Postnatal Smoke Research Articles

Effects of Prenatal Nicotine Exposure on Infant Language Development: A Cohort Follow Up Study.

Objectives To study the longitudinal effects of prenatal nicotine exposure on cognitive development, taking into consideration prenatal and postnatal second-hand smoke exposure. Methods A cohort follow up study was carried out. One hundred and fifty-eight pregnant women and their infants were followed during pregnancy and infant development (at 6, 12, 30months). In each trimester of pregnancy and during postnatal follow-up, a survey was administered to obtain sociodemographic data and the details of maternal and close familial toxic habits. Obstetric and neonatal data were obtained from hospital medical records. To assess cognitive development, the Bayley Scales of Infant Development were applied at 6, 12 and 30months; to assess language development, the MacArthur-Bates Communicative Development Inventories were applied at 12months and the Peabody Picture Vocabulary Test at 30months. Results After adjustment for confounding variables, the results showed that infants prenatally exposed to cigarette smoke recorded poor cognitive development scores. Language development was most consistently affected, specifically those aspects related to auditory function (vocalizations, sound discrimination, word imitation, prelinguistic vocalizations, and word and sentence comprehension). Conclusions for Practice Irrespective of prenatal, perinatal and sociodemographic data (including infant postnatal nicotine exposure), prenatal exposure to cigarette smoke and second-hand smoke affect infant cognitive development, especially language abilities.

Cigarette smoke causes acute airway disease and exacerbates chronic obstructive lung disease in neonatal mice.

Epidemiological evidence demonstrates a strong link between postnatal cigarette smoke (CS) exposure and increased respiratory morbidity in young children. However, how CS induces early onset airway disease in young children, and how it interacts with endogenous risk factors, remains poorly understood. We, therefore, exposed 10-day-old neonatal wild-type and β-epithelial sodium ion channel (β-ENaC)-transgenic mice with cystic fibrosis-like lung disease to CS for 4 days. Neonatal wild-type mice exposed to CS demonstrated increased numbers of macrophages and neutrophils in the bronchoalveolar lavage fluid (BALF), which was accompanied by increased levels of Mmp12 and Cxcl1 BALF from β-ENaC-transgenic mice contained greater numbers of macrophages, which did not increase following acute CS exposure; however, there was significant increase in airway neutrophilia compared with filtered air transgenic and CS-exposed wild-type controls. Interestingly, wild-type and β-ENaC-transgenic mice demonstrated epithelial airway and vascular remodeling following CS exposure. Morphometric analysis of lung sections revealed that CS exposure caused increased mucus accumulation in the airway lumen of neonatal β-ENaC-transgenic mice compared with wild-type controls, which was accompanied by an increase in the number of goblet cells and Muc5ac upregulation. We conclude that short-term CS exposure 1) induces acute airway disease with airway epithelial and vascular remodeling in neonatal wild-type mice; and 2) exacerbates airway inflammation, mucus hypersecretion, and mucus plugging in neonatal β-ENaC-transgenic mice with chronic lung disease. Our results in neonatal mice suggest that young children may be highly susceptible to develop airway disease in response to tobacco smoke exposure, and that adverse effects may be aggravated in children with underlying chronic lung diseases.

Effects of Breastfeeding on Respiratory Symptoms in Infancy

To assess the impact of potential risk factors on the development of respiratory symptoms and their specific modification by breastfeeding in infants in the first year of life. We prospectively studied 436 healthy term infants from the Bern-Basel Infant Lung Development cohort. The breastfeeding status, and incidence and severity of respiratory symptoms (score) were assessed weekly by telephone interview during the first year of life. Risk factors (eg, pre- and postnatal smoking exposure, mode of delivery, gestational age, maternal atopy, and number of older siblings) were obtained using standardized questionnaires. Weekly measurements of particulate matter <10μg were provided by local monitoring stations. The associations were investigated using generalized additive mixed model with quasi Poisson distribution. Breastfeeding reduced the incidence and severity of the respiratory symptom score mainly in the first 27weeks of life (risk ratio 0.70; 95% CI 0.55-0.88). We found a protective effect of breastfeeding in girls but not in boys. During the first 27weeks of life, breastfeeding attenuated the effects of maternal smoking during pregnancy, gestational age, and cesarean delivery on respiratory symptoms. There was no evidence for an interaction between breastfeeding and maternal atopy, number of older siblings, child care attendance, or particulate matter <10μg. This study shows the risk-specific effect of breastfeeding on respiratory symptoms in early life using the comprehensive time-series approach.

The independent role of prenatal and postnatal exposure to active and passive smoking on the development of early wheeze in children.

Maternal smoking during pregnancy increases childhood asthma risk, but health effects in children of nonsmoking mothers passively exposed to tobacco smoke during pregnancy are unclear. We examined the association of maternal passive smoking during pregnancy and wheeze in children aged ≤2 years.Individual data of 27 993 mother-child pairs from 15 European birth cohorts were combined in pooled analyses taking into consideration potential confounders.Children with maternal exposure to passive smoking during pregnancy and no other smoking exposure were more likely to develop wheeze up to the age of 2 years (OR 1.11, 95% CI 1.03-1.20) compared with unexposed children. Risk of wheeze was further increased by children's postnatal passive smoke exposure in addition to their mothers' passive exposure during pregnancy (OR 1.29, 95% CI 1.19-1.40) and highest in children with both sources of passive exposure and mothers who smoked actively during pregnancy (OR 1.73, 95% CI 1.59-1.88). Risk of wheeze associated with tobacco smoke exposure was higher in children with an allergic versus nonallergic family history.Maternal passive smoking exposure during pregnancy is an independent risk factor for wheeze in children up to the age of 2 years. Pregnant females should avoid active and passive exposure to tobacco smoke for the benefit of their children's health.

Effects of paediatric HIV infection on electrical conduction of the heart

ObjectiveTo investigate the effects of HIV infection in children on heart electrical conduction, particularly to delineate the effects of HIV infection from treatment.MethodsOn a 12-lead ECG, available for 37 antiretroviral...

Associations between otitis media and child behavioural and learning difficulties: Results from a Danish cohort

ObjectivesFindings from studies investigating early childhood episodes of otitis media (OM) and developmental outcomes are inconclusive. This may in part be because large-scale prospective studies controlling for relevant confounding factors are sparse. The present study investigates associations between OM in early childhood and later behavioural and learning difficulties controlling for relevant confounding factors. MethodsThe study applied data from the Aarhus Birth Cohort's 10–12-year-old follow-up (N=7578). Associations between retrospective parent-reported OM (no OM; 1–3 episodes of OM with/without tympanostomy tubes; 4+ OM episodes without tympanostomy tubes and; 4+ OM episodes with tympanostomy tubes) one the one hand, and parent- and teacher-reported scores on the Strengths and Difficulties Questionnaire (SDQ) and parent-reported academic difficulties on the other hand, were investigated. The following variables were controlled for: parental educational level, maternal and paternal school problems, parental post-natal smoking, breastfeeding, and age at which the child started walking. All analyses were stratified by gender. ResultsLarge differences in background characteristics were observed for the group of children with 4+ OM episodes with tympanostomy tubes compared to the no OM group. After controlling for relevant confounders, negative associations were consistently observed for the group of children with 4+ episodes of OM with tympanostomy tubes compared to the group of children without OM. This was particularly so for girls. ConclusionThe findings suggest an association between 4+ episodes of early OM with tympanostomy tubes and behavioural and learning difficulties later in childhood. The large inter-group differences, i.e. impact of residual and unmeasured confounding factors, may in part explain the observed associations and underline the need to include these in future studies.

Prenatal and Postnatal Maternal Trajectories of Cigarette Use Predict Adolescent Cigarette Use.

The goal of this study was to identify maternal patterns of prenatal and postnatal cigarette smoking associated with adolescent smoking. We hypothesized that maternal use at multiple time points, especially at later assessments when the offspring were adolescents, would predict offspring use. Pregnant women (N = 456: ages 13-42) were recruited from a prenatal clinic and interviewed during pregnancy and at delivery, providing data on cigarette use (any/none) for the first and third trimesters. Mothers were re-assessed at 6, 10, 14, and 16 years postpartum. Offspring reported cigarette use at age 16. Covariates included maternal race, age, education, family income, child age, parenting behavior, and other maternal and child substance use. A growth mixture model revealed five patterns of tobacco use: infrequent/nonuse (39%), postpartum quitters (5%), later quitters (7%), increasing likelihood of being smokers (17%), and chronic users (32%). Offspring of postpartum quitters and the increasing likelihood of being smokers groups were more likely to use cigarettes, compared to adolescents of mothers from the infrequent/nonuse group, controlling for significant covariates. This is the first study to examine trajectories of maternal cigarette use from pregnancy to 16 years postpartum, linking prenatal and postnatal patterns of maternal use to use in adolescent offspring. Our findings highlight the risk associated with prenatal exposure, because mothers who used during pregnancy but quit by 6 years postpartum still had offspring who were 3.5 times more likely to smoke than non/infrequent users. This is the first study to examine trajectories of maternal cigarette use from the prenatal period to 16 years postpartum, and to link prenatal and postnatal patterns of use to use in adolescent offspring. We identified two long-term patterns of maternal cigarette use that were associated with offspring smoking at age 16, including one where offspring were exposed prenatally, but much less likely to be exposed to maternal cigarette use postpartum. Our findings highlight the risk associated with prenatal exposures for cigarette use in offspring, even if mothers quit in the postpartum.

In Utero Cigarette Smoke Affects Allergic Airway Disease But Does Not Alter the Lung Methylome.

Prenatal and postnatal cigarette smoke exposure enhances the risk of developing asthma. Despite this as well as other smoking related risks, 11% of women still smoke during pregnancy. We hypothesized that cigarette smoke exposure during prenatal development generates long lasting differential methylation altering transcriptional activity that correlates with disease. In a house dust mite (HDM) model of allergic airway disease, we measured airway hyperresponsiveness (AHR) and airway inflammation between mice exposed prenatally to cigarette smoke (CS) or filtered air (FA). DNA methylation and gene expression were then measured in lung tissue. We demonstrate that HDM-treated CS mice develop a more severe allergic airway disease compared to HDM-treated FA mice including increased AHR and airway inflammation. While DNA methylation changes between the two HDM-treated groups failed to reach genome-wide significance, 99 DMRs had an uncorrected p-value < 0.001. 6 of these 99 DMRs were selected for validation, based on the immune function of adjacent genes, and only 2 of the 6 DMRs confirmed the bisulfite sequencing data. Additionally, genes near these 6 DMRs (Lif, Il27ra, Tle4, Ptk7, Nfatc2, and Runx3) are differentially expressed between HDM-treated CS mice and HDM-treated FA mice. Our findings confirm that prenatal exposure to cigarette smoke is sufficient to modify allergic airway disease; however, it is unlikely that specific methylation changes account for the exposure-response relationship. These findings highlight the important role in utero cigarette smoke exposure plays in the development of allergic airway disease.

Prenatal Versus Postnatal Tobacco Smoke Exposure and Intensive Care Use in Children Hospitalized With Bronchiolitis

ObjectiveAmong children hospitalized with bronchiolitis, we examined the associations between in utero exposure to maternal cigarette smoking, postnatal tobacco smoke exposure, and risk of admission to the intensive care unit (ICU). MethodsWe performed a 16-center, prospective cohort study of hospitalized children aged <2 years with a physician admitting diagnosis of bronchiolitis. For 3 consecutive years, from November 1, 2007 until March 31, 2010, site teams collected data from participating families, including information about prenatal maternal smoking and postnatal tobacco exposure. Analyses used chi-square, Fisher's exact, and Kruskal-Wallis tests and multivariable logistic regression. ResultsAmong 2207 enrolled children, 216 (10%) had isolated in utero exposure to maternal smoking, 168 (8%) had isolated postnatal tobacco exposure, and 115 (5%) experienced both. Adjusting for age, sex, race, birth weight, viral etiology, apnea, initial severity of retractions, initial oxygen saturation, oral intake, and postnatal tobacco exposure, children with in utero exposure to maternal smoking had greater odds of being admitted to the ICU (adjusted odds ratio [aOR] 1.51, 95% confidence interval [CI] 1.14–2.00). Among children with in utero exposure to maternal smoking, those with additional postnatal tobacco exposure had a greater likelihood of ICU admission (aOR 1.95, 95% CI 1.13–3.37) compared to children without postnatal tobacco smoke exposure (aOR 1.47, 95% CI 1.05–2.04). ConclusionsMaternal cigarette smoking during pregnancy puts children hospitalized with bronchiolitis at significantly higher risk of intensive care use. Postnatal tobacco smoke exposure may exacerbate this risk. Health care providers should incorporate this information into counseling messages.

Association of prenatal exposure to maternal smoking and postnatal exposure to household smoking with dental caries in 3-year-old Japanese children

BackgroundEpidemiological studies of the association between smoking exposure and dental caries are limited. ObjectiveThe purpose of this cross-sectional study was to examine the association between prenatal and postnatal secondhand smoke (SHS) exposure and the prevalence of dental caries in primary dentition in young Japanese children. MethodsStudy subjects were 6412 children aged 3 years. Information on exposure to maternal smoking during pregnancy and postnatal SHS exposure at home was collected via parent questionnaire. Children were classified as having dental caries if one or more primary teeth had decayed or had been filled. ResultsCompared with never smoking during pregnancy, maternal smoking in the first trimester of pregnancy was significantly associated with an increased prevalence of dental caries in children (adjusted odds ratio=1.37, 95% confidence interval: 1.03–1.80). Postnatal SHS exposure was also positively associated with dental caries, with a significant positive exposure–response relationship. Compared with children not exposed to prenatal maternal smoking or postnatal SHS at home, those exposed to both prenatal and postnatal smoking had higher odds of dental caries (adjusted odds ratio=1.62, 95% confidence interval: 1.23–2.11). ConclusionOur findings suggest that maternal smoking during pregnancy and postnatal SHS exposure may be associated with an increased prevalence of dental caries in primary dentition.

Postpartum depression, a direct and mediating risk factor for preschool wheeze in girls.

Postpartum depression affects over 1 in 10 child-bearing women. A growing body of evidence links maternal distress during the key developmental stages of infants with poor health outcomes, including wheeze and asthma. We sought to investigate whether postpartum depression had an independent association with the development of wheeze in preschool-aged children. A second a priori objective was to ascertain whether postpartum depression functioned as a mediating factor for associations between wheeze, and prenatal distress and nutrition. Data from the Community Perinatal Care Trial on maternal postpartum depression (Edinburgh Postnatal Depression Scale), the dependent variable, wheeze at age 3, and possible confounding factors were obtained for 791 women and their children in Calgary, Canada. Adjusted gender-specific logistic regression analyses were performed to test the association between postpartum depression and child wheeze, which was independent of maternal distress and vitamin use during pregnancy, pre/postnatal smoking, preterm birth, exclusive breastfeeding duration, daycare attendance, and maternal education. The potential mediating effects of postpartum depression were investigated in a path analysis. Wheeze at age 3 was almost 5 times more likely in girls of mothers who experienced postpartum depression. Results from a path analysis suggested that postpartum depression has a direct effect on wheeze (beta-coefficient=0.135, P < 0.05), and also mediates the effects of prenatal distress and vitamin use on wheeze in preschool girls. In boys, only prenatal smoking was a statistically significant predictor of wheeze, mainly through the effects of postnatal smoking. Postpartum depression may be a risk factor for preschool wheeze among girls in a low risk population, directly and indirectly through prenatal distress and vitamin use. Interventions which target postpartum depression and promote a healthy pregnancy may also reduce the risk of wheeze in children.

Postnatal Environmental Tobacco Smoke Exposure Related to Behavioral Problems in Children.

ObjectiveThe purpose of this study was to examine the association between pre and post environmental tobacco smoke (ETS) exposure and behavioral problems in schoolchildren.MethodsIn the cross-sectional 6 cities Study conducted in France, 5221 primary school children were investigated. Pre- and postnatal exposure to secondhand tobacco smoke at home was assessed using a parent questionnaire. Child’s behavioral outcomes (emotional symptoms and conduct problems) were evaluated by the Strengths and Difficulties Questionnaire (SDQ) completed by the parents.ResultsETS exposure during the postnatal period and during both pre- and postnatal periods was associated with behavioral problems in children. Abnormal emotional symptoms (internalizing problems) were related to ETS exposure in children who were exposed during the pre- and postnatal periods with an OR of 1.72 (95% Confidence Interval (CI)= 1.36-2.17), whereas the OR was estimated to be 1.38 (95% CI= 1.12-1.69) in the case of postnatal exposure only. Abnormal conduct problems (externalizing problems) were related to ETS exposure in children who were exposed during the pre- and postnatal periods with an OR of 1.94 (95% CI= 1.51-2.50), whereas the OR was estimated to be 1.47 (95% CI=1.17-1.84) in the case of postnatal exposure only. Effect estimates were adjusted for gender, study center, ethnic origin, child age, low parental education, current physician diagnosed asthma, siblings, preterm birth and single parenthood.ConclusionPostnatal ETS exposure, alone or in association with prenatal exposure, increases the risk of behavioral problems in school-age children.

A couple-focused intervention to prevent postnatal smoking relapse: PRISM study design

BackgroundMaternal smoking is one of the most modifiable factors with clear adverse effects for the fetus and the entire family. Addressing the dearth of pregnancy smoking interventions with partner support, PRISM (Prevent Relapse In SMoking) is a partnership between a research institution and the two largest state-owned obstetrics and gynecology clinics in Cluj-Napoca, Romania. The study will assess the efficacy of a couple-focused telephone-counseling program to prevent smoking relapse among mothers who quit smoking closely before or during pregnancy. Methods/designThe intervention is a program for couples based on motivational interviewing delivered over the phone after birth. The study is an ongoing randomized controlled trial of 250 Romanian women recruited soon after childbirth, who quit smoking in the six months before pregnancy or no later than the end of the first pregnancy trimester and remained abstinent (which was biochemically verified) until delivery. Participants were randomized to: (1) a control arm (usual care); and (2) an intervention arm consisting of up to 4 postnatal counseling calls for mothers and their partners using motivational interviewing to encourage the woman to remain smoke-free and the partner to support her decision. The primary outcome is maternal smoking abstinence at 6months postpartum (biochemically verified). DiscussionPRISM has the potential to identify strategies to reduce maternal postnatal relapse and increase partner quitting. If successful, the program may be an effective method to prevent and reduce smoking, which may lead to improved child, mother, and partner health both in the short and the long term.

Does fetal smoke exposure affect childhood bone mass? The Generation R Study

We assessed the intrauterine influence of maternal smoking on childhood bone mass by comparing parental prenatal and postnatal smoking habits. We observed higher bone mass in children exposed to maternal smoking, explained by higher body weight. Maternal smoking or related lifestyle factors may affect childhood weight gain rather than skeletal growth. Maternal smoking during pregnancy may adversely affect bone health in later life. By comparing the associations of maternal and paternal smoking and of prenatal and postnatal exposure with childhood bone measures, we aimed to explore whether the suggested association could be explained by fetal programming or reflects confounding by familial factors. In 5565 mothers, fathers and children participating in a population-based prospective cohort study, parental smoking habits during pregnancy and current household smoking habits were assessed by postal questionnaires. Total body bone mineral content (BMC), bone area (BA) and bone mineral density (BMD) were measured by dual-energy X-ray absorptiometry (DXA) at the median age of 6.0 years (IQR 0.37). In confounder-adjusted models, maternal smoking during pregnancy was associated with a higher BMC of 11.6 g (95 % confidence interval (CI) 5.6, 17.5), a larger BA of 9.7 cm(2) (95 % CI 3.0, 16.4), a higher BMD of 6.7 g/cm(2) (95 % CI 2.4, 11.0) and a higher BMC of 5.4 g (95 % CI 1.3, 9.6) adjusted for BA of the child. Current weight turned out to mediate these associations. Among mothers who did not smoke, paternal smoking did not show evident associations with childhood bone measures. Also, household smoking practices during childhood were not associated with childhood bone measures. Our results do not support the hypothesis of fetal smoke exposure affecting childhood bone mass via intrauterine mechanisms. Maternal smoking or related lifestyle factors may affect childhood weight gain rather than skeletal growth.

Prenatal exposure to maternal smoking and offspring DNA methylation across the lifecourse: findings from the Avon Longitudinal Study of Parents and Children (ALSPAC).

Maternal smoking during pregnancy has been found to influence newborn DNA methylation in genes involved in fundamental developmental processes. It is pertinent to understand the degree to which the offspring methylome is sensitive to the intensity and duration of prenatal smoking. An investigation of the persistence of offspring methylation associated with maternal smoking and the relative roles of the intrauterine and postnatal environment is also warranted. In the Avon Longitudinal Study of Parents and Children, we investigated associations between prenatal exposure to maternal smoking and offspring DNA methylation at multiple time points in approximately 800 mother–offspring pairs. In cord blood, methylation at 15 CpG sites in seven gene regions (AHRR, MYO1G, GFI1, CYP1A1, CNTNAP2, KLF13 and ATP9A) was associated with maternal smoking, and a dose-dependent response was observed in relation to smoking duration and intensity. Longitudinal analysis of blood DNA methylation in serial samples at birth, age 7 and 17 years demonstrated that some CpG sites showed reversibility of methylation (GFI1, KLF13 and ATP9A), whereas others showed persistently perturbed patterns (AHRR, MYO1G, CYP1A1 and CNTNAP2). Of those showing persistence, we explored the effect of postnatal smoke exposure and found that the major contribution to altered methylation was attributed to a critical window of in utero exposure. A comparison of paternal and maternal smoking and offspring methylation showed consistently stronger maternal associations, providing further evidence for causal intrauterine mechanisms. These findings emphasize the sensitivity of the methylome to maternal smoking during early development and the long-term impact of such exposure.

Smoke exposure as a risk factor for asthma in childhood: a review of current evidence.

Asthma is a common chronic multifactorial disease that affects >300 million people worldwide. Outdoor and indoor pollution exposure has been associated with respiratory health effects in adults and children. Smoking still represents a huge public health problem and millions of children suffer the detrimental effects of passive smoke exposure. This study was designed to review the current evidences on exposure to passive smoke as a risk factor for asthma onset in childhood. A review of the most recent studies on this topic was undertaken to provide evidence about the magnitude of the effect of passive smoking on the risk of incidence of asthma in children. The effects of passive smoking are different depending on individual and environmental factors. Environmental tobacco smoke (ETS) is one of the most important indoor air pollutants and can interact with other air pollutants in eliciting respiratory outcomes during childhood. The increased risk of respiratory outcomes in children exposed to prenatal and early postnatal passive smoke might be caused by an adverse effect on both the immune system and the structural and functional development of the lung; this may explain the subsequent increased risk of incident asthma. The magnitude of the exposure is quite difficult to precisely quantify because it is significantly influenced by the child's daily activities. Because exposure to ETS is a likely cause for asthma onset in childhood, there is a strong need to prevent infants and children from breathing air contaminated with tobacco smoke.

Pre- and postnatal exposure to parental smoking and allergic disease through adolescence.

To examine the role of prenatal and postnatal second-hand tobacco smoke (SHS) exposure on asthma, rhinitis, and eczema development up to 16 years of age. A birth cohort of 4089 children was followed for 16 years. Information on parental smoking habits, lifestyle factors, and symptoms of allergic disease was gathered using repeated parental questionnaires. Generalized estimating equations assessed the overall and age-specific associations between SHS exposure and allergic disease at ages 1 to 16 years. Exposure to SHS in utero was associated with an overall elevated risk of developing asthma up to 16 years (odds ratio [OR] = 1.45; 95% confidence interval [CI], 1.15-1.83) but not for rhinitis or eczema. After additional adjustment for parental smoking throughout childhood, excess overall risks for asthma remained statistically significant. Moreover, a dose-dependent pattern with SHS was observed. Exposure to SHS during infancy was associated with an overall elevated risk of asthma (OR = 1.23; 95% CI, 1.01-1.51), rhinitis (OR = 1.18; 95% CI, 1.01-1.39), and eczema (OR = 1.26; 95% CI, 1.09-1.45) up to 16 years. When age-specific associations were examined, the elevated risks related to SHS exposure in utero or during infancy were mostly confined to early childhood for asthma and rhinitis, whereas the excess risk of eczema appeared greatest at later ages. Our findings indicate that early SHS exposure, in utero or during infancy, influences the development of allergic disease up to adolescence. Excess risks for asthma and rhinitis were seen primarily in early childhood, whereas those for eczema occurred at later ages.

Effect of Prenatal Exposure to Tobacco Smoke on Inhibitory Control

There is accumulating evidence relating maternal smoking during pregnancy to attention-deficit/hyperactivity disorder (ADHD) without elucidating specific mechanisms. Research investigating the neurobiological underpinnings of this disorder has implicated deficits during response inhibition. Attempts to uncover the effect of prenatal exposure to nicotine on inhibitory control may thus be of high clinical importance. To clarify the influence of maternal smoking during pregnancy (hereafter referred to as prenatal smoking) on the neural circuitry of response inhibition and its association with related behavioral phenotypes such as ADHD and novelty seeking in the mother's offspring. Functional magnetic resonance imaging was performed for the offspring at 25 years of age during a modified Eriksen flanker/NoGo task, and voxel-based morphometry was performed to study brain volume differences of the offspring. Prenatal smoking (1-5 cigarettes per day [14 mothers] or >5 cigarettes per day [24 mothers]) and lifetime ADHD symptoms were determined using standardized parent interviews at the offspring's age of 3 months and over a period of 13 years (from 2 to 15 years of age), respectively. Novelty seeking was assessed at 19 years of age. Analyses were adjusted for sex, parental postnatal smoking, psychosocial and obstetric adversity, maternal prenatal stress, and lifetime substance abuse. A total of 178 young adults (73 males) without current psychopathology from a community sample followed since birth (Mannheim, Germany) participated in the study. Functional magnetic resonance imaging response, morphometric data, lifetime ADHD symptoms, and novelty seeking. Participants prenatally exposed to nicotine exhibited a weaker response in the anterior cingulate cortex (t168 = 4.46; peak Montreal Neurological Institute [MNI] coordinates x = -2, y = 20, z = 30; familywise error [FWE]-corrected P = .003), the right inferior frontal gyrus (t168 = 3.65; peak MNI coordinates x = 44, y = 38, z = 12; FWE-corrected P = .04), the left inferior frontal gyrus (t168 = 4.09; peak MNI coordinates x = -38, y = 36, z = 8; FWE-corrected P = .009), and the supramarginal gyrus (t168 = 5.03; peak MNI coordinates x = 64, y = -28, z = 22; FWE-corrected P = .02) during the processing of the NoGo compared to neutral stimuli, while presenting a decreased volume in the right inferior frontal gyrus. These findings were obtained irrespective of the adjustment of confounders, ADHD symptoms, and novelty seeking. There was an inverse relationship between inferior frontal gyrus activity and ADHD symptoms and between anterior cingulate cortex activity and novelty seeking. These findings point to a functional involvement of prenatal exposure to tobacco smoke in neural alterations similar to ADHD, which underlines the importance of smoking prevention treatments.

Physical, Behavioral, and Cognitive Effects of Prenatal Tobacco and Postnatal Secondhand Smoke Exposure

The purpose of this review is to examine the rapidly expanding literature regarding the effects of prenatal tobacco and postnatal secondhand smoke (SHS) exposure on child health and development. Mechanisms of SHS exposure are reviewed, including critical periods during which exposure to tobacco products appears to be particularly harmful to the developing fetus and child. The biological, biochemical, and neurologic effects of the small fraction of identified components of SHS are described. Research describing these adverse effects of both in utero and childhood exposure is reviewed, including findings from both animal models and humans. The following adverse physical outcomes are discussed: sudden infant death syndrome, low birth weight, decreased head circumference, respiratory infections, otitis media, asthma, childhood cancer, hearing loss, dental caries, and the metabolic syndrome. In addition, the association between the following adverse cognitive and behavioral outcomes and such exposures is described: conduct disorder, attention-deficit/hyperactivity disorder, poor academic achievement, and cognitive impairment. The evidence supporting the adverse effects of SHS exposure is extensive yet rapidly expanding due to improving technology and increased awareness of this profound public health problem. The growing use of alternative tobacco products, such as hookahs (a.k.a. waterpipes), and the scant literature on possible effects from prenatal and secondhand smoke exposure from these products are also discussed. A review of the current knowledge of this important subject has implications for future research as well as public policy and clinical practice.

Environmental tobacco smoke exposure and children's intelligence at 8-11 years of age.

Background: Evidence supporting a link between postnatal environmental tobacco smoke (ETS) exposure and cognitive problems among children is mounting, but inconsistent.Objectives: We examined the relationship between ETS exposure, measured using urine cotinine, and IQ scores in Korean school-aged children.Methods: The participants were 996 children 8–11 years of age recruited from five administrative regions in South Korea. We performed a cross-sectional analysis of urinary cotinine concentrations and IQ scores obtained using the abbreviated form of a Korean version of the Wechsler Intelligence Scales for Children. Associations were adjusted for potential confounders, and estimates were derived with and without adjustment for mother’s Full-Scale IQ (FSIQ) score.Results: After adjusting for sociodemographic and developmental covariates, urinary cotinine concentrations were inversely associated with FSIQ, Verbal IQ (VIQ), Performance IQ (PIQ), vocabulary, math, and block design scores. Following further adjustment for maternal IQ, only the VIQ scores remained significantly associated with urinary cotinine concentration (B = –0.31; 95% CI: –0.60, –0.03 for a 1-unit increase in natural log-transformed urine cotinine concentration; p = 0.03).Conclusion: Urine cotinine concentrations were inversely associated with children’s VIQ scores before and after adjusting for maternal IQ. Further prospective studies with serial measurements of cotinine are needed to confirm our findings.Citation: Park S, Cho SC, Hong YC, Kim JW, Shin MS, Yoo HJ, Han DH, Cheong JH, Kim BN. 2014. Environmental tobacco smoke exposure and children’s intelligence at 8–11 years of age. Environ Health Perspect 122:1123–1128; http://dx.doi.org/10.1289/ehp.1307088