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Leptin is produced by the trophoblast and may regulate fetal organogenesis and development. In human term placentas, concentrations of toxic metals and their effects on steroidogenesis were assessed in healthy parturients (109 non\u2010smokers and 99 smokers) in relation to tobacco smoking. Trace elements (cadmium, lead, iron, zinc and copper) were analyzed in placentas using atomic absorption spectroscopy, and steroid hormones (progesterone and estradiol) were assayed in placental samples by an enzyme\u2010immunometric method. Cadmium concentrations were doubled in placentas of smokers as compared with non\u2010smokers, and placental lead and zinc concentrations increased significantly. Placental concentrations of iron, copper, progesterone and estradiol did not differ. In addition, human trophoblast cells were co\u2010cultured with 0, 5, 10 or 20\u2009\u2009\u00b5<jats:sc>m<\/jats:sc> CdCl<jats:sub>2<\/jats:sub> for 96\u2009\u2009h and leptin mRNA assessed by quantitative polymerase chain reaction. Leptin mRNA declined dose\u2010responsively as a result of CdCl<jats:sub>2<\/jats:sub> exposure. Collectively, the results confirm that human placental tissue offers a unique opportunity to biomonitor cadmium exposure in both the maternal and the internal fetal environments. In addition, the results strongly suggest that cadmium may cause a decline in placental leptin synthesis, as we have previously shown for placental progesterone production. This may constitute further evidence of the endocrine\u2010disrupting effects of cadmium, as a constituent of tobacco smoke, on reproduction in women. 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