<p>Cadmium is a widespread and non-biodegradable pollutant that is dangerous to living organisms. The routes of exposure and doses of pollutants are different, and it is extremely important to assess their toxicity. Three experimental groups received a single treatment of CdCl₂ (15 and 30&#xa0;mg/kg orally; 15 OR and 30 OR group and 15&#xa0;mg/kg intraperitoneally; 15 IP group) and one control group (Ctr). The toxic effects of Cd were examined on hematological and biochemical parameters, and histopathological observation of hepatocytes and bone marrow. Leukocytopenia and granulopenia were recorded in 30-OR, and thrombocytopenia in 15-OR and 15-IP. 30-OR causes a decrease in RBC, and 15-IP causes changes in RBC count. Renal markers (CRE and BUN) show a correlation with 15-OR dose, inflammatory marker CRP shows a positive correlation with 15-IP dose, LDH as a biomarker of oxidative stress and CK as a biomarker of membrane damage were significantly increased in all experimental groups. The hepatocyte membrane and the size of the nucleolus have changed in all groups, and the highest degree in 15-IP. Bone marrow hypoplasia was noted with oral doses, and basophilia and an increased number of lymphoblasts and myeloblasts and immature hematopoietic cells with toxic granulations in 15-IP. Single doses of Cd cause serious toxicological changes in blood and tissues. Oral doses cause significant tissue-specific microscopic lesions observed in the liver during histopathology and bone marrow hypoplasia compared with intraperitoneal administration. Intraperitoneal administration shows a strong correlation with renal, inflammatory and stress markers compared to oral administration.</p>