Premature ovarian failure (POF) is a clinical syndrome known to affect approximately 1% of women of reproductive age. A number of genetic, autoimmune, metabolic, infectious and environmental causes have been identified in the etiology of POF. Cadmium is a toxic metal which can accumulate in ovaries and causes a significant decrease in the binding of gonadotropins that regulate steroidogenic enzyme activity in granulosa cells. We aimed to investigate the role of cadmium in the etiology of POF. Thirty-five patients with POF were enrolled in group 1 which was the study group. Two control groups were formed from healthy participants. Thirty-fiveparticipants who were age-matched young women with regular menstruation were included in group 2.Thirty-fivehealthy postmenopausal women were included in group 3. Patients' demographic data were recorded. Serum follicle-stimulating hormone (FSH), luteinizing hormone (LH), estradiol (E2), thyroid-stimulating hormone (TSH), triiodothyronine (T3), thyroxine (T4) and cadmium levels were measured. There was a statistically significant difference between the groups for gravida, parity and living children (p<0.001), but no difference was found for abortion (p=0.430). While there was a statistically significant difference between the groups for serum FSH, LH and E2 levels (p<0.001), no statistically significant difference was found for T3, T4 and TSH. Serum cadmium levels were found to be statistically significantly decreased in group 1 compared to g roups 2 and 3 (p<0.001). This study revealed that cadmium had no direct effect on the development of POF, but it should be kept in mind that the synergistic and antagonistic effects of metals may affect this result.