Lung function growth trajectories in non-asthmatic children aged 4-9 in relation to prenatal exposure to airborne particulate matter and polycyclic aromatic hydrocarbons - Krakow birth cohort study

Background Patterns of lung function development during childhood can be helpful in understanding the pathogenesis of respiratory diseases. A variety of environmental and lifestyle factors, present from the prenatal period to adulthood, may affect or modulate lung function growth. The aim of this study was to investigate, the associations between individual growth trajectories of children's lung function during childhood and prenatal exposure to airborne fine particulate matter (PM2.5) and polycyclic aromatic hydrocarbons (PAH), which were hypothesized to adversely affect spirometry parameters. Material and methods The study group comprised 294 non-asthmatic, full term children from the Krakow birth cohort, who underwent annual spirometry testing at the ages of 4–9 years. Individual personal air monitoring of PM2.5 and PAH were performed over 48 h in the second trimester of pregnancy. Possible confounders or modifiers such as child's gender, height, atopic status and exposure to environmental tobacco smoke (ETS) were considered. Polynomial multilevel mixed models were used to assess the growth rates of children's lung functions. Results Lung function trajectories differed significantly for boys and girls for FVC, FEV1 and FEF25–75. Girls had lower rates of increase than boys: − 20.5 (95%CI: − 32.4; − 8.6) ml/year (FVC); − 19.9 (95%CI: −30.7;−9.0) ml/year (FEV1); and − 32.5 (95%CI: − 56.9; − 8.2) ml/year (FEF25–75). Spirometry functions increased with age; however the growth rate decelerated over time. Significant lung function impairment (lower FVC and FEV1 levels) was observed from 4 to 9 years among subjects prenatally exposed to higher levels of PM2.5 as well as PAH, but not in the case of FEF25-75. No significant differences were observed in the rates of increase over time in relation to prenatal PM2.5 and PAH exposure. Conclusion Our results indicate that in non-asthmatic children high prenatal exposure to airborne PM2.5 and PAH is associated with lower trajectories of FVC and FEV1, but not the rate of increase over time, suggesting that the initial effect is not diminishing in time.