Faculty of Medicine, Nursing, and Health Sciences, Monash University, Melbourne, Victoria, Australia.
Department of Pediatrics, Faculty of Medicine and Dentistry, University of Alberta, Edmonton, Alberta, Canada.
PLoS One. 2014 Jun 6;9(6):e98878. doi: 10.1371/journal.pone.0098878. eCollection 2014.
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.
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.
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.
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.
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.
霉菌暴露与儿童哮喘和支气管高反应性有关。很少有研究评估β-(1,3)-d-葡聚糖(β-葡聚糖),这是真菌细胞壁的重要组成部分,与青春期哮喘的关系。
确定 7-10 岁时从房屋灰尘中获取的β-葡聚糖暴露是否与特应性和非特应性哮喘的发展和持续存在以及 11-14 岁时的支气管高反应性(BHR)有关。
从 1995 年哮喘、基因和环境研究(SAGE)出生队列中采集灰尘样本。该队列来自马尼托巴省医疗保健行政记录中哮喘高风险和低风险的儿童。在 7-10 岁时从 422 名儿童的家中采集样本,并使用β-葡聚糖和内毒素特异性鲎变形细胞溶解物测定法进行分析。在 7-10 岁和 11-14 岁时还评估了每个儿童的哮喘、特应性和 BHR 状况。
7-10 岁时,家中的β-葡聚糖灰尘水平与 11-14 岁时持续性特应性哮喘有关(每增加一个单位的水平,OR 1.79,95%CI 1.14-2.81),独立于内毒素暴露以及交链孢霉或枝孢菌致敏。在哮喘儿童中,β-葡聚糖灰尘每增加一个单位,BHR 的可能性几乎增加一倍。在没有哮喘的儿童中,7-10 岁时暴露于高β-葡聚糖水平也会增加青春期 BHR 的风险(OR 1.74,95%CI 1.05-2.89)。在没有哮喘的儿童中,高β-葡聚糖暴露后,新出现的特应性哮喘的可能性增加了一倍,但关联没有达到统计学意义。在 7-10 岁时没有观察到与同期哮喘表型或 11-14 岁时非特应性哮喘有关的关联。
这些发现表明,学龄期家庭β-葡聚糖暴露是持续性特应性哮喘和新出现的 BHR 的危险因素。城市青少年中 BHR 的更高患病率可能是由这种家庭暴露引起的。