Exposure to tobacco smoke and childhood rhinitis: a population-based study.
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ABSTRACT:
SUBMITTER: Yao TC
PROVIDER: S-EPMC5311963 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Tobacco exposure has been linked with sinonasal pathology and may be associated with allergic sensitization. This study evaluates the association between exposure to active smoking or secondhand smoke (SHS) and the prevalence of rhinitis and allergic sensitization in the US adult population.Cross-sectional study in 4,339 adults aged 20-85 in the National Health and Nutrition Examination Survey, 2005-2006. Never smoking was defined as reported lifetime smoking less than 100 cigarettes and serum cotinine levels <10ng/ml, while active smoking was defined as self-reported smoking or serum cotinine concentrations > 10 ng/mL. Self-reported rhinitis was based on symptoms during the past 12 months, and allergen sensitization was defined as a positive response to any of the 19 specific IgE antigens tested.Almost half of the population (43%) had detectable levels of IgE specific to at least one inhaled allergen and 32% reported a history of rhinitis. After multivariate adjustment, there was a statistically significant association between the highest serum cotinine tertile and rhinitis in active smokers (OR 1.42; 95%CI 1.00-2.00). The association between active smoking and rhinitis was stronger in individuals without allergic sensitization (OR 2.47; 95%CI 1.44-4.23). There was a statistically significant association between increasing cotinine tertiles and decreased odds of inhaled allergen sensitization (p-trend <.01).Tobacco smoke exposure was associated with increased prevalence of rhinitis symptoms, but not with allergic sensitization. The results indicate that the relationship between tobacco smoke exposure and sinonasal pathology in adults may be independent of allergic sensitization.
| S-EPMC4501790 | biostudies-other
Project description:BackgroundSmoking while pregnant is associated with a myriad of negative health outcomes in the child. Some of the detrimental effects may be due to epigenetic modifications, although few studies have investigated this hypothesis in detail.ObjectivesTo characterize site-specific epigenetic modifications conferred by prenatal smoking exposure within asthmatic children.MethodsUsing Illumina HumanMethylation27 microarrays, we estimated the degree of methylation at 27,578 distinct DNA sequences located primarily in gene promoters using whole blood DNA samples from the Childhood Asthma Management Program (CAMP) subset of Asthma BRIDGE childhood asthmatics (n?=?527) ages 5-12 with prenatal smoking exposure data available. Using beta-regression, we screened loci for differential methylation related to prenatal smoke exposure, adjusting for gender, age and clinical site, and accounting for multiple comparisons by FDR.ResultsOf 27,578 loci evaluated, 22,131 (80%) passed quality control assessment and were analyzed. Sixty-five children (12%) had a history of prenatal smoke exposure. At an FDR of 0.05, we identified 19 CpG loci significantly associated with prenatal smoke, of which two replicated in two independent populations. Exposure was associated with a 2% increase in mean CpG methylation in FRMD4A (p?=?0.01) and Cllorf52 (p?=?0.001) compared to no exposure. Four additional genes, XPNPEP1, PPEF2, SMPD3 and CRYGN, were nominally associated in at least one replication group.ConclusionsThese data suggest that prenatal exposure to tobacco smoke is associated with reproducible epigenetic changes that persist well into childhood. However, the biological significance of these altered loci remains unknown.
| S-EPMC4070909 | biostudies-literature
Project description:ObjectivesThis study provides secondhand smoke (SHS) exposure data in utero and after birth when children were at 18 months, 36 months and 66 months old, and it identifies risk factors for the early childhood SHS among 18-month-old infants living in smoker and non-smoker households.Study designThe data come from the Taiwan Birth Cohort Study, a longitudinal survey of a birth cohort born in 2005. This study used the survey wave when children were 18 months old (n=18?845) for statistical analysis of early childhood SHS exposure. Logistic regression was used to identify the risk factors of the SHS exposure.ResultsApproximately 62% of the 18-month-old infants lived in a household with at least one smoker, with the father being the smoker in 84% of those households. Among these infants living in a smoker household, 70% were exposed to SHS and 36% were exposed to heavy SHS in utero, and the prevalence was approximately 66% and 17% after birth for SHS and heavy SHS, respectively. The number and the existence of smokers in the household, parents' smoking status, father's educational attainment and being a first-born baby are strong predictors of early childhood heavy SHS exposure.ConclusionsEncouraging families to have a smoke-free home environment, empowering women to ensure their perspectives and rights are embedded into tobacco control efforts and educating families about the health risks from childhood SHS exposure, especially among people living in households with smokers, will protect non-smoking adults and children from SHS exposure.
| S-EPMC5734351 | biostudies-literature
Project description: Not available
| S-EPMC3969577 | biostudies-literature
Project description:BackgroundEpigenetic modifications, including DNA methylation, act as one potential mechanism underlying the detrimental effects associated with prenatal tobacco smoke (PTS) exposure. Methylation in a gene called AXL was previously reported to differ in response to PTS.MethodsWe investigated the association between PTS and epigenetic changes in AXL and how this was related to childhood asthma phenotypes. We tested the association between PTS and DNA methylation at multiple CpG loci of AXL at birth using Pyrosequencing in two separate study populations, the Children's Health Study (CHS, n = 799) and the Newborn Epigenetic Study (NEST, n = 592). Plasma cotinine concentration was used to validate findings with self-reported smoking status. The inter-relationships among AXL mRNA and miR-199a1 expression, PTS, and AXL methylation were examined. Lastly, we evaluated the joint effects of AXL methylation and PTS on the risk of asthma and related symptoms at age 10 years old.ResultsPTS was associated with higher methylation level in the AXL gene body in both CHS and NEST subjects. In the pooled analysis, exposed subjects had a 0.51% higher methylation level in this region compared to unexposed subjects (95% CI 0.29, 0.74; p < 0.0001). PTS was also associated with 21.2% lower expression of miR-199a1 (95% CI - 37.9, - 0.1; p = 0.05), a microRNA known to regulate AXL expression. Furthermore, the combination of higher AXL methylation and PTS exposure at birth increased the risk of recent episodes of bronchitic symptoms in childhood.ConclusionsPTS was associated with methylation level of AXL and the combination altered the risk of childhood bronchitic symptoms.
| S-EPMC6054742 | biostudies-literature
Project description:BackgroundThirdhand smoke (THS) is the persistent residue resulting from secondhand smoke (SHS) that accumulates in dust, objects, and on surfaces in homes where tobacco has been used, and is reemitted into air. Very little is known about the extent to which THS contributes to children's overall tobacco smoke exposure (OTS) levels, defined as their combined THS and SHS exposure. Even less is known about the effect of OTS and THS on children's health. This project will examine how different home smoking behaviors contribute to THS and OTS and if levels of THS are associated with respiratory illnesses in nonsmoking children.MethodsThis project leverages the experimental design from an ongoing pediatric emergency department-based tobacco cessation trial of caregivers who smoke and their children (NIHR01HD083354). At baseline and follow-up, we will collect urine and handwipe samples from children and samples of dust and air from the homes of smokers who smoke indoors, have smoking bans or who have quit smoking. These samples will be analyzed to examine to what extent THS pollution at home contributes to OTS exposure over and above SHS and to what extent THS continues to persist and contribute to OTS in homes of smokers who have quit or have smoking bans. Targeted and nontargeted chemical analyses of home dust samples will explore which types of THS pollutants are present in homes. Electronic medical record review will examine if THS and OTS levels are associated with child respiratory illness. Additionally, a repository of child and environmental samples will be created.DiscussionThe results of this study will be crucial to help close gaps in our understanding of the types, quantity, and clinical effects of OTS, THS exposure, and THS pollutants in a unique sample of tobacco smoke-exposed ill children and their homes. The potential impact of these findings is substantial, as currently the level of risk in OTS attributable to THS is unknown. This research has the potential to change how we protect children from OTS, by recognizing that SHS and THS exposure needs to be addressed separately and jointly as sources of pollution and exposure.Trial registrationClinicalTrials.gov Identifier: NCT02531594 . Date of registration: August 24, 2015.
| S-EPMC6498613 | biostudies-literature
Project description:BackgroundChildhood exposure to environmental tobacco smoke has been extensively associated with childhood respiratory illness; fewer studies have addressed the effects on adults.MethodsChildhood environmental tobacco smoke exposure in relation to chronic cough, phlegm, and asthma diagnosis was studied in never smokers from a cohort of Singaporeans of Chinese ethnicity aged 45-74 years at enrollment from 1993 to 1998. From 1999 to 2004 subjects were interviewed regarding environmental tobacco smoke exposure before and after the age of 18 and the presence and duration of current symptoms of chronic cough and phlegm production and asthma diagnosis.ResultsAmong 35,000 never smokers, fewer had smoking mothers (19%) than fathers (48%). Although few subjects currently lived (20%) or worked (4%) with smokers, 65% reported living with a daily smoker before the age of 18 years. Living with a smoker before the age of 18 increased the odds of chronic dry cough (149 cases, odds ratio 2.1, 95% CI 1.4 to 3.3) and, to a lesser extent, phlegm, after adjustment for age, sex, dialect group, and current and past exposure to smokers at home and at work after the age of 18. Associations strengthened with higher numbers of smokers in childhood. There was no association with asthma or chronic bronchitis. There was evidence to suggest a stronger association among subjects with a lower adult intake of fibre which has previously been found to be protective for respiratory symptoms.ConclusionsIn this large study of non-smokers, living with a smoker in childhood was associated with chronic dry cough and phlegm in adulthood, independent of later exposures to environmental tobacco smoke.
| S-EPMC1414787 | biostudies-literature
Project description:ObjectiveAssociations between single-nucleotide polymorphisms in the beta2-adrenergic receptor gene and asthma and wheeze have been inconsistent. Recent studies indicated that tobacco smoke affects beta2-adrenergic receptor gene expression and associations of beta2-adrenergic receptor gene variants with asthma in adults. We aimed to investigate the joint effects of in utero and childhood secondhand tobacco smoke exposure and 2 well-characterized functional single-nucleotide polymorphisms (Arg16Gly and Glu27Gln) of beta2-adrenergic receptor gene on asthma and wheezing in 3128 non-Hispanic and Hispanic white children of the Children's Health Study.MethodsWe fitted logistic regression models to estimate odds ratios and 95% confidence intervals for the independent and joint effects of these single-nucleotide polymorphisms and in utero and secondhand tobacco smoke exposure on asthma and wheeze outcomes.ResultsExposures to in utero maternal smoking and secondhand tobacco smoke were associated with wheezing. Children who were homozygous for the Arg16 allele and were exposed to maternal smoking in utero were at a threefold increased risk for lifetime wheeze compared with children who were unexposed and had at least 1 Gly16 allele. We found similar joint effects of secondhand tobacco smoke and Arg16Gly with wheezing. The risk for lifetime, current, and nocturnal wheeze increased with the number of smokers at home among Arg16 homozygous children. The results were consistent in 2 cohorts of children recruited in 1993 and 1996. Diplotype-based analyses were consistent with the single-nucleotide polymorphism-specific results. No associations were found for Glu27Gln.ConclusionsBoth in utero and childhood exposure to tobacco smoke were associated with an increased risk for wheeze in children, and the risks were greater for children with the Arg16Arg genotype or 2 copies of the Arg16-Gln27 diplotype. Exposures to smoking need to be taken into account when evaluating the effects of beta2-adrenergic receptor gene variants on respiratory health outcomes.
| S-EPMC2748980 | biostudies-literature
Project description:Background:Increasing prevalence of childhood allergic diseases including asthma is a global health concern, and we aimed to investigate prenatal risk factors for childhood asthma and to address the potential shared prenatal impacts among childhood asthma, allergic rhinitis (AR) and atopic dermatitis (AD). Methods:We used two claim databases, including Taiwan Birth Cohort Study (TBCS) and National Health Insurance Research Database (NHIRD), to identify independent paired mother-child data (mother-child dyads) between 2006 and 2009. The association between prenatal factors and asthma was determined by calculating adjusted odds ratio (aOR) with 95% confidence interval (CI) using conditional logistic regression analysis. Results:A total of 628,878 mother-child dyads were included, and 43,915 (6.98%) of children developed asthma prior to age 6. We found that male gender (aOR 1.50, 95% CI 1.47-1.53), maternal asthma (aOR 1.80, 95% CI 1.71-1.89), maternal AR (aOR 1.33, 95% CI 1.30-1.37), preterm birth (aOR 1.32, 95% CI 1.27-1.37), low birth weight (aOR 1.14, 95% CI 1.10-1.19) and cesarean section (aOR 1.10, 95% CI 1.08-1.13) were independent predictors for childhood asthma. A high urbanization level and a low number of older siblings were associated with asthma in a dose-response manner. Notably, we identified that the association between maternal asthma and childhood asthma (aOR 1.80, 95% CI 1.71-1.89) was stronger compared with those between maternal asthma and childhood AR (aOR 1.67, 95% CI 1.50-1.87) as well as childhood AD (aOR 1.31, 95% CI 1.22-1.40). Similarly, the association between maternal AR and childhood AR (aOR 1.62, 95% CI 1.53-1.72) was higher than those between maternal AR and childhood asthma (aOR 1.33, 95% CI 1.30-1.37) as well as childhood AD (aOR 1.35, 95% CI 1.31-1.40). Furthermore, the number of maternal allergic diseases was associated with the three childhood allergic diseases in a dose-response manner. Conclusions:In conclusion, this population-based study provided evidence of prenatal impacts on childhood asthma and demonstrated the shared maternal impacts among childhood asthma, AR, and AD. These findings highlight the shared prenatal impacts among allergic diseases, and studies are warranted to address the pivotal pathway in allergic diseases.
| S-EPMC6724237 | biostudies-literature
Project description:(1) Background: Variants of the interleukin-1 receptor antagonist (IL1RN) gene, encoding an anti-inflammatory cytokine, are associated with asthma. Asthma is a chronic inflammatory disease of the airway influenced by interactions between genetic variants and environmental factors. We discovered a gene-environment interaction (GEI) of IL1RN polymorphisms with childhood environmental tobacco smoke (ETS) exposure on asthma susceptibility in an urban adult population. (2) Methods: DNA samples from the NYU/Bellevue Asthma Registry were genotyped for tag SNPs in IL1RN in asthma cases and unrelated healthy controls. Logistic regressions were used to study the GEI between IL1RN variants and childhood ETS exposures on asthma and early onset asthma, respectively, adjusting for population admixture and other covariates. (3) Results: Whereas the rare genotypes of IL1RN SNPs (e.g., GG in SNP rs2234678) were associated with decreased risk for asthma among those without ETS exposure (odds ratio OR = 0.215, p = 0.021), they are associated with increased risk for early onset asthma among those with childhood ETS (OR = 4.467, p = 0.021). (4) Conclusions: We identified a GEI between polymorphisms of IL1RN and childhood ETS exposure in asthma. Analysis of GEI indicated that childhood ETS exposure disrupted the protective effect of some haplotypes/genotypes of IL1RN for asthma and turned them into high-risk polymorphisms for early onset asthma.
| S-EPMC7142766 | biostudies-literature