Pasalic Emilia, Hayat Matthew J, Greenwald Roby
Master of Public Health Program, Georgia State University School of Public Health, Atlanta, GA.
Graduate Division of Epidemiology and Biostatistics, Georgia State University School of Public Health, Atlanta, GA.
J Ga Public Health Assoc. 2016 Fall;6(2 Suppl):314-330. doi: 10.21633/jgpha.6.2s19.
The airway inflammatory response is likely the mechanism for adverse health effects related to exposure to air pollution. Increased ventilation rates during physical activity in the presence of air pollution increases the inhaled dose of pollutants. However, physical activity may moderate the relationship between air pollution and the inflammatory response. The present study aimed to characterize, among healthy adolescents, the relationship between dose of inhaled air pollution, physical activity, and markers of lung function, oxidative stress, and airway inflammation.
With a non-probability sample of adolescents, this observational study estimated the association between air pollution dose and outcome measures by use of general linear mixed models with an unstructured covariance structure and a random intercept for subjects to account for repeated measures within subjects.
A one interquartile range (IQR) (i.e., 345.64 μg) increase in ozone (O) inhaled dose was associated with a 29.16% average decrease in the percentage of total oxidized compounds (%Oxidized). A one IQR (i.e., 2.368E+10 particle) increase in total particle number count in the inhaled dose (PNT) was associated with an average decrease in forced expiratory flow (FEF) of 0.168 L/second. Increasing activity levels attenuated the relationship between PNT inhaled dose and exhaled nitric oxide (eNO). The relationship between O inhaled dose and percent oxidized exhaled breath condensate cystine (%CYSS) was attenuated by activity level, with increasing activity levels corresponding to smaller changes from baseline for a constant O inhaled dose.
The moderating effects of activity level suggest that peaks of high concentration doses of air pollution may overwhelm the endogenous redox balance of cells, resulting in increased airway inflammation. Further research that examines the relationships between dose peaks over time and inflammation could help to determine whether a high concentration dose over a short period of time has a different effect than a lower concentration dose over a longer period of time.
气道炎症反应可能是与空气污染暴露相关的不良健康影响的机制。在空气污染存在的情况下进行体育活动时，通气率增加会增加污染物的吸入剂量。然而，体育活动可能会缓和空气污染与炎症反应之间的关系。本研究旨在描述健康青少年中吸入空气污染剂量、体育活动与肺功能、氧化应激和气道炎症标志物之间的关系。
在一项针对青少年的非概率抽样观察性研究中，我们使用具有非结构化协方差结构和随机截距的一般线性混合模型，以估计空气污染剂量与结果指标之间的关联，随机截距用于考虑个体内的重复测量。
吸入臭氧（O）剂量增加一个四分位数间距（IQR）（即345.64μg）与总氧化化合物百分比（%氧化）平均下降29.16%相关。吸入剂量中总颗粒数计数（PNT）增加一个IQR（即2.368E+10颗粒）与用力呼气流量（FEF）平均下降0.168升/秒相关。活动水平增加减弱了吸入PNT剂量与呼出一氧化氮（eNO）之间的关系。吸入O剂量与呼出呼出气冷凝物胱氨酸百分比（%CYSS）之间的关系因活动水平而减弱，活动水平增加对应于在恒定吸入O剂量下相对于基线的较小变化。
活动水平的缓和作用表明，高浓度空气污染剂量峰值可能会压倒细胞的内源性氧化还原平衡，导致气道炎症增加。进一步研究空气污染剂量峰值随时间与炎症之间的关系，有助于确定短时间内的高浓度剂量与长时间内的低浓度剂量是否具有不同的影响。
