Placenta lead transfer

Roels HA, Hubermont G, Buchet J-P, et al. 1978. Placental transfer of lead, mercury, cadmium, and carbon monoxide in women III. Factors influencing the accumulation of heavy metals in the placenta and the relationship between metal concentration in the placenta and in maternal and cord blood. 

Transfer of uranium across the placenta was investigated in an animal study, but no information is available for humans. In the animal study, only 0.01-0.03% of an intravenous dose of uranium to rat dams crossed the placenta (Sikov and Mahlum 1968) thus if an inhalation, oral, or dermal exposure was sufficient to raise the blood uranium level, a very limited amount of uranium might cross the placenta. No studies were located regarding uranium in breast milk. Based on the chemical properties of uranium, it seems unlikely that there would be preferential distribution from the blood to this high-fat compartment. It is not known if uranium has any effect on the active transport of calcium into breast milk. Most of the adult body burden of uranium is stored in bone (ICRP 1979, 1995, 1996). It is not known if maternal bone stores of uranium (like those of calcium and lead) are mobilized during pregnancy and lactation. 

Transplacental transfer and pharmacokinetics of parathion methyl after dermal application were studied in pregnant rats (Abu-Qare et at., 2000). Both the parent drug and the oxon metabolite were transferred to the fetus, although concentrations were somewhat lower than in maternal tissues. It is clear that the fetus is exposed to a relatively high concentration of parathion methyl even after dermal exposure, and (his exposure leads to a significani degree of cholinesterase inhibition (Abu-Qare and Abou-Donia. 2001) also in placenta tissue (Benjaminov et al., 1992). 

Iodine deficiency results in lowered maternal circulating thyroid hormone concentrations, leading to reduction in placental transfer of thyroxine. The possibility of iodine storage by the placenta compensating for diminished dietary iodine intake has been suggested by Delange (2004), and placental iodine storage has been demonstrated (Smyth et al, 2006). 

In the presence of low body stores of vitamin E, one might expect that marginal dietary intakes could more easily lead to the deficiency state. In various mammalian species, including man, the placenta has a limited capacity to transfer tocopherol to the fetus (Abderhalden, 1945 Dju et al.,... 

Roels H, Hubermont G, Buchet JP, Lauwerys R (1978) Placental transfer of lead, mercury, cadmium, and carbon monoxide in women. III. Factors influencing the accumulation of heavy metals in the placenta and the relationship between metal concentration in the placenta and in maternal and cord blood. Environ. Res. 16 236 Wilson JG (1973) Environment and birth defects. Academic Press, New York - London Wilson JG (1977) Current status in teratology - general principles and mechanisms derived from animal studies. In Handbook of teratology, Vol. 1, eds. Wilson JG, Fraser FC, Plenum Press, New York, p. 75... 

The purpose of this chapter is provide an overview of the mechanisms for transport of two toxic metals, lead and cadmium, and to identify factors that may influence this process. The mechanisms for transfer of these two metals differ in that lead is readily diffusible across the placenta. There is no placental barrier for lead, whereas the placenta provides a protective barrier to fetal exposure to cadmium. Consideration of the placental transport of these two metals is prefaced by a few comments on possible experimental... 

Placental transport of lead may be associated with placental transport of calcium. Barltrop (1969) observed that femur lead increased rapidly in the third trimester, corresponding to onset of ossification and deposition of calcium. There is a question whether the increased deposition of lead in the femur along with calcium is because of some commonality between lead and calcium metabolism. Figure 2 shows the close correlation between size of fetal brain and increase in lead content as the brain matures. Whether the movement of lead into the brain is a matter of simple diffusion or whether there is some relationship to brain calcium is not known. Calcium deficiency does enhance lead absorption and the pathological effects of lead (Mahaffey et al. 1973). The placenta also contains a calcium-binding protein identical to that present in the intestine (Van Dijk 1981). A comparison of placental transfer of toxic metals by Nakano and Kurosa from the Minamata Institute in Japan (unpublished observation) found that lead levels in the placenta were strongly correlated with calcium, suggesting that lead deposition is associated with calcium deposition or with areas of dystrophic calcification that are present in the mature placenta. 

Children and pregnant women appear to be most susceptible to lead poisoning because (1) they are likely to have deficiencies of calcium and iron, minerals which protect against lead toxicity (2) rapidly growing children absorb more lead and excrete less of this metal than other people, and (3) there is a rapid transfer of lead from the blood of pregnant women, through the placenta, to the fetus. 

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