Postnatal Smoke Research Articles

Heavy Metal and Thiol/Disulfide in Children with Attention-Deficit and Hyperactivity Disorder.

In the etiology of attention-deficit and hyperactivity disorder (ADHD), oxidative stress and heavy metal exposure are still controversial topics. In this study, our goal was to examine heavy metal levels and oxidative balance in newly diagnosed patients with ADHD and reveal whether heavy metal levels have an effect on the oxidation balance. The study included 35 patients with newly diagnosed ADHD and 31 healthy control groups of similar age and gender. Participants' parents or caregivers completed a semi-structured questionnaire regarding their children's breastfeeding and prenatal and postnatal smoking exposures. The levels of heavy metals lead (Pb), mercury (Hg), and cadmium were measured with inductively coupled plasma optical emission spectroscopy, and a unique automated spectrophotometric approach was used to quantify serum total thiol, native thiol, and disulfide quantities and ratios. The rate of smoking during pregnancy was significantly higher in the ADHD group than in the control group (P = .030). Compared to the control group, the native and total thiol levels of children with ADHD were significantly higher (P < .001). Likewise, the ADHD group had significantly higher Hg levels compared to the control group (P = .002). Cadmium levels were substantially greater in the control group compared to the ADHD group (P < .001). However, there was no significant difference between Pb levels in the ADHD and the control group (P = .844). Exposure to Hg and prenatal smoking may contribute to the development of ADHD in childhood. In response to oxidative stress, the young brains of children with ADHD may enhance their antioxidant levels.

Prenatal polycyclic aromatic hydrocarbon exposure and asthma at age 8–9 years in a multi-site longitudinal study

Background and aimStudies suggest prenatal exposure to polycyclic aromatic hydrocarbons (PAHs) may influence wheezing or asthma in preschool-aged children. However, the impact of prenatal PAH exposure on asthma and wheeze in middle childhood remain unclear. We investigated these associations in socio-demographically diverse participants from the ECHO PATHWAYS multi-cohort consortium.MethodsWe included 1,081 birth parent–child dyads across five U.S. cities. Maternal urinary mono-hydroxylated PAH metabolite concentrations (OH-PAH) were measured during mid-pregnancy. Asthma at age 8–9 years and wheezing trajectory across childhood were characterized by caregiver reported asthma diagnosis and asthma/wheeze symptoms. We used logistic and multinomial regression to estimate odds ratios of asthma and childhood wheezing trajectories associated with five individual OH-PAHs, adjusting for urine specific gravity, various maternal and child characteristics, study site, prenatal and postnatal smoke exposure, and birth year and season in single metabolite and mutually adjusted models. We used multiplicative interaction terms to evaluate effect modification by child sex and explored OH-PAH mixture effects through Weighted Quantile Sum regression.ResultsThe prevalence of asthma in the study population was 10%. We found limited evidence of adverse associations between pregnancy OH-PAH concentrations and asthma or wheezing trajectories. We observed adverse associations between 1/9-hydroxyphenanthrene and asthma and persistent wheeze among girls, and evidence of inverse associations with asthma for 1-hydroxynathpthalene, which was stronger among boys, though tests for effect modification by child sex were not statistically significant.ConclusionsIn a large, multi-site cohort, we did not find strong evidence of an association between prenatal exposure to PAHs and child asthma at age 8–9 years, though some adverse associations were observed among girls.

Secondhand Smoke Exposure and Risk of Dementia in Nonsmokers: A Population-Based Cohort Study

Background: Large population-based prospective studies are necessary to provide clarification on the associations of panoramic secondhand smoking burden, including prenatal and postnatal secondhand smoke (SHS) exposure, with the risk of developing dementia. Methods: Our study comprised a sample of 353,756 dementia-free individuals from the UK Biobank who were nonsmokers had data on the exposure of maternal smoking as well as SHS exposure in daily life, which was quantified in terms of hours per week (h/week) and whether they lived with household smokers. Multivariable Cox regression models were utilized to analyze the independent and joint associations of maternal smoking and daily life SHS exposure with dementia risk. Results: During a median follow-up of 11.8 years, 4,113 participants developed dementia. Compared with those who lived in the environment without smokers, multivariable-adjusted hazard ratios (HRs) (95% CIs) were 1.11 (1.02, 1.20) and 1.31 (1.13, 1.52) for those who exposed to SHS for >0 but ≤4 h/week and >4 h/week, respectively, and was 1.25 (1.13, 1.39) for those who lived with smokers in the household. A positive history of maternal smoking was associated with a modestly higher risk of dementia (HR = 1.07; 95% CI: 1.01, 1.15). Furthermore, compared with participants with neither history of maternal smoking nor exposure to SHS, a particularly higher risk of dementia was observed among those with both exposures (HR = 1.48; 95% CI: 1.18, 1.86). Additionally, the HR (95% CI) was 1.32 (1.10, 1.59) when comparing participants with a history of maternal smoking who lived with smokers in their households with those who had neither exposures. Conclusions: Having a history of maternal smoking, longer exposure to SHS, and living with smokers in the household were each associated with an increased risk of developing dementia. Individuals who were simultaneously exposed to maternal smoking and SHS or lived with household smokers had a particularly higher dementia risk.

Early-life exposure to cigarette smoke primes lung function and DNA methylation changes at Cyp1a1 upon exposure later in life.

Prenatal and early-life exposure to cigarette smoke (CS) has repeatedly been shown to induce stable, long-term changes in DNA methylation (DNAm) in offspring. It has been hypothesized that these changes might be functionally related to the known outcomes of prenatal and early-life CS exposure, which include impaired lung development, altered lung function, and increased risk of asthma and wheeze. However, to date, few studies have examined DNAm changes induced by prenatal CS in tissues of the lung, and even fewer have attempted to examine the specific influences of prenatal versus early postnatal exposures. Here, we have established a mouse model of CS exposure which isolates the effects of prenatal and early postnatal CS exposures in early life. We have used this model to measure the effects of prenatal and/or postnatal CS exposures on lung function and immune cell infiltration as well as DNAm and expression of Cyp1a1, a candidate gene previously observed to demonstrate DNAm differences on CS exposure in humans. Our study revealed that exposure to CS prenatally and in the early postnatal period causes long-lasting differences in offspring lung function, gene expression, and lung Cyp1a1 DNAm, which wane over time but are reestablished on reexposure to CS in adulthood. This study creates a testable mouse model that can be used to investigate the effects of prenatal and early postnatal CS exposures and will contribute to the design of intervention strategies to mediate these detrimental effects.NEW & NOTEWORTHY Here, we isolated effects of prenatal from early postnatal cigarette smoke and showed that exposure to cigarette smoke early in life causes changes in offspring DNA methylation at Cyp1a1 that last through early adulthood but not into late adulthood. We also showed that smoking in adulthood reestablished these DNA methylation patterns at Cyp1a1, suggesting that a mechanism other than DNA methylation results in long-term memory associated with early-life cigarette smoke exposures at this gene.

The impact of antenatal and postnatal indoor air pollution or tobacco smoke exposure on lung function at 3 years in an African birth cohort.

Indoor air pollution (IAP) and tobacco smoke exposure (ETS) are global health concerns contributing to the burden of childhood respiratory disease. Studies assessing the effects of IAP and ETS in preschool children are limited. We assessed the impact of antenatal and postnatal IAP and ETS exposure on lung function in a South African birth cohort, the Drakenstein Child Health Study. Antenatally enrolled mother-child pairs were followed from birth. Lung function measurements (oscillometry, multiple breath washout and tidal breathing) were performed at 6 weeks and 3 years. Quantitative antenatal and postnatal IAP (particulate matter [PM10 ], volatile organic compounds [VOC]) and ETS exposures were measured. Linear regression models explored the effects of antenatal and postnatal exposures on lung function at 3 years. Five hundred eighty-four children had successful lung function testing, mean (SD) age of 37.3 (0.7) months. Exposure to antenatal PM10 was associated with a decreased lung clearance index (p < 0.01) and postnatally an increase in the difference between resistance at end expiration (ReE) and inspiration (p = 0.05) and decrease in tidal volume (p = 0.06). Exposure to antenatal VOC was associated with an increase in functional residual capacity (p = 0.04) and a decrease in time of expiration over total breath time (tE /tTOT ) (p = 0.03) and postnatally an increase in respiratory rate (p = 0.05). High ETS exposure postnatally was associated with an increase in ReE (p = 0.03). Antenatal and postnatal IAP and ETS exposures were associated with impairment in lung function at 3 years. Strengthened efforts to reduce IAP and ETS exposure are needed.

The association of maternal smoking and other sociobehavioral factors with dental caries in toddlers: A cross-sectional study.

Severe early childhood caries (S-ECC) is a form of dental caries in toddlers, which can strongly affect general health and quality of life. Studies on factors that can contribute to the development of caries immediately after tooth eruption are sparse. The aim of this study was to assess the role of sociobehavioural factors and pre- and postnatal exposure to tobacco smoke in the aetiology of dental caries in children up to 3 years old. A cross-sectional study was conducted between 2011 and 2017 to assess oral health and teething in urban children 0-4 years of age. The number of teeth and surfaces with white spot lesions (d1,2), as well as decayed (d), missing (m), and filled (f) teeth classified according to ICDAS II was evaluated in a dental office setting. d1,2dmft and d1,2dmfs were calculated. Severe early childhood caries was diagnosed for d1,2dmfs > 0. Parents completed a self-administered questionnaire on socioeconomic factors, maternal health, course of pregnancy, child's perinatal parameters, hygiene and dietary practices, as well as maternal smoking during and after pregnancy. Data on children aged 12-36 months were collected and analysed statistically using the t-test, Spearman rank correlations and Poisson regression. Significance level was set at 0.05. Dental caries was found in 46% of 496 children aged 12-36 months. Mean d1,2dmft and d1,2dmfs were 2.62 ± 3.88 and 4.46 ± 8.42, respectively. Tobacco smoking during and after pregnancy was reported by 8.9% and 24.8% of women, respectively. Spearman's rank correlation analysis confirmed a relationship between S-ECC and parental education, maternal smoking, bottle feeding, avoiding springy foods, number of meals, and the age of tooth brushing initiation. Pre- and postnatal exposure to tobacco smoke increased the risk of S-ECC especially in children in age 19-24 months. Maternal smoking was correlated with the level of education and dietary practices. Our study confirmed that prenatal smoking is associated with increased risk of severe-early childhood caries (S-ECC) while the association with post-natal smoking is also evident, the increase in risk is not statistically clear. Both maternal smoking and the child's tooth decay are associated with poor parental education and other improper oral health behaviours. The positive impact of quitting smoking on the oral health in children should be part of anti-smoking advice.

Sex differences in the association between smoking exposure and prevalence of wheeze and asthma in 3-year-old children

Objective We examined independent and joint associations between prenatal and postnatal smoking exposure and the prevalence of wheeze and asthma among 3-year-old Japanese children. Sex differences were also investigated. Methods Smoking exposure, allergic symptoms, and potential confounding factor data were collected using a self-administered questionnaire. Wheeze was defined on the basis of the International Study of Asthma and Allergies in Childhood criteria. Physician-diagnosed asthma was considered to be present if a physician had diagnosed the child with asthma any time before the survey was administered. Results There were 6402 pediatric participants in this study. Maternal smoking throughout pregnancy and household smoking exposure during the first year of life were associated with an increased prevalence of wheeze among girls but not boys (adjusted odds ratio (OR) [95% CI] = 2.00 [1.13–3.42] and 1.34 [1.07–1.68], respectively). Girls exposed to both prenatal maternal smoking and postnatal household smoking exposure had a significantly higher prevalence of wheeze and physician-diagnosed asthma compared with girls without these exposures (adjusted OR [95% CI] = 2.06 [1.39–3.01] and 1.86 [1.01–3.26], respectively). No association was observed between perinatal smoking exposure and the prevalence of wheeze or asthma among boys. Significant interactions between sex and smoking exposure affecting wheeze and asthma were also found (p for interaction = 0.0003 and 0.01, respectively). Conclusion We found a positive association between perinatal smoking exposure and the prevalence of wheeze and asthma only among girls. Effects of perinatal smoking exposure on wheeze and asthma might be sex specific. Further research is required.

Pre- and postnatal exposure to secondhand tobacco smoke and body composition at 12 years: periods of susceptibility.

ObjectiveThe study aimed to identify periods of heightened susceptibility to the effects of pre‐ and postnatal secondhand tobacco smoke (SHS) exposure on body composition at age 12 years.MethodsThe study used data from 217 children from the Health Outcomes and Measures of the Environment (HOME) Study, a prospective cohort in Cincinnati, Ohio. Using multiple informant models, the study estimated associations of maternal serum cotinine (16 and 26 weeks of pregnancy) and child serum cotinine concentrations (at age 12, 24, 36, and 48 months) with measures of body composition obtained with anthropometry and dual‐energy x‐ray absorptiometry at 12 years. We examined whether there were differences between these associations for pre‐ and postnatal exposure periods and potential effect measure modification by sex.ResultsPostnatal cotinine concentrations were associated with higher weight, BMI, body fat and lean mass, waist circumference, and visceral, android, and gynoid fat. Each 10‐fold increase in postnatal cotinine was associated with 76% increased risk of overweight or obesity (95% CI: 1.13‐2.75). Associations between prenatal concentrations and measures of body composition at 12 years were generally null.ConclusionsPostnatal exposure to SHS may increase adolescent adiposity and lean mass. Future studies should determine whether early‐life exposures to SHS are associated with other cardiometabolic risk markers.

Association between prenatal or postpartum exposure to tobacco smoking and allergic rhinitis in the offspring: An updated meta-analysis of nine cohort studies.

INTRODUCTIONPrevious studies have suggested an association between tobacco smoke exposure and allergic rhinitis. This study aimed to investigate if prenatal or postpartum smoke exposure will increase the risk of allergic rhinitis in offspring.METHODSPubMed, EMBASE, and the Cochrane library were searched from inception to July 2020 for eligible studies investigating the association between smoking exposure and allergic rhinitis. The random-effects model was adopted for the meta-analysis to obtain the summary odds ratio (OR) with a 95% confidence interval (CI). Subgroup analysis based on the age of children was performed. Sensitivity analysis was carried out to check the robustness of the results. Publication bias of included studies was assessed.RESULTSThis meta-analysis included nine studies, in which six studies suggested that children exposed to prenatal smoking were more likely to develop allergic rhinitis compared with children who were never exposed (OR=1.12; 95% CI: 1.04–1.21). The subgroup analysis divided children those aged <10 years (OR=1.15; 95% CI: 1.06–1.25) and those aged >10 years (OR=0.99; 95% CI: 0.82–1.20). This meta-analysis revealed a positive relationship between postpartum smoke exposure and the development of allergic rhinitis in offspring (OR=1.19; 95% CI: 1.03–1.39) with marked heterogeneity. The subgroup analysis of age in the postnatal group showed similar results in children aged >10 years (OR=1.17; 95% CI: 1.05–1.30) and children aged <10 years (OR=1.21; 95% CI: 0.91–1.60).CONCLUSIONSThis meta-analysis observed an association between parental smoking exposure and allergic rhinitis in offspring. Our findings indicated that both prenatal and postnatal smoke exposure might be risk factors for allergic rhinitis in the offspring.

Prenatal and Postnatal Cigarette Smoke Exposure Is Associated With Increased Risk of Exacerbated Allergic Airway Immune Responses: A Preclinical Mouse Model

Increased exposure to household air pollution and ambient air pollution has become one of the world’s major environmental health threats. In developing and developed countries, environmental cigarette smoke (CS) exposure is one of the main sources of household air pollution (HAP). Moreover, results from different epidemiological and experimental studies indicate that there is a strong association between HAP, specifically CS exposure, and the development of allergic diseases that often persists into later life. Here, we investigated the impact of prenatal and postnatal CS exposure on offspring susceptibility to the development of allergic airway responses by using a preclinical mouse model. Pregnant BALB/c mice were exposed to either CS or air during pregnancy and lactation and in order to induce allergic asthma the offspring were sensitized and challenged with house dust mite (HDM). Decreased lung function parameters, like dynamic compliance and pleural pressure, were observed in PBS-treated offspring born to CS-exposed mothers compared to offspring from air-exposed mothers. Maternal CS exposure significantly increased the HDM-induced airway eosinophilia and neutrophilia in the offspring. Prenatal and postnatal CS exposure increased the frequency of Th2 cells in the lungs of HDM-treated offspring compared to offspring born to air-exposed mothers. Offspring born to CS-exposed mothers showed increased levels of IL-4, IL-5 and IL-13 in bronchoalveolar lavage fluid compared to offspring from air-exposed mothers. Ex-vivo restimulation of lung cells isolated from HDM-treated offspring born to CS-exposed mothers also resulted in increased IL-4 production. Finally, serum immunoglobulins levels of HDM-specific IgE and HDM-specific IgG1 were significantly increased upon a HDM challenge in offspring born to CS-exposed mothers compared to offspring from air-exposed mothers. In summary, our results reveal a biological plausibility for the epidemiological studies indicating that prenatal and postnatal CS exposure increases the susceptibility of offspring to allergic immune responses.

The Associations of Caesarean Delivery With Risk of Wheezing Diseases and Changes of T Cells in Children.

ObjectivesThis study aimed to assess the associations of caesarean delivery (CD) with risk of wheezing diseases and changes of immune cells in children.DesignThe cross-sectional study was conducted between May, 2020 and April, 2021.Setting and participantsThe study was conducted in Shanghai Children’s Medical Center, Shanghai, China. A total of 2079 children with a mean age of 36.97 ± 40.27 months and their guardians were included in the present study via face-to-face inquiry and physical examination by clinicians.MethodsLogistic regression was applied to estimate odds ratio (ORs) and 95% confidence intervals (CIs) for the association between CD and first episode of wheezing (FEW) or asthma. Models were adjusted for premature or full-term delivery, exclusive breastfeeding (at least 4 months) or not.ResultsAmong the 2079 children, 987 children (47.47%) were born by CD and 1092 (52.53%) by vaginal delivery (VD). Children delivered by caesarean had significantly lower gestational age (P<0.01) compared with those who delivered vaginally. Our results also showed that CD was related to increased risk of FEW by the age of 3(adjusted OR 1.50, 95%CI 1.06, 2.12) and increased tendency to develop asthma by the age of 4 (adjusted OR 3.16, 95%CI 1.25, 9.01). The subgroup analysis revealed that the negative effects of CD on asthma were more obvious in children without exclusive breastfeeding (adjusted OR 4.93, 95%CI 1.53, 21.96) or without postnatal smoking exposure (adjusted OR 3.58, 95%CI 1.20, 13.13). Furthermore, compared with children born through VD, a significant change of the T cells (increased proportion of CD4+ T cells and decreased number and proportion of CD8+ T cells) were observed before the age of one in the CD group. However, the changes were insignificant in children over 1 year old.ConclusionsThis study showed age-dependent associations of CD with asthma and FEW in offspring. Moreover, CD appeared to have an effect on the cellular immunity in infants, the disorder of which may contribute to the development of asthma in children.

Association of prenatal maternal, prenatal secondhand, and postnatal secondhand smoking exposures with the incidence of asthma/atopic dermatitis in children: An epidemiological study using checkup data of mothers and children in Kobe city

Objectives Despite suggested associations among smoking exposures and the prevalence of allergic diseases in children, studies examining the effect of prenatal maternal smoking and secondhand smoking on the occurrence of these diseases in children are limited. Our study aimed to investigate the association between prenatal maternal smoking as well as secondhand smoking and the incidence of asthma or atopic dermatitis in children.Methods We included checkup data of a total of 53,505 children living in Kobe, Japan, without missing values for exposure or outcome, between April 1, 2004, and March 31, 2013. The exposure variables were prenatal maternal smoking, prenatal secondhand smoking, and postnatal secondhand smoking till 4 months, which were assessed by maternal notification form and exclusively classified into eight categories. The outcome variables were the incidence of asthma or atopic dermatitis in the respective children up to 3 years of age assessed by a checkup questionnaire. The association between the smoking exposures and the development of asthma or atopic dermatitis up to 3 years was examined using a generalized linear mixed model with odds ratios and 95% confidence intervals (CI). Additionally, multiple imputation methods were used for the missing covariates.Results Of the 53,505 children, 27,210 (50.9%) were males and 26,218 (49.0%) were females. In total, 5,810 (10.9%) children were diagnosed with asthma and 4,964 (9.3%) with atopic dermatitis up to 3 years of their age. Compared to the children born to nonsmoking mothers during pregnancy and those without exposure to postnatal secondhand smoking, the adjusted odds ratio for the incidence of asthma up to 3 years of their age was found to be 2.04 (95% CI: 1.38-3.01) in children exposed to prenatal maternal smoking. Similarly, the adjusted odds ratio for the incidence of asthma in children exposed to maternal secondhand smoking during pregnancy was 1.12 (95% CI: 1.01-1.25) when compared with children who were never exposed to any smoking. Additionally, the adjusted odds ratio increased to 1.86 (95% CI: 1.42-2.44) in children exposed to both prenatal maternal smoking and secondhand smoking. In contrast, no statistical significance was observed among the smoking exposures and the incidence of atopic dermatitis in the children.Conclusions Our study confirmed that prenatal maternal and secondhand smoking were associated with the incidence of asthma in children. These findings suggest a need to focus on smoking cessation by pregnant women as well as by family members living together to prevent the development of asthma in children.

The Ethics of e-Cigarettes for Smoking Cessation: A Global Challenge

"Tobacco smoking is especially harmful for women because, in addition to its effects on mortality and morbidity, it negatively impacts pregnancy, reproductive, and health of the offspring. Data from our work in Romania revealed that pregnant tobacco smokers are seeking information and clinical advice related to e-cigarette use as a tobacco cessation approach. E-cigarette use increased rapidly in the recent years in the US and in other countries, including LMICs. The tobacco control field is deeply divided on how to respond to the increase in e-cigarette use. Additional evidence on the ethical issues related to e-cigarette use and tobacco cessation will inform our mHealth and other pregnancy tobacco cessation interventions and will guide future tobacco control policy direction. The objective of this study is to identify ethical concerns and associated attitudes and perceptions related to e-cigarette use for tobacco cessation during pregnancy among pregnant smokers, their life partners, medical professionals, and other stakeholders. We will interview (N=20) and conduct two focus groups with women who smoke (one focus group, N=10) and women who quit during pregnancy (one focus group, N=10); interview life partners (N=10) of such women; interview ObGyn physicians (N=10) and nurses (N=10); and interview (N=10) and conduct one focus group (N=10) with perinatal educators. Other relevant stakeholders will be also interviewed including the leadership of 2035 Tobacco Free Romania, the national Stop Smoking program, the Pure Air consortium, the Romanian Pneumology Society, the SAMAS NGO focused on maternal and child health and rights, and others. With respect to expected outcomes, the proposed application is anticipated to advance understanding of the smokers’ and other stakeholders’ ethical concerns and associated attitudes and perceptions related to e-cigarettes use for tobacco smoking cessation. The in-depth new knowledge will have a positive impact on the cessation of prenatal and postnatal tobacco smoking and will inform future tobacco control policy directions. Results will be available and will be presented at the time of the conference. This work is based on research partly funded through six NIH-funded projects (grant no. K01TW009654, R21TW010896, 5R21TW010896-02S1, 5R21TW010896-02S2, 1R21HD103039-0, 1R25TW010518-01A1). "

Household food insecurity and in-utero and early life smoke exposure: Data from NHANES 2003–2016

In-utero, postnatal, and childhood smoke exposure are associated with adverse health consequences, and examining factors related to smoke exposure during these vulnerable periods are critical to inform efforts that promote maternal and child health. This study included pregnant and postpartum women aged 20–44 years and children aged 3–12 years from National Health and Nutrition and Examination Survey (NHANES) 2003–2016 cycles. Logistic regression examined association of household food insecurity with firsthand (FHS) and secondhand (SHS) exposure among pregnant and postpartum women, and SHS exposure among children, based on serum cotinine and respondent-reports. Very low household food security was significantly associated with increased odds of cotinine-based FHS exposure among pregnant (OR(95%CI) = 5.19 (1.75, 15.39)) and postpartum women (OR(95%CI) = 4.75(1.66, 13.57)). Non-smoking, postpartum women from very low food secure households also had significantly greater odds of cotinine-based SHS exposure (OR(95%CI) = 7.40 (2.08, 26.37)) than those from food secure households. Using respondent-reported smoking status, low food security in pregnant and postpartum women was significantly related to increased odds of FHS exposure (OR(95% CI) = 3.75(1.52, 9.23)). Further, children from marginal, low and very low food secure households had significantly higher odds of SHS exposure compared to those from food secure households. Results imply the co-occurrence food insecurity and in-utero and early life smoke exposure.

Effect of prenatal and postnatal exposure to tobacco in the development of acute bronchiolitis in the first two years of life

IntroductionEnvironmental exposure to tobacco increases the risk of respiratory disease in infants. However, the impact of maternal smoking on the development of acute bronchiolitis has hardly been assessed. The aim of this study was to determine the incidence of acute bronchiolitis and to analyse the effect of prenatal and postnatal maternal smoking on the development of this disease. Patients and methodsA prospective, observational study was performed on healthy newborns from a third level hospital born between October 2015 and February 2016. Questionnaires were completed by the mothers at discharge from maternity and followed-up for two years. These collected information about prenatal and postnatal smoking, lifestyle, family and personal history, and the development of bronchiolitis. A bivariate and multivariate logistic regression analysis was performed. ResultsA total of 223 newborns were included, of whom 13.9% were exposed to tobacco smoking during gestation, 21.4% in the postnatal period, and 12.4% in both times. The incidence of bronchiolitis was 28.7% at one year of life, and 34.5% at two years. The multivariate analysis demonstrated that the prenatal and postnatal exposure to tobacco is an independent risk factor for the development of bronchiolitis (OR 4.38; 95% CI; 1.63–11.76), while prolonged breastfeeding is a protective factor (OR 0.13; 95% CI; 0.04–0.48). Other factors that were statistically significant were: atopic dermatitis (OR 2.91; 95% CI; 1.26–6.73), and gestational age (OR 1.42; 95% CI; 1.08–1.88). ConclusionsChildren exposed to prenatal and postnatal maternal smoking have a higher risk of suffering bronchiolitis. Reducing the smoking habit in women that intend to become pregnant must be a priority in preventive medicine.

Evaluation of the relationship between antenatal and postnatal tobacco smoke exposure and childhood cancers.

e22011 Background: The incidence of childhood cancers increased by 1 % per year over the last three decades. Life style changes and increased variety of environmental exposures are accused of this trend. One of these environmental factors is cigarette smoking and parental smoking is the main source of tobacco smoke exposure of children. There are strong reasons for considering parental smoking behaviour as a risk factor for childhood cancers. Many tobacco related compounds are detected in fetal tissues, breast milk and tissues of children of smoking parents. However, it is hard to make causal relationship between parental smoking and childhood cancers. One of the reasons is the difficulty to detect tobacco smoke exposure. Questionnaires, commonly used method to detect tobacco smoke exposure, are prone to biases. Cotinine is the main metabolite of nicotine which is the abundant organic compound in tobacco and a good biomarker to detect tobacco smoke exposure. Methods: 104 newly diagnosed, 0-18 years aged pediatric cancer patients from two pediatric oncology centers ( Ankara University Children’s Hospital and Ankara City Hospital) and 99 healthy children aged 0-18 applied to the Ankara University Children’s Hospital participated our study. Parental smoking behaviours (preconceptional, during pregnancy and current smoking) and environmental tobacco smoke exposures (ETS) of children were compared between two groups. ETS exposures of cancer patients and healthy children were evaluated by hair cotinine ELISA analysis and questionnaire. For hair cotinine analysis, 30 mg of hair samples were taken from occipital part of scalp by a stainless scissors. Samples were processed according to manufacturer's instructions. Parents of two groups were surveyed about their smoking behaviours and ETS exposures of their children. Results: We found no differences between two groups by means of maternal preconceptional smoking, smoking during pregnancy and current smoking behaviours. Paternal preconceptional smoking and smoking during pregnancy rates were significantly low in cancer patients (p &lt; 0,05) according to questionnaire. Environmental tobacco smoke exposures were found statistically low in cancer patients according to questionnaire (p &lt; 0,05). However, quantitative exposure assessment by hair cotinine analysis revealed that cancer patients are exposed to tobacco smoke more than healthy children (p &lt; 0,001). Conclusions: Our findings support that smoking could be a risk factor for childhood cancers. This study also revealed that questionnaires could cause biases. We thought, social desirability bias of father of cancer patients could be a reason of their low smoking rates according to questionnaire. We suggest that cotinine analysis along with validated questionnaires can be used to prevent biases in studies of tobacco smoke in the etiology of childhood cancers.

Pre and postnatal exposure to mercury and respiratory health in preschool children from the Spanish INMA Birth Cohort Study

Effects of mercury on maturing immune system have been reported, however the association with respiratory and allergy problems during infancy remains unclear. The aim of this study is to evaluate the association between pre and postnatal mercury exposure and respiratory and allergy problems among preschool children and to examine the role of potential modifying factors. Study subjects were children participant in Spanish Childhood and Environment Project (INMA, 2003–2008). We measured total mercury levels in cord blood (n = 1868) and hair at 4 years of age (n = 1347). Respiratory outcomes (wheezing, severe wheezing, chestiness, persistent cough, eczema and otitis) were obtained by questionnaires administered to parents. Associations were investigated by logistic regression adjusted for socio-demographic and lifestyle-related variables in each cohort and subsequent meta-analysis. We tested effect modification by factors related to individual susceptibility, diet and co-exposure with other pollutants. The geometric mean of cord blood and hair total mercury was 8.20 μg/L and 0.97 μg/g, respectively. No statistically significant association between pre or postnatal mercury exposure and respiratory and allergy outcomes was found. Notwithstanding, lower maternal intake of fruits and vegetables increased the risk of some respiratory outcomes due to the prenatal exposure to mercury (pint < 0.05). Moreover, an inverse association between prenatal mercury exposure and some respiratory outcomes was observed among children with higher maternal exposure to organocholorine compounds or smoking (pint < 0.05). Also, sex and postnatal smoking exposure modulated mercury postnatal effects on persistent cough (pint < 0.05). In conclusion, no association between pre and postnatal mercury exposure and respiratory and allergy problems among the whole population at study was found. However, diet and other toxicants could modulate this relation, especially during prenatal period. More research on this topic is warranted due to the limited evidence.

Pre- and postnatal maternal smoking and offspring smoking trajectories: Evidence from a 20-year birth cohort

Maternal smoking is associated with increased risk of smoking in the offspring. However, it remains unclear whether this association depends on the timing of exposure to maternal smoking. We investigated the association between prenatal and/or postnatal maternal smoking and offspring smoking during adolescence. Participants (N = 1661) were from the Québec Longitudinal Study of Child Development cohort. We identified longitudinal trajectories of maternal smoking from before pregnancy to child age 12 years using group-based trajectory modeling (GBTM). Adolescent (12–19 years) smoking trajectories were also identified using GBTM. Associations between maternal smoking and offspring smoking trajectories were estimated using multinomial logistic regressions. We used propensity score inverse probability weighting (IPW) to account for the differential distribution of maternal and familial characteristics across exposure groups. We identified four distinct groups for maternal smoking: no (66.1%), decreasing (5.6%), increasing (9.5%) and persistent (18.8%) smoking, and three adolescent smoking trajectories: abstinent, early-onset (before age 15) and late-onset (after age 15). In IPW-adjusted models, youth with mothers with decreasing, increasing and persistent smoking had higher risk of being early-onset smokers compared with youth with mothers in the non-smoking group. We also found that only youth whose mothers were persistent smokers had an increased risk of late-onset smoking. Regardless of timing, offspring exposure to maternal smoking is associated with increased risk of smoking during adolescence. More research is needed on how to create effective smoking cessation campaigns that span preconception, prenatal, and postnatal periods to help prevent intergenerational transmission of smoking behaviors.

Suicidal ideation and attempt in adolescents exposed to maternal smoking across pregnancy and childhood: A 20-year prospective cohort study

BackgroundFew studies investigated the association between maternal smoking during pregnancy and offspring suicide risk, none considering postnatal smoking exposure. We investigated associations between maternal smoking patterns during the pre- and postnatal periods and adolescent suicidal ideation and attempt. MethodsWe identified longitudinal patterns of maternal smoking from the prenatal period to the end of childhood (children's age 12 years, 10 assessments) among participants in the Québec Longitudinal Study of Child Development (N = 1623). We estimated associations between maternal smoking patterns and offspring self-reported suicidal ideation and attempt (ages 13–20). Background confounding factors (e.g., socioeconomic, familial, mental health) were controlled using propensity score inverse-probability weighting (IPW). ResultsParticipants reporting suicidal ideation and attempt were 9.3% and 8.4%, respectively. We identified four maternal smoking patterns: non-smoking (66.5%), increasing (5.5%), decreasing (9.3%), persistent (18.5%). Children exposed to persistent (OR=2.92, CI=1.99–4.30) and increasing (OR=2.06, CI=1.13–3.74) maternal smoking were more likely to attempt suicide, compared to non-exposed children. Accounting for confounding factors using IPW fully explained the association between increasing smoking and suicide attempt (OR=0.95, CI=0.39–2.09) but only reduced the association between persistent exposure and suicide attempt (OR=2.30, CI=1.04–4.99). No increased suicide attempt risk was found for children of mothers with a decreased smoking pattern. We found no associations for suicidal ideation. LimitationsPropensity score cannot account for unmeasured confounding factors; attrition limits generalizability. ConclusionsOffspring of mothers who smoked persistently and heavily prenatally and postnatally were at increased risk of suicide attempt in adolescence. Future studies should elucidate biological and psychosocial mechanisms potentially at play in these associations.

Postnatal Smoke Exposure Further Increases the Hepatic Nicotine Metabolism in Prenatally Smoke Exposed Male Offspring and Is Linked with Aberrant Cyp2a5 Methylation.

Prenatal smoke exposure (PreSE) is a risk factor for nicotine dependence, which is further enhanced by postnatal smoke exposure (PostSE). One susceptibility gene to nicotine dependence is Cytochrome P450 (CYP) 2A6, an enzyme responsible for the conversion of nicotine to cotinine in the liver. Higher CYP2A6 activity is associated with nicotine dependence and could be regulated through DNA methylation. In this study we investigated whether PostSE further impaired PreSE-induced effects on nicotine metabolism, along with Cyp2a5, orthologue of CYP2A6, mRNA expression and DNA methylation. Using a mouse model where prenatally smoke-exposed adult offspring were exposed to cigarette smoke for 3 months, enzyme activity, mRNA levels, and promoter methylation of hepatic Cyp2a5 were evaluated. We found that in male offspring, PostSE increased PreSE-induced cotinine levels and Cyp2a5 mRNA expression. In addition, both PostSE and PreSE changed Cyp2a5 DNA methylation in male groups. PreSE however decreased cotinine levels whereas it had no effect on Cyp2a5 mRNA expression or methylation. These adverse outcomes of PreSE and PostSE were most prominent in males. When considered in the context of the human health aspects, the combined effect of prenatal and adolescent smoke exposure could lead to an accelerated risk for nicotine dependence later in life.