A101-18 Interaction Between Air Pollution and Bronchial Hyperreactivity in Predicting Annual Lung Function Decline Among Individuals With Biomass-COPD in Uganda

Abstract Rationale Bronchial hyperresponsiveness (BHR) is associated with accelerated respiratory decline and increased mortality. Studies have demonstrated a direct association between biomass exposure and BHR. However, few studies, particularly in resource-limited settings where 84% of chronic obstructive pulmonary disease (COPD) related deaths occur and 34% of homes use biomass fuels, have delineated the interaction between air pollution and BHR on lung function decline in a population with biomass-COPD. This study aims to analyze this interaction to better understand the physiological phenotype of biomass-COPD. Methods Participants (n = 30) exposed to biomass fuel were recruited from Nakaseke, Uganda and followed from March 2021 to October 2025 (NCT03984188). Baseline spirometry confirmed COPD. The cohort was stratified by particle matter equal to or less than 2.5 µm (PM2.5) exposure over 24 hours (median=38 µg/m3) via nephelometry. The annualized rate of FEV1 decline was calculated. The cohort was further categorized into low and high bronchodilator response (BDR) (median=7%). Multivariable linear regression was performed, adjusting for age and smoking status, for annual FEV1 decline. Results Participants’ age ranged from 48 to 86 years, 62.1% were women, and 36% were ever smokers. In low BDR groups, eosinophils were lower among individuals exposed to high PM2.5 (152±125cells/µL) compared to low PM2.5 (233±208cells/µL). In high BDR, eosinophils were lower among individuals exposed to high PM2.5 (203 ± 128cells/µL) than low PM2.5 (424±453cells/µL). Lung function decline was greater among high PM2.5 (41mL/yr) compared to low PM2.5 (7mL/yr). High BDR (low PM2.5 = −47.33±22.9mL/yr vs. high PM2.5 = −46.8±27.0mL/yr) trended towards greater decline than low BDR (low PM2.5 = +8.99±32.6mL/yr vs. high PM2.5 = −41.1 ± 20.9mL/yr). Within low BDR, high PM2.5 trended towards greater decline than low PM2.5 ( −41.1 ± 20.9mL/yr vs + 8.9±32.6mL/yr, p = 0.208). In the high BDR group, low PM2.5 and high PM2.5 showed no trend (−47.33±22.9mL/yr vs − 46.8±27.0mL/yr, p = 0.989). Conclusion High BDR is associated with greater annualized lung function decline; PM2.5 has a greater effect on respiratory impairment among individuals with low BDR compared to high BDR. Although prior studies have shown that PM2.5 is associated with eosinophilia and hyper-reactivity in a dose-dependent manner, this study suggests a possible ceiling effect. Along with a larger sample size, future studies should explore Th2 and non-Th2 pathway interactions that could explain these physiological outcomes. This abstract is funded by: None