Postnatal Environmental Tobacco Smoke Research Articles

The impact of exposure to tobacco smoke and e-cigarettes on asthma-related outcomes: Systematic review informing the EAACI guidelines on environmental science for allergic diseases and asthma.

To inform the clinical practice guidelines' recommendations developed by the European Academy of Allergy and Clinical Immunology systematic reviews (SR) assessed using GRADE on the impact of environmental tobacco smoke (ETS) and active smoking on the risk of new-onset asthma/recurrent wheezing (RW)/low lung function (LF), and on asthma-related outcomes. Only longitudinal studies were included, almost all on combustion cigarettes, only one assessing e-cigarettes and LF. According to the first SR (67 studies), prenatal ETS increases the risk of RW (moderate certainty evidence) and may increase the risk of new-onset asthma and of low LF (low certainty evidence). Postnatal ETS increases the risk of new-onset asthma and of RW (moderate certainty evidence) and may impact LF (low certainty evidence). Combined in utero and postnatal ETS may increase the risk of new-onset asthma (low certainty evidence) and increases the risk of RW (moderate certainty evidence). According to the second SR (24 studies), ETS increases the risk of severe asthma exacerbations and impairs asthma control and LF (moderate certainty evidence). According to the third SR (25 studies), active smoking increases the risk of severe asthma exacerbations and of suboptimal asthma control (moderate certainty evidence) and may impact asthma-related quality-of-life and LF (low certainty evidence).

Environmental tobacco smoke and carotid intima-media thickness in healthy children and adolescents: a systematic review.

Thicker carotid intima–media thickness (CIMT) has been a valid predictor for atherosclerosis development. A significant association between environmental tobacco smoke (ETS) and thickening of CIMT has been demonstrated in adults, whereas such association has scarcely been reviewed in paediatric population. The dominate electronic databases, including MEDLINE (Ovid), PubMed, Embase, CINAHL, Web of Science, Scopus, were searched from inception. Reference lists of retrieved articles were further scanned as to avoid any missing literatures. Newcastle-Ottawa scale was used to assess the quality of the included studies. Qualitative synthesis analyses were performed on the selected studies. 331 articles were retrieved, and 4 were finally selected. All four studies investigated the association between postnatal ETS and CIMT in children, and three of them reported a statistically significant positive association. Three studies investigated the association between prenatal maternal ETS and CIMT, and one of the three found a positive association. Two studies explored the association between postnatal maternal ETS and CIMT, one reported a positive association. Two studies used serum cotinine measurement to quantify ETS and demonstrated potential dose-response relationship with CIMT. ETS exposure may play an independent role in the development of cardiovascular risks in healthy children and adolescents. In the consideration of the great burden of respiratory and cardiovascular diseases, there is an urgent need of effective surveillance for paediatric population’s ETS exposure to reduce smoke exposure.

COTININE LEVEL AS A BIOCHEMICAL INDICATOR OF THE TOXIC EFFECTS OF PASSIVE SMOKING EXPOSURE ON INFANTS’ ANTHROPOMETRIC MEASURES

Background: Fetuses, infants and children seem to be the most susceptible populations to the harmful effects of Environmental Tobacco Smoke (ETS). Significant maternal and fetal exposure to ETS inside the home may affect fetal and child health. The aim of the study was to evaluate the toxic effects of perinatal exposure to Second-Hand Smoke (SHS) on the infant’s anthropometric measures and nutritional status and assess the benefit of using serum cotinine level in early childhood as a measurable indicator to such toxic perinatal exposure. Subjects & Methods: an observational cross-sectional study including the mothers and their children (less than two years) attend Monfallout’s Family Medicine Center from the period of October 2017 to October 2018. The questionnaire and serum cotinine of the infants were investigated along with the most important SHS determinants (socio-demographic and environmental). Results: The study included 400 mothers with their infants. The commonest site of SHS exposure was the home and the husband was the main responsible source. SHS infants were classified according to their serum cotinine level as active smokers (14.44%), non-smokers exposed to SHS (75.56%), and non-smokers not exposed (10%). There was a highly statistically significant difference between median birth weight, median birth length of regularly exposed babies to smoking and median birth weight, median birth length of non-exposed babies. There was a dose-dependent decrease in weight and length of babies at birth, as well as associated with reduced weight, length and hemoglobin level in different stages later on in their life with an increase in serum cotinine level. Conclusion: Regular Prenatal and postnatal ETS lead to a dose-dependent decrease in weight and length of babies at birth and later on at early childhood stages. Mothers should take adequate precautions to avoid exposure to such SHS hazards as they and their children may be more susceptible to a series of negative health effects most mothers with their children were regularly exposed to SHS in various places during daily life especially at home and the main source of smoking was husband smoking.

Environmental Tobacco Smoke During the Early Postnatal Period of Mice Interferes With Brain 18 F-FDG Uptake From Infancy to Early Adulthood - A Longitudinal Study.

Exposure to environmental tobacco smoke (ETS) is associated with high morbidity and mortality, mainly in childhood. Our aim was to evaluate the effects of postnatal ETS exposure in the brain 2-deoxy-2-[18F]-fluoro-D-glucose (18F-FDG) uptake of mice by positron emission tomography (PET) neuroimaging in a longitudinal study. C57BL/6J mice were exposed to ETS that was generated from 3R4F cigarettes from postnatal day 3 (P3) to P14. PET analyses were performed in male and female mice during infancy (P15), adolescence (P35), and adulthood (P65). We observed that ETS exposure decreased 18F-FDG uptake in the whole brain, both left and right hemispheres, and frontal cortex in both male and female infant mice, while female infant mice exposed to ETS showed decreased 18F-FDG uptake in the cerebellum. In addition, all mice showed reduced 18F-FDG uptake in infancy, compared to adulthood in all analyzed VOIs. In adulthood, ETS exposure during the early postnatal period decreased brain 18F-FDG uptake in adult male mice in the cortex, striatum, hippocampus, cingulate cortex, and thalamus when compared to control group. ETS induced an increase in 18F-FDG uptake in adult female mice when compared to control group in the brainstem and cingulate cortex. Moreover, male ETS-exposed animals showed decreased 18F-FDG uptake when compared to female ETS-exposed in the whole brain, brainstem, cortex, left amygdala, striatum, hippocampus, cingulate cortex, basal forebrain and septum, thalamus, hypothalamus, and midbrain. The present study shows that several brain regions are vulnerable to ETS exposure during the early postnatal period and these effects on 18F-FDG uptake are observed even a long time after the last exposure. This study corroborates our previous findings, strengthening the idea that exposure to tobacco smoke in a critical period interferes with brain development of mice from late infancy to early adulthood.

In utero and postnatal exposure to environmental tobacco smoke, blood pressure, and hypertension in children: the Seven Northeastern Cities study

ABSTRACT To evaluate the association of environmental tobacco smoke (ETS) exposure with hypertension and blood pressure (BP) in children, a sample of 9,354 children, aged 5–17 years, was studied from seven northeastern cities of China in 2012–2013. The results showesd that significant associations were observed for hypertension with ETS exposure in utero [odds ratio (OR) 1.36, 95% confidence interval (CI) 1.18–1.57], with current major ETS exposure from fathers (1.38, 1.21–1.57) or anyone (1.26, 1.12–1.42), and with intensity of ETS exposure greater than 1 cigarette per day (ORs ranged from 1.20 to 1.35). For SBP, significant associations were only observed in children with major ETS exposure from father and with cigarettes smoking >10/day. When stratified by sex, more significant associations were found in girls than in boys. In conclusion, prenatal and postnatal ETS exposure was significantly associated with increased odds of hypertension in children, especially in girls.

Indoor air pollution and tobacco smoke exposure: impact on nasopharyngeal bacterial carriage in mothers and infants in an African birth cohort study.

Indoor air pollution (IAP) or environmental tobacco smoke (ETS) exposure may influence nasopharyngeal carriage of bacterial species and development of lower respiratory tract infection (LRTI). The aim of this study was to longitudinally investigate the impact of antenatal or postnatal IAP/ETS exposure on nasopharyngeal bacteria in mothers and infants.A South African cohort study followed mother–infant pairs from birth through the first year. Nasopharyngeal swabs were taken at birth, 6 and 12 months for bacterial culture. Multivariable and multivariate Poisson regression investigated associations between nasopharyngeal bacterial species and IAP/ETS. IAP exposures (particulate matter, carbon monoxide, nitrogen dioxide, volatile organic compounds) were measured at home visits. ETS exposure was measured through maternal and infant urine cotinine. Infants received the 13-valent pneumococcal and Haemophilus influenzae B conjugate vaccines.There were 881 maternal and 2605 infant nasopharyngeal swabs. Antenatal ETS exposure was associated with Streptococcus pneumoniae carriage in mothers (adjusted risk ratio (aRR) 1.73 (95% CI 1.03–2.92)) while postnatal ETS exposure was associated with carriage in infants (aRR 1.14 (95% CI 1.00–1.30)) Postnatal particulate matter exposure was associated with the nasopharyngeal carriage of H. influenzae (aRR 1.68 (95% CI 1.10– 2.57)) or Moraxella catarrhalis (aRR 1.42 (95% CI 1.03–1.97)) in infants.Early-life environmental exposures are associated with an increased prevalence of specific nasopharyngeal bacteria during infancy, which may predispose to LRTI.

Exposure to tobacco smoke during the early postnatal period modifies receptors and enzymes of the endocannabinoid system in the brainstem and striatum in mice

Environmental tobacco smoke (ETS) exposure during brain development has been associated with several disorders, such as depression, anxiety, sudden infant death syndrome, and the predisposition to addiction. The endocannabinoid system plays an essential role in neuronal development. We investigated the effects of early postnatal ETS exposure on the endocannabinoid system in different brain regions. C57BL/6 J mice were exposed to ETS that was generated from 3R4F cigarettes from postnatal day 3 (P3) to P14. Receptors and enzymes of the endocannabinoid system were assessed in infancy, adolescence, and adulthood by Western blot. In the brainstem, ETS exposure decreased cannabinoid 1 (CB1) receptor, CB2 receptor, N-arachidonoyl phosphatidyl ethanol-specific phospholipase D (NAPE-PLD), and fatty acid amino hydrolase (FAAH) levels and increased in diacylglycerol lipase (DAGL) and monoacylglycerol lipase (MAGL) levels during infancy and decreased CB2 and FAAH levels during adulthood. In the striatum, ETS decreased in the NAPE-PLD and MAGL levels and increased FAAH levels during infancy, increased FAAH levels during adolescence, and decreased NAPE-PLD levels during adulthood. The present findings indicate that exposure to ETS during a critical period of brain development can disturb the endocannabinoid system in the brainstem and striatum, regions that are involved in the pathogenesis of sudden infant death syndrome and the susceptibility to addiction.

Assessment of tobacco smoke effects on neonatal cardiorespiratory control using a semi-automated processing approach.

A semi-automated processing approach was developed to assess the effects of early postnatal environmental tobacco smoke (ETS) on the cardiorespiratory control of newborn lambs. The system consists of several steps beginning with artifact rejection, followed by the selection of stationary segments, and ending with feature extraction. This approach was used in six lambs exposed to 20 cigarettes/day for the first 15days of life, while another six control lambs were exposed to room air. On postnatal day 16, electrocardiograph and respiratory signals were obtained from a 6-h polysomnographic recording. The effects of postnatal ETS exposure on heart rate variability, respiratory rate variability, and cardiorespiratory interrelations were explored. The unique results suggest that early postnatal ETS exposure increases respiratory rate variability and decreases the coupling between cardiac and respiratory systems. Potentially harmful consequences in early life include unstable breathing and decreased adaptability of cardiorespiratory function, particularly during early life challenges, such as prematurity or viral infection. Graphical abstract ᅟ.

Exposure of Neonatal Mice to Tobacco Smoke Disturbs Synaptic Proteins and Spatial Learning and Memory from Late Infancy to Early Adulthood.

Exposure to environmental tobacco smoke (ETS) in the early postnatal period has been associated with several diseases; however, little is known about the brain effects of ETS exposure during this critical developmental period or the long-term consequences of this exposure. This study investigated the effects of the early postnatal ETS exposure on both reference and working memory, synaptic proteins and BDNF from late infancy to early adulthood (P3-P73). BALB/c mice were exposed to ETS generated from 3R4F reference research cigarettes (0.73 mg of nicotine/cigarette) from P3 to P14. Spatial reference and working memory were evaluated in the Morris water maze during infancy (P20-P29), adolescence (P37-P42) and adulthood (P67-P72). Synapsin, synaptophysin, PSD95 and brain-derived neurotrophic factor (BDNF) were assessed at P15, P35 and P65 by immunohistochemistry and immunoblotting. Mice that were exposed to ETS during the early postnatal period showed poorer performance in the spatial reference memory task. Specifically, the ETS-exposed mice exhibited a significantly reduced time and distance traveled in the target quadrant and in the platform location area than the controls at all ages evaluated. In the spatial working memory task, ETS disrupted the maintenance but not the acquisition of the critical spatial information in both infancy and adolescence. ETS also induced changes in synaptic components, including decreases in synapsin, synaptophysin, PSD95 and BDNF levels in the hippocampus. Exposure to ETS in the early postnatal period disrupts both spatial reference and working memory; these results may be related to changes in synaptogenesis in the hippocampus. Importantly, most of these effects were not reversed even after a long exposure-free period.

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.

Environmental tobacco smoke in the early postnatal period induces impairment in brain myelination.

Environmental tobacco smoke (ETS) is associated with high morbidity and mortality, mainly in children. However, few studies focus on the brain development effects of ETS exposure. Myelination mainly occurs in the early years of life in humans and the first three postnatal weeks in rodents and is sensitive to xenobiotics exposure. This study investigated the effects of early postnatal ETS exposure on myelination. BALB/c mice were exposed to ETS generated from 3R4F reference research cigarettes from the third to the fourteenth days of life. The myelination of nerve fibers in the optic nerve by morphometric analysis and the levels of Olig1 and myelin basic protein (MBP) were evaluated in the cerebellum, diencephalon, telencephalon, and brainstem in infancy, adolescence, and adulthood. Infant mice exposed to ETS showed a decrease in the percentage of myelinated fibers in the optic nerve, compared with controls. ETS induced a decrease in Olig1 protein levels in the cerebellum and brainstem and an increase in MBP levels in the cerebellum at infant. It was also found a decrease in MBP levels in the telencephalon and brainstem at adolescence and in the cerebellum and diencephalon at adulthood. The present study demonstrates that exposure to ETS, in a critical phase of development, affects the percentage of myelinated fibers and myelin-specific proteins in infant mice. Although we did not observe differences in the morphological analysis in adolescence and adulthood, there was a decrease in MBP levels in distinctive brain regions suggesting a delayed effect in adolescence and adulthood.

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

Perfluorinated Compound Levels in Cord Blood and Neurodevelopment at 2 Years of Age

Epidemiologic data regarding the potential neurotoxicity of perfluorinated compounds (PFCs) are inconclusive. We investigated the associations between in utero exposure to perfluorooctanoic acid (PFOA) and perfluorooctyl sulfonate (PFOS) and early childhood neurodevelopment. We recruited 239 mother-infant pairs in northern Taiwan from the Taiwan Birth Panel Study, which was established in 2004. We examined the association between PFCs in cord blood and children's neurodevelopment at 2 years of age, using the Comprehensive Developmental Inventory for Infants and Toddlers. This tool contains cognitive, language, motor, social, and self-help domains; test scores were further transformed into developmental quotients according to standardized norms. All multivariate regression models were adjusted for infant sex and gestational age, maternal education, family income, cord blood cotinine levels, postnatal environmental tobacco smoke exposure, and breastfeeding. Prenatal PFOS concentrations in both untransformed and natural log (Ln)-transformed values were associated with adverse performance on the whole test and the domains related to development. A dose-response relationship was observed when PFOS levels were categorized into four groups. This association was most obvious in relation to the gross-motor subdomain. Across the PFOS interquartile range, the quotients of the gross-motor subdomain decreased by 3.7 points (95% confidence interval [CI] = -6.0 to -1.5), with an increasing odds ratio of poor performance (2.4; 95% CI = 1.3 to 4.2). In contrast, measures of association between PFOA concentrations and test scores were close to null. Prenatal exposure to PFOS, but not PFOA, may affect children's development, especially gross-motor development at 2 years of age.

Intrauterine exposure to fine particulate matter as a risk factor for increased susceptibility to acute broncho-pulmonary infections in early childhood

Over the last decades many epidemiologic studies considered the morbidity patterns for respiratory diseases and lung function of children in the context of ambient air pollution usually measured in the postnatal period. The main purpose of this study is to assess the impact of prenatal exposure to fine particulate matter (PM2.5) on the recurrent broncho-pulmonary infections in early childhood. The study included 214 children who had measurements of personal prenatal PM2.5 exposure and regularly collected data on the occurrence of acute bronchitis and pneumonia diagnosed by a physician from birth over the seven-year follow-up. The effect of prenatal exposure to PM2.5 was adjusted in the multivariable logistic models for potential confounders, such as prenatal and postnatal ETS (environmental tobacco smoke), city residence area as a proxy of postnatal urban exposure, children's sensitization to domestic aeroallergens, and asthma. In the subgroup of children with available PM2.5 indoor levels, the effect of prenatal exposure was additionally adjusted for indoor exposure as well. The adjusted odds ratio (OR) for incidence of recurrent broncho-pulmonary infections (five or more spells of bronchitis and/or pneumonia) recorded in the follow-up significantly correlated in a dose-response manner with the prenatal PM2.5 level (OR=2.44, 95%CI: 1.12-5.36). In conclusion, the study suggests that prenatal exposure to PM2.5 increases susceptibility to respiratory infections and may program respiratory morbidity in early childhood. The study also provides evidence that the target value of 20μg/m(3) for the 24-h mean level of PM2.5 protects unborn babies better than earlier established EPA guidelines.

Effects of postnatal environmental tobacco smoke on non-nutritive swallowing-breathing coordination in newborn lambs

While prenatal environmental tobacco smoke (ETS) exposure is a well-known risk factor for sudden infant death syndrome, the effect of postnatal ETS exposure is less clear. The objective of this study was to investigate the effect of postnatal ETS exposure on non-nutritive swallowing (NNS) and NNS-breathing coordination, which are crucial to prevent aspiration related-cardiorespiratory events. Eighteen newborn lambs (6 per group) were randomly exposed to either 10 cigarettes/day, 20 cigarettes/day or room air for 15 days. Lambs were instrumented for recording states of alertness, swallowing, electrocardiogram and breathing; recordings were performed in non-sedated lambs at the end of ETS exposure. Urinary cotinine/creatinine ratio confirmed relevant real-life exposure. Postnatal ETS exposure had no effect on NNS frequency but tended to decrease inspiratory NNS (p=0.07) during quiet sleep. No effect on respiratory or heart rate (p>0.6), apnea index (p=0.2) or sleep states (p=0.3) was observed. In conclusion, postnatal ETS exposure in lambs had only mild effects on NNS-breathing coordination.

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.

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.

Maternal cigarette smoking is associated with reduced high-density lipoprotein cholesterol in healthy 8-year-old children

Smoking in pregnancy is common. Its effects on lipoprotein levels and arterial structure in childhood are not well characterized. We aimed to determine the effects of maternal smoking in pregnancy on lipoprotein levels and arterial wall thickness in healthy pre-pubertal children. A community-based longitudinal study with prospective ascertainment of exposure to smoking in pregnancy and environmental tobacco smoke (ETS) since birth and then lipoprotein and arterial measurements at age 8 years. In 616 newborn infants (gestation >36 weeks and birth weight >2.5 kg) data were collected prospectively by questionnaire on smoking in pregnancy and ETS exposure in childhood. At age 8-years, 405 of the children had measurements of lipoproteins, blood pressure (BP) and carotid intima-media thickness. Children born to mothers who smoked in pregnancy had lower HDL cholesterol [1.32 vs. 1.50 mmol/L, 95% confidence interval (CI) for difference -0.28 to -0.08, P = 0.0005], higher triglycerides (1.36 vs. 1.20 mmol/L, 95% CI for ratio 1.01-1.30, P = 0.04) and higher systolic BP (102.1 vs. 99.9 mmHg, 95% CI for difference 0.6-3.8, P = 0.006). After adjustment for maternal passive smoking, post-natal ETS exposure, gender, breast feeding duration, physical inactivity, and adiposity, smoking in pregnancy remained significantly associated with lower HDL cholesterol (difference = -0.22 mmol/L, 95% CI -0.36 to -0.08, P = 0.003) but not with higher systolic BP. Neither smoking in pregnancy nor post-natal ETS exposure was associated with alterations of carotid artery wall thickness. Smoking in pregnancy is independently associated with significantly lower HDL cholesterol in healthy 8-year-old children.

Association between Prenatal and Postnatal Tobacco Smoke Exposure and Allergies in Young Children

Background. Many studies have shown a positive association between environmental tobacco smoke (ETS) exposure and allergic disorders, whereas epidemiological evidence of the effect of maternal smoking during pregnancy on allergic diseases is inconsistent. We investigated the independent and joint effects of in utero exposure to maternal smoking and postnatal ETS exposure at home on allergic disorders among Japanese children. Methods. Study subjects were 1951 children aged 3 years. Data on maternal smoking during pregnancy and postnatal exposure to ETS at home, allergic symptoms, and potential confounders were collected through the use of a questionnaire. Outcomes were defined according to the criteria of the International Study of Asthma and Allergies in Childhood (ISAAC). Results. The prevalence values of symptoms of wheeze, asthma, and eczema in the previous 12 months were 22.0%, 8.8%, and 17.2%, respectively. We found that postnatal ETS exposure at home in the absence of in utero exposure to maternal smoking was associated with a higher prevalence of wheeze (adjusted odds ratio (OR) = 1.30, 95% confidence interval (CI): 1.01–1.67). In contrast, in utero exposure without subsequent postnatal ETS exposure at home or exposure to postnatal ETS at home in addition to in utero exposure to maternal smoking was not associated with the prevalence of wheeze. No measurable associations were observed between fetal, postnatal, or joint exposure and the prevalence of asthma or eczema. Conclusions. Data from this study indicate that ETS at home may be associated with a higher prevalence of wheeze among young Japanese 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.