Development Of Asthma In Children Research Articles

A Comprehensive Look at the Development of Asthma in Children.

Asthma, a prevalent chronic respiratory condition affecting millions of children globally, presents a significant health challenge. This review critically examines the developmental pathways of asthma in children, focusing on genetic, environmental, and early-life determinants. Specifically, we explore the impact of prenatal and postnatal factors such as maternal smoking, nutrition, respiratory infections, and allergen exposure on asthma development. Our analysis highlights the intricate interplay of these influences and their contribution to childhood asthma. Moreover, we emphasize targeted strategies and interventions to mitigate its burden, including genetic counseling for at-risk families, environmental modifications to reduce triggers, and early-life immunomodulation. By delving into these preventive measures and interventions, our review aims to provide actionable insights for healthcare professionals in developing tailored strategies to address the complexities of childhood asthma. In summary, this article offers a detailed examination of asthma development in children, aiming to enhance understanding and inform efforts to reduce its burden through targeted interventions.

ST2 and IL-33 polymorphisms and the development of childhood asthma: a prospective birth cohort study in Finnish children.

The ST2/IL-33 signaling pathway has an important role in the host inflammatory response. Here we aimed to study the association of ST2 and IL-33 polymorphisms with serum soluble (s) ST2 and IL-33 concentrations in healthy Finnish children and, in addition, their association with childhood asthma. In total, 146 children were followed from birth to the age 7 years for the development of asthma. Single-nucleotide polymorphisms (SNPs) in ST2 and IL-33 were determined, and associations of the SNP variants with serum levels of sST2 and IL-33 at age of 13 months and with recurrent wheezing and childhood asthma at 7 years of age were analyzed. Children with ST2 rs1041973 AC/AA genotypes had significantly lower level of serum sST2 (2453 pg/mL; IQR 2265) than those with CC genotype (5437 pg/mL; IQR 2575; p = < 0.0001). Similar difference was also observed with ST2 rs13408661. No differences were observed between subjects with studied IL-33 SNPs. Children who carried genetic variants of ST2 rs1041973 or rs13408661 seemed to have a higher risk of asthma. In contrast, children who carried genetic variants of IL-33 rs12551268 were less often diagnosed with asthma. Even though these SNPs seemed to associate with asthma, the differences were not statistically significant.

The association of infant urinary adrenal steroids with the risk of childhood asthma development

BackgroundAdrenal steroids play important roles in early-life development. However, our understanding of the effects of perinatal adrenal steroids on the development of childhood asthma is incomplete. ObjectiveTo evaluate the associations between early-life adrenal steroid levels and childhood asthma. MethodsParticipants included the Infant Susceptibility to Pulmonary Infections and Asthma following Respiratory Syncytial Virus Exposure birth cohort children with untargeted urinary metabolomics data measured during early infancy (n = 264) and nasal immune mediator data measured concurrently at age 2 to 6 months (n = 76). A total of 11 adrenal steroid compounds were identified using untargeted metabolomics and 6 asthma-relevant nasal immune mediators from multiplex assays were a priori selected. Current asthma at ages 5 and 6 years was ascertained using validated questionnaires. Associations were tested using logistic and linear regression with confounders adjustment. ResultsPregnenetriol disulfate (adjusted odds ratio [aOR] = 0.20, 95% CI = 0.06-0.68) and 3a,21-dihydroxy-5b-pregnane-11,20-dione-21-glucuronide (aOR = 0.34, 95% CI = 0.14-0.75) were inversely associated with childhood asthma at 5 and 6 years after multiple testing adjustment. There was a significant interaction effect of pregnanediol-3-glucuronide by biological sex assigned at birth (aOR = 0.11, 95% CI = 0.02-0.51, for those with female sex) on childhood asthma. Pregnenetriol disulfate was inversely associated with granulocyte-macrophage colony-stimulating factor (β = −0.45, q-value = 0.05). 3a,21-dihydroxy-5b-pregnane-11,20-dione 21-glucuronide was inversely associated with interleukin [IL]-4 (β = −0.29, q-value = 0.02), IL-5 (β = −0.35, q-value = 0.006), IL-13 (β = −0.26, q-value = 0.02), granulocyte-macrophage colony-stimulating factor (β = −0.35, q-value = 0.006), and fibroblast growth factor-β (β = −0.24, q-value = 0.01) after multiple testing adjustment. ConclusionThe inverse association between adrenal steroids downstream of progesterone and 17-hydroxypregnenolone and the odds of childhood asthma and nasopharyngeal type 2 immune biomarkers suggest that increased early-life adrenal steroids may suppress type 2 inflammation and protect against the development of childhood asthma.

Recent Insights into the Environmental Determinants of Childhood Asthma.

Ubiquitous environmental exposures, including ambient air pollutants, are linked to the development and severity of childhood asthma. Advances in our understanding of these links have increasingly led to clinical interventions to reduce asthma morbidity. We review recent work untangling the complex relationship between air pollutants, including particulate matter, nitrogen dioxide, and ozone and asthma, such as vulnerable windows of pediatric exposure and their interaction with other factors influencing asthma development and severity. These have led to interventions to reduce air pollutant levels in children's homes and schools. We also highlight emerging environmental exposures increasingly associated with childhood asthma. Growing evidence supports the present threat of climate change to children with asthma. Environmental factors play a large role in the pathogenesis and persistence of pediatric asthma; in turn, this poses an opportunity to intervene to change the course of disease early in life.

Early-Life Exposure to Air Pollution and Childhood Asthma Cumulative Incidence in the ECHO CREW Consortium

Exposure to outdoor air pollution contributes to childhood asthma development, but many studies lack the geographic, racial and ethnic, and socioeconomic diversity to evaluate susceptibility by individual-level and community-level contextual factors. To examine early life exposure to fine particulate matter (PM2.5) and nitrogen oxide (NO2) air pollution and asthma risk by early and middle childhood, and whether individual and community-level characteristics modify associations between air pollution exposure and asthma. This cohort study included children enrolled in cohorts participating in the Children's Respiratory and Environmental Workgroup consortium. The birth cohorts were located throughout the US, recruited between 1987 and 2007, and followed up through age 11 years. The survival analysis was adjusted for mother's education, parental asthma, smoking during pregnancy, child's race and ethnicity, sex, neighborhood characteristics, and cohort. Statistical analysis was performed from February 2022 to December 2023. Early-life exposures to PM2.5 and NO2 according to participants' birth address. Caregiver report of physician-diagnosed asthma through early (age 4 years) and middle (age 11 years) childhood. Among 5279 children included, 1659 (31.4%) were Black, 835 (15.8%) were Hispanic, 2555 (48.4%) where White, and 229 (4.3%) were other race or ethnicity; 2721 (51.5%) were male and 2596 (49.2%) were female; 1305 children (24.7%) had asthma by 11 years of age and 954 (18.1%) had asthma by 4 years of age. Mean values of pollutants over the first 3 years of life were associated with asthma incidence. A 1 IQR increase in NO2 (6.1 μg/m3) was associated with increased asthma incidence among children younger than 5 years (HR, 1.25 [95% CI, 1.03-1.52]) and children younger than 11 years (HR, 1.22 [95% CI, 1.04-1.44]). A 1 IQR increase in PM2.5 (3.4 μg/m3) was associated with increased asthma incidence among children younger than 5 years (HR, 1.31 [95% CI, 1.04-1.66]) and children younger than 11 years (OR, 1.23 [95% CI, 1.01-1.50]). Associations of PM2.5 or NO2 with asthma were increased when mothers had less than a high school diploma, among Black children, in communities with fewer child opportunities, and in census tracts with higher percentage Black population and population density; for example, there was a significantly higher association between PM2.5 and asthma incidence by younger than 5 years of age in Black children (HR, 1.60 [95% CI, 1.15-2.22]) compared with White children (HR, 1.17 [95% CI, 0.90-1.52]). In this cohort study, early life air pollution was associated with increased asthma incidence by early and middle childhood, with higher risk among minoritized families living in urban communities characterized by fewer opportunities and resources and multiple environmental coexposures. Reducing asthma risk in the US requires air pollution regulation and reduction combined with greater environmental, educational, and health equity at the community level.

Pidotimod as an Immunomodulator: An Unsung Warrior to Restore Immune Dysregulation in Acute and Chronic Lung Disease

Immune dysregulation has been observed in the majority of the infective and non-infectious respiratory illnesses with impact on the natural course of illness in pediatric to geriatric age groups. Immune regulation between Th1 and Th2 is altered and reversal of proportion between these two differential cells and ultimately homeostasis, with predominance Th2 cells will increase susceptibility for recurrent illnesses; is typically documented in pediatric age groups with first respiratory infection during early neonatal period with respiratory viral etiologies. Apart from recurrent childhood infections, pediatric cases with immune dysregulation will have recurrent wheezing in childhood and are prone for development of childhood asthma in adolescent age groups; if immune dysregulation does not restore in time. In adults, respiratory illnesses due acute viral infective etiology will cause immune dysregulation as documented after coronavirus, influenza and respiratory syncytial virus infections. Immune dysregulation has also been documented in chronic respiratory illnesses such bronchial asthma, chronic bronchitis and COPD. Immune dysregulation will cause recurrent exacerbations in these inflammatory conditions. Pidotimod is an immunomodulator which will work as an immunostimulant molecule due to its unique pharmacological actions on antigen presenting cells, and have novel action on immune cell proliferation and differentiation. In spite of three decades of research of this novel drug Pidotimod, still; it is less used as of today for respiratory ailments in spite of need of a molecule with an immunomodulatory effect for prevention and or cure of illnesses; and modification of natural course of recurrent or relapsing course of chronic illnesses. COVID-19 pandemic has taught us many pathways of immune dysregulation which evolved during natural course of disease and now documented with respiratory viral illnesses such as RSV; and its long-term impact as long covid presenting due to immune dysregulation occurred as a natural course in recovered cases. It’s unclear whether long covid is reversible as of now, but the majority of symptoms have been resolved and shown response to versatile molecules such as steroid, multivitamins, L-arginine, Paxlovid, beta blockers with variable results and long-term outcomes. Pidotimod can be used in acute COVID-19 illness without pneumonia and comorbidities in stable cases in outdoor settings, and also; considered as potential option in long covid cases with recurrent respiratory infections. In this review we have discussed basic aspects of Pidotimod, and its role in immunomodulatory effects in acute and chronic respiratory illness which have shown positive outcomes.

Deep T-Cell Profiling Implicates Lung-Resident Rhinovirus-Specific Cells in the Development and Persistence of Severe Childhood Asthma

Deep T-Cell Profiling Implicates Lung-Resident Rhinovirus-Specific Cells in the Development and Persistence of Severe Childhood Asthma

Early-life pulmonary viral infection leads to long-term functional and lower airway structural changes in the lungs.

Early-life respiratory virus infections have been correlated with enhanced development of childhood asthma. In particular, significant numbers of respiratory syncytial virus (RSV)-hospitalized infants go on to develop lung disease. It has been suggested that early-life viral infections may lead to altered lung development or repair that negatively impacts lung function later in life. Our data demonstrate that early-life RSV infection modifies lung structure, leading to decreased lung function. At 5 wk postneonatal RSV infection, significant defects are observed in baseline pulmonary function test (PFT) parameters consistent with decreased lung function as well as enlarged alveolar spaces. Lung function changes in the early-life RSV-infected group continue at 3 mo of age. The altered PFT and structural changes induced by early-life RSV were mitigated in TSLPR-/- mice that have previously been shown to have reduced immune cell accumulation associated with a persistent Th2 environment. Importantly, long-term effects were demonstrated using a secondary RSV infection 3 mo following the initial early-life RSV infection and led to significant additional defects in lung function, with severe mucus deposition within the airways, and consolidation of the alveolar spaces. These studies suggest that early-life respiratory viral infection leads to alterations in lung structure/repair that predispose to diminished lung function later in life.NEW & NOTEWORTHY These studies outline a novel finding that early-life respiratory virus infection can alter lung structure and function long-term. Importantly, the data also indicate that there are critical links between inflammatory responses and subsequent events that produce a more severe pathogenic response later in life. The findings provide additional data to support that early-life infections during lung development can alter the trajectory of airway function.

The urinary metabolites of volatile organic compounds and asthma in young children: NHANES 2011–2018

The vast majority of volatile organic compounds (VOCs) are of biological origin and do not affect human health, while some VOCs or their oxidation products can damage the respiratory system, nervous system, digestive system and blood system after long-term inhalation by humans. There is limited evidence regarding the association of VOCs exposure with childhood asthma. In this study, we examined the associations between metabolites of VOCs (mVOCs) in urine and childhood asthma. We included a total of 1542 children aged 3–12 years who had information on urinary mVOCs, asthma and essential covariates in the current analyses. After controlling for covariates, we used logistic regression to assess the association between urinary mVOCs and childhood asthma. Then, we examined effect measure modification by child age, gender, race/ethnicity and serum cotinine. 2-Methylhippuric acid (xylene metabolites) (OR: 1.14; 95 % CI: 0.87, 1.59), N-acetyl-S-(benzyl)-l-cysteine (toluene metabolites) (OR: 1.15 95 % CI: 0.76, 1.71), N-acetyl-S-(2-carboxyethyl)-l-cysteine (acrolein metabolites) (OR: 1.09; 95 % CI: 0.61, 1.75), N-acetyl-S-(3-hydroxypropyl)-l-cysteine (acrolein metabolites) (OR: 1.10; 95 % CI: 0.66, 1.80), and N-acetyl-S-(3-hydroxypropyl-1-methyl)-l-cysteine (crotonaldehyde metabolites) (OR: 1.18; 95 % CI: 0.68, 2.01) were weakly associated with the prevalence of asthma in children. Among female children, 2MHA (2-methylhippuric acid) in urine was significantly associated with the prevalence of asthma (OR: 1.81 95 % CI: 1.07, 3.05). At the same time, BMA (N-acetyl-S-(benzyl)-l-cysteine) was significantly associated with the prevalence of asthma in non-Hispanic White (OR:2.09 95 % CI: 0.91, 4.66) and Black (OR:1.90 95 % CI: 0.96, 3.71) children. We found that gender modified the associations between urinary 2MHA and the odds of asthma (interaction term p value = 0.03). Therefore, exposure to VOCs and the development of childhood asthma remains controversial, and the interpretation of these results needs to be treated with caution and should be confirmed in future studies.Therefore, exposure to VOCs and the development of childhood asthma remains controversial, and the interpretation of these results needs to be treated with caution and should be confirmed in future studies.

Beyond bacteria: early-life gut virome link with childhood asthma development.

Beyond bacteria: early-life gut virome link with childhood asthma development.

The influence of urban trees and total vegetation on asthma development in children

Objective: We aimed to assess whether the influence of urban vegetation on asthma development in children (&lt;13 years) varies by type (e.g., total vegetation, tree type, and grass) and season. Methods: We used a cohort of all children born in Montreal, Canada, between 2000 and 2015. Children and cases were identified from linked medico-administrative databases. Exposure to residential vegetation was estimated using the Normalized Difference Vegetation Index (NDVI) for total vegetation and using the total area covered by deciduous and evergreen crowns for trees in 250 m buffers centered on residential postal codes. Seasonal variations in vegetation were modeled by setting values to zero on days outside of pollen and leaf-on seasons. Cox models with vegetation exposures, age as a time axis, and adjusted for sex, material deprivation, and health region were used to estimate hazard ratios (HR) for asthma development. Results: We followed 352,946 children for a total of 1,732,064 person-years and identified 30,816 incident cases of asthma. While annual vegetation (total and trees) measures did not appear to be associated with asthma development, models for pollen and leaf-on seasons yielded significant nonlinear associations. The risk of developing asthma was lower in children exposed to high levels (&gt;33,300 m2) of deciduous crown area for the leaf-on season (HR = 0.69; 95% confidence interval [CI] = 0.67, 0.72) and increased for the pollen season (HR = 1.07; 95% CI =1.02, 1.12), compared with unexposed children. Similar results were found with the Normalized Difference Vegetation Index. Conclusion: The relationship between urban vegetation and childhood asthma development is nonlinear and influenced by vegetation characteristics, from protective during the leaf-on season to harmful during the pollen season.

Greater fruit and vegetables consumption, and adherence to a Mediterranean type of diet reduces the risk for asthma in children; a systematic review and meta-analysis

The objective of this study was to explore the relationship between the consumption of fruits, vegetables and adherence to the Mediterranean diet with childhood asthma development and severity. A systematic literature search and synthesis of the results was performed throughout the last two decades. A total of 45 studies were analysed and 392,797 children were included. Greater adherence to a Mediterranean type of diet was inversely associated with asthmatic outcomes (OR:0.71,95% CI:0.54,0.88). Regarding fruits, vegetables consumption, a significant inverse association between increased fruits or vegetable intake and asthma was found (OR:0.82,95% CI:0.77,0.86; 0.84,95% CI:0.77,0.91, respectively). Fruits and vegetables consumption combined was also inversely related to all asthmatic outcomes (OR:0.65,95% CI:0.49,0.78). The level of heterogeneity was moderate-to-high (30%–97%). The present review and meta-analysis show a trend to an inverse association between adherence to the Mediterranean diet or a healthy diet rich in fruits and vegetables and the occurrence of childhood asthma but with a low level of certainty.

The re-emerging role of linoleic acid in paediatric asthma.

Asthma is the most common chronic disease within the paediatric population. Although it is multifactorial, its onset may be linked to early-life exposures with subsequent impact on immune system development. Microbial and dietary metabolic products have been implicated in the development and exacerbation of paediatric asthma. Linoleic acid is the most common omega-6 polyunsaturated fatty acid in the Western diet. In this review, we summarise the literature regarding the involvement of linoleic acid in the development of and its impact on existing paediatric asthma. First, we summarise the existing knowledge surrounding the relationship between human microbial metabolism and allergic diseases in children. Next, we examine cellular or animal model-based mechanistic studies that investigated the impact of dietary- and microbial-derived linoleic acid metabolites on asthma. Finally, we review the literature investigating the impact of linoleic acid metabolites on the development and exacerbation of childhood asthma. While there is conflicting evidence, there is growing support for a role of linoleic acid in the onset and pathophysiology of asthma. We recommend that additional cellular, animal, and longitudinal studies are performed that target linoleic acid and its metabolites.

Association between household cleaning product exposure in infancy and development of recurrent wheeze and asthma.

Household chemicals may act as irritants in the lungs; however, their association with recurrent wheeze and asthma in children remains controversial. We aimed to investigate if household cleaning product exposure in infancy is associated with recurrent wheezing and asthma development in children. We analyzed data from two cohorts: MARC-35 consisting of 815 children with history of severe bronchiolitis in infancy, and MARC-43 consisting of 525 healthy children in infancy. Frequency of use of cleaning product at the child's home during infancy was collected via telephone interview with parents. Outcomes were recurrent wheezing by age 3years and asthma diagnosis at age 6years. In MARC-35, there was no association between cleaning product exposure in infancy and recurrent wheeze (adjusted HR = 1.01 [95% CI 0.66-1.54] for 4-7days/week exposure frequency), nor asthma (adjusted OR = 0.91 [95% CI 0.51-1.63]). In MARC-43, there was also no association between cleaning product exposure in infancy and recurrent wheeze (adjusted HR = 0.69 [95% CI 0.29-1.67] for 4-7days/week exposure frequency). We found no association between household cleaning product exposure in infancy and later development of recurrent wheeze or asthma, even among children who are at high risk for asthma due to history of severe bronchiolitis.

From preschool wheezing to asthma: Immunological determinants.

Asthma represents a chronic respiratory disease affecting millions of children worldwide. The transition from preschool wheezing to school-age asthma involves a multifaceted interplay of various factors, including immunological aspects in early childhood. These factors include complex cellular interactions among different immune cell subsets, induction of pro-inflammatory mediators and the molecular impact of environmental factors like allergens or viral infections on the developing immune system. Furthermore, the activation of specific genes and signalling pathways during this early phase plays a pivotal role in the manifestation of symptoms and subsequent development of asthma. Early identification of the propensity or risk for asthma development, for example by allergen sensitisation and viral infections during this critical period, is crucial for understanding the transition from wheeze to asthma. Favourable immune regulation during a critical 'window of opportunity' in early childhood can induce persistent changes in immune cell behaviour. In this context, trained immunity, including memory function of innate immune cells, has significant implications for understanding immune responses, potentially shaping long-term immunological outcomes based on early-life environmental exposures. Exploration of these underlying immune mechanisms that drive disease progression will provide valuable insights to understand childhood asthma development. This will be instrumental to develop preventive strategies at different stages of disease development for (i) inhibiting progression from wheeze to asthma or (ii) reducing disease severity and (iii) uncovering novel therapeutic strategies and contributing to more tailored and effective treatments for childhood asthma. In the long term, this shall empower healthcare professionals to develop evidence-based interventions that reduce the burden of asthma for children, families and society overall.

Exploring impacts of greenness accessibility on childhood asthma development: An Ontario birth cohort study

Exploring impacts of greenness accessibility on childhood asthma development: An Ontario birth cohort study

Fungi in Early-Life House Dust Samples and the Development of Asthma: A Birth Cohort Study.

Rationale: Fungal exposure has been associated with predisposing and protective effects on the development of childhood asthma. Objectives: To study whether early-life house dust mycobiota composition is associated with the development of asthma. Methods: Mycobiota were determined by amplicon sequencing from 382 dust samples collected from living room floors 2 months after birth in homes of the LUKAS cohort. Asthma status by 10.5 years of age was defined from questionnaires and assigned as ever asthma (n = 68) or current asthma (n = 27). Inhalant atopy was clinically determined at the same age. β-composition was analyzed using PERMANOVA-S, and asthma and atopy analyses were performed using discrete time hazard models and logistic regression, respectively. Results: The house dust mycobiota composition based on Bray-Curtis distance was different in the homes of children who later did or did not develop asthma. The first and the fourth axes scores of principal coordinates analysis based on Bray-Curtis were associated with ever asthma. Of the genera with the strongest correlation with these axes, the relative abundance of Boeremia, Cladosporium, Microdochium, Mycosphaerella, and Pyrenochaetopsis showed protective associations with asthma. None of these associations remained significant after mutual adjustment among the five genera or when mutually adjusted for other microbial cell wall markers and previously identified asthma-protective bacterial indices. Neither fungal α-diversity nor load was associated with asthma in the whole population, but higher fungal richness was a risk factor among children on farms. Higher fungal loads (measured via quantitative polymerase chain reaction) in house dust were associated with the risk of inhalant atopy. Conclusions: The results of our analyses from this well-characterized birth cohort suggest that the early-life house dust mycobiota in Finnish homes, characterized via DNA amplicon sequencing, do not have strong predisposing or protective effects on asthma development.

Managing Asthma During Pregnancy and the Postpartum Period

Asthma is one of the most common chronic diseases in pregnancy and is associated with adverse perinatal outcomes. Asthma symptoms worsen in approximately 40% of women, and exacerbations requiring medical intervention occur in at least 20% of women. Factors associated with exacerbation and worsening asthma include multiparity, obesity, black race, exacerbations prior to pregnancy and poor asthma control. Exacerbations are associated with further increased risks for poor perinatal outcomes including low birth weight, preterm birth and small for gestational age, as well as an increase in the development of asthma in early childhood. Common medications used for asthma, including short acting beta agonists and inhaled corticosteroids are considered safe to use in pregnancy. While guidelines generally suggest traditional step therapy for the management of asthma in pregnancy, there are alternative models of care and management approaches which may be effective in pregnancy, but require more research. These include single inhaler maintenance and reliever (SMART) therapy, treatment adjustment with fractional exhaled nitric oxide (FeNO), treatable traits personalised medicine approaches and telemedicine. Little is known about changes to asthma in the postpartum period, however, low adherence to medication, and potential effects of postpartum depression on asthma exacerbation risk warrant further research.

Salivary microbiome and asthma risk in children with orofacial defects.

Patients with congenital orofacial defects, cleft lip (CL),cleft palate (CP),and cleft lip and palate (CLP)have continuous exposure of the respiratory system to the microbiome from the oral environment, offering opportunities to develop mucosal immunity in the airway. This two-part study aims to analyze data on asthma occurrence in CL, CP, and CLP infants and the composition of the salivary microbiome, and to evaluate the oral microbiota and its association with the risk of developing childhood asthma. Patient data from the research database of Chang Gung Memorial Hospital from 2004 to 2015 were retrospectively analyzed by multivariable regression. Diseases diagnoses were defined by ICD codes. Asthma must also meet the criteria for receiving selective β2 agonistic or/and inhaled corticosteroid treatments twice within 1 year. Analysis of the saliva microbiome was performed prospectively from 2016 to 2020 in 10 healthy term infants and 10 CLP infants on postnatal 7th day, 1 month, and 6 months by next-generation sequencing. Asthma and nonasthma groups included 988 and 3952 patients, respectively. The incidence of asthma development was higher in patients with CP than in CL and CLP groups (aOR: 5.644, CI: 1.423-22.376). The species composition of the microbiome at 1 and 6 months was significantly different between infants with CLP and healthy infants. Children with orofacial defects have a higher risk of developing asthma with a possible contribution from oral microbiota in the early months of life.

Early-Life Weight Status and Risk of Childhood Asthma or Recurrent Wheeze in Preterm and Term Offspring.

Excessive weight is associated with the development of childhood asthma. However, trends among preterm and term offspring may differ. To assess whether the association of longitudinal weight for age (WFA) and odds of asthma/recurrent wheeze in early life differs between children born preterm and those born at term. This study used prospectively collected data from the Vitamin D Antenatal Asthma Reduction Trial. Children (n= 804) were followed-up and anthropometric measurements, including WFA, were taken at birth and annually until the age of 6 years. The primary outcome was asthma/recurrent wheeze by age 3 and 6 years. Among the offspring, 71 (8.8%) were premature. In all the children, the odds of asthma/recurrent wheeze increased by 15% (adjusted odds ratio [aOR], 1.15; 95% CI, 1.10-1.20; P < .001) by age 3 years and 9% (aOR, 1.09; 95% CI, 1.07-1.11; P < .001) by age 6 years for each unit increase in WFA z score. Odds were different between term and preterm offspring (Pinteraction < .001). In term offspring, the odds of having asthma/recurrent wheeze by age 3 and 6 years increased by 22% and 15%, respectively (aOR, 1.22, 95% CI, 1.16-1.27, P < .001, and aOR, 1.15, 95% CI, 1.11-1.18, P < .001). In preterm offspring, by age 3 years, odds of asthma/recurrent wheeze decreased by 10% for each unit increase in WFA z score (aOR, 0.90; 95% CI, 0.81-0.99; P= .030) and decreased by 27% by age 6 years (aOR, .73; 95% CI, 0.61-0.86; P < .001). During early life, increasing standardized WFA is associated with higher odds of asthma/recurrent wheeze in term children. In contrast, in preterm children, a higher standardized WFA during catch-up growth may decrease the odds of asthma/recurrent wheeze associated with prematurity.