Lower birth weight and growth retardation has been found in studies with laboratory animals, in children born of mothers exposed to accidental high levels of polychlorinated biphenyls (PCBs) and related compounds, and in children born of mothers who consumed PCB-contaminated fish. The effect of background exposure to PCBs and dioxins on birth size and growth in human newborns, however, is still unknown. This study examined birth size and postnatal growth of term newborns in relation to their background PCB and dioxin exposure. Birth weight and weight, length, and head circumference were measured at 10 d and 3, 7, 18, and 42 mo of age in 207 children, of whom 105 were breast-fed and 102 were formula-fed during infancy. The effect of in utero exposure to PCBs on birth size, assessed by cord and maternal plasma PCB levels, was investigated in the whole group. The effect of prenatal PCB exposure on postnatal growth was studied in the formula-fed group, whereas the effect of prenatal as well as lactational exposure to PCBs and dioxins on postnatal growth was studied in the breast-fed group. After adjustment for covariates, cord and maternal plasma PCB levels where both negatively associated with birth weight. Infants with high cord plasma PCB levels (P90 = 0.80 µg/L) weighed 165 g less compared with infants with low cord plasma PCB levels (P10 = 0.20 µg/L). Cord and maternal plasma PCB levels where both significantly associated with lower growth rate, defined as change in SD score (SDS) of weight, length, and head circumference from birth to 3 mo in the formula-fed group (all p values <0.05). No negative effects of prenatal PCB exposure on growth rate were found from 3 to 42 months of age. Postnatal PCB and dioxin exposure was not negatively associated with growth rate in the breast-fed group. In utero exposure to environmental levels of PCBs is negatively associated with birth weight and postnatal growth until 3 mo of age. Although this growth delay was described in healthy term born infants, intrauterine and postnatal growth retardation are potentially harmful to the developing human and should be avoided by reducing maternal PCB and dioxin body burden, and consequently fetal exposure to these pollutants.