Despite considering cisplatin as one of the most efficient antineoplasticdrugs, it has been classified as Group 2A, probably carcinogenic to humans. Itstoxicity is executed through DNA damage ending in cell death or mutation.Objectives: This study aims at evaluation of the hazardous health effects ofcisplatin exposure among healthcare workers at the oncology department, KasrEl Aini hospital, by assessing DNA damage, repair and immune body responseto that damage among those exposed workers.Subjects and Methods: The exposed group included all 32 nurses workingin the chemotherapeutic section of the oncology department at Kasr El Ainihospital. They were exposed to cisplatin drug through preparation andadministration. The exposed group was composed of 25 female and 7 maleswith age range between 22-64 years and with duration of employment rangingfrom 2-29 years. The unexposed group was composed of 37 nurses randomlyselected from other departments of Kasr El Aini hospital, who have never beenexposed to antineoplastic drugs. The group consisted of 35 female and 2 maleswith age range between 22-52years, and was matched with the exposed group asregards gender, socioeconomic standard and special habits of medicalimportance. Both groups were subjected to clinical examination, routinelaboratory investigations, estimation of DNA adduct blood level, plasma levelof Rad52, IL-15, levels of Bcl2 and glutathione , using ELISA techniques.Results: The study showed highly significant elevation in cisplatin DNAadducts, Rad52 as well as highly significant increase in IL-15 and Bcl2 amongexposed workers. There was highly significant reduction in glutathione levelsamong exposed workers. It also showed significant positive correlation betweencisplatin DNA adducts level and that of IL-15 and Rad52 while it showed significant negative correlation between glutathione level and cisplatin DNAadducts level.Conclusion: Occupational exposure to cisplatin is associated with seriousDNA damage and DNA adduct formation, with an attempt of the body to repairthat damage and prevent apoptosis through expression of IL-15 and Bcl2. Thepossibility of failure to repair and increased susceptibility to mutagenesis andcarcinogenesis necessitaties the use of IL-15, Bcl2 or DNA adducts as earlybioindicator for follow up.