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MERCURY 352<br />

2. HEALTH EFFECTS<br />

In general, quantitative data are available to evaluate the rate <strong>and</strong> extent of distribution, metabolism, <strong>and</strong><br />

elimination of mercury in humans <strong>and</strong> animals following inhalation <strong>and</strong> oral exposure. Data on<br />

distribution, metabolism, <strong>and</strong> excretion following dermal exposure are lacking <strong>for</strong> all <strong>for</strong>ms of mercury.<br />

The distribution data <strong>for</strong> metallic, inorganic <strong>and</strong> organic mercury are similar in humans <strong>and</strong> animals<br />

(Aschner <strong>and</strong> Aschner 1990; Berlin 1963; Cherian <strong>and</strong> Clarkson 1976; Cherian et al. 1978; Clarkson 1989;<br />

Clarkson <strong>and</strong> Magos 1978; Danscher et al. 1990; Gr<strong>and</strong>jean et al. 1992; Nielsen <strong>and</strong> Andersen 1990,<br />

1991a, 1991b; Nordberg 1976; Schionning et al. 1991; Sin et al. 1983; Suzuki et al. 1992; Warfvinge et al.<br />

1992; Yeoh et al. 1989; Yoshida et al. 1990, 1992). No quantitative distribution data were located <strong>for</strong><br />

organic mercury compounds following inhalation exposure. The oxidation <strong>and</strong> reduction reactions that<br />

control the disposition of elemental mercury were identified in both animals <strong>and</strong> humans (Clarkson 1989;<br />

Halbach <strong>and</strong> Clarkson 1978; Nielsen-Kudsk 1973). Quantitative data on the biotrans<strong>for</strong>mation of organic<br />

mercury are limited (Norseth <strong>and</strong> Clarkson 1970). Reliable quantitative evidence on excretion of metallic<br />

<strong>and</strong> inorganic mercury in humans <strong>and</strong> animals following inhalation exposure is available (Cherian et al.<br />

1978; Hursh et al. 1976; Joselow et al. 1968b; Lovejoy et al. 1974).<br />

As discussed in the section on data needs <strong>for</strong> biomarkers, further study is needed on the effects that the<br />

exposure level of methylmercury (as well as other <strong>for</strong>ms of mercury) has on tissue distributions <strong>and</strong> the<br />

correlation to biomarkers of exposure. Age appears to be a factor in the elimination of mercury in rats<br />

following inorganic <strong>and</strong> organic mercury exposures (Daston et al. 1986; Thomas et al. 1982). Elimination<br />

of methylmercury in rats may also be sex-related (Ballatori <strong>and</strong> Clarkson 1982). Nielson et al. (1994)<br />

observed a significant sex-related differences in the toxicokinetics of methylmercury in mice following<br />

administration of a single radiolabeled dose. Drasch et al. (1997) reported that mercury levels in all tissues<br />

assayed in their human cadaver study had higher levels compared to male tissues. Nakagawa (1995) also<br />

report higher mean mercury hair levels in males (2.98 µg/g) compared with females (2.02 µg/g) in a<br />

Japanese population. Further research is, there<strong>for</strong>e, needed to characterize potential sex related difference<br />

in the toxicokinetics of mercury under different exposure scenarios.<br />

Insufficient data are available to assess whether or not there are any differences in absorption, distribution,<br />

metabolism, <strong>and</strong> excretion of mercury with respect to time or dose (i.e., if saturation phenomena occur).<br />

The majority of the available toxicokinetic data involve acute exposures to single doses. For all three<br />

routes, studies are needed that compare various dose levels <strong>and</strong> durations in order to determine if there are<br />

any differences in the toxicokinetics of mercury. Little is known about how mercurials are eliminated<br />

from specific organs. In particular, the mechanism by which mercury is eliminated from the brain is

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