CaNa2EDTA), and oral chelating agents, such as 2,3-dimercaptosuccinic acid (commonly referred to as DMSA) (Graziano et al. 1985). A much smaller proportion of absorbed lead is excreted in feces, sweat, breast milk, seminal fluid, and hair.

A number of factors can influence the toxicokinetics of lead. Several aspects of nutrition—including iron, zinc, and calcium status and supplementation—can influence the gastrointestinal absorption and distribution of lead. Diets low in calcium or high in lactose or fat have been reported to enhance lead accumulation (Goyer 1995). Studies have shown that iron-deficient children have higher gastrointestinal absorption of lead (Barton et al. 1978). Sex differences in lead toxicokinetics have also been reported. Some studies have shown that blood lead levels (BLLs) varied by geographic areas, were higher in men than in women, and were higher in smokers than in nonsmokers (Friberg and Vahter 1983). Analysis of BLLs in monozygotic and dizygotic twins provided evidence of a genetic factor’s regulating BLLs in females but not in males (Bjorkman et al. 2000). Yang et al. (2007) reported a small but statistically significant increase in BLLs of about 7.6% from a baseline of 2.64 μg/dL in teenage girls during menstruation, but the underlying factors related to this observation remain unknown. Lactating and postmenopausal women can mobilize lead stores from bone (Hernandez-Avila et al. 2000; Ettinger et al. 2004).


FIGURE 3-1 Compartmental model for lead (modified from O’Flaherty 1993). The percentages shown represent the fractions of lead found in different tissue compartments. Used with permission of Brian Schwartz, Johns Hopkins Bloomberg School of Public Health.

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