Rare earth elements, including yttrium, which have been used in clinical therapy and magnetic resonance imaging, have also been applied to farmlands in past decades, polluting the environment. This study aimed to investigate the effect of early exposure to yttrium nitrate on the peripheral blood of offspring. Pregnant Sprague Dawley (SD) rats (10 per dosage group) and their offspring (10 females and 10 males per dosage group, from different dams) were gavaged with different doses of yttrium (0, 2, 8, and 32 mg/kg.bw , respectively) from gestation day 0 to postnatal day 70. The offspring were evaluated using hemograms, the apoptosis/necrosis were evaluated using alkaline comet assays, and the oxidative damage parameters of malondialdehyde (MDA), carbonyl protein (CP) and monoamine oxidase (MAO), and their antioxidative abilities, including total antioxidative capacity (TAOC), and the catalase (CAT) of the offspring's serum were used in a colorimetric determination. Rats fed 2 and 8 mg/kg.bw of yttrium have elevated platelet distribution widths, platelets, mean platelet volumes, and thrombocytocrit; but those fed 32 mg/kg.bw of yttrium had in a decrease in the number of blood cells and lymphocytes. The hemoglobin, neutrophilic granulocyte, and eosinophil counts were all reduced when the rats were fed 8 mg/kg.bw or 32 mg/kg.bw of yttrium. A dose of 32 mg/kg.bw yttrium significantly raised the levels of CP, MAO, and the cellular apoptosis/necrosis rates of the peripheral blood cells, but the TAOC and CAT levels increased. A high dose of yttrium nitrate induced oxidative stress and cellular apoptosis in the peripheral blood, accompanied by an enhanced antioxidant ability.