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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.

Maheswaran D, Zeng Y, Chan-Yeung M, Scott J, Osornio-Vargas A, Becker AB, Kozyrskyj AL - PLoS ONE (2014)

Bottom Line: At 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.These 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.

View Article: PubMed Central - PubMed

Affiliation: Faculty of Medicine, Nursing, and Health Sciences, Monash University, Melbourne, Victoria, Australia.

ABSTRACT

Background: Mould 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.

Objective: To 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.

Methods: Dust 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.

Results: At 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.

Conclusion: These 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.

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Related in: MedlinePlus

Flowchart of recruitment design.All parents of children from the 1995 Manitoba birth cohort who were alive and still resided in Manitoba were sent a short recruitment survey to which 3598 responded. These were grouped into cases and controls based on asthma status. Non-asthmatic controls were stratified according to urban or rural residence. Dust samples were collected from 190 and 394 cases and controls respectively. Of these, 77% of asthmatic children (n = 147) and 70% of control children (n = 275) were followed up for re-assessment by a pediatric allergist at age 11–14.
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pone-0098878-g001: Flowchart of recruitment design.All parents of children from the 1995 Manitoba birth cohort who were alive and still resided in Manitoba were sent a short recruitment survey to which 3598 responded. These were grouped into cases and controls based on asthma status. Non-asthmatic controls were stratified according to urban or rural residence. Dust samples were collected from 190 and 394 cases and controls respectively. Of these, 77% of asthmatic children (n = 147) and 70% of control children (n = 275) were followed up for re-assessment by a pediatric allergist at age 11–14.

Mentions: This was a planned, longitudinal follow-up of a nested case-control study of children in the 1995 SAGE birth cohort to study home environmental risk factors for asthma development in adolescence. This cohort was created from healthcare registry records of all children born in the province of Manitoba, Canada. Details of the study design for the SAGE cohort and nested case-control study have been published [32]. In brief, a short recruitment survey was sent to cohort households, including general health and home environment questions, as well as permission to be contacted. From the 3598 returned surveys (Figure 1) and following written consent from their parents, children aged 7–10 with and without asthma were recruited for the case-control study. This included all asthma cases (n = 246) and almost twice as many controls (n = 477), which had been randomly selected within urban-rural strata. Home dust samples were collected in 190 (77%) of homes of asthmatic children and in 394 (83%) of control homes. Seventy seven percent of asthmatic children (n = 147) and 70% of control children (n = 275) were seen at age 11–14 years (Figure 1). To test hypotheses on incidence and persistence, as others have [8], associations between dust beta-glucan and subsequent asthma and BHR were determined separately within each of the asthma and control arms.


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.

Maheswaran D, Zeng Y, Chan-Yeung M, Scott J, Osornio-Vargas A, Becker AB, Kozyrskyj AL - PLoS ONE (2014)

Flowchart of recruitment design.All parents of children from the 1995 Manitoba birth cohort who were alive and still resided in Manitoba were sent a short recruitment survey to which 3598 responded. These were grouped into cases and controls based on asthma status. Non-asthmatic controls were stratified according to urban or rural residence. Dust samples were collected from 190 and 394 cases and controls respectively. Of these, 77% of asthmatic children (n = 147) and 70% of control children (n = 275) were followed up for re-assessment by a pediatric allergist at age 11–14.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4048218&req=5

pone-0098878-g001: Flowchart of recruitment design.All parents of children from the 1995 Manitoba birth cohort who were alive and still resided in Manitoba were sent a short recruitment survey to which 3598 responded. These were grouped into cases and controls based on asthma status. Non-asthmatic controls were stratified according to urban or rural residence. Dust samples were collected from 190 and 394 cases and controls respectively. Of these, 77% of asthmatic children (n = 147) and 70% of control children (n = 275) were followed up for re-assessment by a pediatric allergist at age 11–14.
Mentions: This was a planned, longitudinal follow-up of a nested case-control study of children in the 1995 SAGE birth cohort to study home environmental risk factors for asthma development in adolescence. This cohort was created from healthcare registry records of all children born in the province of Manitoba, Canada. Details of the study design for the SAGE cohort and nested case-control study have been published [32]. In brief, a short recruitment survey was sent to cohort households, including general health and home environment questions, as well as permission to be contacted. From the 3598 returned surveys (Figure 1) and following written consent from their parents, children aged 7–10 with and without asthma were recruited for the case-control study. This included all asthma cases (n = 246) and almost twice as many controls (n = 477), which had been randomly selected within urban-rural strata. Home dust samples were collected in 190 (77%) of homes of asthmatic children and in 394 (83%) of control homes. Seventy seven percent of asthmatic children (n = 147) and 70% of control children (n = 275) were seen at age 11–14 years (Figure 1). To test hypotheses on incidence and persistence, as others have [8], associations between dust beta-glucan and subsequent asthma and BHR were determined separately within each of the asthma and control arms.

Bottom Line: At 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.These 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.

View Article: PubMed Central - PubMed

Affiliation: Faculty of Medicine, Nursing, and Health Sciences, Monash University, Melbourne, Victoria, Australia.

ABSTRACT

Background: Mould 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.

Objective: To 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.

Methods: Dust 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.

Results: At 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.

Conclusion: These 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.

Show MeSH
Related in: MedlinePlus