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空气污染在婴儿期毛细支气管炎史患儿哮喘发展中的作用。

Role of Air Pollution in the Development of Asthma Among Children with a History of Bronchiolitis in Infancy.

机构信息

From the Department of Environmental and Occupational Health Sciences, School of Public Health, University of Washington, Seattle, WA.

Department of Biostatistics, School of Public Health, University of Washington, Seattle, WA.

出版信息

Epidemiology. 2023 Jul 1;34(4):554-564. doi: 10.1097/EDE.0000000000001613. Epub 2023 Apr 11.

Abstract

BACKGROUND

Infants experiencing bronchiolitis are at increased risk for asthma, but few studies have identified modifiable risk factors. We assessed whether early life air pollution influenced child asthma and wheeze at age 4-6 years among children with a history of bronchiolitis in the first postnatal year.

METHODS

Children with caregiver-reported physician-diagnosed bronchiolitis were drawn from ECHO-PATHWAYS, a pooled longitudinal cohort from six US cities. We estimated their air pollution exposure from age 1 to 3 years from validated spatiotemporal models of fine particulate matter (PM 2.5 ), nitrogen dioxide (NO 2 ), and ozone (O 3 ). Caregivers reported children's current wheeze and asthma at age 4-6 years. We used modified Poisson regression to estimate relative risks (RR) and 95% confidence intervals (CI), adjusting for child, maternal, and home environmental factors. We assessed effect modification by child sex and maternal history of asthma with interaction models.

RESULTS

A total of 224 children had caregiver-reported bronchiolitis. Median (interquartile range) 2-year pollutant concentrations were 9.3 (7.8-9.9) µg/m 3 PM 2.5 , 8.5 (6.4-9.9) ppb NO 2 , and 26.6 (25.6-27.7) ppb O 3 . RRs (CI) for current wheeze per 2-ppb higher O 3 were 1.3 (1.0-1.7) and 1.4 (1.1-1.8) for asthma. NO 2 was inversely associated with wheeze and asthma whereas associations with PM 2.5 were null. We observed interactions between NO 2 and PM 2.5 and maternal history of asthma, with lower risks observed among children with a maternal history of asthma.

CONCLUSION

Our results are consistent with the hypothesis that exposure to modest postnatal O 3 concentrations increases the risk of asthma and wheeze among the vulnerable subpopulation of infants experiencing bronchiolitis.

摘要

背景

患有细支气管炎的婴儿患哮喘的风险增加,但很少有研究确定可改变的危险因素。我们评估了在婴儿期后第一年有细支气管炎病史的儿童中,早期生活中的空气污染是否会影响 4-6 岁时儿童的哮喘和喘息。

方法

从美国六个城市的汇集纵向队列 ECHO-PATHWAYS 中抽取有 caregiver 报告的经医生诊断的细支气管炎的儿童。我们使用经过验证的细颗粒物(PM 2.5 )、二氧化氮(NO 2 )和臭氧(O 3 )时空模型来估计他们从 1 岁到 3 岁的空气污染暴露水平。caregiver 在 4-6 岁时报告儿童当前的喘息和哮喘情况。我们使用修正后的泊松回归来估计相对风险(RR)和 95%置信区间(CI),并调整了儿童、产妇和家庭环境因素。我们通过交互模型评估了儿童性别和产妇哮喘史的效应修饰作用。

结果

共有 224 名儿童有 caregiver 报告的细支气管炎。中位数(四分位距)2 年污染物浓度分别为 9.3(7.8-9.9)µg/m 3 PM 2.5 、8.5(6.4-9.9)ppb NO 2 和 26.6(25.6-27.7)ppb O 3 。每增加 2-ppb 的 O 3 ,当前喘息的 RR(CI)分别为 1.3(1.0-1.7)和 1.4(1.1-1.8),哮喘为 1.4(1.1-1.8)。NO 2 与喘息和哮喘呈负相关,而与 PM 2.5 无关。我们观察到 NO 2 和 PM 2.5 与产妇哮喘史之间存在交互作用,在有产妇哮喘史的儿童中,风险较低。

结论

我们的结果与假设一致,即暴露于适度的新生儿 O 3 浓度会增加患有细支气管炎的脆弱亚群婴儿患哮喘和喘息的风险。

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