltreatment and antenatal depression were exposed to significantly greater levels of childhood maltreatment and exhibited significantly higher levels of adolescent antisocial behaviour compared with offspring not so exposed. Furthermore, maternal childhood maltreatment accounted for a significant proportion of the variance in offspring childhood maltreatment in only those offspring exposed to depression in utero.
Maternal childhood maltreatment and maternal antenatal depression are highly associated. The co-occurrence of both insults significantly increases the risk of offspring adversity. The antenatal period is an optimum period to identify vulnerable women and to provide interventions.
Adolescents; antisocial behaviour; maltreatment; pregnancy; prenatal stress
Although several studies have suggested an association between maternal smoking during pregnancy and both attention-deficit/hyperactivity disorder (ADHD) and conduct disorder (CD) in their offspring. However, it is unclear whether one or both of the documented links are spurious given the considerable comorbidity between these disorders. The main aim of this study was to disentangle the association between maternal smoking during pregnancy with psychopathological outcomes, adjusting for possible confounders.
Two large, identically designed, longitudinal, case-control family studies of male and female probands with and without ADHD were combined. We used data from the non-referred siblings of the probands from both studies (n=536). All subjects were blindly assessed with structured diagnostic interviews. Logistic regression analysis was used to determine the adjusted effect of exposure to maternal smoking during pregnancy.
Among all siblings, maternal smoking during pregnancy was significantly associated with ADHD, independent of CD and other covariates. In contrast, maternal smoking during pregnancy was a risk factor for CD only in siblings of Control probands, after adjusting for covariates.
These results support the hypothesis that maternal smoking during pregnancy is a risk factor for both ADHD and CD, independently of each other. However, the risk for CD appears to be conditional on family risk status.
To examine the relationship between prenatal secondhand smoke (SHS) exposure, preterm birth and immediate neonatal outcomes by measuring maternal hair nicotine.
Cross-sectional, observational design.
A metropolitan Kentucky birthing center.
Two hundred ten (210) mother-baby couplets
Nicotine in maternal hair was used as the biomarker for prenatal SHS exposure collected within 48 hours of birth. Smoking status was confirmed by urine cotinine analysis.
Smoking status (nonsmoking, passive smoking, and smoking) strongly correlated with low, medium, and high hair nicotine tertiles (rho = .74; p < .001). Women exposed to prenatal SHS were more at risk for preterm birth (OR = 2.3; 95% CI: .96–5.96), and their infants were more likely to have immediate newborn complications (OR = 2.4; 95% CI 1.09–5.33) than non-exposed women. Infants of passive smoking mothers were at increased risk for respiratory distress syndrome (RDS) (OR = 4.9; 95% CI 1.45–10.5) and admission to a neonatal intensive care unit (NICU) (OR= 6.5; CI: 1.29 to 9.7) when compared to infants of smoking mothers (OR 3.9; 95% CI: 1.61–14.9; OR 3.5; 95% CI: 2.09–20.4; respectively). Passive smokers and/or women with hair nicotine levels greater than .35 ng/ml were more likely to deliver earlier (1 week); give birth to infants weighing less (decrease of 200 to 300 grams); and deliver shorter infants (decrease of 1.1 to 1.7 cm).
Prenatal SHS exposure places women at greater risk for preterm birth and their newborns are more likely to have RDS, NICU admissions and immediate newborn complications.
Preterm birth; Secondhand smoke exposure; Hair nicotine biomarkers; Smoking and pregnancy
Exposure to prenatal stress is associated with later adverse health and adjustment outcomes. This is generally presumed to arise through early environmentally mediated programming effects on the foetus. However, associations could arise through factors that influence mothers' characteristics and behaviour during pregnancy which are inherited by offspring.
A ‘prenatal cross-fostering’ design where pregnant mothers are related or unrelated to their child as a result of in vitro fertilization (IVF) was used to disentangle maternally inherited and environmental influences. If links between prenatal stress and offspring outcome are environmental, association should be observed in unrelated as well as related mother–child pairs. Offspring birth weight and gestational age as well as mental health were the outcomes assessed.
Associations between prenatal stress and offspring birth weight, gestational age and antisocial behaviour were seen in both related and unrelated mother–offspring pairs, consistent with there being environmental links. The association between prenatal stress and offspring anxiety in related and unrelated groups appeared to be due to current maternal anxiety/depression rather than prenatal stress. In contrast, the link between prenatal stress and offspring attention deficit hyperactivity disorder was only present in related mother–offspring pairs and therefore was attributable to inherited factors.
Genetically informative designs can be helpful in testing whether inherited factors contribute to the association between environmental risk factors and health outcomes. These results suggest that associations between prenatal stress and offspring outcomes could arise from inherited factors and post-natal environmental factors in addition to causal prenatal risk effects.
ADHD; anxiety; birth weight; child; conduct
We prospectively examined the relationship between prenatal tobacco exposure (PTE) and child behavior in a birth cohort of 357 offspring of teenage mothers. PTE was defined as any exposure across pregnancy and, in separate analyses, exposure within each trimester. Outcomes included measures of behavior problems, activity, and attention. On average, the children were 6.4 years of age, 48% were females, and 69% were Black. Data on maternal tobacco and other substance use were collected prenatally and postnatally: 46% of the mothers smoked in the first trimester and 58% smoked 6 years later. Child urinary cotinine measured exposure to environmental tobacco smoke (ETS). Stepwise multiple regressions were run. PTE predicted significantly increased offspring activity; impulsivity; and aggression, externalizing, and total behavior problems in step 1. PTE remained a significant predictor of increased activity when maternal psychological characteristics, home environment, and ETS were added. The results were similar when PTE was examined by trimesters, although later pregnancy tobacco exposure predicted the most behavioral outcomes. In the final model, PTE (all three trimesters) and PTE (second trimester) were significant predictors of increased activity and attention problems, respectively. Other predictors of child behavior included maternal anxiety, depression, hostility, and home environment. ETS was not a significant predictor of child behavior when PTE was considered. Smoking during pregnancy among adolescents is a significant predictor of increased activity and attention problems in their offspring after controlling for covariates in the prenatal and current environments. Smoking cessation interventions are recommended for this population to avoid the effects of PTE on the offspring of pregnant adolescents. This is particularly important because these mothers will likely become pregnant again and many will increase their level of tobacco use as they mature.
OBJECTIVE--To determine whether maternal smoking during pregnancy causes impairment in growth after birth. DESIGN--Longitudinal study. SETTING--Six medical university centres of six towns of north, central, and south Italy. SUBJECTS--12,987 babies (10,238 born from non-smoking mothers, 2276 from mothers smoking one to nine cigarettes a day, and 473 from mothers smoking > or = 10 cigarettes a day) entered the study. MAIN OUTCOME MEASURES--Difference in weight gain between children born to smoking mothers and those born to non-smoking mothers. Weight was measured at birth and at 3 and 6 months of age. Maternal smoking habit was derived from interview on third or fourth day after delivery. RESULTS--Compared with children born to mothers who did not smoke during pregnancy, the birth weights of children born to mothers who smoked up to nine cigarettes a day were 88 g (girls) and 107 g (boys) lower; in children born to mothers who smoked > or = 10 cigarettes a day weights were 168 g and 247 g lower. At six months of age for the first group the mean weight for girls was 9 g (95% confidence interval -47 g to 65 g) higher and for boys 64 g (-118 g to -10 g) lower than that of children born to mothers who did not smoke. The corresponding figures for the second group were 28 g (-141 g to 85 g) lower for girls and 24 g (-136 g to 88 g) lower for boys. CONCLUSIONS--The deficits of weight at birth in children born to mothers who smoked during pregnancy are overcome by 6 months of age. These deficits are probably not permanent when smoking habit during pregnancy is not associated with other unfavourable variables (such as lower socioeconomic class).
Maternal smoking during pregnancy is associated with low birth weight and adverse pregnancy outcomes. Women are more likely to quit smoking during pregnancy than at any other time in their lives, but some pregnant women continue to smoke. A recent genome-wide association study demonstrated an association between a common polymorphism (rs1051730) in the nicotinic acetylcholine receptor gene cluster (CHRNA5–CHRNA3–CHRNB4) and both smoking quantity and nicotine dependence. We aimed to test whether the same polymorphism that predisposes to greater cigarette consumption would also reduce the likelihood of smoking cessation in pregnancy. We studied 7845 pregnant women of European descent from the South-West of England. Using 2474 women who smoked regularly immediately pre-pregnancy, we analysed the association between the rs1051730 risk allele and both smoking cessation during pregnancy and smoking quantity. Each additional copy of the risk allele was associated with a 1.27-fold higher odds (95% CI 1.11–1.45) of continued smoking during pregnancy (P = 0.0006). Adjustment for pre-pregnancy smoking quantity weakened, but did not remove this association [odds ratio (OR) 1.20 (95% CI 1.03–1.39); P = 0.018]. The same risk allele was also associated with heavier smoking before pregnancy and in the first, but not the last, trimester [OR for smoking 10+ cigarettes/day versus 1–9/day in first trimester = 1.30 (95% CI 1.13–1.50); P = 0.0003]. To conclude, we have found strong evidence of association between the rs1051730 variant and an increased likelihood of continued smoking in pregnancy and have confirmed the previously observed association with smoking quantity. Our data support the role of genetic factors in influencing smoking cessation during pregnancy.
To examine the association between maternal smoking during pregnancy and the development of smoking behaviour patterns among young adult offspring.
Data were from the Mater‐University of Queensland Study of Pregnancy (MUSP), a birth cohort of 7223 mothers and children enrolled in Brisbane, Australia, in 1981. The development of smoking behaviours (early or late onset, or combination of onset and prevalence patterns) among offspring at age 21 years with different patterns of maternal smoking (never smoked, smoked before or after pregnancy but not during pregnancy, or smoked during pregnancy) were compared. Maternal smoking information was derived from the prospectively collected data from the beginning of pregnancy until the child was 14 years of age. Analyses were restricted to the 3058 mothers and children whose smoking status was reported.
The proportion of young adults who smoked regularly, either with early onset or late onset, was greater among those whose mothers had smoked during pregnancy compared with those whose mothers had never smoked. The smoking patterns among those adolescent offspring whose mothers stopped smoking during pregnancy, but who then smoked at other times during the child's life, were similar to those whose mothers had never smoked. This association was robust to adjustment for a variety of potential covariates.
The findings provide some evidence for a direct effect of maternal smoking in utero on the development of smoking behaviour patterns of offspring and provide yet another incentive to persuade pregnant women not to smoke.
Individuals who quit smoking frequently experience symptoms of anxiety and/or depression. It is not clear whether these symptoms index liability to negative affect generally or whether such symptoms are a function of nicotine withdrawal and are thus indexed by nicotine dependence (ND).
A population-based sample of twins (N = 4,777 individuals) reported their lifetime history of psychopathology, ND, and symptoms of anxiety and depression experienced after attempts to quit smoking. Co-twin phenotype was used to predict withdrawal-induced symptoms of negative affect and to test whether genetic factors influence liability to these symptoms.
Co-twin's ND was significantly associated with nicotine withdrawal-induced symptoms of anxiety and depression. Furthermore, monozygotic co-twins more strongly predicted outcome than did dizygotic co-twins, indicating that genetic factors contribute to risk. Co-twins’ history of psychopathology did not predict outcome, suggesting that liability to withdrawal-induced negative affect is independent of a liability to negative affect outside the context of nicotine withdrawal.
These findings indicate that symptoms of anxiety or depression experienced in the context of nicotine withdrawal are best conceptualized as a component of the withdrawal syndrome, with the severity of symptoms indexed by level of ND. Genetic influences underlying ND contribute to the liability to these symptoms. Though psychopathology might be indirectly related to withdrawal-induced symptoms through its correlation with ND, it is not directly predictive of withdrawal symptoms.
There is strong evidence for an association between maternal smoking in pregnancy and psychological problems in offspring. The problems most frequently associated are attention problems, hyperactivity, and conduct problems, although there is some evidence for an association with substance use problems as well. The nature of this association is unclear, but it is likely the result of a number of different mechanisms. Animal studies provide evidence for a causal relationship, in which exposure to nicotine has detrimental effects on foetal development. Other studies suggest that factors that correlate with maternal prenatal smoking may be the real risk factors for behavioural problems, although evidence that the associations remain after controlling for such risks goes some way to dispel this as the only explanation. Finally, maternal prenatal smoking may index underlying psychological problems in the mother that are inherited by the offspring. In all likelihood, a combination of these mechanisms may contribute to observed relationships between prenatal smoking and offspring psychological problems. Now that the association is well established, future research needs to focus more strongly on disentangling underlying mechanisms. Although animal studies demonstrate a casual relationship, it appears from other research that this may not be the whole story in human samples. Furthermore, the relationship may only exist under certain conditions (i.e. against a certain genetic background), and this possibility warrants further examination, particularly in relation to other genetic risks, and outcomes other than ADHD. Application of the children-of-twins design may also cast further light on the processes involved.
Prenatal Smoking; ADHD; antisocial behaviour; substance use; genes
There have been a few studies that examined the oxidative stress effects of nicotine during pregnancy and lactation. The adverse effect of prenatal smoking exposure on human fetal development and growth has been a major public health issue. Active or passive smoking during pregnancy can result in a wide variety of adverse outcomes, including intrauterine growth retardation (IUGR), prematurity, stillbirth, and the sudden infant death syndrome. Smoking in pregnancy has also been associated with an increased risk of attention deficit and learning problems in childhood. Some studies argued that as a principal component of tobacco smoke, nicotine alone is responsible for the majority of negative reproductive outcomes. Nicotine and its major metabolite cotinine can cross the placental barrier. The level of nicotine in fetal tissues was found to be equal to or greater than the plasma nicotine level in the mothers. The oxidative stress induce by nicotine has been increasingly postulated as a major contributor to endothelial dysfunction. A large body of research has investigated the potential role of antioxidant nutrients in the prevention of endothelial dysfunction in women. Therefore, the present study was undertaken to assess the potential benefit of antioxidant supplementation on markers of placental oxidative stress in an in vitro model of endothelial dysfunction induced by nicotine, since it was previously found that nicotine is able to trigger the placental secretion of stress molecules. In this regard, we evaluated the effects of vitamin C, vitamin E and N-acetylcysteine (NAC), alone or in combination, in placental villi culture after exposure to nicotine. The effect of antioxidant nutrients on trophoblast cells proliferation and vitality was also evaluated. The results obtained suggest that in a patho-physiological condition, such as endothelial dysfunction induced by nicotine, the deleterious effect of reactive oxygen species may be counteracted by an antioxidant therapy, and there is the need to investigate the optimum dosing and timing of antioxidants administration, since an inappropriate antioxidant treatment in pregnant women may have deleterious consequences, reducing placental cells proliferation until to cell death.
Nicotine; oxidative stress; vitamins.
There is a significant association between maternal cigarette smoking during pregnancy and greater subsequent risk of smoking in female offspring. In animal models, prenatal nicotine exposure causes persistent alterations in cholinergic and monoaminergic systems, both of which are important for nicotine actions underlying tobacco addiction. Accordingly, the current study was conducted to determine if there is a cause-and-effect relationship between prenatal nicotine exposure and nicotine self-administration starting in adolescence. Pregnant rats were administered nicotine (6 mg/kg/day) by osmotic minipump infusion throughout gestation and then, beginning in adolescence and continuing into adulthood, female offspring were given access to nicotine via a standard operant IV self-administration procedure (0.03 mg/kg/infusion). Gestational nicotine exposure did not alter the initial rate of nicotine self-administration. However, when animals underwent one week of forced abstinence and then had a second opportunity to self-administer nicotine, the prenatally-exposed animals showed a significantly greater rate of self-administration than did the controls. Prenatal nicotine exposure causes increased nicotine self-administration, which is revealed only when the animals are allowed to experience a period of nicotine abstinence. This supports a cause-and-effect relationship between the higher rates of smoking in the daughters of women who smoke cigarettes during pregnancy and implicates a role for nicotine in this effect. Our results further characterize the long-term liabilities of maternal smoking but also point to the potential liabilities of nicotine-based treatments for smoking cessation during pregnancy.
Nicotine; Self-administration; Prenatal; Adolescent; Prenatal Nicotine Exposure