Cadmium and other metallic ions can act as metalloestrogens and endocrine disruptors of reproductive tissues and fetal development in mammals, including humans. The detrimental effects occur with respect to the synthesis of both steroid and polypeptide hormones in the placenta. 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-smokers 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-immunometric method. Cadmium concentrations were doubled in placentas of smokers as compared with non-smokers, 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-cultured with 0, 5, 10 or 20 microm CdCl(2) for 96 h and leptin mRNA assessed by quantitative polymerase chain reaction. Leptin mRNA declined dose-responsively as a result of CdCl(2) 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-disrupting effects of cadmium, as a constituent of tobacco smoke, on reproduction in women.

This study was conducted to determine if vitamin D supplementation is required to prevent rickets in breast-fed infants. Breast-feeding rates are increasing, and there are concerns about whether the vitamin D content of breast milk is sufficient. There are a few treatment trials of vitamin D supplementation in breast-fed infants; these were conducted in northern climates. The authors therefore performed a prospective clinical trial comparing vitamin D supplementation with placebo as control in southern Louisiana. Blood samples and questionnaires were collected at birth, 2, 4, and 6 months of age. There were no cases of rickets observed, and no differences in alkaline phosphatase levels between groups. Thus, there was no evidence that vitamin D supplementation reduced rickets risk in the authors' study population. This suggests that the current recommendations for universal vitamin D supplementation of breast-fed infants throughout the United States may need to be revised.

Vitamin D is critical in bone and mineral homeostasis, particularly in the prevention of rickets in children. Levels of vitamin D in cord blood were measured in a population from New Orleans as an index of maternal vitamin D status at the time of delivery. Cord blood samples from infants born during the summer and winter showed lower 25-hydroxyvitamin D levels compared with those from infants born during fall and spring, indicating an unusual pattern of seasonality where vitamin D levels were among the lowest in the season with the greatest sunlight. It is important to establish screening and supplementation guidelines based on observed regional trends and risk factors, in addition to considerations based on global recommendations.