Oxidative damage to DNA has been associated with neurodegenerative diseases. Developmental exposure to lead (Pb) has been shown to elevate the Alzheimer's disease (AD) related β‐amyloid peptide (Aβ), which is known to generate reactive oxygen species in the aging brain. This study measures the lifetime cerebral 8‐hydroxy‐2'‐deoxyguanosine (oxo⁸dG) levels and the activity of the DNA repair enzyme 8‐oxoguanine DNA glycosylase (Ogg1) in rats developmentally exposed to Pb. Oxo⁸dG was transiently modulated early in life (Postnatal day 5), but was later elevated 20 months after exposure to Pb had ceased, while Ogg1 activity was not altered. Furthermore, an age‐dependent loss in the inverse correlation between Ogg1 activity and oxo⁸dG accumulation was observed. The effect of Pb on oxo⁸dG levels did not occur if animals were exposed to Pb in old age. These increases in DNA damage occurred in the absence of any Pb‐induced changes in copper/zinc‐superoxide dismutase (SOD1), manganese‐SOD (SOD2), and reduced‐form glutathion (GSH). These data suggest that oxidative damage and neurodegeneration in the aging brain could be impacted by the developmental disturbances.