Electroretinographic and cyclic nucleotide metabolism studies have established that low-level lead exposure during early postnatal development results in long-term selective rod deficits. To determine whether there was a corresponding selective rod photoreceptor cell degeneration we examined retinas of adult rats exposed to low-level lead during development using light and electron microscopy. In all retinal regions, a rod but not cone cell degeneration was observed. Overall, 20% of the rod cells were lost. Moreover, two specific regional differences were found. Degeneration was much greater in the inferior (-25%) than superior (-15%) retina and greater in the posterior (-22%) than peripheral (-17%) retina. The latter pattern indicates a central-peripheral gradient of degeneration. Total retinal thickness decreased 15-20%, which reflects cell loss in the outer and inner nuclear layers. Ultrastructurally, the most obvious lead-induced alterations were swollen and disorganized rod outer segments and large accumulations of beta-glycogen particles in rod photoreceptor mitochondria. Glycogen accumulations were heaviest in rod inner segment mitochondria followed by rod axon and synaptic terminal mitochondria. Possible cellular mechanisms of action responsible for these lead-induced retinal alterations include an inhibition of retinal cyclic GMP phosphodiesterase and the resultant elevation of cyclic GMP, an inhibition of intermediary metabolism, and/or an alteration in calcium metabolism. In addition, the thinning of the inner nuclear layers could be due to transneuronal degeneration. As noted in our preceding paper, the first possibility has been demonstrated in rats similarly exposed to lead. These quantitative histological results, in combination with the ERG and biochemical results in the preceding paper, demonstrate that low-level lead exposure during early postnatal development produces long-term selective rod functional deficits and degeneration.