Department of Epidemiology and Biostatistics, Dornsife School of Public Health, Drexel University, Philadelphia, PA, USA.
Department of Environmental and Occupational Health, Dornsife School of Public Health, Drexel University, PA, USA; Urban Health Collaborative, Dornsife School of Public Health, Drexel University, Philadelphia, PA, USA.
Environ Res. 2023 Oct 1;234:116395. doi: 10.1016/j.envres.2023.116395. Epub 2023 Jun 28.
Fine particulate matter (PM) and aeroallergens (i.e., pollen, molds) are known triggers of asthma exacerbation. Despite mechanistic evidence suggesting synergistic effects between PM and asthma exacerbation, little epidemiologic work has been performed in children, which has exhibited inconsistency. We conducted a time-series study to explore their interactions using electronic health records (EHR) data in Philadelphia, PA, for asthma diagnoses in outpatient, emergency department [ED], and inpatient settings. Daily asthma exacerbation cases (28,540 asthma exacerbation case encounters) were linked to daily ambient PM and daily aeroallergen levels during the aeroallergen season of a six-year period (mid-March to October 2011-2016). Asthma exacerbation counts were modeled using quasi-Poisson regression, where PM and aeroallergens were fitted with distributed lag non-linear functions (lagged from 0 to 14-days), respectively, when modeled as the primary exposure variables. Regression models were adjusted for mean daily temperature/relative humidity, long-term and seasonal trends, day-of-week, and major U.S. holidays. Increasing gradient of RR estimates were observed for only a few primary exposure risk factors [PM (90th vs. 5th percentile)/aeroallergens (90th percentile vs. 0)], across different levels of effect modifiers. For example, RRs for the association between late-season grass pollen (lag1) and asthma exacerbation were higher at higher levels of PM, 5-days preceding the exacerbation event (low PM: RR = 1.01, 95% CI: 0.93-1.09; medium PM: 1.04, 95% CI: 0.96-1.12; high PM: 1.09, 95% CI: 1.01-1.19). However, most of the highest RRs for aeroallergens were instead observed for days with low- or medium- PM levels; likewise, when PM was modeled as the primary exposure with aeroallergens as the effect modifier. Most of the RR estimates did not exhibit gradients that suggested synergism, and were of relatively high imprecision. Overall, our study suggested no evidence for interactions between PM and aeroallergens in their relationships with childhood asthma exacerbation.
细颗粒物（PM）和空气过敏原（即花粉、霉菌）已知是哮喘恶化的诱因。尽管有机制证据表明 PM 和哮喘恶化之间存在协同作用，但在儿童中进行的流行病学研究很少，结果不一致。我们在宾夕法尼亚州费城进行了一项时间序列研究，利用电子健康记录（EHR）数据，在门诊、急诊部[ED]和住院环境中探索哮喘诊断的 PM 和空气过敏原水平之间的相互作用。在六年的空气过敏原季节（2011 年至 2016 年 3 月中旬至 10 月）中，将每日哮喘恶化病例（28540 例哮喘恶化病例）与每日环境 PM 和每日空气过敏原水平相关联。使用准泊松回归对哮喘恶化计数进行建模，当将 PM 和空气过敏原分别拟合为主要暴露变量时，PM 和空气过敏原分别采用分布式滞后非线性函数（滞后 0-14 天）进行拟合。回归模型调整了每日平均温度/相对湿度、长期和季节性趋势、星期几和美国主要节假日。仅观察到几个主要暴露危险因素[PM（第 90 百分位数与第 5 百分位数）/空气过敏原（第 90 百分位数与 0）]的递增梯度 RR 估计值，在不同的效应修饰剂水平下。例如，在较高水平的 PM 下，晚期草花粉（滞后 1）与哮喘恶化之间关联的 RR 更高，在哮喘恶化事件发生前 5 天（低 PM：RR=1.01，95%CI：0.93-1.09；中 PM：1.04，95%CI：0.96-1.12；高 PM：1.09，95%CI：1.01-1.19）。然而，空气过敏原的大多数最高 RR 则出现在 PM 水平较低或中等的日子；同样，当 PM 作为主要暴露物建模，空气过敏原作为效应修饰剂时。大多数 RR 估计值没有表现出协同作用的梯度，并且相对精度较高。总体而言，我们的研究表明，在 PM 和空气过敏原与儿童哮喘恶化的关系中，没有证据表明它们之间存在相互作用。
