Postnatal Smoke Research Articles

Fetal Exposure to Maternal and Paternal Smoking and the Risks of Wheezing in Preschool Children

Previous studies have suggested that fetal smoke exposure is associated with increased risks of wheezing during childhood. The underlying pathways are unknown. We examined the associations of parental smoking during pregnancy with wheezing in preschool children and whether these associations are explained by postnatal smoke exposure or small for gestational age at birth. This study was embedded in a population-based prospective cohort study. Parental smoking was prospectively assessed by questionnaires. Wheezing was reported at 1 to 4 years. Small for gestational age at birth was available from registries. The analyses were based on 4,574 subjects. Maternal smoking during the first trimester only was not associated with wheezing. Continued maternal smoking in pregnancy was associated with the risk of wheezing at 1 to 4 years (P for trends < .05). The strongest effect estimates were observed for frequent wheezing (four or more episodes of wheezing per year) until age 3 years (OR [95% CI]: age 1,1.64 [1.12-2.40]; age 2, 1.64 [1.01-2.64]; age 3, 2.19 [1.24-3.86]). Among children of nonsmoking mothers, fetal exposure to paternal smoking was not consistently associated with the risks of wheezing. The associations of continued maternal smoking during pregnancy with wheezing symptoms were independent of postnatal smoke exposure or small for gestational age at birth. Fetal exposure to continued maternal smoking is associated with increased risks of wheezing in preschool children. Further research is needed to explore the effects of paternal smoking. Diminishing maternal smoking before conception or in early pregnancy is likely to have the greatest impact on reducing childhood wheezing.

Maternal smoking during pregnancy and offspring trajectories of height and adiposity: comparing maternal and paternal associations

Background Maternal smoking during pregnancy is associated with reduced offspring birth length and has been postulated as a risk factor for obesity. Causality for obesity is not established. Causality is well-supported for birth length, but evidence on persistence of height deficits is inconsistent.Methods We examined the association between maternal smoking during pregnancy and trajectories of offspring height (0–10 years, N = 9424), ponderal index (PI) (0–2 years, N = 9321) and body mass index (BMI) (2–10 years, N = 8887) in the Avon Longitudinal Study of Parents and Children. To strengthen inference, measured confounders were controlled for, maternal and partner smoking associations were compared, dose–response and associations with post-natal smoking were examined.Results Maternal smoking during pregnancy was associated with shorter birth length, faster height growth in infancy and slower growth in later childhood. By 10 years, daughters of women who smoke during pregnancy are on average 1.11 cm (SE = 0.27) shorter after adjustment for confounders and partner smoking; the difference is 0.22 cm (SE = 0.22) for partner's smoking. Maternal smoking was associated with lower PI at birth, faster PI increase in infancy, but not with BMI changes 2–10 years. Associations were stronger for maternal than partner smoking for PI at birth and PI changes in infancy, but not for BMI changes after 2 years. A similar dose–response in both maternal and partner smoking was seen for BMI change 2–10 years.Conclusion Maternal smoking during pregnancy has an intrauterine effect on birth length, and possibly on adiposity at birth and changes in height and adiposity in infancy. We do not find evidence of a specific intrauterine effect on height or adiposity changes after the age of 2 years.

Prenatal exposure to tobacco and future nicotine dependence: population-based cohort study

Maternal smoking during pregnancy may increase the risk of nicotine dependence, especially in girls, but data are conflicting and confounding by other familial factors cannot be ruled out. To clarify the relationship between prenatal tobacco exposure and adolescent tobacco uptake and dependence in boys and girls respectively, while taking confounding factors into close consideration. We conducted a prospective longitudinal study, comprising 3020 Swedish youths followed from 11 to 18 years of age. Exposure and outcome information was elicited via self-administered parental and repeated youth questionnaires. Hazard ratios (HRs), odds ratios (ORs) and corresponding 95% confidence intervals (CIs) were calculated as measures of associations. Girls prenatally exposed to maternal tobacco use had a two- to threefold increased odds of experiencing a high number of withdrawal symptoms (OR = 2.83, 95% CI 1.68-4.87), craving for tobacco (OR = 2.04, 95% CI 1.28-3.32) and heavy tobacco use (five or more cigarettes or snus dips per day) (OR = 1.93, 95% CI 1.30-2.86). These associations were weaker among boys, and did not reach formal statistical significance. Associations between prenatal tobacco exposure and onset of regular tobacco use in both genders appeared to be mostly explained by parents' social position and postnatal smoking behaviour. Prenatal exposure to tobacco is linked to an increased risk of nicotine dependence among adolescent girls.

Negative Control Exposures in Epidemiologic Studies

The authors respond: We thank George Davey Smith1 for his thoughtful comments on our paper2 and for drawing attention to his previous use of a negative control exposure. We agree with his interpretation that the lack of association of paternal smoking during pregnancy (negative control exposure B as shown in Fig. 3 in our original paper,2 and reproduced here in simplified form as the Figure) with birth weight strengthens the causal interpretation of an observed association of maternal smoking (A) with low birth weight (Y). Comparing Figure 1a and b of Davey Smith, paternal smoking has a univariate association with low birth weight, but this association disappears in a model including maternal smoking. This example emphasizes why the negative control exposure (B) should be evaluated in a model including the exposure of interest (A). The negative control is used to see whether there is evidence for a causal arrow from unobserved confounders (U) to the outcome (Y). Even if no U→Y arrow exists, B will be associated with Y under the alternative hypothesis (A→Y) through the path B←U→A→Y. Conditioning on (A) by including it in the model will close this path.Figure: Causal diagram showing an ideal negative control exposure B for use in evaluating studies of the causal relationship between exposure A and outcome Y, with measured confounders L and possible unmeasured confounders U. This figure is simplified from Figure 3 of Reference 2.This example also nicely illustrates the subject-matter knowledge needed to interpret negative controls. A potential problem with paternal smoking as a negative control for maternal smoking is that paternal smoking causes maternal passive smoking; therefore, paternal smoking might be associated with the outcome causally. Observing an association of paternal smoking with birth weight would thus not invalidate in utero effects interpretation of the maternal smoking-birth weight association in this study. Nonetheless, the lack of association with paternal smoking in the birth weight case is reassuring. The later-life BMI outcome in offspring discussed by Davey Smith is possibly more complicated. Postnatal outcomes could be associated with in utero and postnatal exposures. The finding of an association with paternal smoking during pregnancy (B) after adjustment for in utero exposure to maternal smoking during pregnancy (A) could reflect any combination of three nonmutually exclusive possibilities: (i) uncontrolled confounding of the A→Y association; (ii) an additional causal link B→Y via in utero exposure to passive smoke; or (iii) that some or all of the association A-Y and B-Y is due to effects of postnatal exposure to smoke from either parent. That is, the observed association between parental smoking during pregnancy and adiposity may reflect a causal relationship between postnatal parental smoking and adiposity, combined with a tendency of parents who smoke during pregnancy to continue smoking after the baby is born. Marc Lipsitch Department of Epidemiology Harvard School of Public Health Boston, MA Department of Immunology and Infectious Diseases Harvard School of Public Health Boston, MA Center for Communicable Disease Dynamics Harvard School of Public Health Boston, MA [email protected] Eric Tchetgen Tchetgen Department of Epidemiology Harvard School of Public Health Boston, MA Center for Communicable Disease Dynamics Harvard School of Public Health Boston, MA Department of Biostatistics Harvard School of Public Health Boston, MA Ted Cohen Department of Epidemiology Harvard School of Public Health Boston, MA Center for Communicable Disease Dynamics Harvard School of Public Health Boston, MA Division of Global Health Equity Brigham and Women's Hospital Boston, MA

Physiological Regulation at 9 Months of Age in Infants Prenatally Exposed to Cigarettes.

The primary purpose of this study was to examine the association between prenatal cigarette exposure and physiological regulation at 9 months of age. Specifically, we explored the possibility that any association between prenatal cigarette exposure and infant physiological regulation was moderated by postnatal environmental tobacco smoke (ETS) exposure or infant gender. We evaluated whether male infants with prenatal cigarette exposure or infants who were also exposed to ETS after birth had the highest levels of physiological dysregulation. Respiratory sinus arrhythmia (RSA) was obtained from 206 (142 exposed and 64 nonexposed) infants during a baseline period and during procedures designed to elicit both positive and negative affect. There was a significant suppression of RSA during the negative affect task for nonexposed infants but not for exposed infants. Postnatal ETS exposure did not moderate this association; however, gender did moderate this association such that boys with prenatal cigarette exposure had a significant increase in RSA rather than the suppression seen among both nonexposed boys and girls. These results provide additional support for the idea that boys are particularly vulnerable to the effects of prenatal cigarette exposure.

Effects of Tobacco Smoking in Pregnancy on Offspring Intelligence at the Age of 5

The aim of the study was to examine the effects of tobacco smoking in pregnancy on children's IQ at the age of 5. A prospective follow-up study was conducted on 1,782 women, and their offspring were sampled from the Danish National Birth Cohort. At 5 years of age, the children were tested with the Wechsler Preschool and Primary Scale of Intelligence-Revised. Parental education, maternal IQ, maternal alcohol consumption in pregnancy, the sex and age of the child, and tester were considered core confounders, but the full model also controlled for prenatal paternal smoking, maternal age and Bodymass Mass Index, parity, family/home environment, postnatal parental smoking, breast feeding, the child's health status, and indicators for hearing and vision impairments. Unadjusted analyses showed a statistically significant decrement of 4 points on full-scale IQ (FSIQ) associated with smoking 10+ cigarettes per day compared to nonsmoking. After adjustment for potential confounders, no significant effects of prenatal exposure to tobacco smoking were found. Considering the indisputable teratogenic effects of tobacco smoking, these findings should be interpreted with caution. Still, the results may indicate that previous studies that failed to control for important confounders, particularly maternal intelligence, may be subject to substantial residual confounding.

Parental and household smoking and the increased risk of bronchitis, bronchiolitis and other lower respiratory infections in infancy: systematic review and meta-analysis

BackgroundPassive smoke exposure increases the risk of lower respiratory infection (LRI) in infants, but the extensive literature on this association has not been systematically reviewed for nearly ten years. The aim of this paper is to provide an updated systematic review and meta-analysis of studies of the association between passive smoking and LRI, and with diagnostic subcategories including bronchiolitis, in infants aged two years and under.MethodsWe searched MEDLINE and EMBASE (to November 2010), reference lists from publications and abstracts from major conference proceedings to identify all relevant publications. Random effect pooled odds ratios (OR) with 95% confidence intervals (CI) were estimated.ResultsWe identified 60 studies suitable for inclusion in the meta-analysis. Smoking by either parent or other household members significantly increased the risk of LRI; odds ratios (OR) were 1.22 (95% CI 1.10 to 1.35) for paternal smoking, 1.62 (95% CI 1.38 to 1.89) if both parents smoked, and 1.54 (95% CI 1.40 to 1.69) for any household member smoking. Pre-natal maternal smoking (OR 1.24, 95% CI 1.11 to 1.38) had a weaker effect than post-natal smoking (OR 1.58, 95% CI 1.45 to 1.73). The strongest effect was on bronchiolitis, where the risk of any household smoking was increased by an OR of 2.51 (95% CI 1.96 to 3.21).ConclusionsPassive smoking in the family home is a major influence on the risk of LRI in infants, and especially on bronchiolitis. Risk is particularly strong in relation to post-natal maternal smoking. Strategies to prevent passive smoke exposure in young children are an urgent public and child health priority.

Low to Moderate Alcohol Intake During Pregnancy and Risk of Psychomotor Deficits

To examine the effects of low to moderate alcohol consumption during pregnancy on child motor function at age 5. A prospective follow-up study of 685 women and their children sampled from the Danish National Birth Cohort based on maternal alcohol consumption during pregnancy. At 5 years of age, the children were tested with the "Movement Assessment Battery for Children" (MABC). Parental education, maternal IQ, prenatal maternal smoking, the child's age at testing, and gender of child were considered core confounders, while the full model also controlled for prenatal maternal binge drinking episodes, age, maternal prepregnancy body mass index, parity, home environment, postnatal parental smoking, health status, and indicators for hearing and vision impairment. There were no systematic or significant differences in motor function between children of mothers reporting low to moderate levels of average alcohol consumption during pregnancy and children of mothers who abstained. In this study, we found no systematic association between low to moderate maternal alcohol intake during pregnancy and child motor function at age 5.

ASSOCIATION BETWEEN TRAFFIC-RELATED BLACK CARBON EXPOSURE AND THE CONNER’S CONTINUOUS PERFORMANCE TEST (CPT) AMONG URBAN CHILDREN IN A PROSPECTIVE BIRTH COHORT

Background and Aims: Associations between ambient air pollution exposure and children’s cognitive domains are only beginning to be examined and analyses have not accounted for community-level psychosocial stressors that may co-vary with pollution exposures. We assessed the relationship of exposure to black carbon (BC), a marker of traffic particles, with attention and vigilance domains while adjusting for exposure to community violence (ETV), among 192 children aged 6-12 years in a Boston-based prospective birth cohort. Methods: BC levels were estimated using a validated spatio-temporal land-use regression model based on residence during the child’s lifetime, then categorized into quartiles. Exposure to violence (ETV) in these neighborhoods was ascertained using the My Exposure to Violence survey, which was categorized into tertiles. Attention and vigilance were measured using the Conner’s Continuous Performance Test (CPT). Primary outcomes included: omission errors, commission errors, hit reaction time (HRT), HRT standard error (SE), HRT block change, and HRT SE block change (higher scores indicating worse performance or slower reaction time). Multiple regression analyses were used to determine effects of BC levels on outcomes. Results: Children were primarily Hispanic (55%) and Caucasians (42%). We found a positive association between BC levels with commission errors and HRT (p&lt;0.05), adjusting for age, gender, maternal education, ETV, and blood lead level. Higher-level ETV was associated with lower commission errors (p&lt;0.05). Additional inclusion of children’s IQ, prenatal smoking, and postnatal secondhand smoke exposure did not alter these results. Gender-stratified analysis suggested that the effects of BC on CPT measures were stronger in boys (p&lt;0.05) for both commission errors and HRT, than in girls (p&gt;0.2). Conclusions: In this population of urban children, we found a relationship between increased BC exposure with increased commission errors and slower reaction time. Effects of traffic-related pollution on attention domains may be stronger in boys.

Parental Smoking and the Risk of Middle Ear Disease in Children

A systematic review and meta-analysis of studies of the association between secondhand tobacco smoke (SHTS) and middle ear disease (MED) in children. MEDLINE, EMBASE, and CAB abstracts (through December 2010) and reference lists. Sixty-one epidemiological studies of children assessing the effect of SHTS on outcomes of MED. Articles were reviewed, and the data were extracted and synthesized by 2 researchers. MAIN OUTCOME EXPOSURES: Children's SHTS exposure. Middle ear disease in children. Living with a smoker was associated with an increased risk of MED in children by an odds ratio (OR) of 1.62 (95% CI, 1.33-1.97) for maternal postnatal smoking and by 1.37 (95% CI, 1.25-1.50) for any household member smoking. Prenatal maternal smoking (OR, 1.11; 95% CI, 0.93-1.31) and paternal smoking (OR, 1.24; 95% CI, 0.98-1.57) were associated with a nonsignificant increase in the risk of MED. The strongest effect was on the risk of surgery for MED, where maternal postnatal smoking increased the risk by an OR of 1.86 (95% CI, 1.31-2.63) and paternal smoking by 1.83 (95% CI, 1.61-2.07). Exposure to SHTS, particularly to smoking by the mother, significantly increases the risk of MED in childhood; this risk is particularly strong for MED requiring surgery. We have shown that per year 130 200 of child MED episodes in the United Kingdom and 292 950 of child frequent ear infections in the United States are directly attributable to SHTS exposure in the home.

Secondhand Smoke Exposure and Neurobehavioral Disorders Among Children in the United States

The association between parent-reported postnatal secondhand tobacco smoke exposure in the home and neurobehavioral disorders (attention-deficit/hyperactivity disorder, learning disabilities, and conduct disorders) among children younger than 12 years in the United States was examined using the 2007 National Survey on Children's Health. Excess neurobehavioral disorders attributable to secondhand smoke (SHS) exposure in the home in 2007 were further investigated. The methods used in this study were multivariable logistic regression models that accounted for potential confounders and complex survey designs to evaluate associations. A total of 6% of 55 358 children (aged < 12 years), corresponding to a weighted total of 4.8 million children across the United States, were exposed to SHS in the home. The weighted prevalence and 95% confidence intervals of each of the children's neurobehavioral outcomes were 8.2% (7.5-8.8) with learning disabilities, 5.9% (5.5-6.4) with attention-deficit/hyperactivity disorder, and 3.6% (3.1-4.0) with behavioral and conduct disorders. Children exposed to SHS at home had a 50% increased odds of having ≥2 childhood neurobehavioral disorders compared with children who were not exposed to SHS. Boys had a significantly higher risk. Older children, especially those aged 9 to 11 years, and those living in households with the highest poverty levels were at greater risk. In absolute terms, 274 100 excess cases in total of these 3 disorders could have been prevented if children had not been exposed to SHS in their homes. The findings of the study, which are associational and not necessarily causal, underscore the health burden of childhood neurobehavioral disorders that may be attributable to SHS exposure in homes in the United States.

Physiological regulation in cigarette exposed infants: An examination of potential moderators

The primary purpose of this study was to examine pathways from prenatal cigarette exposure to physiological regulation at 2 months of age. Specifically, we explored the possibility that any association between prenatal cigarette exposure and infant physiological regulation was moderated by fetal growth, prenatal or postnatal environmental tobacco smoke (ETS) exposure or maternal depressive symptomatology during pregnancy. We evaluated whether exposed infants who were also exposed to ETS after birth, were small for gestational age (SGA) or had mothers with higher depressive symptoms during pregnancy had the highest levels of physiological dysregulation. Respiratory sinus arrhythmia (RSA) was obtained from 234 (166 exposed and 68 nonexposed) infants during sleep. As expected, cigarette-exposed infants had significantly lower RSA than nonexposed infants. This association was not moderated by prenatal or postnatal ETS exposure, or maternal depressive symptomatology during pregnancy. However, small for gestational age status did moderate this association such that nonexposed infants who were not small for gestational age had a significantly higher RSA than nonexposed small for gestational age infants and exposed infants. These findings provide additional evidence that prenatal cigarette exposure is directly associated with dysregulation during infancy.

Prenatal and postnatal tobacco smoke exposure and development of insulin resistance in 10 year old children

In this study, we evaluated the association between prenatal and postnatal exposure to environmental tobacco smoke and the development of insulin resistance in 10 year old children. Fasting blood samples were collected from 470 children participating in two prospective birth cohorts. Of those 276 were selected population based and enriched with 194 children exceeding the 85th percentile of body mass index in this age group. Children already having diabetes type 1 or 2 at the age of 10 years were excluded. Fasting blood insulin and glucose levels and calculated HOMA index for insulin resistance assessment were analysed using generalised additive models. Potential confounders were adjusted for. Insulin resistance was increased by 24% in children frequently exposed to environmental tobacco smoke during childhood (MR(adj) = 1.24, p = 0.001), while glucose levels were not. Exclusion of prenatally exposed children did not attenuate the association (MR(adj) = 1.25, p = 0.006). After stratification, the effect sizes were identical within overweight children and the population based sample of children. Insulin resistance and fasting insulin levels were increasing with increasing numbers of cigarettes smoked in children's home. Maternal smoking during the third trimester of pregnancy increased children's insulin levels (MR(adj) = 1.19, p = 0.037), and even more so, if children were exclusively breastfed after birth (MR(adj) = 1.31, p = 0.016). Increased mean ratios were found for smoking of a third person in addition to maternal smoking. Positive dose-dependent associations and independent effects of postnatal exposure suggest involvement of environmental tobacco smoke in the risk for development of insulin resistance in children.

Gender-specific differences in effects of prenatal and postnatal environmental tobacco smoke exposure on respiratory symptoms in 23,474 children with and without allergic predisposition: results from 25 districts of northeast China

To assess the interaction of environmental tobacco smoke (ETS) exposure and allergic predisposition regarding respiratory health among Chinese children, a sample of 23,474 children (6–13 years old) was studied from 25 districts in Liaoning province, China. The results showed that children without allergic predisposition were more susceptible to ETS than children with allergic predisposition. Among children without allergic predisposition, ETS exposure was associated with more respiratory symptoms and diseases in boys than in girls; In utero ETS exposure was associated with history of asthma (OR, 1.86; 95% CI, 1.44–2.40) and current asthma (OR, 2.25; 95% CI, 1.48–3.44) only among boys without allergic predisposition. Among children with allergic predisposition, more associations between ETS exposure and respiratory symptoms and diseases were detected in girls. In conclusion, ETS exposure was more evident in boys without family atopy history and more associations were detected in girls with family atopy history.

Postnatal parental smoking: an important risk factor for SIDS

BackgroundSudden infant death syndrome (SIDS) is the unexpected death of an infant that remains unexplained after a thorough investigation of the circumstances, family history, paediatric investigation and complete autopsy. In Western society, it is the leading cause of post-neonatal death below 1 year of age. In the Netherlands, the SIDS incidence is very low, which offers opportunities to assess the importance of old and new environmental risk factors. For this purpose, cases were collected through pathology departments and the working group on SIDS of the Dutch Paediatrician Foundation. A total of 142 cases were included; these occurred after the parental education on sleeping position (1987), restricted to the international age criteria and had no histological explanation. Age-matched healthy controls (N = 2,841) came from a survey of the Netherlands Paediatric Surveillance Unit, completed between November 2002 and April 2003. A multivariate analysis was performed to determine the risk factors for SIDS, including sleeping position, antenatal maternal smoking, postnatal parental smoking, premature birth, gender, lack of breastfeeding and socio-economic status. Postnatal smoking was identified as an important environmental risk factor for SIDS (OR one parent = 2.5 [1.2, 5.0]; both parents = 5.77 [2.2, 15.5]; maternal = 2.7 [1.0, 6.4]; paternal = 2.4 [1.3, 4.5] ) as was prone sleeping (OR put prone to sleep = 21.5 [10.6, 43.5]; turned prone during sleep = 100 [46, 219]). Premature birth was also significantly associated with SIDS (OR = 2.4 [1.2, 4.8]).ConclusionPostnatal parental smoking is currently a major environmental risk factor for SIDS in the Netherlands together with the long-established risk of prone sleeping.

Secondhand smoke exposure during pregnancy and infantile neurodevelopment

During prenatal development, the nervous system may be more susceptible to environmental toxicants, such as secondhand smoke. The authors assessed the effects of prenatal and postnatal secondhand smoke exposure on the neurodevelopment of 6-month infants. The subjects were 414 mother and infant pairs with no medical problems, taken from the Mothers' and Children's Environmental Health study. Prenatal and postnatal exposures to secondhand smoke were determined using maternal self-reports. Examiners, unaware of exposure history, assessed the infants at 6 months of age using the Bayley Scales of Infant Development. Bayley scores were compared for secondhand smoke exposed and unexposed groups after adjusting for potential confounders. Multiple logistic regression analysis was carried out to estimate the risk of developmental delay posed by SHS exposure. The multivariate model included residential area, maternal age, pre-pregnancy body mass index, education, income, infant sex, parity, birth weight, and type of feeding. After adjusting for covariates, secondhand smoke exposure during pregnancy was found to be related to a decrease in mental developmental index score, but not to a decrease in psychomotor developmental index score. In addition, secondhand smoke exposure during pregnancy was found to increase the risk of developmental delay (mental developmental index score ≤85) at 6 months. This study suggests that the infants of non-smoking women exposed to secondhand smoke are at risk of neurodevelopmental delay.

Indoor Coal Use and Early Childhood Growth

To examine whether indoor coal combustion for heating, which releases pollutants into the air, affects early childhood growth. A prospective longitudinal study, with growth measurements extracted from medical records of the children's well-child care visits at age 36 months. Data were compiled from self-administered questionnaires and medical records, both completed at 2 time points: delivery and follow-up. Teplice and Prachatice districts in the Czech Republic. A total of 1133 children followed from birth to age 36 months. Maternally reported use of coal for heating. The z score for height for age and sex at age 36 months. Adjusted for covariates, indoor coal use was significantly associated with a lower z score for height for age and sex at age 36 months (z score = -0.37; 95% confidence interval, -0.60 to -0.14). This finding translates into a reduction in height of about 1.34 cm (95% confidence interval, 0.51 to 2.16) for boys and 1.30 cm (95% confidence interval, 0.50 to 2.10) for girls raised in homes that used coal. The association between coal use and height was modified by postnatal cigarette smoke exposure. Pollution from indoor coal use may impair early childhood skeletal growth to age 36 months. Because a significant proportion of the world population still uses coal indoors, the finding has public health consequences.

Environmental tobacco smoke (ETS) exposure and respiratory morbidity in school age children

IntroductionTobacco smoke is a risk factor for Chronic Obstructive Pulmonary Disease and a major public health problem. Prenatal maternal smoking and post-natal environmental tobacco smoke (ETS) lead to dose-dependent decrease in lung function and respiratory morbidity. Influence of different socioeconomic indicators and ETS in the home has also been suggested. MethodsData on 313 children (52 % male) from 4 public schools in Lisbon was analyzed [1st (46 %) and 4th graders]. ETS assessment and respiratory symptoms were based on a self-answered questionnaire. All children performed standard spirometry in the school setting and 54 % were acceptable according to ATS/ERS criteria. Descriptive and bivariate analysis of the most relevant variables was done, followed by multiple logistic regression analysis adjusted to the variables with clinical/statistical relevance. ResultsETS in the home was found in 41 % (maternal smoking during pregnancy 18 %, smoking mother 32 %, smoking father 38 %). Smoking fathers had lower education and less qualified occupation. Cough was more frequent in children with a smoking mother (adjusted OR=2.1; 95 %CI, 1.1–4) and wheezing in children with maternal smoking during pregnancy and smoking parents. All differences were significant (p<0.05). No association was found between parental education and cough/wheeze or ETS and respiratory infections/asthma/decreased spirometric values. ConclusionsChildren in Lisbon are frequently exposed to ETS which results in significant respiratory morbidity. Targeted interventions must have social conditions in consideration. In this study, field spirometry was not helpful in early detection of lung function disability in children associated with ETS.

Exposição ao fumo do tabaco (EFT) e morbilidade respiratória em crianças em idade escolar

Introduction Tobacco smoke is a risk factor for Chronic Obstructive Pulmonary Disease and a major public health problem. Prenatal maternal smoking and post-natal environmental tobacco smoke (ETS) lead to dose-dependent decrease in lung function and respiratory morbidity. Influence of different socioeconomic indicators and ETS in the home has also been suggested. Methods Data on 313 children (52% male) from 4 public schools in Lisbon was analyzed [1st (46%) and 4th graders]. ETS assessment and respiratory symptoms were based on a self-answered questionnaire. All children performed standard spirometry in the school setting and 54% were acceptable according to ATS/ERS criteria. Descriptive and bivariate analysis of the most relevant variables was done, followed by multiple logistic regression analysis adjusted to the variables with clinical/statistical relevance. Results ETS in the home was found in 41% (maternal smoking during pregnancy 18%, smoking mother 32%, smoking father 38%). Smoking fathers had lower education and less qualified occupation. Cough was more frequent in children with a smoking mother (adjusted OR = 2.1 95CI 1.1–4.0) and wheezing in children with maternal smoking during pregnancy and smoking parents. All differences were significant (p < 0.05). No association was found between parental education and cough/wheeze or ETS and respiratory infections/asthma/decreased spirometric values. Conclusions Children in Lisbon are frequently exposed to ETS which results in significant respiratory morbidity. Targeted interventions must have social conditions in consideration. In this study, field spirometry was not helpful in early detection of lung function disability in children associated with ETS.

Prenatal exposure to polycyclic aromatic hydrocarbons, environmental tobacco smoke and asthma

Previously, we reported that prenatal exposures to polycyclic aromatic hydrocarbons (PAH) and postnatal environmental tobacco smoke (ETS) in combination were associated with respiratory symptoms at ages 1 and 2 years. Here, we hypothesized that children exposed to both prenatal PAH and ETS may be at greater risk of asthma and seroatopy at ages 5-6 years, after controlling for current pollution exposure. Prenatal PAH exposure was measured by personal air monitoring over 48h. ETS exposure, respiratory symptoms and asthma at ages 5-6 years were assessed through questionnaire. Immunoglobulin (Ig) E was measured by Immunocap. A significant interaction between prenatal PAH and prenatal (but not postnatal) ETS exposure on asthma (p<0.05), but not IgE, was detected. Among children exposed to prenatal ETS, a positive nonsignificant association was found between prenatal PAH exposure and asthma (OR 1.96, 95% CI [0.95-4.05]). Among children without exposure to prenatal ETS, a negative nonsignificant association was found between prenatal PAH exposure and asthma (OR 0.65, 95% CI [0.41-1.01]). Prenatal PAH exposure was not associated with asthma or IgE at age 5-6 years. Combined prenatal exposure to PAH and ETS appears to be associated with asthma but not seroatopy at age 5-6. Exposure to PAH alone does not appear associated with either asthma or seroatopy at age 5-6 years. Discerning the differential effects between ETS exposed and ETS nonexposed children requires further study.