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Mobilization of maternal bone lead stores has been suggested as a potential endogenous source of lead in breast milk.
Calcium supplementation may attenuate fetal exposure by inhibiting mobilization of maternal bone lead and/or intestinal absorption of ingested lead.
Background: Mobilization of maternal bone mineral partly supplies calcium for fetal and neonatal bone growth and development.
In lactation, the calcium requirement for breast milk production is largely met by mobilization of maternal bone mineral and renal calcium conservation (2, 4, 5).
Inadequate level of maternal body fat may result in higher rates of mobilization of maternal fat stores in the last trimester of pregnancy (Haggarty 2010).
The effect of calcium may be exerted, at least in part, by decreasing bone resorption and the consequent mobilization of maternal bone lead stores.
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Consequently, it is now appreciated that prenatal lead exposure can occur not only through current maternal environmental exposures, but also through the mobilization of cumulative maternal bone lead stores during pregnancy and lactation (Gulson et al. 1997, 2003; Tellez-Rojo et al. 2002).
Substantial fetal lead exposure can occur from mobilization of cumulative maternal skeletal lead stores into the circulation during pregnancy (Hu 1998; Tellez-Rojo et al. 2004).
Nonetheless, dietary calcium intake likely plays a limited, but still important, role in suppressing mobilization of lead from maternal bone and/or decreasing gastrointestinal absorption of ingested lead, thereby decreasing the risk of fetal and infant exposure.
In pregnancy, the calcium for fetal bone growth and mineralization is supplied by increases in maternal calcium absorption and mobilization of mineral from the maternal skeleton (1– 3).
Previous studies have demonstrated that there is increased mobilization of lead from the maternal skeleton at this time and that calcium supplementation may have a protective effect.
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