Exposure to Beta-(1,3)-D-Glucan in House Dust at Age 7–10 Is Associated with Airway Hyperresponsiveness and Atopic Asthma by Age 11–14

Abstract

BackgroundMould exposure has been linked to childhood asthma and bronchial hyper-responsiveness. Few studies have assessed beta-(1,3)-d-glucan (beta-glucan), a significant fungal cell wall constituent, in relation to asthma in adolescence.ObjectiveTo determine whether house dust-derived beta-glucan exposure at age 7–10 is associated with the development and persistence of atopic and non-atopic asthma, and bronchial hyper-responsiveness (BHR) by age 11–14.MethodsDust samples were collected from the 1995 Study of Asthma, Genes, and Environment (SAGE) birth cohort. This cohort was derived from Manitoba provincial healthcare administrative records of children high and low risk for asthma. Samples were collected from the homes of 422 children at age 7–10 and analyzed using beta-glucan and endotoxin-specific Limulus Amoebocyte Lysate assays. Asthma, atopy, and BHR status of each child were also assessed at ages 7–10 and 11–14.ResultsAt age 7–10, beta-glucan dust levels in the home were associated with persistent atopic asthma at age 11–14 (OR 1.79 for each unit increase in levels, 95% CI 1.14–2.81), independent of endotoxin exposure, and Alternaria or Cladosporium sensitization. The likelihood of BHR almost doubled with unit increases in dust beta-glucan in asthmatic children. In children without asthma, exposure to high beta-glucan levels at age 7–10 also elevated risk for BHR in adolescence (OR 1.74, 95% CI 1.05–2.89). New-onset atopic asthma was twice more likely following high beta-glucan exposure in children without asthma but the association did not reach statistical significance. No associations were evident with concurrent asthma phenotype at age 7–10 or non-atopic asthma at age 11–14.ConclusionThese findings implicate home beta-glucan exposure at school-age as a risk factor for persistent atopic asthma and new-onset BHR. The higher prevalence of BHR in urban adolescents may be propagated by this home exposure.

Environmental determinants of allergy and asthma in early life

“…Qualitative assessments of fungal exposure in the form of mildew odor or visible mold have been linked with increased risk of allergic rhinitis and asthma 96-98 . This finding is corroborated by studies using quantitative fungal measures, such as DNA-based analyses 99 and β-1,3-glucan measurements 100, 101 . In a longitudinal birth cohort of high-risk infants, Iossifova et al demonstrated an increased risk of asthma with exposure to low levels of β-1,3-glucan but a protective effect upon exposure to levels of β-1,3-glucan greater than 60 micrograms per gram of dust 97, 100 , suggesting a possible nonlinear dose-response relationship similar to that observed for HDM allergen.…”

Associations between evaporative cooling and dust‐mite allergens, endotoxins, and β‐(1 → 3)‐d‐glucans in house dust: A study of low‐income homes

“…59 Certain types of fungi have been shown to be associated with protection from asthma and may also play a key role in influencing the composition of the microbiota and immune system. 62 High levels of fungal exposure have been strongly implicated in the development and prevalence of asthma. 62 High levels of fungal exposure have been strongly implicated in the development and prevalence of asthma.…”

Fungal Exposure and Asthma: IgE and Non-IgE-Mediated Mechanisms

“…Similarly, no difference was found in any of the concentrations between sensitized and non-sensitized cases. In contrast, Maheswaran et al [56] found that increased β−1,3-glucan concentration was significantly associated with increased prevalence of atopic asthma. No association was found between β−1,3-glucan and non-atopic asthma.…”