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Updated: Jul 4, 2026

Measuring Carbon Content in Airway Macrophages Exposed to Carbon-Containing Particulate Matters
Published on: July 12, 2024
Air pollution, airway inflammation, and lung function in a cohort study of Mexico City schoolchildren
Albino Barraza-Villarreal1, Jordi Sunyer, Leticia Hernandez-Cadena
1Instituto Nacional de Salud Pública, Cuernavaca, México.
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.
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