Pulmonary effects of indoor- and outdoor-generated particles in children with asthma.
Pulmonary effects of indoor- and outdoor-generated particles in children with asthma.
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哮喘儿童室内和室外生成的颗粒的肺作用。
DOI：
10.1289/ehp.7511
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发表时间：
2005-04
影响因子：
10.4
通讯作者：
中科院分区：
文献类型：
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作者：
大多数颗粒物（PM）健康影响研究使用室外（环境）PM作为个人暴露量的替代。然而，人们大部分时间都在室内，暴露在室内产生的颗粒和已渗透的环境颗粒的组合中。因此，研究室内和环境产生的颗粒对健康的不同影响是很重要的。我们结合我们最近采用的递归模型和估算渗透效率的预测模型，将个人暴露(E) PM2.5（空气动力学直径≤2.5 μm的PM）分为室内产生（Eig）和环境产生（Eag）两部分，研究了19名哮喘儿童。然后，我们比较了Eig和Eag与呼出的一氧化氮（eNO）的变化，一氧化氮是气道炎症的标志。基于样本量为8名儿童的递归模型，Eag与eNO的增加存在边际关联[PM2.5每增加10-μg/m3增加5.6 ppb；95%置信区间（CI），−0.6 ~ 11.9；P = 0.08]。Eig与eNO无关（每10μg/m3变化- 0.19 ppb）。我们的预测模型使我们能够估计所有19名儿童的Eag和Eig。对于这些综合估计，只有Eag与eNO的增加显著相关（Eag: PM2.5每增加10-μg/m3增加5.0 ppb; 95% CI， 0.3至9.7;p = 0.04; Eag: PM2.5每增加10-μg/m3增加3.3 ppb; 95% CI, - 1.1至7.7;p = 0.15）。仅在未使用皮质类固醇治疗的儿童中观察到效果。我们得出的结论是，PM2.5暴露的环境产生的成分与eNO的增加始终相关，而室内产生的成分与eNO的相关性较弱。
Most particulate matter (PM) health effects studies use outdoor (ambient) PM as a surrogate for personal exposure. However, people spend most of their time indoors exposed to a combination of indoor-generated particles and ambient particles that have infiltrated. Thus, it is important to investigate the differential health effects of indoor- and ambient-generated particles. We combined our recently adapted recursive model and a predictive model for estimating infiltration efficiency to separate personal exposure (E) to PM2.5 (PM with aerodynamic diameter ≤2.5 μm) into its indoor-generated (Eig) and ambient-generated (Eag) components for 19 children with asthma. We then compared Eig and Eag to changes in exhaled nitric oxide (eNO), a marker of airway inflammation. Based on the recursive model with a sample size of eight children, Eag was marginally associated with increases in eNO [5.6 ppb per 10-μg/m3 increase in PM2.5; 95% confidence interval (CI), −0.6 to 11.9; p = 0.08]. Eig was not associated with eNO (−0.19 ppb change per 10μg/m3). Our predictive model allowed us to estimate Eag and Eig for all 19 children. For those combined estimates, only Eag was significantly associated with an increase in eNO (Eag: 5.0 ppb per 10-μg/m3 increase in PM2.5; 95% CI, 0.3 to 9.7; p = 0.04; Eig: 3.3 ppb per 10-μg/m3 increase in PM2.5; 95% CI, −1.1 to 7.7; p = 0.15). Effects were seen only in children who were not using corticosteroid therapy. We conclude that the ambient-generated component of PM2.5 exposure is consistently associated with increases in eNO and the indoor-generated component is less strongly associated with eNO.