Rats were exposed to cadmium (Cd) during pregnancy orally (50 ppm Cd in drinking water from gestation day [GD] 1–20) or parenterally (5 mg/kg sc during GD 1–19 or on GD 16). Cadmium levels were measured in blood, placenta, and fetus at the end of exposure. Human studies comprised of two cohorts of healthy Croatian postpartum women in the continental versus coastal area; in these women, Cd levels were measured in maternal blood, placenta, and cord blood. Cadmium in rat placenta was 10-fold higher following parenteral versus oral exposure, with highest value after exposure in mid pregnancy. The values were 10-fold higher in placenta than blood, and the fetus had ≤10% of blood metal levels. Cadmium levels in human placenta noted increased values in smokers that were 10- to 20-fold higher than in maternal blood and in cord blood were very low (<0.1 ppb). In nonsmokers, different Cd levels in placenta and blood in coastal versus continental area were found due to dietary intake. Data showed that Cd in placenta is a reliable biomarker of exposure following oral and parenteral treatment during pregnancy in rats and in human biomonitoring that includes prenatal assessment. In addition, tobacco smoking is a prominent source of metal exposure. Cd levels in placenta are also a valuable biomarker of metal dietary exposure related to specific dietary habits and soil characteristics.

The effect of maternal smoking as a source of exposure to toxic metals Cd and Pb on superoxide dismutase (SOD) and glutathione peroxidase (GPx) activity, metallothionein (MT), Cd, Pb, Cu, Fe, Mn, Se and Zn concentrations were assessed in maternal and umbilical cord blood and placenta in 74 healthy mother-newborn pairs after term delivery. Sparse discriminant analysis (SDA) was used to identify elements with the strongest impact on the SOD, GPx and MT in the measured compartments, which was then quantified by multiple regression analysis. SOD activity was lower in maternal and cord plasma, and higher in the placenta of smokers compared to non-smokers, whereas GPx activity and MT concentration did not differ between the groups. Although active smoking during pregnancy contributed to higher maternal Cd and Pb concentrations, its contribution to the variability of SOD, GPx or MT after control for other elements identified by SDA was not significant. However, an impaired balance in the antioxidant defence observed in the conditions of relatively low-to-moderate exposure levels to Cd and Pb could contribute to an increased susceptibility of offspring to oxidative stress and risk of disease development later in life. Further study on a larger number of subjects will help to better understand complex interactions between exposure to toxic elements and oxidative stress related to maternal cigarette smoking.