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 (Rrs 5 and Xrs 5 ), 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/m 3 , respectively. The mean ± SD Z‐scores for Rrs 5 , Xrs 5 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/m 3 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/m 3 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.