Risk Of Early Childhood Asthma Research Articles

Pre-eclampsia and risk of early-childhood asthma: a register study with sibling comparison and an exploration of intermediate variables.

BackgroundWe aimed to study whether pre-eclampsia is associated with childhood asthma, allergic and non-allergic asthma, accounting for family factors and intermediate variables.MethodsThe study population comprised 779 711 children born in 2005–2012, identified from Swedish national health registers (n = 14 823/7410 exposed to mild/moderate and severe pre-eclampsia, respectively). We used Cox regression to estimate the associations of mild/moderate and severe pre-eclampsia with incident asthma, before and after age 2 years. Cox regressions were controlled for familial factors using sibling comparisons, then stratified on high and low risk for intermediate variables: caesarean section, prematurity and small for gestational age. We used logistic regression for allergic and non-allergic prevalent asthma at 6 years as a measure of more established asthma.ResultsThe incidence of asthma in children was 7.7% (n = 60 239). The associations varied from adjusted hazard ratio (adjHR) 1.11, 95% confidence interval (CI): 1.00, 1.24 for mild/moderate pre-eclampsia and asthma at >2 years age, to adjHR 1.78, 95% CI: 1.64, 1.95 for severe pre-eclampsia and asthma at <2 years age. Sibling comparisons attenuated most estimates except for the association between severe pre-eclampsia and asthma at <2 years age (adjHR 1.45, 95% CI: 1.10, 1.90), which also remained when stratifying for the risk of intermediates. Mild/moderate and severe pre-eclampsia were associated with prevalent non-allergic (but not allergic) asthma at 6 years, with adjusted odds ratio (adjOR) 1.17, 95% CI: 1.00, 1.36 and adjOR 1.51, 95% CI: 1.23, 1.84, respectively.ConclusionsWe found evidence that severe, but not mild/moderate, pre-eclampsia is associated with asthma regardless of familial factors and confounders.

FUT2\u2013ABO epistasis increases the risk of early childhood asthma and Streptococcus pneumoniae respiratory illnesses

Asthma with severe exacerbation is the most common cause of hospitalization among young children. We aim to increase the understanding of this clinically important disease entity through a genome-wide association study. The discovery analysis comprises 2866 children experiencing severe asthma exacerbation between ages 2 and 6 years, and 65,415 non-asthmatic controls, and we replicate findings in 918 children from the Copenhagen Prospective Studies on Asthma in Childhood (COPSAC) birth cohorts. We identify rs281379 near FUT2/MAMSTR on chromosome 19 as a novel risk locus (OR = 1.18 (95% CI = 1.11–1.25), Pdiscovery = 2.6 × 10−9) as well as a biologically plausible interaction between functional variants in FUT2 and ABO. We further discover and replicate a potential causal mechanism behind this interaction related to S. pneumoniae respiratory illnesses. These results suggest a novel mechanism of early childhood asthma and demonstrates the importance of phenotype-specificity for discovery of asthma genes and epistasis.

Prenatal polycyclic aromatic hydrocarbon (PAH) exposure and early childhood asthma in a diverse US pregnancy cohort

Background/AimExposure to polycyclic aromatic hydrocarbons (PAH) may increase risk of pediatric asthma. Effects of prenatal PAH exposure, specifically, are hypothesized but understudied. The ECHO PATHWAYS Consortium investigated these relationships in a large, diverse prospective cohort study.MethodsWe included 919 mother-child dyads from the CANDLE Study, a longitudinal pregnancy cohort set in Shelby County, TN. PAH metabolites were measured in second trimester urine and adjusted for specific gravity. Seven metabolites detected in &gt;80% of women were included in analysis. When children were 4-6 years old, mothers completed the International Study on Allergies and Asthma in Childhood survey. Poisson regression with robust standard errors was used to estimate relative risk of current wheeze, current asthma, and ever asthma associated with each metabolite in separate models, adjusted for maternal age, race, education and other asthma risk factors. Effect modification by child sex and maternal asthma was assessed using interaction models. We did not adjust for multiple comparisons.ResultsParticipants were 66% Black, 44% White; 58% with high school education or less. On average, urinary PAH metabolite concentrations were higher than in other US cohorts. Mean (SD) child age at assessment was 4.3 (0.4) years. Prevalence of reported current wheeze and asthma and ever asthma was 19.4%, 16.1%, and 14.6%, respectively. In multivariable models, we observed no evidence that any metabolite was associated with any outcome. No differences by child sex were observed. Maternal asthma modified associations between 1/9-hydroxyphenanthrene and current asthma (RRmaternal asthma = 0.88; 95%CI: 0.78, 0.99 versus RRwithout maternal asthma = 1.09; 95%CI: 0.97, 1.23 per two-fold increase in exposure; pinteraction=0.012).ConclusionsResults of our analysis, the largest cohort study of prenatal PAH and childhood airway outcomes conducted to date, did not support the hypothesis that prenatal PAHs increases risk of early childhood asthma.

New Risk Factors for Transient Tachypnea of the Newborn and Childhood Asthma: A Study of Clinical Data and a Survey of Parents.

Objectives: It is established that transient tachypnea of the newborn (TTN) is associated with an increased risk of early childhood asthma. However, the question remains whether both asthma and TTN have common risk factors as well as the same underlying etiology. This study aims to determine possible risk factors for TTN as well as early childhood asthma.Methods: This study was carried out in two phases. While the first phase included medical records of 1318 newborns, the second phase consisted of a phone survey.Results: Elective cesarean section (ECS), maternal asthma, gestational age (GA), babies with large and small birth weight, number of pregnancies, and number of children were found to be significantly associated with TTN. ECS, maternal asthma, length of the hospital stay due to TTN, and O2 treatment were statistically significant for asthma. TTN was found to be associated with a subsequent diagnosis of childhood asthma after adjusting for ECS and maternal asthma.Conclusions: Both ECS and maternal asthma are the common risk factors for the development of both TTN and childhood asthma as previously reported. In order to uncover this association, when ECS is taken out, it is seen that the association between TTN and asthma is stronger. Furthermore, O2 treatment and duration of hospital stay due to TTN were also found to be associated with childhood asthma. Association of maternal allergic rhinitis and eczema with TTN was investigated and there was no relationship between maternal allergic rhinitis or maternal eczema and the subsequent diagnosis of TTN.

The severity-dependent relationship of infant bronchiolitis on the risk and morbidity of early childhood asthma

Infants hospitalized for bronchiolitis have a high rate of early childhood asthma. It is not known whether bronchiolitis severity correlates with the risk of early childhood asthma or with asthma-specific morbidity. We sought to determine whether a dose-response relationship exists between severity of infant bronchiolitis and both the odds of early childhood asthma and asthma-specific morbidity. We conducted a population-based retrospective birth cohort study of term healthy infants born from 1995-2000 and enrolled in a statewide Medicaid program. We defined bronchiolitis severity by categorizing infants into mutually exclusive groups based on the most advanced level of health care for bronchiolitis. Health care visits, asthma-specific medications, and demographics were identified entirely from Medicaid and linked vital records files. Asthma was ascertained at between 4 and 5.5 years of age, and 1-year asthma morbidity (hospitalization, emergency department visit, or oral corticosteroid course) was determined between 4.5 and 5.5 years among children with prevalent asthma. Among 90,341 children, 18% had an infant bronchiolitis visit, and these infants contributed to 31% of early childhood asthma diagnoses. Relative to children with no infant bronchiolitis visit, the adjusted odds ratios for asthma were 1.86 (95% CI, 1.74-1.99), 2.41 (95% CI, 2.21-2.62), and 2.82 (95% CI, 2.61-3.03) in the outpatient, emergency department, and hospitalization groups, respectively. Children hospitalized with bronchiolitis during infancy had increased early childhood asthma morbidity compared with that seen in children with no bronchiolitis visit. To our knowledge, this is the first study to demonstrate the dose-response relationship between the severity of infant bronchiolitis and the increased odds of both early childhood asthma and asthma-specific morbidity.

Maternal Fish Consumption During Pregnancy and Risk of Early Childhood Asthma

Maternal Fish Consumption During Pregnancy and Risk of Early Childhood Asthma

Maternal Fish Consumption During Pregnancy and Risk of Early Childhood Asthma

Maternal fish consumption during pregnancy may affect children's asthma risk by modulating early-life immune development. Type of fish intake may be important because of differences in fatty acid content. To test this hypothesis, we conducted a nested case-control study, selecting subjects from the Children's Health Study, a population-based study of school-aged children in southern California. Cases had physician-diagnosed asthma and controls were asthma-free by age 5 years. Mothers or guardians provided information on fish consumption during pregnancy in telephone interviews. We computed odds ratio (OR) and 95% confidence interval (CI) by using conditional logistic regression models that accounted for the sampling. In children born to mothers with a history of asthma, the OR of asthma was 0.20 (95% CI = 0.06–0.65) when mothers ate oily fish at least monthly during pregnancy compared with no consumption (ptrend = 0.006). Maternal oily fish consumption during pregnancy did not benefit children of non-asthmatic mothers. In contrast, fish stick (a source of trans-fats) consumption during pregnancy increased asthma risk in children (OR = 2.04; 95% CI = 1.18–3.51). Our results suggest that maternal oily fish intake during pregnancy may protect offspring from asthma; however, eating fish sticks during pregnancy may increase asthma risk in children.

Parental asthma, parental eczema and asthma and eczema in early childhood

The relationship between parental asthma, parental eczema and asthma and eczema in early childhood was studied in a birth cohort of New Zealand 4-yr-olds. Application of logistic regression and log linear modelling methods revealed the presence of a complicated system of relationships between asthma and eczema in parents and the occurrence of these conditions in early childhood. For boys, the presence of parental asthma increased the risk of early childhood asthma by nearly 2 1 2 times, whereas parental asthma was unrelated to early asthma in girls. For both sexes the presence of parental eczema increased the risks of childhood eczema. Analysis of the joint parental asthma, parental eczema, child asthma, child eczema distributions suggested that the presence of a specific component of inheritance in childhood asthma and childhood eczema so that asthma in parents was associated with asthma but not eczema in boys and eczema in parents was associated with eczema but not asthma in both sexes. However, there was an additional generalised tendency for both asthma and eczema in children to occur together. It is concluded that the widely held belief that asthma and eczema in parents are non-specifically related to the occurrence of these conditions in early childhood reflecting the presence of a general and undifferentiated familial tendency to atopic disease is, at best, an oversimplification of the complex relationships which exist between parental asthma, parental eczema and the occurrence of these conditions in early childhood.