Chronic traffic-related air pollution and stress interact to predict biologic and clinical outcomes in asthma.
Chronic traffic-related air pollution and stress interact to predict biologic and clinical outcomes in asthma.
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DOI：
10.1289/ehp.11076
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发表时间：
2008-07
影响因子：
10.4
通讯作者：
Brauer M
中科院分区：
文献类型：
--
作者：
Chen E;Schreier HM;Strunk RC;Brauer M
先前的研究已经记录了身体和社会环境暴露对儿童哮喘的影响。然而，很少有研究考虑这两种环境如何相互作用影响哮喘。本研究旨在测试长期暴露于交通相关空气污染和长期家庭压力之间的相互作用，以预测哮喘儿童的生物学和临床结局。对哮喘儿童（n = 73，9-18岁）进行生活压力访谈，并测量哮喘相关炎症标志物[细胞因子产生，免疫球蛋白E（IgE），嗜酸性粒细胞计数]。家长报告孩子的症状。在基线和6个月后，儿童完成每日症状日记和呼气峰流速（PEFR）测量。暴露于交通相关的空气污染进行了评估，使用土地利用回归模型二氧化氮浓度。NO2与应激的相互作用见于白细胞介素-5（相互作用项β =-0.31，p = 0.02）、IgE（相互作用β =-0.29，p = 0.02）和嗜酸性粒细胞计数（相互作用β =-0.24，p = 0.04）。这些相互作用表明，随着污染水平的降低，更高的慢性压力与更高的炎症特征相关。纵向上，NO2与压力的相互作用出现在日常日记症状（相互作用β =-0.28，p = 0.02）、父母报告的症状（相互作用β =-0.25，p = 0.07）和PEFR（相互作用β = 0.30，p = 0.03）中。这些相互作用表明，较高的慢性压力与随着时间的推移，在症状和减少随着时间的推移，随着污染水平的下降PEFR。在预测哮喘儿童的生物学和临床结果方面，物理和社会环境相互作用，这表明当污染暴露较温和时，慢性压力较高的儿童哮喘急性发作的脆弱性可能会增加。
Previous research has documented effects of both physical and social environmental exposures on childhood asthma. However, few studies have considered how these two environments might interact to affect asthma. This study aimed to test interactions between chronic exposure to traffic-related air pollution and chronic family stress in predicting biologic and clinical outcomes in children with asthma. Children with asthma (n = 73, 9–18 years of age) were interviewed about life stress, and asthma-relevant inflammatory markers [cytokine production, immunoglobulin E (IgE), eosinophil counts] were measured. Parents reported on children’s symptoms. Children completed daily diaries of symptoms and peak expiratory flow rate (PEFR) measures at baseline and 6 months later. Exposure to traffic-related air pollution was assessed using a land use regression model for nitrogen dioxide concentrations. NO2 by stress interactions were found for interleukin-5 (β for interaction term = −0.31, p = 0.02), IgE (interaction β = −0.29, p = 0.02), and eosinophil counts (interaction β = −0.24, p = 0.04). These interactions showed that higher chronic stress was associated with heightened inflammatory profiles as pollution levels decreased. Longitudinally, NO2 by stress interactions emerged for daily diary symptoms (interaction β = −0.28, p = 0.02), parent-reported symptoms (interaction β = −0.25, p = 0.07), and PEFR (interaction β = 0.30, p = 0.03). These interactions indicated that higher chronic stress was associated with increases over time in symptoms and decreases over time in PEFR as pollution levels decreased. The physical and social environments interacted in predicting both biologic and clinical outcomes in children with asthma, suggesting that when pollution exposure is more modest, vulnerability to asthma exacerbations may be heightened in children with higher chronic stress.
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影响因子：
14.2
作者：
Chen, Edith;Hanson, Margaret D.;Miller, Gregory E.
通讯作者：
Miller, Gregory E.
影响因子：
10.4
作者：
Gee, Gilbert C;Payne-Sturges, Devon C
通讯作者：
Payne-Sturges, Devon C
DOI：
10.1164/rccm.200308-1178oc
发表时间：
2004-08-15
影响因子：
24.7
作者：
Bacharier, LB;Strunk, RC;Sorkness, CA
通讯作者：
Sorkness, CA
影响因子：
10.4
作者：
Crain, EF;Walter, M;Stout, JW
通讯作者：
Stout, JW
影响因子：
11.4
作者：
Henderson, Sarah B.;Beckerman, Bernardo;Brauer, Michael
通讯作者：
Brauer, Michael