Risk Of Childhood Asthma Research Articles

Peak weight velocity in infancy is negatively associated with lung function in adolescence. Results from the GINIplus study.

Background: Weight gain during infancy increases the risk of asthma in childhood which might be related to lower lung function. This study aimed to investigate the association between dynamics of growth (peak weight velocity) during the first two years of life and spirometric lung function indices measured at 15 years of age.

Childhood Asthma Hospital Discharge Medication Fills and Risk of Subsequent Readmission

To assess the relationship between posthospitalization prescription fills for recommended asthma discharge medication classes and subsequent hospital readmission. This was a retrospective cohort analysis of Medicaid Analytic Extract files from 12 geographically diverse states from 2005-2007. We linked inpatient hospitalization, outpatient, and prescription claims records for children ages 2-18 years with an index hospitalization for asthma to identify those who filled a short-acting beta agonist, oral corticosteroid, or inhaled corticosteroid within 3 days of discharge. We used a multivariable extended Cox model to investigate the association of recommended medication fills and hospital readmission within 90 days. Of 31,658 children hospitalized, 55% filled a beta agonist prescription, 57% an oral steroid, and 37% an inhaled steroid. Readmission occurred for 1.3% of patients by 14 days and 6.3% by 90 days. Adjusting for patient and billing provider factors, beta agonist (hazard ratio [HR] 0.67, 95% CI 0.51, 0.87) and inhaled steroid (HR 0.59, 95% CI 0.42, 0.85) fill were associated with a reduction in readmission at 14 days. Between 15 and 90 days, inhaled steroid fill was associated with decreased readmission (HR 0.87, 95% CI 0.77, 0.98). Patients who filled all 3 medications had the lowest readmission hazard within both intervals. Filling of beta agonists and inhaled steroids was associated with diminished hazard of early readmission. For inhaled steroids, this effect persisted up to 90 days. Efforts to improve discharge care for asthma should include enhancing recommended discharge medication fill rates.

Childhood body mass index and wheezing disorders: a systematic review and meta-analysis.

It has been claimed that overweight/obesity, childhood asthma and wheezing disorders are associated, although the results of observational studies have remained inconsistent. We conducted a systematic review and meta-analysis to investigate this. An online search of published papers linking childhood asthma and wheezing with overweight/obesity up to May 2014 using EMBASE and MEDLINE medical research databases was carried out. Summary odds ratios (OR) were estimated using random-effects models. Subgroup meta-analyses were performed to assess the robustness of risk associations and between-study heterogeneity. A total of 38 studies comprising 1,411,335 participants were included in our meta-analysis. The summary ORs of underweight (<5th percentile), overweight (>85th to <95th percentile) and obesity (≥ 95 th percentile) were 0.85 (95% CI: 0.75 to 0.97; p = 0.02), 1.23 (95% CI: 1.17 to 1.29; p < 0.001) and 1.46 (95% CI: 1.36 to 1.57, p < 0.001), respectively. Heterogeneity was significant and substantial in all three weight categories, and not accounted for by pre-defined study characteristics. Our results suggest that underweight is associated with a reduced risk of childhood asthma, and overweight and obesity are associated with an increased risk of childhood asthma. Although our findings assert that overweight/obesity and childhood asthma are associated, the causal pathway and temporal aspects of this relationship remain unanswered and deserve further epidemiological investigation.

Influence of childhood growth on asthma and lung function in adolescence

BackgroundLow birth weight and rapid infant growth in early infancy are associated with increased risk of childhood asthma, but little is known about the role of postinfancy growth in asthmatic children.ObjectivesWe sought to examine the associations of children's growth patterns with asthma, bronchial responsiveness, and lung function until adolescence.MethodsIndividual growth trajectories from birth until 10 years of age were estimated by using linear spline multilevel models for 9723 children participating in a population-based prospective cohort study. Current asthma at 8, 14, and 17 years of age was based on questionnaires. Lung function and bronchial responsiveness or reversibility were measured during clinic visits at 8 and 15 years of age.ResultsRapid weight growth between 0 and 3 months of age was most consistently associated with increased risks of current asthma at the ages of 8 and 17 years, bronchial responsiveness at age 8 years, and bronchial reversibility at age 15 years. Rapid weight growth was associated with lung function values, with the strongest associations for weight gain between 3 and 7 years of age and higher forced vital capacity (FVC) and FEV1 values at age 15 years (0.12 [95% CI, 0.08 to 0.17] and 0.11 [95% CI, 0.07 to 0.15], z score per SD, respectively) and weight growth between 0 and 3 months of age and lower FEV1/FVC ratios at age 8 and 15 years (−0.13 [95% CI, −0.16 to −0.10] and −0.04 [95% CI, −0.07 to −0.01], z score per SD, respectively). Rapid length growth was associated with lower FVC and FVC1 values at age 15 years.ConclusionFaster weight growth in early childhood is associated with asthma and bronchial hyperresponsiveness, and faster weight growth across childhood is associated with higher FVC and FEV1 values.

Asthma Risk Profiles of Children Participating in an Asthma Education and Management Program

BackgroundFocused risk assessment is essential in the effective management of asthma.PurposeThis study identified and examined correlations among areas of pediatric asthma risk and determined associations between these risks and demographic characteristics.MethodsThis exploratory study identified risk factors that affect asthma management among pediatric asthmatics using the Child Asthma Risk Assessment Tool. Results were analyzed using descriptive frequencies and tests of correlation and association.ResultsRisk assessments were completed for 155 children. The most prominent areas of risk were responsibility in medication administration (46%), caregiver well-being (35%), child well-being (33%), and medication adherence (28%). Correlations and associations were found among areas of risk and demographic characteristics.DiscussionAs a result of the assessment, participants were able to receive tailored asthma education sessions to address asthma risks and promote effective asthma self-management.Translation to Health Education PracticeConducting standardized asthma risk assessment offers health educators and healthcare providers valuable information to understand the relationships between various areas of risk and tailor asthma education and management activities in efforts to eliminate those risks and improve asthma health outcomes.

Gene-Environment Interactions Should be Considered in Future Studies to Understand the Association Between Prenatal Folate Supplementation and Asthma Development.

Because the increasing prevalence of allergies within the last 20 to 30 years cannot be explained by genetic changes, most allergists have tried to find answers in environmental and lifestyle changes, as reflected by the hygiene hypothesis. Environmental exposures during pregnancy and early infancy during critical periods of immune development can have profound effects on allergy development. Food intake is a well-known environmental factor that influences allergy development and three specific nutrients-vitamin D, omega 3 polyunsaturated fatty acids and folate-have recently attracted attention.1 The methyl donor folate is a well-known nutrient supplement given during early pregnancy to prevent neutral tube defects in the developing fetus. A recent murine study has reported however that a maternal diet supplemented with folate increased the prevalence of allergic airway disease in offspring.2 Of the 82 genes that were found in that mouse study to be differentially methylated after in utero supplementation with a methyl-rich diet, runt-related transcription factor 3, which regulates allergic airway disease, was shown to be excessively methylated. These results suggest that prenatal dietary factors can increase the risk of allergy development in offspring through epigenetic mechanisms. Other nutrients, including methionine, vitamin B12, choline, and betaine, are also known to induce methylation changes in genes.3 In contrast to the results in a mouse model, a number of human studies have tried to identify an association between an increased intake of folate during pregnancy and the risk of asthma in childhood but have not produced any solid evidence to support such an association. A previous meta-analysis of the effect of prenatal folate on the risk of postnatal asthma also found no evidence of this association, although only 14 articles were assessed in that analysis.4 Likewise, in this current issue of Allergy, Asthma & Immunology Research, Wang et al.5 did not find any association between prenatal folate and a risk of asthma, other than a risk of wheeze in early childhood. A previous large cohort study by Haberg et al.6 reported that maternal folic acid supplementation during early pregnancy increased the risk of wheeze at 6-18 months postnatally. The weight of that study was calculated at 92% in the present meta-analysis of the relationship between maternal folic acid supplementation during pregnancy and the risk of wheeze in childhood, whereas the weights of the other 2 studies that found no relationship between these 2 factors were just 1.83% and 6.18%, respectively. However, 59.2% of children who developed a wheeze in the first 3 years after birth did not show this condition at the age of 6 years.7 Indeed, although wheeze is the main symptom of childhood asthma, it is not diagnostic for asthma. Moreover, in another earlier meta-analysis,4 when the data of Haberg et al. were removed, the association between prenatal folate and the risk of childhood wheeze became non-significant. We conclude from the reported evidence to date that gene-environmental interactions affect the development of asthma and should therefore be considered when investigating the association between prenatal folate and asthma development. The data in many epidemiologic studies have been inconsistent in this regard. A single nucleotide polymorphism (C677T) in the methylenetetrahydrofolate reductase gene has been associated with folate metabolism, resulting in different blood concentrations of folate in individuals with different genotypes.8 The risk of asthma should be evaluated in offspring with differing genotypes to determine how the genotype interacts with prenatal folate intake. Given that folate is a well-known methyl donor, epigenetic changes should also be evaluated in a future study. Prenatal folate intake may alter the methylation of genes involved in the development of the immune system, increasing the risk of asthma in humans, as found in mouse studies. The limitations of previous epidemiologic studies should also be considered in any future study. Because most pregnant women take folate to prevent neural tube defects in their offspring, a randomized control trial of the relationship between prenatal folate intake and asthma development in children could not be conducted within ethical guidelines. Indeed, there has been no previous randomized control trial in this area, which is an obstacle to any meta-analysis conclusion supported by strong evidence. Previous studies of the association between prenatal folate and asthma development have varied in terms of the type, time, dose, duration, and method for measuring folate exposure, the definition of outcomes, and the child's age at the evaluation of outcomes. Given these factors, a detailed and well-considered study design is needed.

Association between a functional single nucleotide polymorphism in the brain-derived neurotrophic factor gene and risk of child asthma

Brain-derived neurotrophic factor (BDNF) promotes synaptic remodeling and modulates the function of other neurotransmitters. Allergic inflammation triggers neuronal dysfunction and structural changes in the airways. Genetic polymorphisms in functional regions of the BDNF gene have a plausible role in modulating the risk of child asthma (CA). This study examined the potential association between CA and three single nucleotide polymorphisms (SNPs) in BDNF (rs2030323, rs6265, and rs16917204 in the promoter, exon 4, and 3'-untranslated regions, respectively). The study was conducted in 350 children with asthma and 356 healthy controls. The genotype and allele frequencies and difference between groups were analyzed using HaploView 4.0 and SPSS 20.0 software platforms. The analysis revealed a strong association between the rs6265 genotype distribution and CA. The frequency of the G allele was significantly higher in CA patients than in healthy controls (P = 0.0007, odds ratio = 1.323, 95% confidence interval = 1.073-1.632). Strong linkage disequilibrium was observed between rs16917204 and rs6265. A significantly higher number of G-G haplotypes were observed in CA patients than in controls (P = 0.024 after Bonferroni correction), while the G-A haplotypes were more significant in controls (P = 0.013 after Bonferroni correction). This suggested that BDNF gene polymorphisms confer susceptibility to CA, and also support the notion that BDNF dysfunction is involved in the pathophysiological process of CA.

The influence of childhood traffic-related air pollution exposure on asthma, allergy and sensitization: a systematic review and a meta-analysis of birth cohort studies.

The impact of early childhood traffic-related air pollution (TRAP) exposure on development of asthma and allergies remains unclear. Birth cohort studies are the best available study design to answer this question, but the evidence from such studies has not been synthesized to date. We conducted a systematic review and meta-analyses of published birth cohort studies to understand the association between early childhood TRAP exposure, and subsequent asthma, allergies and sensitization. Increased longitudinal childhood exposure to PM2.5 and black carbon was associated with increasing risk of subsequent asthma in childhood (PM2.5 : OR 1.14, 95%CI 1.00 to 1.30 per 2 μg/m(3) and black carbon: OR 1.20, 95%CI 1.05 to 1.38 per 1 × 10(-5) m(-1) ). Also, early childhood exposure to TRAP was associated with development of asthma across childhood up to 12 years of age. The magnitude of these associations increased with age, and the pattern was prominent for PM2.5 . Increasing exposure to PM2.5 was associated with sensitization to both aero- and food allergens. There was some evidence that TRAP was associated with eczema and hay fever. In summary, exposure to TRAP was related to asthma and allergic diseases. However, the substantial variability across studies warrants long-term birth cohort studies with regular repeated follow-ups to confirm these findings.

Prenatal and post‐natal exposure to antibiotics and risk of asthma in childhood

Evidence on the association between post-natal exposure to antibiotics and the development of asthma is extensive, but inconsistent and even less is known about prenatal exposure. The aim of this study was to examine the associations between prenatal and post-natal exposure to different antibiotics and the risk of childhood asthma in a population- and register-based nested case-control study. All children who were born in 1996-2004 in Finland and diagnosed with asthma by 2006 were identified from a national health register. For each case, one matched control was selected. Information on asthma diagnoses, purchased anti-asthmatic drugs and antibiotics as well as putative confounders was obtained from national health registries. The associations were analysed using conditional logistic regression for children diagnosed at the age of 3 years or later (n = 6 690 case-control pairs). Maternal use of any antibiotics during pregnancy was associated with an increased risk of asthma in the offspring [adjusted odds ratio (OR) = 1.31 (95% confidence interval (CI): 1.21-1.42)]. Several maternal specific antibiotics were associated with the risk of asthma, and the strongest association was observed for cephalosporins [OR = 1.46 (95% CI 1.30-1.64)]. Child's use of antibiotics during the first year of life was associated with an increased risk of asthma [OR = 1.60 (95% CI 1.48-1.73)]. Child's use of cephalosporins [OR = 1.79 (95% CI 1.59-2.01)], sulphonamides and trimethoprim [OR = 1.65 (95% CI 1.34-2.02)], macrolides [OR = 1.61 (95% CI 1.46-1.78)] and amoxicillin [OR = 1.46 (95% CI 1.35-1.58)] was associated with an increased risk of asthma. Both prenatal and post-natal exposure to antibiotics was associated with an increased risk of asthma. The potential role of adverse effects of antibiotics on the gut microbiota and the development of asthma should be further explored.

Perennial aeroallergens sensitisation and risk of asthma in African children and adolescents: a case-control study

Objectives: The distribution and impact of various aeroallergens on asthma occurrence vary across regions. We investigated the association between sensitisation to perennial aeroallergens and asthma risk in children and adolescents in Yaounde, Cameroon. Methods: This was a case-control study involving children and adolescents with asthma (cases) vs. non-allergic counterparts (controls). Children/adolescents with doctor-diagnosed asthma were included over a period of 30 months, and controls were selected from the community through random sampling. Logistic regression models were used to relate perennial aeroallergens sensitisation with asthma. Results: The asthma and control groups included, respectively, 151 and 372 participants, with no sex ratio difference. The mean age (standard deviation) was 11.9 (4.4) years in cases and 11.3 (3.7) years in controls. The prevalence of sensitisation to any aeroallergen (cases vs. controls) was 76.8% (116/151) and 32.3% (120/372), p < 0.001. Sensitisation to mites was found in 104 (68.9%) cases vs. 56 (15.1%) controls, p < 0.001. In multivariable analysis, sensitisation to Alternaria alternata, Blattella germanica and dander (cat and dog) was not associated with asthma. However, sensitisation to mites was significantly associated with asthma. Odds ratios (95% CI) for sensitisation to Dermatophagoides pteronyssinus, Dermatophagoides farinae and Blomia tropicalis in relation with asthma were 7.28 (3.75–14.15), 2.65 (1.27–5.45) and 3.23 (1.68–6.21), respectively. Conclusions: Sensitisation to mites was the main perennial allergenic factor associated with asthma in children and adolescents in this setting. This has application for the selection of patients with asthma who could benefit from the control of exposure to mites and specific immunotherapy.

Environmental and socioeconomic data do not improve the Predicting Asthma Risk in Children (PARC) tool

Environmental and socioeconomic data do not improve the Predicting Asthma Risk in Children (PARC) tool

Maternal intimate partner violence exposure, child cortisol reactivity and child asthma

Psychosocial stressors like intimate partner violence (IPV) exposure are associated with increased risk of childhood asthma. Longitudinal studies have not investigated the role of hypothalamic-pituitary-adrenal (HPA) axis reactivity (and associated alterations in cortisol release) in the child IPV exposure–asthma association. We sought to investigate this association, and to assess whether this relationship differs by child HPA reactivity. This secondary analysis used longitudinal cohort data from the Family Life Project. Participants included 1,292 low-income children and mothers; maternal interview and child biomarker data, including maternal report of IPV and child asthma, and child salivary cortisol obtained with validated stress reactivity paradigms, were collected when the child was 7, 15, 24, 35, and 48 months. Using structural equation modeling, maternal IPV when the child was 7 months of age predicted subsequent reports of childhood asthma (B=0.18, p=.002). This association differed according to the child's HPA reactivity status, with IPV exposed children who were HPA reactors at 7 and 15 months of age – defined as a ≥10% increase in cortisol level twenty minutes post peak arousal during the challenge tasks and a raw increase of at least .02μg/dl – being significantly at risk for asthma (7 months: B=0.17, p=.02; 15 months: B=0.17, p=.02). Our findings provide support that children who are physiologically reactive are the most vulnerable to adverse health outcomes when faced with environmental stressors.

Paracetamol exposure in pregnancy and early childhood and development of childhood asthma: a systematic review and meta-analysis

Background and objectiveWhile paracetamol exposure in pregnancy and early infancy has been associated with asthma, it remains unclear whether this is confounded by respiratory tract infections, which have been suggested...

Prenatal and infant exposure to acetaminophen and ibuprofen and the risk for wheeze and asthma in children

Several studies have reported an association between use of over-the-counter antipyretics during pregnancy or infancy and increased asthma risk. An important potential limitation of these observational studies is confounding by indication. We investigated the association of antipyretic intake during pregnancy and during the first year of life (infancy) with asthma-related outcomes before and after controlling for early-life respiratory tract infections. We included 1490 mother-child pairs in Project Viva, a longitudinal prebirth cohort study. We categorized prenatal acetaminophen exposure as the maximum intake (never, 1-9 times, or ≥10 times) in early pregnancy or midpregnancy and ibuprofen intake as presence or absence in early pregnancy. We expressed intake of antipyretics in infancy as never, 1 to 5 times, 6 to 10 times, or more than 10 times. We examined the associations of acetaminophen and ibuprofen (per unit increase in exposure category) during pregnancy and infancy with wheeze, asthma, and allergen sensitization in early childhood (3-5 years of age, n = 1419) and midchildhood (7-10 years of age, n = 1220). Unadjusted models showed an increased asthma risk in early childhood for higher infant acetaminophen (odds ratio [OR], 1.21; 95% CI 1.04-1.41) and ibuprofen (OR, 1.35; 95% CI, 1.19-1.52) intake. Controlling for respiratory tract infections attenuated estimates for acetaminophen (OR, 1.03; 95% CI, 0.88-1.22) and ibuprofen (OR, 1.19; 95% CI, 1.05-1.36). Prenatal acetaminophen was associated with increased asthma (OR, 1.26; 95% CI, 1.02-1.58) in early childhood but not midchildhood. Adjustment for respiratory tract infections in early life substantially diminished associations between infant antipyretic use and early childhood asthma. Respiratory tract infections should be accounted for in studies of antipyretics and asthma to mitigate bias caused by confounding by indication.

Effect of low birth weight on childhood asthma: a meta-analysis.

BackgroundLow birth weight is strongly correlated with an increased risk of adult diseases. Additionally, low birth weight might be a risk factor for asthma later in life.MethodsA systematic literature search of the PubMed database from 1966 to November 2013 was conducted. The criteria for inclusion of papers were as follows: case–control or cohort studies; the odds ratio (OR) or risk ratio (RR) estimates with the corresponding 95% confidence intervals (CIs) were presented, or there were sufficient data for calculation; and studies were published in English up to October 2013. Random-effect and fixed-effect meta-analyses, meta-regression, and cumulative meta-analysis were conducted.ResultsThirteen cohort studies and 1,105,703 subjects were included. The overall pooled RRs (95% CIs) of asthma risk for low birth weight were 1.162 (fixed-effects model, 95% CI, 1.128–1.197) and 1.152 (random-effects model, 95% CI, 1.082–1.222). In stratified analyses, the effect of low birth weight on childhood asthma was strong, particularly in studies conducted in Europe, those with a small sample size, and those published recently. A meta-regression analysis did not find significant determinants.ConclusionsThis meta-analysis shows that low birth weight significantly increases the risk of childhood asthma.

PS-061 Maternal Fatty Acid Composition During Early Pregnancy And Asthma At Age 7 Years In The Amsterdam Born Children And Their Development (abcd) Cohort

<h3>Background and aims</h3> Fetal exposure to polyunsaturated fatty acids (PUFAs) might influence the risk of childhood asthma. Epidemiologic studies suggest decreased risks of asthma after high intake of omega-3 and many women take omega-3 supplements during pregnancy. Few studies have maternal PUFA blood levels. We examined the relationship between maternal PUFA blood levels during early pregnancy and asthma in the offspring at age 7 years in a population based prospective cohort. <h3>Methods</h3> In 2,105 women, we determined maternal PUFA levels in plasma phospholipids drawn at about week 13 of pregnancy. Child asthma at age 7 (n = 154 cases) was based on parental report of physician diagnosis. We categorised PUFA levels and omega-3 to omega-6 ratios in quartiles with the lowest quartile as the reference category in multivariate logistic regression. Risk ratios were adjusted for: gestational age at blood draw; maternal education; western ethnicity; maternal age; parental asthma; and prepregnancy body mass index. <h3>Results</h3> Higher omega-3 levels were related to lower asthma risk with a trend across the quartiles (risk ratio for the top quartile = 0.73, 95% CI (0.45–1.17, P trend across quartiles = 0.04) and higher omega-6 levels showed opposite associations but also not statistically significant and with no significant trend. Higher ratios of omega-3 to omega-6 were associated with slightly lower risks of asthma with a trend across quartiles (risk ratio for top quartile = 0.80, 95% CI 0.50–1.27, P trend across quartiles = 0.04). <h3>Conclusions</h3> We found some suggestion of a reduced risk of childhood asthma at age 7 with higher maternal plasma levels of omega-3 and a higher ratio of omega-3 to omega-6 PUFAs.

Risk of childhood asthma is associated with CpG-site polymorphisms, regional DNA methylation and mRNA levels at the GSDMB/ORMDL3 locus.

Single-nucleotide polymorphisms (SNPs) in GSDMB (Gasdermin B) and ORMDL3 (ORMDL sphingolipid biosynthesis regulator 3) are strongly associated with childhood asthma, but the molecular alterations contributing to disease remain unknown. We investigated the effects of asthma-associated SNPs on DNA methylation and mRNA levels of GSDMB and ORMDL3. Genetic association between GSDMB/ORMDL3 and physician-diagnosed childhood asthma was confirmed in the Swedish birth-cohort BAMSE. CpG-site SNPs (rs7216389 and rs4065275) showed differences in DNA methylation depending on carrier status of the risk alleles, and were significantly associated with methylation levels in two CpG sites in the 5′ UTR (untranslated region) of ORMDL3. In the Swedish Search study, we found significant differences in DNA methylation between asthmatics and controls in five CpG sites; after adjusting for lymphocyte and neutrophil cell counts, three remained significant: one in IKZF3 [IKAROS family zinc finger 3 (Aiolos); cg16293631] and two in the CpG island (CGI) of ORMDL3 (cg02305874 and cg16638648). Also, cg16293631 and cg02305874 correlated with mRNA levels of ORMDL3. The association between methylation and asthma was independent of the genotype in rs7216389, rs4065275 and rs12603332. Both SNPs and CpG sites showed significant associations with ORMDL3 mRNA levels. SNPs influenced expression independently of methylation, and the residual association between methylation and expression was not mediated by these SNPs. We found a differentially methylated region in the CGI shore of ORMDL3 with six CpG sites less methylated in CD8+ T-cells. In summary, this study supports that there are differences in DNA methylation at this locus between asthmatics and controls; and both SNPs and CpG sites are independently associated with ORMDL3 expression.

Parental socioeconomic status, childhood asthma and medication use--a population-based study.

BackgroundLittle is known about how parental socioeconomic status affects offspring asthma risk in the general population, or its relation to healthcare and medication use among diagnosed children.MethodsThis register-based cohort study included 211,520 children born between April 2006 and December 2008 followed until December 2010. Asthma diagnoses were retrieved from the National Patient Register, and dispensed asthma medications from the Prescribed Drug Register. Parental socioeconomic status (income and education) were retrieved from Statistics Sweden. The associations between parental socioeconomic status and outcomes were estimated by Cox proportional hazard regression.ResultsCompared to the highest parental income level, children exposed to all other levels had increased risk of asthma during their first year of life (e.g. hazard ratio, HR 1.19, 95% confidence interval, CI 1.09–1.31 for diagnosis and HR 1.17, 95% CI 1.08–1.26 for medications for the lowest quintile) and the risk was decreased after the first year, especially among children from the lowest parental income quintile (HR 0.84, 95% CI 0.77–0.92 for diagnosis, and HR 0.80, 95% CI 0.74–0.86 for medications). Further, compared to children with college-educated parents, those whose parents had lower education had increased risk of childhood asthma regardless of age. Children with the lowest parental education had increased risk of an inpatient (HR 2.07, 95% CI 1.61–2.65) and outpatient (HR 1.32, 95% CI 1.18–1.47) asthma diagnosis. Among diagnosed children, those from families with lower education used fewer controller medications than those whose parents were college graduates.ConclusionsOur findings indicate an age-varying association between parental income and childhood asthma and consistent inverse association regardless of age between parental education and asthma incidence, dispensed controller medications and inpatient care which should be further investigated and remedied.

Is elective cesarean section associated with a higher risk of asthma? A meta-analysis

Background: Recent meta-analyses indicate that children delivered by cesarean section have increased risk for asthma. However, the studies included in these previous meta-analyses showed significant heterogeneity. Furthermore, no previous meta-analysis has distinguished the association of elective and emergency CS, spontaneous and instrumental vaginal deliveries (VD) with the odds of asthma. Objective: To examine the association between specific mode of delivery and the prevalence of asthma. Methods: PUBMED, Google Scholar, EMBASE, and MEDLINE were searched to identify relevant studies. Odds ratio (OR) and 95% confidence interval (CI) were calculated from the prevalence of asthma in children born by elective CS, emergent CS, instrumental VD and spontaneous VD. Meta-analysis was then used to derive a combined OR. Heterogeneity between studies was also tested in the findings. Results: A total of 26 studies were identified. The overall meta-analysis revealed an increase in the risk of asthma in children delivered by CS (OR = 1.16, 95% CI 1.14, 1.29), and no evidence of heterogeneity was found (I2 = 24.6%). Elective and emergency CS moderately increased the risk of asthma (OR = 1.21, 95% CI 1.17, 1.25; I2 = 39.9%; OR = 1.23, 95% CI 1.19–1.26). The risk of asthma was also higher in the children born by instrumental VD (OR = 1.07, 95% CI, 1.04–1.11) but with evidence of heterogeneity (I2 = 54.9%). Conclusion: About 20% increase in the subsequent risk of asthma was both found in children delivered by elective and emergency CS. The increasing rates of CS worldwide might partly explain the concomitant rise in asthma during the same time period.

Associations of sugar-containing beverages with asthma prevalence in 11-year-old children: the PIAMA birth cohort.

Recently, a few studies have linked soft drink consumption to increased asthma risk, but the contribution of different types of soft drinks is unknown. We investigated cross-sectional associations between six different types of soft drinks and asthma in 11-year-old children. We analyzed data of 2406 children participating in the Dutch Prevention and Incidence of Asthma and Mite Allergy birth cohort. At age 11, children self-reported consumption of sugar-added drinks, diet drinks, sweetened milk drinks, 100% fruit juice, energy drinks and sport drinks. The definition of asthma was based on parental reports of wheezing, prescription of inhaled corticosteroids and doctor's diagnosis of asthma. The prevalence of asthma in this study was 5.8%. In adjusted logistic regression analyses, asthma risk was increased for high (⩾10 glasses/week (gl/wk) versus low (<4 gl/wk) consumption of 100% fruit juice (odds ratio (OR): 2.09, 95% confidence interval (CI): 1.21-3.60), sugar-added drinks (OR: 1.56, 95%CI: 0.95-2.56) and for very high (>21.5 gl/wk) versus low (<12.5 gl/wk) total sugar-containing beverage (SCB) consumption (OR: 1.91, 95%CI: 1.04-3.48). Consumption of other beverages and consumption of fruit were not associated with increased asthma risk. No evidence for mediation of the observed associations by body mass index was found. This study indicates that high consumption of 100% fruit juice and total SCBs is associated with increased asthma risk in children. The positive association between consumption of 100% fruit juice and asthma is an unexpected finding that needs confirmation in future studies.