Moore Camille M, Thornburg Jonathan, Secor Elizabeth A, Hamlington Katharine L, Schiltz Allison M, Freeman Kristy L, Everman Jamie L, Fingerlin Tasha E, Liu Andrew H, Seibold Max A
Center for Genes, Environment, and Health, National Jewish Health, Denver, CO, USA.
Department of Biostatistics and Informatics, University of Colorado-AMC, Aurora, CO, USA.
Respir Res. 2025 Jan 27;26(1):40. doi: 10.1186/s12931-025-03114-y.
Air pollution is associated with poor asthma outcomes in children. However, most studies focus on ambient or indoor monitor pollution levels. Few studies evaluate breathing zone exposures, which may be more consequential for asthma outcomes.
We measured personal exposures to NO, O, PM and PM constituents, including black carbon (BC), brown carbon (BrC), environmental tobacco smoke (ETS), endotoxins, and 𝛽-glucan, in a cohort of children with exacerbation-prone asthma for 72 h using wearable monitors. Personal exposures were compared to concentrations from in-home monitors in the child's bedroom and ambient EPA air quality monitoring using correlation analyses. Personal exposures were tested for association with lung function and compared between participants with and without well-controlled asthma and signs of exacerbation in the prior 60 days using censored regression with robust standard errors.
81 children completed 219 monitoring sessions. Personal NO, O, and PM exposures ranged from < 2 to 99.1 parts per billion (ppb), < 1.5 to 23.3 ppb, and < 1 to 141.9 𝜇g/m, respectively. Personal endotoxin ranged from 0.04 to 101.3 EU/m, 𝛽-glucan from 18.5 to 1,162 pg/m, BC from < 0.3 to 46.9 𝜇g/m, BrC from < 0.3 to 6.1 𝜇g/m, and ETS from < 0.3 to 56.6 𝜇g/m. Correlations between personal and ambient PM, NO, and O concentrations were poor, whereas personal PM and NO correlated with in-home concentrations. In-home monitoring less frequently detected BrC (Personal:79% > lower limit of detection, Home:36.8%) and ETS (Personal:83.7%, Home:4.1%) than personal exposures, and detected BC in participants without personal exposure (Personal: 26.5%, Home: 96%). Personal exposures were not significantly associated with lung function or daily asthma control. Children requiring corticosteroid treatment for asthma exacerbation within 60 days of exposure monitoring had 1.98, 2.21 and 2.04 times higher personal exposures to BrC (p < 0.001; 95% CI: 1.43-2.37), ETS (p = 0.007; 95% CI: 1.25-3.91), and endotoxin (p = 0.012; 95% CI: 1.14-3.68), respectively.
Although in-home monitoring was correlated with personal exposure to PM and NO, in-home detection of ETS and BrC was not associated with personal exposures. Personal PM exposures in general, as well as BrC, ETS, and endotoxin levels were associated with recent childhood asthma exacerbations.
Not applicable.
空气污染与儿童哮喘不良预后相关。然而，大多数研究关注的是环境或室内监测污染水平。很少有研究评估呼吸带暴露情况，而这可能对哮喘预后更具影响。
我们使用可穿戴监测器，对一组易加重哮喘儿童进行了72小时的个人暴露于一氧化氮（NO）、臭氧（O）、细颗粒物（PM）及其成分（包括黑碳（BC）、棕碳（BrC）、环境烟草烟雾（ETS）、内毒素和β-葡聚糖）的测量。通过相关性分析，将个人暴露水平与儿童卧室中的家庭监测器浓度以及美国环境保护局（EPA）的环境空气质量监测浓度进行比较。使用稳健标准误差的删失回归法，检验个人暴露与肺功能的关联，并比较在过去60天内哮喘控制良好与未控制且有加重迹象的参与者之间的个人暴露情况。
81名儿童完成了219次监测。个人NO、O和PM暴露范围分别为<2至99.1十亿分比（ppb）、<1.5至23.3 ppb和<1至141.9微克/立方米。个人内毒素范围为0.04至101.3 EU/立方米，β-葡聚糖为18.5至1162皮克/立方米，BC为<0.3至46.9微克/立方米，BrC为<0.3至6.1微克/立方米，ETS为<0.3至56.6微克/立方米。个人与环境PM、NO和O浓度之间的相关性较差，而个人PM和NO与家庭监测浓度相关。家庭监测比个人暴露更少检测到BrC（个人：79%高于检测下限，家庭：36.8%）和ETS（个人：83.7%，家庭：4.1%），并且在没有个人暴露的参与者中检测到了BC（个人：26.5%，家庭：96%）。个人暴露与肺功能或每日哮喘控制无显著关联。在暴露监测的60天内需要使用皮质类固醇治疗哮喘加重的儿童，其个人BrC暴露（p<0.001；95%置信区间：1.43 - 2.37）、ETS暴露（p = 0.007；95%置信区间：1.25 - 3.91）和内毒素暴露（p = 0.012；95%置信区间：1.14 - 3.68）分别高出1.98倍、2.21倍和2.04倍。
尽管家庭监测与个人对PM和NO的暴露相关，但家庭对ETS和BrC的检测与个人暴露无关。总体而言，个人PM暴露以及BrC、ETS和内毒素水平与近期儿童哮喘加重相关。
不适用。
