Department of Occupational Safety and Health, College of Public Health, China Medical University, Taichung, Taiwan; Japan Environment and Children's Study Programme Office, National Institute for Environmental Studies, Tsukuba, Japan.
Department of Atmospheric Sciences, National Taiwan University, Taipei, Taiwan.
J Allergy Clin Immunol. 2019 Jun;143(6):2254-2262.e5. doi: 10.1016/j.jaci.2019.03.024. Epub 2019 Apr 5.
Lung development is a multistage process from conception to the postnatal period, disruption of which by air pollutants can trigger later respiratory morbidity.
We sought to evaluate the effects of weekly average fine particulate matter (particulate matter with an aerodynamic diameter less than 2.5 μm [PM]) exposure during pregnancy and infancy on asthma and identify vulnerable times to help elucidate possible mechanisms of the effects of PM on asthma symptoms.
A birth cohort study including 184,604 children born during 2004-2011 in Taichung City was retrieved from the Taiwan Maternal and Child Health Database and followed until 2014. A daily satellite-based hybrid model was applied to estimate PM exposure for each subject. A Cox proportional hazard model combined with a distributed lag nonlinear model was used to evaluate the associations of asthma with PM exposure during pregnancy and infancy.
The birth cohort contained 34,336 asthmatic patients, and the mean age of children given a diagnosis of asthma was 3.39 ± 1.78 years. Increased exposure to PM during gestational weeks 6 to 22 and 9 to 46 weeks after birth were significantly associated with an increased incidence of asthma. The exposure-response relationship indicated that the hazard ratio (HR) of asthma increased steeply at PM exposure of greater than 93 μg/m during pregnancy. Additionally, the HRs remained significant with postnatal exposure to PM between 26 and 72 μg/m (range, 1.01-1.07 μg/m), followed by a sharp increase in HRs at PM exposure of greater than 73 μg/m.
Both prenatal and postnatal exposures to PM were associated with later development of asthma. The vulnerable time windows might be within early gestation and midgestation and infancy.
肺发育是一个从受孕到出生后时期的多阶段过程,空气污染物的干扰可能会引发后期的呼吸道发病率。
我们旨在评估孕妇和婴儿期每周平均细颗粒物(空气动力学直径小于 2.5μm 的颗粒物 [PM])暴露对哮喘的影响,并确定易受影响的时期,以帮助阐明 PM 对哮喘症状影响的可能机制。
从台湾母婴健康数据库中检索到一项包括 2004-2011 年在台中市出生的 184604 名儿童的出生队列研究,并随访至 2014 年。应用基于卫星的混合模型每日估计每个研究对象的 PM 暴露量。采用 Cox 比例风险模型结合分布式滞后非线性模型来评估哮喘与孕期和婴儿期 PM 暴露的关联。
该出生队列包含 34336 例哮喘患者,儿童被诊断为哮喘的平均年龄为 3.39±1.78 岁。妊娠第 6 至 22 周和出生后第 9 至 46 周期间 PM 暴露增加与哮喘发病率增加显著相关。暴露-反应关系表明,妊娠期间 PM 暴露大于 93μg/m 时,哮喘的危险比(HR)急剧增加。此外,产后 PM 暴露在 26 至 72μg/m 之间(范围为 1.01-1.07μg/m)时,HR 仍保持显著,随后 PM 暴露大于 73μg/m 时 HR 急剧增加。
产前和产后 PM 暴露均与后期哮喘的发展有关。易受影响的时间窗可能在妊娠早期和中期以及婴儿期。