In utero, CO readily crosses the placenta, and the circulating fetal hemoglobin (Hgb) has a higher affinity for CO than oxygen. As a result, CO elimination takes longer in the fetal circulatory system when compared to maternal circulation, leading to fetal hypoxia and potentially resulting in permanent fetal brain damage and stillbirth at high maternal CO exposures.^6,16 Similarly, prenatal CO exposure has been shown to result in decreased birth weight, in-utero growth restriction, perinatal asphyxia, small infant head circumference, behavioral abnormalities, and disruption in cognitive function.^7,5,34,25 Children born to mothers with increased CO exposure during pregnancy appear to have a reduced lung function at age one month.²