Barraza-Villarreal Albino, Sunyer Jordi, Hernandez-Cadena Leticia, Escamilla-Nuñez Maria Consuelo, Sienra-Monge Juan Jose, Ramírez-Aguilar Matiana, Cortez-Lugo Marlene, Holguin Fernando, Diaz-Sánchez David, Olin Anna Carin, Romieu Isabelle
Instituto Nacional de Salud Pública, Cuernavaca, México.
Environ Health Perspect. 2008 Jun;116(6):832-8. doi: 10.1289/ehp.10926.
The biological mechanisms involved in inflammatory response to air pollution are not clearly understood.
In this study we assessed the association of short-term air pollutant exposure with inflammatory markers and lung function.
We studied a cohort of 158 asthmatic and 50 nonasthmatic school-age children, followed an average of 22 weeks. We conducted spirometric tests, measurements of fractional exhaled nitric oxide (Fe(NO)), interleukin-8 (IL-8) in nasal lavage, and pH of exhaled breath condensate every 15 days during follow-up. Data were analyzed using linear mixed-effects models.
An increase of 17.5 microg/m(3) in the 8-hr moving average of PM(2.5) levels (interquartile range) was associated with a 1.08-ppb increase in Fe(NO) [95% confidence interval (CI), 1.01-1.16] and a 1.07-pg/mL increase in IL-8 (95% CI 0.98-1.19) in asthmatic children and a 1.16 pg/ml increase in IL-8 (95% CI, 1.00-1.36) in nonasthmatic children. The 5-day accumulated average of exposure to particulate matter <2.5 microm in aerodynamic diamter (PM(2.5)) was significantly inversely associated with forced expiratory volume in 1 sec (FEV(1)) (p=0.048) and forced vital capacity (FVC) (p=0.012) in asthmatic children and with FVC (p=0.021) in nonasthmatic children. Fe(NO) and FEV(1) were inversely associated (p=0.005) in asthmatic children.
Exposure to PM(2.5) resulted in acute airway inflammation and decrease in lung function in both asthmatic and nonasthmatic children.
空气污染炎症反应所涉及的生物学机制尚不清楚。
在本研究中，我们评估了短期接触空气污染物与炎症标志物及肺功能之间的关联。
我们对158名哮喘学龄儿童和50名非哮喘学龄儿童组成的队列进行了研究，平均随访22周。在随访期间，每15天进行一次肺功能测试、呼出一氧化氮分数（Fe(NO)）测量、鼻腔灌洗白细胞介素-8（IL-8）检测以及呼出气冷凝液pH值检测。使用线性混合效应模型对数据进行分析。
PM(2.5)水平8小时移动平均值（四分位间距）每增加17.5微克/立方米，哮喘儿童的Fe(NO)增加1.08 ppb [95%置信区间（CI），1.01 - 1.16]，IL-8增加1.07 pg/mL（95% CI 0.98 - 1.19）；非哮喘儿童的IL-8增加1.16 pg/ml（95% CI，1.00 - 1.36）。空气动力学直径<2.5微米颗粒物（PM(2.5)）的5天累积平均暴露量与哮喘儿童的第1秒用力呼气量（FEV(1)）（p = 0.048）和用力肺活量（FVC）（p = 0.012）以及非哮喘儿童的FVC（p = 0.021）显著负相关。哮喘儿童中Fe(NO)与FEV(1)呈负相关（p = 0.005）。
接触PM(2.5)导致哮喘和非哮喘儿童出现急性气道炎症并使肺功能下降。
