Diverging prevalences and different risk factors for childhood asthma and eczema: a cross-sectional study

This is the final version of the article. Available from BMJ Publishing Groupvia the DOI in this record.OBJECTIVE: To compare the prevalences of and risk factors for asthma, wheeze, hay fever and eczema in primary schoolchildren in Aberdeen in 2014. DESIGN: Cross-sectional survey. SETTING: Primary schools in Aberdeen, North-East Scotland. PARTICIPANTS: Children in Scottish school years primary 1-7 were handed a questionnaire by their class teacher to be completed by their parents and returned to the researchers by post or online. MAIN OUTCOME MEASURES: Lifetime history of asthma, eczema and hay fever, and recent history of wheeze. RESULTS: 41 schools agreed to participate (87%). 11,249 questionnaires were distributed and 3935 returned (35%). A parent-reported lifetime history of asthma, eczema and hay fever was present in 14%, 30% and 24% of children, respectively. The odds of lifetime asthma increased with age (OR 1.1 per year, 95% CI 1.1 to 1.2), male sex (OR 1.89, 95% CI 1.4 to 2.3), parental smoking (OR 1.7, 95% CI 1.2 to 2.3) and eczema (OR 6.6, 95% CI 5.2 to 8.4). Prevalence of recent wheeze was also reported to be 14% and was positively associated with male sex, parental smoking and eczema. In contrast, parental eczema was the only identified predictor of childhood eczema risk. CONCLUSIONS: The lifetime prevalence of asthma in primary schoolchildren was 14% in this survey, approximately half the prevalence of eczema. We report diverging prevalences in relation to previous studies in our locality, and different risk factors for asthma and eczema. These findings suggest that asthma and eczema are unlikely to have a common origin.This study was funded by Chest Heart and Stroke Scotland and a private donation from the family of Blanche Dawson, who conducted the initial 1964 Aberdeen Schools Asthma Survey

Pulmonary epithelial barrier and immunological functions at birth and in early life - key determinants of the development of asthma? A description of the protocol for the Breathing Together study

Acknowledgements The authors are indebted to the participants and parents who have already been recruited. We also acknowledge the enthusiasm and endeavour of the research nurse team which includes: Stephen Main, Margaret Connon, Catherine Beveridge, Julie Baggott, Kay Riding, Ellie McCamie, Maria Larsson, Lynda Melvin, Mumtaz Idris, Tara Murray, Nicky Tongue, Nicolene Plaatjies, Sheila Mortimer, Sally Spedding, Susy Grevatt, Victoria Welch, Morag Zelisko, Jillian Doherty, Jane Martin, Emma Macleod and Cilla Snape. We are also delighted to be working alongside the following colleagues in laboratories: Marie Craigon, Marie McWilliam, Maria Zarconi, Judit Barabas, Lindsay Broadbent, Ceyda Oksel and Sheerien Manzoor. Grant information The study is supported by the Wellcome Trust [108818]; and the PHA HSC R&D Division, Northern Ireland.Peer reviewedPublisher PD

Duration of total and exclusive breastfeeding, timing of solid food introduction and risk of allergic diseases: a systematic review and meta-analysis [Abstract]

Background Allergic diseases are the leading causes of chronic illness in children and young adults in the UK. Aim To undertake a comprehensive review of the evidence on the effect of breastfeeding (BF) duration and timing of solid food introduction (SFI), on the risk of wheeze, atopic dermatitis, rhino-conjunctivitis, food allergy, allergic sensitisation and measures of lung function or bronchial hyper-responsiveness. Methods We carried out a systematic review following the PRISMA guidelines (International Prospective Register of Systematic Reviews [PROSPERO] CRD42013003802). We included intervention, cohort, case-control and cross-sectional studies. Following literature searches (July 2013), study eligibility, data extraction and risk of bias assessments were conducted independently by two investigators. Random effects meta-analyses were used to pool results. Five levels of comparison of total or exclusive BF duration were used to assess disease risk in children at age 0–4 yrs, 5–15 yrs or 15+yrs: ‘never vs ever’,’≥1–2 months vs. <1–2 months’, ‘≥3–4 months vs. <3–4 months’, ‘≥5–7 months vs. <5–7 months’, and ‘≥8–12 months vs. <8–12 months’. Exclusive BF (EBF; BF without formula or solid food supplementation) was categorised as ‘≥0–2 months vs. <0–2 months’, ‘≥3–4 months vs. <3–4 months’ and ‘≥5+ months vs. <5+ months’, and SFI as ‘≥3–4 months vs. <3–4 months’. Publication bias was assessed using Egger’s asymmetry test. Results Of 16,289 identified studies, 564 met the inclusion criteria and were eligible for analysis. We found reduced risk of wheezing in children aged 5–14 yrs with longer BF or EBF duration, which was dose-dependent, but there was evidence of publication bias (BF and odds of recurrent wheezing P = 0.007). Similar results were found for recurrent wheeze at age 5–14 yrs but not in other ages. Measures of lung function were also increased with increased BF or EBF duration. We found no evidence that BF duration influences other allergic outcomes, and no evidence that timing of SFI influences any of the outcomes assessed. Conclusion Longer breastfeeding duration may protect against wheezing later in childhood. Any effect is likely to be through effects on lung function rather than allergic sensitisati

Intestinal interstitial fluid isolation provides novel insight into the human host-microbiome interface

AIMS: The gastrointestinal (GI) tract is composed of distinct sub-regions, which exhibit segment-specific differences in microbial colonization and (patho)physiological characteristics. Gut microbes can be collectively considered as an active endocrine organ. Microbes produce metabolites, which can be taken up by the host and can actively communicate with the immune cells in the gut lamina propria with consequences for cardiovascular health. Variation in bacterial load and composition along the GI tract may influence the mucosal microenvironment and thus be reflected its interstitial fluid (IF). Characterization of the segment-specific microenvironment is challenging and largely unexplored because of lack of available tools. METHODS AND RESULTS: Here, we developed methods, namely tissue centrifugation and elution, to collect IF from the mucosa of different intestinal segments. These methods were first validated in rats and mice, and the tissue elution method was subsequently translated for use in humans. These new methods allowed us to quantify microbiota-derived metabolites, mucosa-derived cytokines, and proteins at their site-of-action. Quantification of short-chain fatty acids showed enrichment in the colonic IF. Metabolite and cytokine analyses revealed differential abundances within segments, often significantly increased compared to plasma, and proteomics revealed that proteins annotated to the extracellular phase were site-specifically identifiable in IF. Lipopolysaccharide injections in rats showed significantly higher ileal IL-1β levels in IF compared to the systemic circulation, suggesting the potential of local as well as systemic effect. CONCLUSION: Collection of IF from defined segments and the direct measurement of mediators at the site-of-action in rodents and humans bypasses the limitations of indirect analysis of faecal samples or serum, providing direct insight into this understudied compartment

The Canadian Healthy Infant Longitudinal Development (CHILD) birth cohort study: Assessment of environmental exposures

The Canadian Healthy Infant Longitudinal Development birth cohort was designed to elucidate interactions between environment and genetics underlying development of asthma and allergy. Over 3600 pregnant mothers were recruited from the general population in four provinces with diverse environments. The child is followed to age 5 years, with prospective characterization of diverse exposures during this critical period. Key exposure domains include indoor and outdoor air pollutants, inhalation, ingestion and dermal uptake of chemicals, mold, dampness, biological allergens, pets and pests, housing structure, and living behavior, together with infections, nutrition, psychosocial environment, and medications. Assessments of early life exposures are focused on those linked to inflammatory responses driven by the acquired and innate immune systems. Mothers complete extensive environmental questionnaires including time-activity behavior at recruitment and when the child is 3, 6, 12, 24, 30, 36, 48, and 60 months old. House dust collected during a thorough home assessment at 3–4 months, and biological specimens obtained for multiple exposure-related measurements, are archived for analyses. Geo-locations of homes and daycares and land-use regression for estimating traffic-related air pollution complement time-activity-behavior data to provide comprehensive individual exposure profiles. Several analytical frameworks are proposed to address the many interacting exposure variables and potential issues of co-linearity in this complex data set

Asthma Is a Risk Factor for Respiratory Exacerbations Without Increased Rate of Lung Function Decline:Five-Year Follow-up in Adult Smokers From the COPDGene Study

BACKGROUND: Previous investigations in adult smokers from the COPDGene Study have shown that early-life respiratory disease is associated with reduced lung function, COPD, and airway thickening. Using 5-year follow-up data, we assessed disease progression in subjects who had experienced early-life respiratory disease. We hypothesized that there are alternative pathways to reaching reduced FEV1 and that subjects who had childhood pneumonia, childhood asthma, or asthma-COPD overlap (ACO) would have less lung function decline than subjects without these conditions.METHODS: Subjects returning for 5-year follow-up were assessed. Childhood pneumonia was defined by self-reported pneumonia at &lt; 16 years. Childhood asthma was defined as self-reported asthma diagnosed by a health professional at &lt; 16 years. ACO was defined as subjects with COPD who self-reported asthma diagnosed by a health-professional at ≤ 40 years. Smokers with and those without these early-life respiratory diseases were compared on measures of disease progression.RESULTS: Follow-up data from 4,915 subjects were examined, including 407 subjects who had childhood pneumonia, 323 subjects who had childhood asthma, and 242 subjects with ACO. History of childhood asthma or ACO was associated with an increased exacerbation frequency (childhood asthma, P &lt; .001; ACO, P = .006) and odds of severe exacerbations (childhood asthma, OR, 1.41; ACO, OR, 1.42). A history of childhood pneumonia was associated with increased exacerbations of COPD (absolute difference [β], 0.17; P = .04). None of these early-life respiratory diseases were associated with an increased rate of lung function decline or progression on CT scans.CONCLUSIONS: Subjects who had early-life asthma are at increased risk of COPD developing and of having more active disease with more frequent and severe respiratory exacerbations without an increased rate of lung function decline over a 5-year period.TRIAL REGISTRY: ClinicalTrials.gov; No. NCT00608764; https://clinicaltrials.gov.</p