D2.165 - Geographic Disparities in Air Pollution and Th2-Mediated Airway Inflammation in Pediatric Asthma: A Cross-Sectional Study from Mexico City

Mexico City is one of the most polluted megacities worldwide and exhibits marked geographic heterogeneity in ambient air pollution across its boroughs. Traffic- and industry-related emissions have been linked to asthma morbidity and type 2 (Th2) airway inflammation. Fractional exhaled nitric oxide (FeNO) is a non-invasive biomarker of Th2-mediated airway inflammation and is particularly relevant in pediatric asthma. However, data exploring geographical disparities in FeNO levels in relation to ambient air pollution in highly urbanized settings remain limited.

A cross-sectional observational study was conducted including 47 children and adolescents (>6 years) with persistent asthma receiving GINA step 2–3 maintenance therapy. FeNO was measured during routine outpatient visits using a standardized electrochemical analyzer (NIOX VERO). Daily concentrations of PM2.5, NO₂, and O₃ were obtained from the Mexico City Atmospheric Monitoring System according to borough of residence, using 7-day averages prior to FeNO measurement. Descriptive analyses, borough-level comparisons, and correlation analyses were performed. Multivariable linear regression models were constructed with FeNO as the dependent variable, adjusting for age, sex, GINA treatment step, and borough of residence. Statistical significance was set at p < 0.05.

FeNO levels showed substantial variability across individuals and boroughs of Mexico City. Among the evaluated boroughs, Benito Juárez exhibited the highest mean FeNO levels, coinciding with the highest average NO₂ concentrations, suggesting a greater burden of Th2-mediated airway inflammation in areas with higher traffic-related pollution. Boroughs with mixed urban and industrial characteristics, including Iztapalapa and Venustiano Carranza, also demonstrated elevated FeNO levels alongside increased PM2.5 concentrations, indicating potential cumulative effects of multiple urban pollution sources. Higher NO₂ concentrations were additionally associated with an increased frequency of asthma exacerbations over the previous 12 months. Associations between FeNO and O₃ were weaker and less consistent across boroughs.

This cross-sectional study identifies geographic disparities in Th2-mediated airway inflammation among children and adolescents with asthma living in Mexico City. Higher FeNO levels were observed in boroughs with increased traffic-related air pollution, particularly Benito Juárez, where elevated NO₂ concentrations coincided with the greatest inflammatory burden. Boroughs characterized by mixed urban and industrial emissions also demonstrated elevated FeNO levels, suggesting a potential cumulative effect of multiple pollution sources. Although causal inferences cannot be established due to the study design, these findings support the use of FeNO as a biomarker of community-level inflammatory burden in urban pediatric asthma. Identifying boroughs with higher inflammatory profiles may help inform targeted environmental policies and tailored clinical interventions aimed at reducing pollution-related asthma morbidity in vulnerable pediatric populations.