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 (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. RESULTS: 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. CONCLUSIONS: Exposure to PM(2.5) resulted in acute airway inflammation and decrease in lung function in both asthmatic and nonasthmatic children.

Exhaled breath malondialdehyde as a marker of effect of exposure to air pollution in children with asthma.

BACKGROUND: Assessment of the adverse effects of oxidative stress related to air pollution is limited by the lack of biological markers of dose to the lungs. OBJECTIVE: We evaluated the use of exhaled breath condensate (EBC) malondialdehyde as a biomarker of exposure to traffic-related pollution in children with asthma as part of a panel study in Mexico City. METHODS: Standard spirometry and collection of EBC and nasal lavage were performed. Environmental monitoring sites were located within 5 km of the children's homes and schools. Data were analyzed by using generalized estimating equations. RESULTS: A total of 480 samples of malondialdehyde were obtained from 107 patients with asthma, with a median level of 18.7 (interquartile range [IQR], 12.4-28.7) nmol. Ambient particulates less than 2.5 microg/m(3) and ozone levels on the day of sampling were significantly associated with higher malondialdehyde levels. A 14.2-microg/m(3) (IQR) increase in 8-hour moving average particulates less than 2.5 microg/m(3) in size was associated with a 1.12-nmol increase in malondialdehyde and a 15.9-ppb (IQR) increase in 8-hour moving average ozone with a 1.16-nmol increase in malondialdehyde. Malondialdehyde levels were inversely associated with forced vital capacity and FEV(1) and positively associated with IL-8 levels in nasal lavage. CONCLUSION: Exhaled breath condensate malondialdehyde was related to both air pollution exposure and changes in lung function and inflammatory markers.