Air Pollution, Airway Inflammation, and Lung Function in a Cohort Study of Mexico City Schoolchildren

Background: The biological mechanisms involved in inflammatory response to air pollution are not clearly understood. Objective: In this study we assessed the association of short-term air pollutant exposure with inflammatory markers and lung function. Methods: 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 $({\rm Fe}_{{\rm NO}})$, 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. Results: An increase of $17.5\ \mu {\rm g}/{\rm m}^{3}$ in the 8-hr moving average of ${\rm PM}_{2.5}$ levels (interquartile range) was associated with a 1.08-ppb increase in ${\rm Fe}_{{\rm NO}}$ [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 μm in aerodynamic diamter $({\rm PM}_{2.5})$ was significantly inversely associated with forced expiratory volume in 1 sec $({\rm FEV}_{1})$ (p = 0.048) and forced vital capacity (FVC) (p = 0.012) in asthmatic children and with FVC (p = 0.021) in nonasthmatic children. ${\rm Fe}_{{\rm NO}}$ and ${\rm FEV}_{1}$ were inversely associated (p = 0.005) in asthmatic children. Conclusions: Exposure to ${\rm PM}_{2.5}$ resulted in acute airway inflammation and decrease in lung function in both asthmatic and nonasthmatic children.