Objectives: The main goal of the study was to assess possible association between fetal exposure to fi ne particulate matter (PM2.5) and exhaled carbon monoxide (eCO) measured in non-asthmatic children. Material and Methods: The subjects include 118 children taking part in an ongoing population-based birth cohort study in Kraków. Personal samplers of PM2.5 were used to measure fi ne particle mass in the fetal period and carbon monoxide (CO) in exhaled breath from a single exhalation effort at the age of 7. In the statistical analysis of the effect of prenatal PM2.5 exposure on eCO, a set of potential confounders, such as environmental tobacco smoke (ETS), city residence area, sensitization to house dust allergens and the occurrence of respiratory symptoms monitored over the seven-year follow-up was considered. Results: The level of eCO did not correlate with the self-reported ETS exposure recorded over the follow-up, however, there was a positive signifi cant relationship with the prenatal PM2.5 exposure (non-parametric trend p = 0.042). The eCO mean level was higher in atopic children (geometric mean = 2.06 ppm, 95% CI: 1.58–2.66 ppm) than in non-atopic ones (geometric mean = 1.57 ppm, 95% CI: 1.47–1.73 ppm) and the difference was statistically signifi cant (p = 0.036). As for the respiratory symptoms, eCO values were associated positively only with the cough severity score recorded in the follow-up (nonparametric trend p = 0.057). In the nested multivariable linear regression model, only the effects of prenatal PM2.5 and cough severity recorded in the follow-up were related to eCO level. The prenatal PM2.5 exposure represented 5.1%, while children’s cough represented only 2.6% of the eCO variability. Conclusion: Our study suggests that elevated eCO in non-asthmatic children may result from oxidative stress experienced in the fetal period and that heme oxygenase (HO) activity in body tissues may be programmed in the fetal period by the exposure to fi ne particulate matter.