SUMMARY
Impaired fetal development is associated with a number of adult chronic diseases and it is believed that these associations arise as a result of the phenomenon of “epigenetic programming”, which involves persisting changes in structure and function of various body organs caused by ambient factors during critical and vulnerable periods of early development. The main goal of the study was to assess the association between lung function in early childhood and prenatal exposure to fine particulate matter (PM2.5 ), which represents a wide range of chemical compounds potentially hazardous for fetal development. Among pregnant women recruited prenatally to the study personal measurements of PM2.5 was performed over 48 hours in the second trimester of pregnancy. After delivery, infants were followed over five years and the interviewers visited participants at their homes to record children’s respiratory symptoms every three months in the child’s first two years of life and every 6 months later. In the fifth year of the follow-up, children were invited for standard lung function testing and quantified by FVC, FEV1 and FEV05 levels. Material consisted of 176 children of nonsmoking mothers, who performed at least two acceptable spirometry measurements. Multivariable linear regression model showed a significant deficit of FVC at the highest quartile of PM2.5 exposure (beta coefficient = − 91.9 , P = 0.008), after adjustment for covariates (age, gender, birth weight, height and wheezing). Also FEV1 level in children was inversely correlated with prenatal exposure to PM2.5, and the average FEV1 deficit amounted to 87.7 ml (P = 0.008) at the higher level of exposure. Although the effect of PM2.5 exposure on FEV05 was proportionally weaker (−72.7, P = 0.026) it was significant as well. The lung function level was inversely and significantly associated with the wheezing recorded over the follow-up. The findings showed that significant lung function deficits in early childhood is associated with prenatal exposure to fine particulate matter, which may affect fetal lung growth.