The association between maternal smoking during pregnancy and childhood antisocial outcomes has been demonstrated repeatedly across a variety of outcomes. Yet debate continues as to whether this association reflects a direct programming effect of nicotine on fetal brain development, or a phenotypic indicator of heritable liability passed from mother to child. In the current study, we examine relations between maternal smoking and child behavior among 133 women and their 7–15-year-olds, who were recruited for clinical levels of psychopathology. In order to disentangle correlates of maternal smoking, women who smoked during pregnancy were compared with (a) those who did not smoke, and (b) those who did not smoke but experienced significant second-hand exposure. Second-hand exposure was associated with increased externalizing psychopathology in participant mothers’ offspring. Moreover, regression analyses indicated that smoke exposure during pregnancy predicted conduct disorder symptoms, over and above the effects of income, parental antisocial tendencies, prematurity, birth weight, and poor parenting practices. This is the first study to extend the findings of externalizing vulnerability to second hand smoke exposure.
Maternal smoking; Conduct disorder; Aggression; Second hand smoke; ADHD
environmental tobacco smoke (ETS) during childhood and in utero
exposure to maternal smoking are associated with adverse effects on
lung growth and development.
METHODS—A study was
undertaken of the associations between maternal smoking during
pregnancy, exposure to ETS, and pulmonary function in 3357 school
children residing in 12 Southern California communities. Current and
past exposure to household ETS and exposure to maternal smoking in
utero were assessed by a self-administered questionnaire completed by
parents of 4th, 7th, and 10th grade students in 1993.Standard linear
regression techniques were used to estimate the effects of in utero and
ETS exposure on lung function, adjusting for age, sex, race, Hispanic
ethnicity, height, weight, asthma, personal smoking, and selected
exposure to maternal smoking was associated with reduced peak
expiratory flow rate (PEFR) (-3.0%, 95% CI -4.4 to -1.4), mean mid
expiratory flow (MMEF) (-4.6%, 95% CI -7.0 to -2.3), and forced
expiratory flow (FEF75) (-6.2%, 95% CI -9.1 to -3.1),
but not forced expiratory volume in one second (FEV1). Adjusting for household ETS exposure did not substantially change these
estimates. The reductions in flows associated with in utero exposure
did not significantly vary with sex, race, grade, income, parental
education, or personal smoking. Exposure to two or more current
household smokers was associated with reduced MMEF (-4.1%, 95% CI
-7.6 to -0.4) and FEF75 (-4.4%, 95% CI -9.0 to 0.4).
Current or past maternal smoking was associated with reductions in PEFR and MMEF; however, after adjustment for in utero exposure, deficits in
MMEF and FEF75 associated with all measurements of ETS were substantially reduced and were not statistically significant.
exposure to maternal smoking is independently associated with decreased
lung function in children of school age, especially for small airway flows.
The glutathione S-transferase M1 (GSTM1) null variant is a common copy number variant associated with adverse pulmonary outcomes, including asthma and airflow obstruction, with evidence of important gene-by-environment interactions with exposures to oxidative stress.
To explore the joint interactive effects of GSTM1 copy number and tobacco smoke exposure on the development of asthma and asthma-related phenotypes in a family-based cohort of childhood asthmatics.
We performed quantitative PCR-based genotyping for GSTM1 copy number in children of self-reported white ancestry with mild to moderate asthma in the Childhood Asthma Management Program. Questionnaire data regarding intrauterine (IUS) and postnatal, longitudinal environmental tobacco smoke exposure were available. We performed both family-based and population-based tests of association for the interaction between GSTM1 copy number and tobacco smoke exposure with asthma and asthma-related phenotypes.
Associations of GSTM1 null variants with asthma (p= .03), younger age of asthma symptom onset (p=.03), and greater airflow obstruction (reduced FEV1/FVC, p=.01) were observed among the 50 children (10% of the cohort) with exposure to IUS. In contrast, no associations were observed between GSTM1 null variants and asthma-related phenotypes among children without IUS exposure. Presence of at least one copy of GSTM1 conferred protection.
These findings support an important gene-by-environment interaction between two common factors: increased risk of asthma and asthma-related phenotypes conferred by GSTM1-null homozygosity in children is restricted to those with a history of IUS exposure.
Asthma; GSTM1; copy number variation (CNV); gene by environment; intrauterine smoke exposure; tobacco smoke
Prenatal factors such as prenatal psychological stress might influence the development of childhood asthma.
Methodology and Principal Findings
We assessed the association between maternal bereavement shortly before and during pregnancy, as a proxy for prenatal stress, and the risk of childhood asthma in the offspring, based on two samples of children 1–4 (n = 426 334) and 7–12 (n = 493 813) years assembled from the Swedish Medical Birth Register. Exposure was maternal bereavement of a close relative from one year before pregnancy to child birth. Asthma event was defined by a hospital contact for asthma or at least two dispenses of inhaled corticosteroids or montelukast. In the younger sample we calculated hazards ratios (HRs) of a first-ever asthma event using Cox models and in the older sample odds ratio (ORs) of an asthma attack during 12 months using logistic regression. Compared to unexposed boys, exposed boys seemed to have a weakly higher risk of first-ever asthma event at 1–4 years (HR: 1.09; 95% confidence interval [CI]: 0.98, 1.22) as well as an asthma attack during 12 months at 7–12 years (OR: 1.10; 95% CI: 0.96, 1.24). No association was suggested for girls. Boys exposed during the second trimester had a significantly higher risk of asthma event at 1–4 years (HR: 1.55; 95% CI: 1.19, 2.02) and asthma attack at 7–12 years if the bereavement was an older child (OR: 1.58; 95% CI: 1.11, 2.25). The associations tended to be stronger if the bereavement was due to a traumatic death compared to natural death, but the difference was not statistically significant.
Our results showed some evidence for a positive association between prenatal stress and childhood asthma among boys but not girls.
The effects of in utero tobacco smoke exposure on childhood respiratory health have been investigated, and outcomes have been inconsistent.
To determine if in utero tobacco smoke exposure is associated with childhood persistent asthma in Mexican, Puerto Rican, and black children.
PATIENTS AND METHODS:
There were 295 Mexican, Puerto Rican, and black asthmatic children, aged 8 to 16 years, who underwent spirometry, and clinical data were collected from the parents during a standardized interview. The effect of in utero tobacco smoke exposure on the development of persistent asthma and related clinical outcomes was evaluated by logistic regression.
Children with persistent asthma had a higher odds of exposure to in utero tobacco smoke, but not current tobacco smoke, than did children with intermittent asthma (odds ratio [OR]: 3.57; P = .029). Tobacco smoke exposure from parents in the first 2 years of life did not alter this association. Furthermore, there were higher odds of in utero tobacco smoke exposure in children experiencing nocturnal symptoms (OR: 2.77; P = .048), daily asthma symptoms (OR: 2.73; P = .046), and emergency department visits (OR: 3.85; P = .015) within the year.
Exposure to tobacco smoke in utero was significantly associated with persistent asthma among Mexican, Puerto Rican, and black children compared with those with intermittent asthma. These results suggest that smoking cessation during pregnancy may lead to a decrease in the incidence of persistent asthma in these populations.
asthma; tobacco; Latino; African American; pregnancy
To examine the association of social and environmental factors with levels of second hand smoke (SHS) exposure, as measured by salivary cotinine, in young inner city children with asthma.
We used data drawn from a home-based behavioral intervention for young high risk children with persistent asthma post emergency department (ED) treatment (N=198). SHS exposure was measured by salivary cotinine and caregiver report. Caregiver demographic and psychological functioning, household smoking behavior and asthma morbidity were compared with child cotinine concentrations. Chi-square and ANOVA tests and multivariate regression models were used to determine the association between cotinine concentrations with household smoking behavior and asthma morbidity.
Over half (53%) of the children had cotinine levels compatible with SHS exposure and mean cotinine concentrations were high at 2.42 ng/ml (SD 3.2). The caregiver was the predominant smoker in the home (57%) and (63%) reported a total home smoking ban. Preschool age children, and those with caregivers reporting depressive symptoms and high stress had higher cotinine concentrations than their counterparts. Among children living in a home with a total home smoking ban, younger children had significantly higher mean cotinine concentration than older children (Cotinine: 3–5 year olds, 2.24 ng/ml (SD 3.5); 6–10 year olds, 0.63 ng/ml (SD 1.0); p <0.05). In multivariate models, the factors most strongly associated with high child cotinine concentrations were increased number of household smokers (β = 0.24) and younger child age (3–5 years) (β = 0.23; P <0.001, R2 = 0.35).
Over half of young inner-city children with asthma were exposed to second hand smoke and caregivers are the predominant household smoker. Younger children and children with depressed and stressed caregivers are at significant risk of smoke exposures, even when a household smoking ban is reported. Further advocacy for these high-risk children is needed to help caregivers quit and to mitigate smoke exposure.
asthma; children; cotinine; second hand smoke
Among people with asthma, the clinical impact and relative contribution of maternal smoking during pregnancy (in utero smoking) and current secondhand smoke exposure on asthma control is poorly documented, and there is a paucity of research involving minority populations.
To examine the association between poor asthma control and in utero smoking and current secondhand smoke exposure among Latino and Black children with asthma.
Case-only analysis of 2 multi-center case-control studies conducted from 2008–2010 using similar protocols. We recruited 2,481 Latinos and Blacks with asthma (ages 8–17) from the mainland United States and Puerto Rico. Ordinal logistic regression was used to estimate the effect of in utero smoking and current secondhand smoke exposures on National Heart Lung and Blood Institute-defined asthma control.
Poor asthma control among children 8–17 years of age was independently associated with in utero smoking (odds ratio; 95% confidence interval = 1.5; 1.1–2.0). In utero smoking via the mother was also associated with secondary asthma outcomes, including early onset asthma (1.7; 1.1–2.4), daytime symptoms (1.6; 1.1–2.1), and asthma-related limitation of activities (1.6; 1.2–2.2).
Maternal smoking while in utero is associated with poor asthma control in Black and Latino subjects assessed at 8–17 years of age.
Secondhand smoke; prenatal exposure delayed effects; asthma; health status disparities
Both environmental tobacco smoke and indoor allergens can exacerbate already established childhood albeit primarily through quite disparate mechanisms. In infancy and childhood, environmental tobacco smoke (ETS) exposure is associated with measures of decreased flow in the airways, bronchial hyperresponsiveness, and increased respiratory infections, but the relationship between ETS and allergy is poorly understood. Indoor allergens from dust mite, cockroach, and cat can be associated with asthma exacerbation in children sensitized to the specific allergens. The precise role of either ETS or indoor allergens in the development of asthma is less well understood. The strong and consistent association between ETS and asthma development in young children may relate to both prenatal and postnatal influences on airway caliber or bronchial responsiveness. Dust mite allergen levels predict asthma in children sensitized to dust mite. The tendency to develop specific IgE antibodies to allergens (sensitization) is associated with and may be preceded by the development of a T-helper (Th)2 profile of cytokine release. The importance of either ETS or indoor allergens in the differentiation of T cells into a Th2-type profile of cytokine release or in the localization of immediate-type allergic responses to the lung is unknown. This article evaluates the strength of the evidence that ETS or indoor allergens influence asthma exacerbation and asthma development in children. We also selectively review data for the effectiveness of allergen reduction in reducing asthma symptoms and present a potential research agenda regarding these two broad areas of environmental exposure and their relationship to childhood asthma.
Environmental tobacco smoke (ETS) exposure is associated with poor asthma outcomes in children. However, little is known about natural changes in ETS exposure over time in children with asthma and how these changes may affect health-care utilization. This article documents the relationship between changes in ETS exposure and childhood asthma morbidity among children enrolled in a clinical trial of supervised asthma therapy.
Data for this analysis come from a large randomized clinical trial of supervised asthma therapy in which 290 children with persistent asthma were randomized to receive either usual care or supervised asthma therapy. No smoking cessation counseling or ETS exposure education was provided to caregivers; however, children were given 20 min of asthma education, which incorporated discussion of the avoidance of asthma triggers, including ETS. Asthma morbidity and ETS exposure data were collected from caregivers via telephone interviews at baseline and at the 1-year follow-up.
At baseline, 28% of caregivers reported ETS exposure in the home and 19% reported exposure outside of the primary household only. Among children whose ETS exposure decreased from baseline, fewer hospitalizations (p = 0.034) and emergency department (ED) visits (p ≤ 0.001) were reported in the 12 months prior to the second interview compared to the 12 months prior to the first interview. Additionally, these children were 48% less likely (p = 0.042) to experience an episode of poor asthma control (EPAC).
This is the first study to demonstrate an association between ETS exposure reduction and fewer EPACs, respiratory-related ED visits, and hospitalizations. These findings emphasize the importance of ETS exposure reduction as a mechanism to improve asthma control and morbidity. Potential policy implications include supporting ETS reductions and smoking cessation interventions for parents and caregivers of children with asthma. Research to identify the most cost-effective strategy is warranted.
Clinicaltrials.gov Identifier: NCT00110383
asthma; children; environmental tobacco smoke; tobacco smoke pollution
To determine the association between type, chronicity, and severity of childhood hardships and smoking status during pregnancy, preterm birth, and low birth weight.
Prospective cohort study
The National Child Development Study, a nationally representative study of births in Britain in 1958
4865 women with at least one singleton live birth
Hardship during childhood, indicated by several variables, including financial/structural hardship, lack of parental interest in education, family dysfunction, violence/mental health issues, and family structure.
Main outcome measures
Smoking in pregnancy, low birthweight (LBW), preterm birth (PTB).
A consistent and graded association was seen between all types of childhood hardships and smoking status during pregnancy (odd ratio (OR) and 95% confidence interval (CI) for 4 or more hardships 2.02, 1.58–2.58; p<0.001 for all comparisons). Most hardships were also associated with risk of LBW and PTB, with associations between number of hardships and both outcomes persisting after controlling for smoking status and adult social class (for LBW, OR 1.51, 95% CI 1.10–2.06; for PTB, OR 1.44, 95% CI 1.08–1.92).
Childhood hardships have an enduring impact on future pregnancy outcomes, in part through their association with smoking during pregnancy and adult socioeconomic position.
Second-hand smoke (SHS) exposure is estimated to kill 600 000 people worldwide annually. The WHO recommends that smoke-free indoor public environments are enforced through national legislation. Such regulations have been shown to reduce SHS exposure and, consequently, respiratory and cardiovascular morbidity. Evidence of particular health benefit in children is now emerging, including reductions in low birthweight deliveries, preterm birth and asthma exacerbations. We aim to comprehensively assess the impact of smoke-free legislation on fetal, infant and childhood outcomes. This can inform further development and implementation of global policy and strategies to reduce early life SHS exposure.
Two authors will search online databases (1975–present; no language restrictions) of published and unpublished/in-progress studies, and references and citations to articles of interest. We will consult experts in the field to identify additional studies. Studies should describe associations between comprehensive or partial smoking bans in public places and health outcomes among children (0–12 years): stillbirth, preterm birth, low birth weight, small for gestational age, perinatal mortality, congenital anomalies, bronchopulmonary dysplasia, upper and lower respiratory infections and wheezing disorders including asthma. The Cochrane Effectiveness Practice and Organisational Care (EPOC)-defined study designs are eligible. Study quality will be assessed using the Cochrane 7-domain-based evaluation for randomised and clinical trials, and EPOC criteria for quasiexperimental studies. Data will be extracted by two reviewers and presented in tabular and narrative form. Meta-analysis will be undertaken using random-effects models, and generic inverse variance analysis for adjusted effect estimates. We will report sensitivity analyses according to study quality and design characteristics, and subgroup analyses according to coverage of ban, age group and parental/maternal smoking status. Publication bias will be assessed.
Ethics and dissemination
Ethics assessment is not required.
Will be presented in one manuscript. The protocol is registered with PROSPERO, registration number CRD42013003522.
The goal of the study was to examine the association between biomarkers and environmental measures of second hand smoke (SHS) with caregiver, i.e. parent or legal guardian, report of household smoking behavior and morbidity measures among children with asthma. Baseline data were drawn from a longitudinal intervention for 126 inner city children with asthma, residing with a smoker. Most children met criteria for moderate to severe persistent asthma (63%) versus mild intermittent (20%) or mild persistent (17%). Household smoking behavior and asthma morbidity were compared with child urine cotinine and indoor measures of air quality including fine particulate matter (PM2.5) and air nicotine (AN). Kruskal–Wallis, Wilcoxon rank-sum and Spearman rho correlation tests were used to determine the level of association between biomarkers of SHS exposure and household smoking behavior and asthma morbidity. Most children had uncontrolled asthma (62%). The primary household smoker was the child's caregiver (86/126, 68%) of which 66 (77%) were the child's mother. Significantly higher mean PM2.5, AN and cotinine concentrations were detected in households where the caregiver was the smoker (caregiver smoker: PM2.5 μg/m3: 44.16, AN: 1.79 μg/m3, cotinine: 27.39 ng/ml; caregiver non-smoker: PM2.5: 28.88 μg/m3, AN: 0.71 μg/m3, cotinine:10.78 ng/ml, all P ≤ 0.01). Urine cotinine concentrations trended higher in children who reported 5 or more symptom days within the past 2 weeks (>5 days/past 2 weeks, cotinine: 28.1 ng/ml vs. <5 days/past 2 weeks, cotinine: 16.2 ng/ml; P = 0.08). However, environmental measures of SHS exposures were not associated with asthma symptoms. Urban children with persistent asthma, residing with a smoker are exposed to high levels of SHS predominantly from their primary caregiver. Because cotinine was more strongly associated with asthma symptoms than environmental measures of SHS exposure and is independent of the site of exposure, it remains the gold standard for SHS exposure assessment in children with asthma.
Asthma; Children; Cotinine; Particulate matter; Air Nicotine
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
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.
This study was designed to test the hypothesis that fetal exposure to corticosteroids in the antenatal period is an independent risk factor for the development of asthma in early childhood with little or no effect in later childhood. A population-based cohort study of all pregnant women who resided in Nova Scotia, Canada, and gave birth to a singleton fetus between 1989 and 1998
was undertaken. After a priori specified exclusions, 80,448 infants were available for analysis.
Using linked health care utilization records, incident asthma cases developed after 36 months of
age were identified. Extended Cox proportional hazards models were used to estimate hazard
ratios while controlling for confounders. Exposure to corticosteroids during pregnancy was
associated with a risk of asthma in childhood between 3–5 years of age: adjusted hazard ratio of
1.19 (95% confidence interval: 1.03, 1.39), with no association noted after 5 years of age:
adjusted hazard ratio for 5–7 years was 1.06 (95% confidence interval: 0.86, 1.30)
and for 8 or greater years was 0.74 (95% confidence interval: 0.54, 1.03). Antenatal steroid therapy appears to be an independent risk factor for the development of asthma between 3 and 5 years of age.
Cardiovascular disease is a major cause of morbidity and mortality in the United States. While many studies have focused upon the effects of adult second-hand smoke exposure on cardiovascular disease development, disease development occurs over decades and is likely influenced by childhood exposure. The impacts of in utero versus neonatal second-hand smoke exposure on adult atherosclerotic disease development are not known. The objective of the current study was to determine the effects of in utero versus neonatal exposure to a low dose (1 mg/m3 total suspended particulate) of second-hand smoke on adult atherosclerotic lesion development using the apolipoprotein E null mouse model. Consequently, apolipoprotein E null mice were exposed to either filtered air or second-hand smoke: (i) in utero from gestation days 1–19, or (ii) from birth until 3 weeks of age (neonatal). Subsequently, all animals were exposed to filtered air and sacrificed at 12–14 weeks of age. Oil red-O staining of whole aortas, measures of mitochondrial damage, and oxidative stress were performed. Results show that both in utero and neonatal second-hand smoke exposure significantly increased adult atherogenesis in mice compared to filtered air controls. These changes were associated with changes in aconitase and mitochondrial superoxide dismutase activities consistent with increased oxidative stress in the aorta, changes in mitochondrial DNA copy number and deletion levels. These studies show that in utero or neonatal exposure to second-hand smoke significantly influences adult atherosclerotic lesion development and results in significant alterations to the mitochondrion and its genome that may contribute to atherogenesis.
Studies on the associations between smoking and allergic diseases have mostly focused on asthma. Epidemiological studies in adults on the effects of smoking on allergic diseases other than asthma, such as eczema and rhinoconjunctivitis, have been limited, and the information that is available has been inconsistent. The aim of this study was to investigate the association between smoking status and environmental tobacco smoke (ETS) exposure and the prevalence of allergic diseases.
Study subjects were 1743 pregnant Japanese women. The definitions of wheeze and asthma were based on criteria from the European Community Respiratory Health Survey whereas those of eczema and rhinoconjunctivitis were based on criteria from the International Study of Asthma and Allergies in Childhood. Adjustment was made for age; region of residence; family history of asthma, atopic eczema, and allergic rhinitis; household income; and education.
Compared with never smoking, current smoking and ≥ 4 pack-years of smoking were independently positively associated with the prevalence of wheeze. There were no associations between smoking status and the prevalence of asthma, eczema, or rhinoconjunctivitis. When subjects who had never smoked were classified into four categories based on the source of ETS exposure (never, only at home, only at work, and both), exposure occurring both at home and at work was independently associated with an increased prevalence of two outcomes: wheeze and rhinoconjunctivitis. No relationships were observed between exposure to ETS and the prevalence of asthma or eczema.
Our results provide evidence that current smoking and ETS exposure may increase the likelihood of wheeze. The possibility of a positive association between ETS exposure and rhinoconjunctivitis was also suggested.
Asthma; Cross-sectional studies; Eczema; Environmental tobacco smoke; Smoking; Wheeze; Rhinoconjunctivitis
Background: An emerging literature suggests that environmental chemicals may play a role in the development of childhood obesity and metabolic disorders, especially when exposure occurs early in life.
Objective: Here we assess the association between these health outcomes and exposure to maternal smoking during pregnancy as part of a broader effort to develop a research agenda to better understand the role of environmental chemicals as potential risk factors for obesity and metabolic disorders.
Methods: PubMed was searched up to 8 March 2012 for epidemiological and experimental animal studies related to maternal smoking or nicotine exposure during pregnancy and childhood obesity or metabolic disorders at any age. A total of 101 studies—83 in humans and 18 in animals—were identified as the primary literature.
Discussion: Current epidemiological data support a positive association between maternal smoking and increased risk of obesity or overweight in offspring. The data strongly suggest a causal relation, although the possibility that the association is attributable to unmeasured residual confounding cannot be completely ruled out. This conclusion is supported by findings from laboratory animals exposed to nicotine during development. The existing literature on human exposures does not support an association between maternal smoking during pregnancy and type 1 diabetes in offspring. Too few human studies have assessed outcomes related to type 2 diabetes or metabolic syndrome to reach conclusions based on patterns of findings. There may be a number of mechanistic pathways important for the development of aberrant metabolic outcomes following perinatal exposure to cigarette smoke, which remain largely unexplored.
Conclusions: From a toxicological perspective, the linkages between maternal smoking during pregnancy and childhood overweight/obesity provide proof-of-concept of how early-life exposure to an environmental toxicant can be a risk factor for childhood obesity.
animal; chemically induced/epidemiology; diabetes; environmental epidemiology; glucose; insulin; maternal smoking toxicity; metabolism; nicotine toxicity; obesity
One of the mechanisms supposed to explain the increasing prevalence of asthma, among children in particular, is the use of antibiotics because they may modify natural microbial exposure and development of the immune system in early childhood. The aim of this study is to investigate the association between the use of various classes of antibiotics (penicillin, cephalosporin and macrolide derivatives) in early childhood and the medical diagnosis of asthma or wheezing reported by mothers over the follow-up after adjustment for potential confounders and respiratory infections. In a population-based sample of 5-year-olds, a part of the ongoing birth cohort study, the standardized interviews on health outcomes, potential confounders (child’s gender, maternal atopy, parity, prenatal and postnatal environmental tobacco smoke) and the use of antibiotics were gathered from mothers of 310 children. While the overall use of antibiotics during the early childhood was insignificantly associated with asthma (adjusted OR = 1.65, 95%CI: 0.93 – 2.93), the risk estimates were significant both for macrolide antibiotics (adjusted OR=2.14, 95%CI: 1.16–3.95) and cephalosporins (OR=1.98, 95%CI: 1.14–3.37). The significant excess in IRR (incident risk ratio) of wheezing episodes was related only to the use of macrolide antibiotics (adjusted IRR=1.91, 95%CI: 1.12–3.27). The use of other classes of antibiotics was found not to be associated with the medical diagnosis of asthma or wheezing episodes recorded in the study period. Conclusion: as early childhood use of broad spectrum antibiotics is associated with an increased risk of developing asthma in 5-year-olds, it may be hypothesized that the antibiotic- related suppression of allergic inflammatory responses in the course of treatment may later lead to greater than before atopic immune response in Th2 children or an impairment of Th1 immune responses in early childhood.
antibiotics; asthma; childhood; wheezing; Th1 immune responses; allergic reactions
Asthma constitutes a serious public health problem in many regions of the world, including the city of Salvador, State of Bahia – Brazil. The purpose of this study was to analyse the factors associated with poor asthma control.
Two definitions were used for asthma: 1) wheezing in the last 12 months; 2) wheezing in the last 12 months plus other asthma symptoms or asthma diagnosis ever. The definition of poorly controlled asthma was: at least one reported hospitalisation due to asthma and/or high frequency of symptoms, in the last year. Children with poorly controlled asthma (N = 187/374) were compared with wheezing children with controlled asthma regarding age, gender, atopy, parental asthma, rhinitis, eczema, exposure to second hand tobacco smoke, presence of moulds, pets and pests in the house, helminth infections and body mass index. Crude and logistic regression adjusted odds ratios were used as measures of association. There was a higher proportion of poorly controlled asthma among children with eczema (OR = 1.55; 95% CI 1.02; 2.37). The strength of the association was greater among children with eczema and rhinitis (42.6%, 53.4% and 57.7%, respectively, in children who had no rhinitis nor eczema, had only one of those, and had both (p = 0.02 for trend test). The presence of mould in the houses was inversely associated with poorly controlled asthma (OR = 0.54; 95% CI 0.34; 0.87).
Our results indicate an association between eczema and poor asthma control in this environment, but emphasize the role of various other individual and environmental factors as determinants of poor control.
Tobacco smoke has both carcinogenic effects and anti-estrogenic properties and its inconsistent association with breast cancer risk in observational studies may be because of these competing effects across the lifecourse. We conducted a prospective study of prenatal smoke exposure, childhood household smoke exposure, and adult active smoke exposure and mammographic density, a strong intermediate marker of breast cancer risk, in an adult follow-up of existing US birth cohorts. Specifically, we followed up women who were born between 1959 and 1967 and whose mothers participated in either the Collaborative Perinatal Project (Boston and Providence sites) or the Childhood Health and Development Study in California. Of the 1134 women interviewed in adulthood (ranging in age from 39 to 49 years at interview), 79% had a screening mammogram. Cigarette smoking was reported by mothers at the time of their pregnancy; 40% of mothers smoked while pregnant. Women whose mothers smoked during pregnancy had a 3.1% (95% confidence interval (CI) = −6.0%, −0.2%) lower mammographic density than women whose mothers did not smoke during pregnancy. When we further accounted for adult body mass index and adult smoking status, the association remained (β = −2.7, 95% CI = −5.0, −0.3).When we examined patterns of smoking, prenatal smoke exposure without adult smoke exposure was associated with a 5.6% decrease in mammographic density (β = −5.6, 95% CI = −9.6, −1.6). Given the strength of mammographic density as an intermediate marker for breast cancer, the inverse associations between mammographic density and smoking patterns across the lifecourse may help explain the complex association between cigarette smoking and breast cancer risk.
breast cancer; mammographic density; prenatal smoke exposure
The link between chest illnesses in childhood to age 7 and the prevalence of cough and phlegm in the winter reported at age 23 was investigated in a cohort of 10 557 British children born in one week in 1958 (national child development study). Both pneumonia and asthma or wheezy bronchitis to age 7 were associated with a significant excess in the prevalence of chronic cough and phlegm at age 23 after controlling for current smoking. This excess was largely attributable to the association of cough and phlegm at age 23 with a history of asthma or wheezy bronchitis from age 16. When adjustment was made for recent wheezing, current cigarette consumption, previous smoking habit, and passive exposure to smoke the relative odds of cough or phlegm, or both, in subjects with a history of childhood chest illness was 1·11 (95% confidence interval 0·97 to 1·27). When analysed separately asthma, wheezy bronchitis, and pneumonia up to age 7 did not significantly increase the prevalence of either cough or phlegm.
The explanation for the observed continuity between chest illness in childhood and respiratory symptoms in later life may lie more in the time course of functional disturbances related to asthma than in the persistence of structural lung damage.
Studies have shown diverse strength of evidence for the associations between air pollutants and childhood asthma, but these associations have scarcely been documented in the early life. The purpose of this study was to evaluate the impacts of various air pollutants on the development of asthma phenotypes in the first year of life.
Adjusted odds ratios were estimated to assess the relationships between exposures to air pollutants and single and multi-dimensional asthma phenotypes in the first year of life in children of the EDEN mother-child cohort study (n = 1,765 mother-child pairs). The Generalized Estimating Equation (GEE) model was used to determine the associations between prenatal maternal smoking and in utero exposure to traffic-related air pollution and asthma phenotypes (data were collected when children were at birth, and at 4, 8 and 12 months of age). Adjusted Population Attributable Risk (aPAR) was estimated to measure the impacts of air pollutants on health outcomes.
In the first year of life, both single and multi-dimensional asthma phenotypes were positively related to heavy parental smoking, traffic-related air pollution and dampness, but negatively associated with contact with cats and domestic wood heating. Adjusted odds ratios (aORs) for traffic-related air pollution were the highest [1.71 (95% Confidence Interval (CI): 1.08-2.72) for ever doctor-diagnosed asthma, 1.44 (95% CI: 1.05-1.99) for bronchiolitis with wheezing, 2.01 (95% CI: 1.23-3.30) for doctor-diagnosed asthma with a history of bronchiolitis]. The aPARs based on these aORs were 13.52%, 9.39%, and 17.78%, respectively. Results persisted for prenatal maternal smoking and in utero exposure to traffic-related air pollution, although statistically significant associations were observed only with the asthma phenotype of ever bronchiolitis.
After adjusting for potential confounders, traffic-related air pollution in utero life and in the first year of life, had a greater impact on the development of asthma phenotypes compared to other factors.
Environment; Traffic-related air pollution; Environmental Tobacco Smoke (ETS); Pets; Moulds; Asthma; Children
The prevalence of asthma in adolescents markedly varies between different localities as found by the International Study of Asthma and Allergies in Childhood (ISAAC) and this may be due to environmental factors. Although tobacco smoke exposure is related to an increase in the prevalence of asthma, there is lack of information on that respect in children from developing countries, where active tobacco smoking usually starts early in adolescence. This study was undertaken to assess the effect of tobacco smoking on the prevalence of asthma symptoms in a random sample of 4738 adolescents aged 13.4 ± 1.05 years who responded the ISAAC video questionnaires plus questions on tobacco smoking. The prevalence of tobacco smoking in the last 12 months was 16.2%, with significant female predominance. The persistent smokers had a significantly higher prevalence of asthma-like symptoms ever and in the last 12 months (wheezing, wheezing with exercise, nocturnal wheezing, severe wheezing, and dry nocturnal cough) than ex-smokers and nonsmokers. More than 27% of asthma symptoms in our adolescents are attributable to active tobacco consumption (population attributable risk). This study strongly suggests that potent and more effective campaigns against tobacco smoking should be implemented in developing countries, where active tobacco smoking is dramatically increasing in children.
asthma; prevalence; ISAAC; tobacco; video questionnaires
This paper explores the possible association between antibiotics prescribed in infancy and allergic disorders, mainly eczema and asthma, in childhood.
No-one fully understands why childhood asthma and eczema have become so common. Some authorities suggest that there may be an association between eczema and asthma and antibiotics prescribed in childhood; however, others disagree.
The available literature was reviewed to examine the links between prescribed antibiotics and childhood eczema and asthma.
Some, but not all, research indicates that antibiotic administration in pregnancy, childbirth or infancy may be linked to childhood asthma and eczema, but much uncertainty remains. None of the papers identified stated the doses of antibiotics prescribed. In addition, we were unable to locate studies reporting the interactions between antibiotics and the developing immune system.
Health care professionals should be selective when prescribing antibiotics. Further prospective work is needed to guide the prescribing of antibiotics in childbirth and infancy.
Allergic disorders; antibiotics; prescribing; adverse drug reactions; evidence based practice.