Risk Of Childhood Asthma Research Articles

Is Neighborhood Green Space Protective against Associations between Child Asthma, Neighborhood Traffic Volume and Perceived Lack of Area Safety? Multilevel Analysis of 4447 Australian Children.

Heavy traffic is a source of air pollution and a safety concern with important public health implications. We investigated whether green space lowers child asthma risk by buffering the effects of heavy traffic and a lack of neighborhood safety. Multilevel models were used to analyze affirmative asthma cases in nationally representative cross-sectional data from 4447 children aged 6–7 years old in Australia. Case-finding was based upon a triangulation of affirmative responses to three questions on doctor-diagnosed asthma, asthma-related medications and illness with wheezing lasting for at least 1 week within the 12 months prior. Among children considered to be exposed to high traffic volumes and areas with 0 to 20% green space quantity, the odds ratio of affirmative asthma was 1.87 (95% CI 1.37 to 2.55). However, the association between heavy traffic and asthma was significantly lower for participants living in areas with over 40% green space coverage (odds ratio for interaction 0.32, 95% CI 0.12 to 0.84). No association between affirmative asthma and green space coverage was observed for participants not exposed to heavy traffic, nor for the area safety variable. Protecting existing and investing in new green space may help to promote child respiratory health through the buffering of traffic-related air pollution.

Lead exposure, IgE, and the risk of asthma in children.

Lead (Pb) has adverse effects on our nervous system and renal systems. Young children are more vulnerable to Pb exposure. However, the role of low-level Pb exposure in the immune system and allergic diseases in children is not well established. The aims of this study are to investigate the associations between Pb exposure and allergic diseases; between Pb and immunoglobulin E (IgE) as an intervening variable; and gender-based differences. We used multistage stratified random sampling to recruit kindergarten children nationwide in Taiwan. Information about allergic diseases and environmental exposures was collected by questionnaire. We compared children with and without allergic diseases for blood Pb levels measured by inductively coupled plasma mass spectrometry. The association between blood Pb and allergic diseases was assessed by logistic regression and those between Pb and IgE by generalized linear models. We also conducted mediation analysis to evaluate how much risk of allergic diseases related to Pb exposure is explained by IgE. A total of 930 children completed specimen collections. There was a positive association between Pb and asthma. Blood Pb were also positively linked with serum IgE (β=0.26 kU/l per ln-unit increase Pb concentration; 95% CI 0.009-0.50 kU/l), after adjusting for potential confounders. Analyses stratified by gender revealed that blood Pb correlated with IgE only in boys (β=0.40 kU/l; 95% CI 0.03-0.76 kU/l). We estimated that 38% of the total effect of Pb exposure on asthma is mediated by IgE levels. In conclusion, Pb exposure is associated with both blood IgE and asthma in boys. Moreover, the effect of Pb exposure on asthma may be mediated by IgE levels.

Pediatric Asthma and Food Allergy.

To quantitatively summarize the evidence from observational studies on the relation between pediatric asthma and food allergy. A literature search was conducted in Medline and EMBASE (August 2016). Two independent reviewers appraised the studies and extracted the estimates of interest. Methodological quality of the included studies was assessed using National Heart Lung and Blood Institute (NHLBI) Quality Assessment Tools. Data were pooled using random-effects meta-analysis. A total of 32 relevant studies were identified but only 8 studies met the inclusion criteria. Using random-effect model, food allergy showed strong association with asthma in children (OR=2.87 [95% CI: 2.05-4.00]; P<0.0001). This study suggested that food allergy is associated with an increased risk of asthma in children.

Maternal vitamin D status during pregnancy and risk of childhood asthma: A meta-analysis of prospective studies.

Mounting evidence suggests that maternal vitamin D status during pregnancy may be associated with development of childhood asthma, but the results are still inconsistent. A dose-response meta-analysis was performed to quantitatively summarize evidence on the association of maternal vitamin D status during pregnancy with the risk of childhood asthma. A systematic search was conducted to identify all studies assessing the association of maternal 25-hydroxyvitamin D (25(OH)D) during pregnancy with risk of childhood asthma. The fixed or random-effect model was selected based on the heterogeneity test among studies. Nonlinear dose-response relationship was assessed by restricted cubic spline model. Fifteen prospective studies with 12758 participants and 1795 cases were included in the meta-analysis. The pooled relative risk of childhood asthma comparing the highest versus lowest category of maternal 25(OH)D levels was 0.87 (95% confidence interval, CI, 0.75-1.02). For dose-response analysis, evidence of a U-shaped relationship was found between maternal 25(OH)D levels and risk of childhood asthma (Pnonlinearity = 0.02), with the lowest risk at approximately 70 nmol/L of 25(OH)D. This dose-response meta-analysis suggested a U-shaped relationship between maternal blood 25(OH)D levels and risk of childhood asthma. Further studies are needed to confirm the association.

Rapid adiposity growth increases risks of new-onset asthma and airway inflammation in children.

We aim to (1) examine the influence of long-term adiposity status/short-term adiposity changes on asthma with high or low fractional exhaled nitric oxide (FeNO), and (2) to determine the differences in long-term adiposity status/short-term adiposity changes on atopy, airway inflammation and pulmonary function. We recruited 2450 fourth- to sixth-grade children from the nationwide Taiwan Children Health Study. Data regarding various adiposity indicators, atopic status, pulmonary function tests and asthma outcomes were collected annually. New-onset asthma was stratified by airway inflammation status using FeNO. The generalized estimating equation was used for analyzing longitudinal relationships between long-term adiposity status/short-term adiposity changes and new-onset asthma. Individual adiposity growth slopes were obtained using a hierarchical linear model to establish the relationships between short-term adiposity changes and asthma among children with high airway inflammation. We found long-term adiposity status predicted childhood asthma with low FeNO, whereas short-term adiposity changes may increase risks of childhood asthma with high FeNO. Long-term adiposity status reduced pulmonary function, whereas short-term adiposity increase were associated with atopic diseases and airway inflammation. Obesity-induced asthma could be mediated by high or low airway inflammation, depending on the velocity of increase in adiposity. Rapid adiposity growth may increase risks of childhood asthma and airway inflammation.

T1 polymorphism in a disintegrin and metalloproteinase 33 (ADAM33) gene may contribute to the risk of childhood asthma in Asians.

Polymorphisms in ADAM33 gene have been implicated in susceptibility to the risk of childhood asthma. However, the results remain controversial. We performed meta-analyses to clarify the relationship between them. Relevant articles were searched in PubMed, Embase, Wanfang, and China National Knowledge Infrastructure. The Odds ratio (OR) with 95% confidence interval (CI) was used to assess the strength of the associations. Fourteen studies with five ADAM33 polymorphisms (F + 1, T1, T2, S2, and V4) were identified, involving 2687 cases and 2996 controls. ADAM33 F + 1, T2, and T1 polymorphisms showed significant associations with asthma risks in the overall and Caucasian children, Asian children, and Caucasian and Chinese children, respectively; however, these significant results were unstable in sensitivity analysis. T1 revealed significant and stable associations with asthma risks among Asian children in the dominant (OR = 2.00, 95% CI = 1.40-2.87, P = 0.0002) and codominant (OR = 3.06, 95% CI = 1.71-5.50, P = 0.0002) models; in cumulative meta-analyses, these significant results were robust. Concerning S2 or V4 polymorphism, no significant associations were observed. These findings demonstrate that ADAM33 T1 polymorphism might be a potential susceptible predictor of asthma for Asian children. Further functional studies between this polymorphism and asthma risks are warranted.

Association of Mycoplasma pneumoniae infection with increased risk of asthma in children.

The present study was conducted to investigate the relationship between Mycoplasma pneumoniae (MP) infection and the risk of asthma among children by detecting the rate of MP immunoglobulin M (MP-IgM) and the eosinophil (EOS) count. A total of 139 asthmatic children were enrolled as the case group and assigned into three groups: Group A (aged <3 years, n=42), group B (aged 3–8 years, n=45) and group C (aged >8 years, n=52). Additionally, 115 healthy children were enrolled in the control group. Enzyme-linked immunosorbent assay was used to measure the MP-IgM-positive rate. EOS count was detected in the experimental and control groups by using a hemocytometer analyzer. A meta-analysis was performed by using the Comprehensive Meta-Analysis version 2.0 software. The positive rates of the MP-IgM and EOS count in the experimental group were significantly higher than those in control group (both P<0.001). Furthermore, the asthmatic children in group C had a higher MP-IgM-positive rate and EOS count as compared to those in groups A and B, respectively (all P<0.05). Results from groups A and B were not statistically significant (all P>0.05). The meta-analysis further confirmed that asthmatic children had a higher MP-IgM-positive rate as compared to the healthy controls (P<0.001). Age-stratified analysis revealed that the MP-IgM-positive rate in asthmatic children aged ≥8 and <8 years was significantly higher than that in the healthy controls (P=0.003 and P<0.001). Asthmatic children had a higher MP-IgM-positive rate and EOS count as compared with controls, suggesting that the MP infection may be closely associated with the risk of asthma. Additionally, the positive rate of MP-IgM may indicate an important biological marker in predicting the development of asthma.

Polymorphisms of TGFB1, TLE4 and MUC22 are associated with childhood asthma in Chinese population

ObjectiveTo investigate whether the genetic variants of TGFB1, TLE4, MUC22 and IKZF3 are associated with the development of asthma in Chinese children. Methods572 adolescent asthma patients and 590 age-matched healthy controls were included in this study. A total of four SNPs were genotyped, including rs2241715 of TGFB1, rs2378383 of TLE4, rs2523924 of MUC22, and rs907092 of IKZF3. Allele frequencies of the patients and the control group were compared by the Chi-square test. The Student t test was used to analyse the relationship between genotypes and clinical feature of the patients. ResultsPatients were found to have significantly different frequencies of allele A of rs2241715, allele G of rs2378383 and allele A of rs2523924 as compared with the controls (40.4% vs. 45.9%, p=0.01 for rs2241715; 17.2% vs. 13.4%, p=0.01 for rs2378383; 15.3% vs. 11.9%, p=0.02 for rs2523924). For patients with severe asthma, those with genotype AA/AG of rs2241715 had remarkably higher FEV1% as compared with those with genotype GG (59.1±4.3% vs. 55.4±3.7%, p<0.001). Moreover, those with genotype GG/GA of rs2378383 had remarkably lower FEV1% as compared with those with genotype AA (54.6±2.9% vs. 58.6±4.1%, p<0.001). ConclusionsGenes TGFB1, TLE4 and MUC22 are associated with the risk of childhood asthma in Chinese population. Our results associating TGFB1 and TLE4 with clinical features of asthma suggest potential application of these parameters in the management of asthma children.

Serum carotenoid and tocopherol concentrations and risk of asthma in childhood: a nested case-control study.

The antioxidant hypothesis regarding the risk of asthma in childhood has resulted in inconsistent findings. Some data indicate that the role of antioxidants in childhood asthma risk may have a critical time window of effect, but only a well-designed longitudinal cohort study can clarify this hypothesis. To study the longitudinal associations between serum carotenoid and tocopherol concentrations during the first 4years of life and asthma risk by the age of 5years. Based on a case-control design nested within a Finnish birth cohort, 146 asthma cases were matched to 270 controls on birth time, sex, genetic risk, and birth place. Non-fasting blood samples were collected at the ages of 1, 1.5, 2, 3, and 4years and serum carotenoids and tocopherols were analysed. Parents reported the presence and age at start of persistent doctor-diagnosed asthma in the child at the age of 5years. Data analyses were conducted using generalized estimating equations. We did not find strong associations between serum carotenoids and tocopherols and the risk of asthma based on age-specific and longitudinal analyses. Both lower and higher quarters of α-carotene and γ-tocopherol increased the risk of asthma. The current findings do not support the suggestion that the increased prevalence of asthma may be a consequence of decreased intake of antioxidant nutrients. Moreover, we did not confirm any critical time window of impact of antioxidants on asthma risk. Replication of these findings in similar longitudinal settings will strengthen this evidence base.

Fish and seafood consumption during pregnancy and the risk of asthma and allergic rhinitis in childhood: a pooled analysis of 18 European and US birth cohorts.

It has been suggested that prenatal exposure to n-3 long-chain fatty acids protects against asthma and other allergy-related diseases later in childhood. The extent to which fish intake in pregnancy protects against child asthma and rhinitis symptoms remains unclear. We aimed to assess whether fish and seafood consumption in pregnancy is associated with childhood wheeze, asthma and allergic rhinitis. We pooled individual data from 60 774 mother-child pairs participating in 18 European and US birth cohort studies. Information on wheeze, asthma and allergic rhinitis prevalence was collected using validated questionnaires. The time periods of interest were: infancy (0-2 years), preschool age (3-4 years), and school age (5-8 years). We used multivariable generalized models to assess associations of fish and seafood (other than fish) consumption during pregnancy with child respiratory outcomes in cohort-specific analyses, with subsequent random-effects meta-analyses. The median fish consumption during pregnancy ranged from 0.44 times/week in The Netherlands to 4.46 times/week in Spain. Maternal fish intake during pregnancy was not associated with offspring wheeze symptoms in any age group nor with the risk of child asthma [adjusted meta-analysis relative risk (RR) per 1-time/week = 1.01, 95% confidence interval 0.97-1.05)] and allergic rhinitis at school age (RR = 1.01, 0.99-1.03). These results were consistently found in further analyses by type of fish and seafood consumption and in sensitivity analyses. We found no evidence supporting a protective association of fish and seafood consumption during pregnancy with offspring symptoms of wheeze, asthma and allergic rhinitis from infancy to mid childhood.

Lifetime secondhand smoke exposure and childhood and adolescent asthma: findings from the PIAMA cohort

BackgroundSecondhand smoke (SHS) exposure is a modifiable risk factor associated with childhood asthma. Associations with adolescent asthma and the relevance of the timing and patterns of exposure are unclear. Knowledge of critical windows of exposure is important for targeted interventions.MethodsWe used data until age 17 from 1454 children of the Dutch population-based PIAMA birth cohort. Residential SHS exposure was assessed through parental questionnaires completed at ages 3 months, 1–8 (yearly), 11, 14, and 17 years. Lifetime exposure was determined as; a) time window-specific exposure (prenatal, infancy, preschool, primary school, and secondary school); b) lifetime cumulative exposure; c) longitudinal exposure patterns using latent class growth modeling (LCGM). Generalized estimation equations and logistic regression were used to analyze associations between exposure and asthma at ages 4 to 17 years, adjusting for potential confounders.ResultsWith all three methods, we consistently found no association between SHS exposure and asthma at ages 4 to 17 years e.g. adjusted overall odds ratio (95% confidence interval) 0.67 (0.41–1.12), 1.00 (0.66–1.51) and 0.67 (0.41–1.11) for prenatal maternal active smoking, infancy, and preschool school time window exposures, respectively.ConclusionWe assessed lifetime SHS exposure using different methods. Different timing and patterns of SHS exposure were not associated with an increased risk of asthma in childhood and adolescence in our study. More longitudinal studies could investigate effects of lifetime SHS exposure on asthma in adolescence and later life.

Prenatal paracetamol use and asthma in childhood: A systematic review and meta-analysis

ObjectivesSome studies have suggested that prenatal paracetamol exposure might associate with the risk of child asthma. However, other studies have not confirmed this result. Therefore, we conducted a meta-analysis to investigate their relationship. MethodsTwo authors searched Pubmed and Embase databases up to June 2016. The strength of the association was calculated with the OR and respective 95% CIs. The random-effects model was chosen to calculate the pooled OR. ResultsA total of 13 articles of more than 1,043,109 individuals were included in the meta-analysis. A statistically significant association between prenatal paracetamol exposure and child asthma risk was found. The data showed that prenatal paracetamol exposure could increase the risk of child asthma (OR=1.19; 95% CI, 1.12–1.27; P<0.00001) in a random-effect model. Six studies reported paracetamol exposure during the first trimester of pregnancy. We found that paracetamol exposure during the first trimester of pregnancy was associated with increased risk of child asthma (OR=1.21; 95% CI, 1.14–1.28; P<0.00001). Furthermore, we observed that paracetamol exposure during the 2–3 trimesters of pregnancy was also associated with child asthma risk (OR=1.13; 95% CI, 1.04–1.23; P=0.005). ConclusionsThis study suggested that prenatal paracetamol exposure was significantly associated with the increased risk of child asthma.

Maternal Folate Intake during Pregnancy and Childhood Asthma in a Population-based Cohort

A potential adverse effect of high folate intake during pregnancy on children's asthma development remains controversial. To prospectively investigate folate intake from both food and supplements during pregnancy and asthma at age 7 years when the diagnosis is more reliable than at preschool age. This study included eligible children born 2002-2006 from the Norwegian Mother and Child Cohort Study, a population-based pregnancy cohort, linked to the Norwegian Prescription Database. Current asthma at age 7 was defined by asthma medications dispensed at least twice in the year (1,901 cases; n = 39,846) or by maternal questionnaire report (1,624 cases; n = 28,872). Maternal folate intake was assessed with a food frequency questionnaire validated against plasma folate. We used log-binomial and multinomial regression to calculate adjusted relative risks with 95% confidence intervals. Risk of asthma was increased in the highest versus lowest quintile of total folate intake with an adjusted relative risk of 1.23 (95% confidence interval, 1.06-1.44) that was similar for maternally reported asthma. Mothers in the highest quintile had a relatively high intake of food folate (median, 308; interquartile range, 241-366 μg/d) and nearly all took at least 400 μg/d of supplemental folic acid (median, 500; interquartile range, 400-600 μg/d). In this large prospective population-based cohort with essentially complete follow-up, pregnant women taking supplemental folic acid at or above the recommended dose, combined with a diet rich in folate, reach a total folate intake level associated with a slightly increased risk of asthma in children.

Association between ADAM metallopeptidase domain 33 gene polymorphism and risk of childhood asthma: a meta-analysis.

This study aimed to investigate the association between ADAM metallopeptidase domain 33 (ADAM33) gene polymorphisms and the risk of childhood asthma. The relevant studies about the relationship between ADAM33 gene polymorphisms and childhood asthma were searched from electronic databases and the deadline of retrieval was May 2016. The single nucleotide polymorphisms (SNPs) of ADAM33 (rs511898, rs2280092, rs3918396, rs528557, rs2853209, rs44707, rs2280091 and rs2280089) were analyzed based on several models including the allele, codominant, recessive and dominant models. The results showed that the ADAM33 rs2280091 polymorphism in all four genetic models was associated with an increased risk of childhood asthma. Positive associations were also found between the polymorphisms rs2280090, rs2787094, rs44707 and rs528557 and childhood asthma in some genetic models. This meta-analysis suggested that ADAM33 polymorphisms rs2280091, rs2280090, rs2787094, rs44707 and rs528557 were significantly associated with a high risk of childhood asthma.

Fish oil supplement in pregnancy cuts child asthma risk

Fish oil supplement in pregnancy cuts child asthma risk

17q21 locus rs7216389 polymorphism and childhood asthma risk: a meta-analysis.

Recently, a genome-wide association study (GWAS) indicated that rs7216389 polymorphism on chromosome 17q21 was associated with paediatric asthma risk. However, the results remained controversial. Therefore, a meta-analysis was performed. A comprehensive literature retrieve was performed on PubMed, Embase and Science Direct databases up to Feb 20, 2016. The strength of association between 17q21 locus rs7216389 polymorphism and pediatric asthma risk was assessed by computing odds ratio (OR) with its corresponding 95% confidence interval (CI). A total of 10 studies with 7797 cases and 38757 controls were included. A statistically significant association of rs7216389 polymorphism and pediatric asthma risk was found (OR=1.41, 95%CI=1.34-1.49, P<0.00001). Furthermore, both Caucasians (OR=1.41, 95%CI=1.33-1.49, P<0.00001) and Asians (OR=1.43, 95%CI=1.25-1.63, P<0.00001) with rs7216389 polymorphism showed significant association, respectively. A significantly increased susceptibility was identified in atopic asthma (OR=1.45, 95%CI=1.22-1.72, P<0.00001). In the stratification analysis by study design, both case-control studies (OR=1.40, 95%CI=1.33-1.48, P<0.00001) and cohort studies (OR=2.05, 95%CI=1.32-3.17, P=0.001) showed significant association, respectively. In conclusion, this meta-analysis suggests that 17q21 locus rs7216389 polymorphism was significantly associated with paediatric asthma risk.

Epigenome-wide analysis links SMAD3 methylation at birth to asthma in children of asthmatic mothers

The timing and mechanisms of asthma inception remain imprecisely defined. Although epigenetic mechanisms likely contribute to asthma pathogenesis, little is known about their role in asthma inception. We sought to assess whether the trajectory to asthma begins already at birth and whether epigenetic mechanisms, specifically DNA methylation, contribute to asthma inception. We used the Methylated CpG Island Recovery Assay chip to survey DNA methylation in cord blood mononuclear cells from 36 children (18 nonasthmatic and 18 asthmatic subjects by age 9years) from the Infant Immune Study (IIS), an unselected birth cohort closely monitored for asthma for a decade. SMAD3 methylation in IIS (n=60) and in 2 replication cohorts (the Manchester Asthma and Allergy Study [n=30] and the Childhood Origins of Asthma Study [n=28]) was analyzed by using bisulfite sequencing or Illumina 450K arrays. Cord blood mononuclear cell-derived IL-1β levels were measured by means of ELISA. Neonatal immune cells harbored 589 differentially methylated regions that distinguished IIS children who did and did not have asthma by age 9years. In all 3 cohorts methylation in SMAD3, the most connected node within the network of asthma-associated, differentially methylated regions, was selectively increased in asthmatic children of asthmatic mothers and was associated with childhood asthma risk. Moreover, SMAD3 methylation in IIS neonates with maternal asthma was strongly and positively associated with neonatal production of IL-1β, an innate inflammatory mediator. The trajectory to childhood asthma begins at birth and involves epigenetic modifications in immunoregulatory and proinflammatory pathways. Maternal asthma influences epigenetic mechanisms that contribute to the inception of this trajectory.

Maternal depressive symptoms, maternal asthma, and asthma in school-aged children

BackgroundLittle is known about the joint effects of maternal asthma and maternal depression on childhood asthma. ObjectiveTo examine whether maternal depression and maternal asthma lead to greater risk of childhood asthma than maternal asthma alone. MethodsCross-sectional studies of children (6–14 years old) in San Juan, Puerto Rico (n = 655) and Sweden (n = 6,887) were conducted. In Puerto Rico, maternal depressive symptoms were defined using the Center for Epidemiologic Studies Depression Scale (CES-D) questionnaire. In Sweden, maternal physician-diagnosed depression was derived from national registries, and maternal depressive symptoms were defined using an abbreviated CES-D questionnaire. Childhood asthma was defined as physician-diagnosed asthma plus current wheeze (in Puerto Rico) or plus medication use (in Sweden). Logistic regression was used for multivariable analysis. ResultsCompared with Puerto Rican children whose mothers had neither asthma nor depressive symptoms, those whose mothers had asthma but no depressive symptoms had 3.2 times increased odds of asthma (95% confidence interval [CI] = 2.1–4.8) and those whose mothers had asthma and depressive symptoms had 6.5 times increased odds of asthma (95% CI = 3.3–13.0). Similar results were obtained for maternal depression and maternal asthma in the Swedish cohort (odds ratio for maternal asthma without maternal depression = 2.8, 95% CI = 2.1–3.7; odds ratio for maternal asthma and maternal depression = 4.0, 95% CI = 1.7–9.6). Although the estimated effect of maternal asthma on childhood asthma was increased when maternal depressive symptoms (Puerto Rico) or maternal depression (Sweden) was present, there were no statistically significant additive interactions. ConclusionMaternal depression can further increase the risk of asthma in children whose mothers have a history of asthma.

Vitamin D deficiency and its impact on asthma severity in asthmatic children.

BackgroundDespite obtaining evidences on association between vitamin D and development of lung in fetus, little is known about vitamin D level and its impact on severity of asthma in children. The present study aimed to assess the relationship between the asthma severity and vitamin D deficiency in asthmatic children.MethodsThis case-control study was conducted on 106 individuals including asthmatic (n = 53) and healthy children (n = 53) who referred to Mofid hospital in Tehran in 2013. The level of serum vitamin D in both groups was measured by radioimmunoassay method at the reference lab and was categorized as sufficient (> 30 ng/ml), insufficient (20 to 30 ng/ml), or deficient (< 20 ng/ml). The control status of asthma in patients group was classified as controlled, partially controlled, and uncontrolled.ResultsIn the groups with and without asthma, the prevalence of vitamin D deficiency was 73.6 and 49.1%, and the prevalence of vitamin D insufficiency was 18.9 and 18.9%, while normal vitamin D level was revealed in 7.5 and 32.1%, respectively with a significant difference (p = 0.005). Using the multivariate logistic regression analysis, the presence of asthma was associated with reduced level of vitamin D (OR = 1.068, 95% CI: 1.027–1.110, P = 0.001). In this context, the risk for asthma in the children with vitamin D deficiency was 6.3 times of those with normal vitamin D level. Although the presence of asthma was strongly associated with reduced level of vitamin D in serum, neither severity of asthma nor control status of asthma were associated with vitamin D deficiency.ConclusionThe presence of vitamin D deficiency effectively predict increased risk for childhood asthma; however the severity or control status of this event may not be predicted by confirming vitamin D deficiency.

Association between Caesarean Delivery and Childhood Asthma in India and Vietnam.

While there is evidence of an association between caesarean birth and increased asthma in children in high-income countries, it is unknown whether this association exists in low-to-middle-income countries (LMICs). We investigated whether children born through caesarean in India and Vietnam are at increased risk of caregiver-reported asthma by 8 years of age. Data from an ongoing multi-national longitudinal cohort study (the Young Lives Study) in two LMICs (India n = 2026; Vietnam n = 2000) were used. Caregiver questionnaires captured information on caregiver-reported long-term respiratory problems such as asthma or wheeze at age 8 years, birth mode and a range of sociodemographic factors. Multivariable logistic regression models using propensity score adjustment were used to explore birth mode and asthma at age 8 years adjusted for a range of known confounders. Children delivered by caesarean in India (odds ratio (OR) 2.6, 95% confidence interval (CI) 1.3, 5.4) and Vietnam (OR 2.0, 95% CI 1.2, 3.3) had greater odds of asthma at age 8 years, after adjustment for other risk factors including wealth, liveborn parity, low birthweight, geographic location, cooking fuel used, livestock ownership, household size, housing quality and parental smoking. The study suggests that caesarean birth may be associated with an increased risk of childhood asthma in India and Vietnam. The underlying mechanisms of this finding need to be further elucidated.