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MERCURY 458<br />

5. POTENTIAL FOR HUMAN EXPOSURE<br />

concentrations in breast milk from women in the Faroe Isl<strong>and</strong>s, a population that consumes large quantities<br />

of fish <strong>and</strong> marine mammal tissue, were 2.45 <strong>and</strong> 8.7 ppb, respectively (Gr<strong>and</strong>jean et al. 1995a). Breast milk<br />

mercury concentrations reported by these authors were significantly associated with mercury concentrations<br />

in cord blood <strong>and</strong> with the frequency of pilot whale dinners during pregnancy. These are relatively low<br />

values in contrast to the values reported in Minamata, Japan, <strong>for</strong> women who ate<br />

contaminated seafood in the Minamata episode, which resulted in total mercury concentrations in breast milk<br />

of 63 ppb (Fujita <strong>and</strong> Takabatake 1977), <strong>and</strong> in Iraq, where consumption of homemade bread prepared from<br />

methylmercury-contaminated wheat occurred, resulted in breast milk concentrations of up to 200 ppb (about<br />

60%) methylmercury (Amin-Zaki et al. 1976; Bakir et al. 1973).<br />

Children can be exposed to mercury by many of the same pathways as adults as discussed in<br />

Sections 5.4.4., 5.5, <strong>and</strong> 5.7. Children can receive mercury exposures from oral or dermal contact with<br />

mercury-contaminated soils <strong>and</strong> sediments or mercury-contaminated objects. Exposure analysis of<br />

individuals living near an ab<strong>and</strong>oned mercury-contaminated industrial site suggested that children were<br />

exposed primarily via soil ingestion (Nublein et al. 1995). Little experimental in<strong>for</strong>mation on the<br />

bioavailability of mercury via oral or dermal exposure was found relative to mercury or mercury compounds<br />

sorbed to contaminated soils <strong>and</strong> sediments (De Rosa et al. 1996). Paustenbach et al. (1997) noted that, due<br />

to the presence of mercury at a number of major contaminated sites in the United States, the bioavailability<br />

of inorganic mercury following ingestion has emerged as an important public health issue. Although precise<br />

estimates are not available, in vivo <strong>and</strong> in vitro estimates of the bioavailability of different inorganic<br />

mercury species in different matrices suggest that the bioavailability of these mercury species in soil is likely<br />

to be significantly less (on the order of 3 to 10 fold), than the bioavailability of mercuric chloride, the<br />

mercury species used to derive the toxicity criteria <strong>for</strong> inorganic mercury (Paustenbach et al. 1997). These<br />

authors suggest that site specific estimates of bioavailability be conducted of various mercury compounds<br />

because bioavailability can vary significantly with soil type, soil aging, the presence of co-contaminants <strong>and</strong><br />

other factors. Canady et al. (1997) concluded that the “100% bioavailability assumption” <strong>for</strong> mercurycontaminated<br />

soils is excessively conservative. These authors note that various mercury compounds have<br />

distinctly different bioavailability. For example, mercuric chloride has been reported to be approximately<br />

20–25% bioavailable in adult animals (Nielsen <strong>and</strong> Andersen 1990; Schoof <strong>and</strong> Nielsen 1997).<br />

Methylmercury is thought to be nearly completely absorbed (Aberg et al. 1969; Miettinen et al. 1971; Rice<br />

1989a, 1989b). Mercuric nitrate was reported to be only 15% bioavailable in humans (Rahola et al. 1973)<br />

<strong>and</strong> elemental mercury is thought to be very poorly absorbed, although experimental evidence is lacking <strong>for</strong><br />

the latter. Recently, Barnett et al. (1997) reported that analysis of mercury contaminated soil from the flood

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