Early life exposure to coal mine fire smoke emissions and altered lung function in young children

Background and objective: Long-term respiratory risks following exposure to relatively short periods of poor air quality early in life are unknown. We aimed to evaluate the association between exposure to a 6-week episode of air pollution from a coal mine fire in children aged <2 years, and their lung function 3 years after the fire. Methods: We conducted a prospective cohort study. Individual exposure to 24-h average and peak concentrations of particulate matter with an aerodynamic diameter <2.5 μm in diameter (PM_2.5) during the fire were estimated using dispersion and chemical transport modelling. Lung function was measured using the forced oscillation technique (FOT), generating standardized Z-scores for resistance and reactance at a frequency of 5 Hz (Rrs₅ and Xrs₅), and area under the reactance curve (AX). We used linear regression models to assess the associations between PM_2.5 exposure and lung function, adjusted for potential confounders. Results: Of the 203 infants originally recruited, 84 aged 4.3 ± 0.5 years completed FOT testing. Median (interquartile range, IQR) for average and peak PM_2.5 were 7.9 (6.8–16.8) and 103.4 (60.6–150.7) μg/m³, respectively. The mean ± SD Z-scores for Rrs₅, Xrs₅ and AX were 0.56 ± 0.80, –0.76 ± 0.88 and 0.72 ± 0.92, respectively. After adjustment for potential confounders including maternal smoking during pregnancy, a 10 μg/m³ increase in average PM_2.5 was significantly associated with worsening AX (β-coefficient: 0.260; 95% CI: 0.019, 0.502), while the association between a 100-μg/m³ increase in peak PM_2.5 and AX was borderline (0.166; 95% CI: −0.002, 0.334). Conclusion: Infant exposure to coal mine fire emissions could be associated with long-term impairment of lung reactance.