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BackgroundPreventing exacerbations of asthma is a major goal in current guidelines. We aimed to develop a prediction model enabling practitioners to identify patients at risk of severe exacerbations who could potentially benefit from a change in management.MethodsWe used data from a 12-month primary care pragmatic trial; candidate predictors were identified from GINA 2014 and selected with a multivariable bootstrapping procedure. Three models were constructed, based on: (1) history, (2) history+spirometry and (3) history+spirometry+FeNO. Final models were corrected for overoptimism by shrinking the regression coefficients; predictive performance was assessed by the area under the receiver operating characteristic curve (AUROC) and Hosmer–Lemeshow test. Models were externally validated in a data set including patients with severe asthma (Unbiased BIOmarkers in PREDiction of respiratory disease outcomes).Results80/611 (13.1%) participants experienced ≥1 severe exacerbation. Five predictors (Asthma Control Questionnaire score, current smoking, chronic sinusitis, previous hospital admission for asthma and ≥1 severe exacerbation in the previous year) were retained in the history model (AUROC 0.77 (95% CI 0.75 to 0.80); Hosmer–Lemeshow p value 0.35). Adding spirometry and FeNO subsequently improved discrimination slightly (AUROC 0.79 (95% CI 0.77 to 0.81) and 0.80 (95% CI 0.78 to 0.81), respectively). External validation yielded AUROCs of 0.72 (95% CI 0.70 to 0.73; 71 to 0.74 and 0.71 to 0.73) for the three models, respectively; calibration was best for the spirometry model.ConclusionsA simple history-based model extended with spirometry identifies patients who are prone to asthma exacerbations. The additional value of FeNO is modest. These models merit an implementation study in clinical practice to assess their utility.Trial registration numberNTR 1756.

IntroductionEarly infant diet might influence the risk of subsequent allergic disease.MethodsThe Merthyr Allergy Prevention Study (MAPS) was a randomised controlled trial in infants at high risk of allergic disease. The trial determined whether a cow’s milk exclusion diet for the first 4 months of life decreased the risk of allergic disease including asthma compared with a normal diet. A soya milk preparation was offered to those in the intervention group. A standardised questionnaire for allergic disease was completed at ages 1, 7, 15 and 23 years, with clinical assessment at 1, 7 and 23 years. The effect of the intervention on the risk of atopy, asthma and wheeze at age 23 years was determined.Findings487 subjects entered the study; at age 23 years 299 completed the questionnaire, of which 119 attended clinical assessment. Subjects randomised to the intervention group had a significantly increased risk of atopy (adjusted OR 2.97, 95% CI 1.30 to 6.80; p=0.01) and asthma (OR 2.07, 95%CI 1.09 to 3.91; p=0.03) at age 23 years, but not wheeze (OR 1.43, 95%CI 0.87 to 2.37; p=0.16). Earlier exposure to cow’s milk was associated with a decreased risk of wheeze and asthma at age 23 years, while earlier exposure to soya milk was associated with an increased risk of atopy and asthma.InterpretationIn infants at high risk of allergic disease, either cow’s milk exclusion or early soya milk introduction for the first 4 months of life increases the risk of atopy, wheeze and asthma in adulthood.

The school is a complex microenvironment of indoor allergens, pollutants, and other exposures. The school represents an occupational model for children and exposures in this environment have a significant health effect. Current research establishes an association between school exposure and asthma morbidity in children. This review will focus on common school environmental exposures (cockroach, rodents, cat, dog, classroom pets, dust mite, fungus, and pollution) and their impact on children with allergies and asthma. Understanding and evaluation of school-based environments is needed to help guide school-based interventions. School-based interventions have the potential for substantial benefit to the individual, school, community, and public health. However, there is a paucity data on school-based environmental interventions and health outcomes. The studies performed to date are small and cross-sectional with no control for home exposures. Randomized controlled school-based environmental intervention trials are needed to assess health outcomes and the cost-effectiveness of these interventions. The School Inner-City Asthma Intervention Study (SICAS 2), a NIH/NIAID randomized controlled clinical trial using environmental interventions modeled from successful home-based interventions, is currently underway with health outcome results pending. If efficacious, these interventions could potentially help further guide school-based interventions potentially with policy implications. In the meanwhile, the allergist/immunologist can continue to play a vital role in improving the quality of life in children with allergies and asthma at school through the use of the ADA policy and Section 504 of the Rehabilitation Act as well as encouraging adoption of toolkits to build successful school-based asthma programs and asthma-friendly schools.

Laboratory exposures of persons with asthma to diesel exhaust are associated with physiological and clinical changes that are consistent with diminished disease control. In this trial, which involved persons with mild or moderate asthma, exposure to diesel exhaust during a walk on a London street was associated with physiological changes in lung function as compared with a walk in a nearby park. Exposure to diesel exhaust can result in worsening of asthma. In persons with mild or moderate asthma, exposure to diesel exhaust during a walk on a London street was associated with physiological changes in lung function as compared with a walk in a nearby park. Air pollution from road traffic is a serious health hazard, and particulates from diesel exhaust have become cause for increasing concern. Epidemiologic studies have demonstrated associations between ambient particulate matter and respiratory-associated morbidity and mortality; these effects may be greater among persons with preexisting respiratory disease, including asthma. 1 , 2 Diesel engines emit relatively low concentrations of carbon monoxide and carbon dioxide, but as compared with gasoline engines of similar size, diesel engines can generate more than 100 times the number of particles per distance traveled 3 and are major contributors to atmospheric particulate pollution. In urban environments, almost 90% of traffic-generated . . .

IntroductionAsthma is a leading cause of morbidity and healthcare use among children. Risk factors of childhood asthma include atopic predisposition and severe wheezing episodes caused by rhinovirus infection in early life. In children with first-time rhinovirus-induced wheezing, we aim to study the response of a short corticosteroid treatment to prevent recurrent wheezing and asthma.Method and analysisThis is a double-blind, randomised, placebo-controlled, phase IV, international multicentre trial involving eight sites in Norway, Sweden and Finland. Two hundred and eighty 3–23 months old steroid-naïve children are randomised 1:1 to receive oral dexamethasone (0.3 mg/kg/day) versus placebo in 3 days for their first wheezing episode and rhinovirus infection. Rhinovirus is diagnosed with multiplex PCR. The two co-primary outcomes are time to next physician-confirmed wheezing episode, and time to asthma, within 24 months from inclusion. Asthma is defined as fulfilment of the 2007 National Asthma Education and Prevention Program—criteria for initiating asthma controller medication in children aged 0–4 years. Primary interaction analyses are age, gender, atopic predisposition, risk genotypes and viral co-detection. The optimal cut-off on the rhinovirus genome load used to define a true rhinovirus infection will be assessed by exploring interactions between rhinovirus genomic loads and study drug on the co-primary outcomes. Secondary outcomes are number of wheezing episodes, duration and severity of each wheezing episode, bronchial hyperreactivity, quality of life and safety (height/weight development) at 24 months from inclusion.Ethics and disseminationRhinovirus positive children with acute wheezing fulfilling inclusion and exclusion criteria are enrolled after informed consent from both caregivers. This trial has received ethical approval from all sites. Results will be submitted to Competent Authorities and disseminated via peer-reviewed publications and conferences within paediatrics and other relevant fields. If proven effective, findings may be implemented directly into paediatric clinical guidelines.Trial registration number NCT03889743.

Objective Maternal asthma is the most common chronic disease complicating pregnancy and is a risk factor for bronchiolitis in infancy. Recurrent episodes of bronchiolitis are strongly associated with the development of childhood asthma. Methods We conducted a follow-up study of infants born to women with asthma who completed a double-blind randomised controlled trial during pregnancy. In this trial, pregnant women with asthma were assigned to treatment adjustment by an algorithm using clinical symptoms (clinical group) or the fraction of exhaled nitric oxide (FeNO group) and we showed that the FeNO group had significantly lower asthma exacerbation rates in pregnancy. Results 146 infants attended the 12-month follow-up visit. Infants born to mothers from the FeNO group were significantly less likely to have recurrent episodes of bronchiolitis in the first year of life (OR 0.08, 95% CI 0.01 to 0.62; p=0.016) as compared with the clinical group. Conclusions Optimised management of asthma during pregnancy may reduce recurrent episodes of bronchiolitis in infancy, which could potentially modulate the risk to develop or the severity of emerging childhood asthma.

ObjectivesThe risk of incident asthma and bronchial hyper-reactivity associated with early life exposure to traffic-related air pollution has not been fully elucidated. We aimed to evaluate the hypothesis that the risk of new onset asthma is positively associated with early exposure to traffic-related air pollution in a well-characterised high-risk birth cohort.MethodsInfants at high-risk for asthma were recruited for an intervention study. Birth year exposures to NO, NO2, black carbon and PM2.5 were estimated by land use regression. At 7 years of age, asthma was assessed by a paediatric allergist and bronchial hyper-reactivity was measured by methacholine challenge. Associations between exposures and outcomes were analysed by stepwise multiple logistic regression, adjusted for potential confounding variables.ResultsExposure estimates were available for 184 children; 23 were diagnosed with asthma and 68 with bronchial hyper-reactivity. The IQR (4.1 μg/m3) of birth year PM2.5 was associated with a significantly increased risk of asthma (OR 3.1, 95% CI 1.3 to 7.4) and with a trend to increased risk of bronchial hyper-reactivity. Similar findings were noted in association with NO and NO2, while black carbon did not appear to confer increased risk.ConclusionModest elevations in exposure to some traffic-related air pollutants during the year of birth are associated with new onset asthma assessed at age 7. That significant associations were revealed in spite of a limited sample size emphasises the strengths of a high-risk birth cohort model, along with individual air pollution exposure estimates and well-characterised data on covariates and outcomes.

ObjectiveTo determine whether environmental control using nocturnal temperature controlled laminar airflow (TLA) treatment could improve the quality of life of patients with persistent atopic asthma.DesignRandomised, double-blind, placebo-controlled, parallel-group trial.SettingNineteen European asthma clinics.Participants312 patients aged 7–70 with inadequately controlled persistent atopic asthma.Main outcome measureProportion of patients with an increase of ≥0.5 points in asthma quality of life score after 1 year of treatment.ResultsTLA devices were successfully installed in the bedrooms of 282 (90%) patients included in the primary efficacy analysis. There was a difference in treatment response rate between active (143 of 189, 76%) and placebo (56 of 92, 61%) groups, difference 14.8% (95% CI 3.1 to 26.5, p=0.02).3 In patients aged ≥12, on whom the study was powered, the difference in response rate was similar-active 106 of 143 (74%), placebo 42 of 70 (60%), difference 14.1% (0.6 to 27.7, p=0.059). There was a difference between groups in fractional exhaled nitric oxide change of −7.1 ppb (−13.6 to −0.7, p=0.03). Active treatment was associated with less increase in cat-specific IgE than placebo. There was no difference in adverse event rates between treatment groups.ConclusionInhalant exposure reduction with TLA improves quality of life, airway inflammation and systemic allergy in patients with persistent atopic asthma. TLA may be a treatment option for patients with inadequately controlled persistent atopic asthma.Trial registration numberClinical Trials NCT00986323.

Background: low vitamin D status in pregnancy can influence the offspring’s lung function and contribute to childhood asthma development. The objective of this study was to examine the influence of neonatal vitamin D status on the development of asthma among children age 3–9 years in a large population sample. Method: in a case-cohort study utilizing a Danish biobank and register data we examined the association between neonatal 25-hydroxyvitamin D3 (25(OH)D3) concentrations and incidence of asthma among children aged 3–9 years. Cases of asthma (n = 911) were randomly selected among all cases of asthma in the Danish National Patient Register from children born between 1992 and 2002. The sub-cohort (n = 1423) was randomly selected among all children born in the same period. We used a weighted Cox proportional hazard model assessing the hazard of first asthma diagnoses by quintiles of 25(OH)D3. Results: the median 25(OH)D3 (interquartile range) for asthma cases was 23 nmol/L (14–35) and the sub-cohort 25 nmol/L (14–40). The hazard ratio for developing asthma between ages 3 and 9 years was lower for children in the fifth quintile of neonatal 25(OH)D3 compared to children in the first quintile, both in the unadjusted (0.61 95% CI: 0.46–0.80) and adjusted (0.55 95% CI: 0.39–0.77) analyses. Conclusion: the results from our study suggest that higher neonatal vitamin D concentration may reduce the risk of developing childhood asthma at ages 3–9 years, indicating that neonatal vitamin D status as a proxy of vitamin D status during the prenatal period is important for normal immune- and lung development.

It is hypothesized that the metabolic syndrome explains the association between body mass index (BMI) and asthma in adults. Our objective was to longitudinally compare the relative strengths of the associations of the metabolic syndrome and BMI with incident asthma in adults. We included 4,619 eligible participants in the Coronary Artery Risk Development in Young Adults (CARDIA) cohort followed over 25 years. Incident asthma was defined by a new self-reported provider asthma diagnosis plus either the presence of asthma symptoms and/or use of asthma medications. Cox proportional hazard analyses were performed. Six hundred two subjects (417 women and 185 men) developed incident asthma over 25 years of follow-up. Metabolic syndrome predicted incident asthma among women but not men (unadjusted hazard ratios, 1.50 and 0.98; P = 0.01 and 0.93, respectively). BMI had a similar predictive association among women but not men (unadjusted hazard ratios, 1.19 and 1.04 per 5 units of BMI; P < 0.001 and 0.60, respectively). The association of metabolic syndrome with incident asthma in women was no longer statistically significant after adjustment for BMI (P = 0.44). In contrast, the association of BMI with incident asthma in women remained statistically significant after adjusting for the metabolic syndrome (P = 0.01). In a stepwise model, BMI was a stronger predictor than the metabolic syndrome (P = 0.001). BMI is a stronger predictor of incident asthma among women than the metabolic syndrome. Other obesity-associated factors that are not a part of the metabolic syndrome may play a role in the BMI-asthma association in women.