revised final - Agency for Toxic Substances and Disease Registry ...

MERCURY 208
2. HEALTH EFFECTS
Oral absorption of metallic mercury is low, possibly because of an in vivo conversion to divalent mercury
and subsequent binding to sulfhydral groups, or possibly because of poor absorption of the elemental form.
For inorganic mercuric compounds, the low absorption in the lungs is probably due to the deposition of
particles in the upper respiratory system that should be cleared rapidly (Friberg and Nordberg 1973).
Solubility and other chemical properties may also be factors in the absorption. The mechanism for
intestinal absorption of inorganic mercuric mercury may also involve the process of diffusion, and the
absorption rate is proportional to the concentration of mercury in the lumen of the intestines (Piotrowski et
al. 1992). The extent of transport of inorganic mercury across the intestinal tract may depend on its
solubility (Friberg and Nordberg 1973) or on how easily the compounds dissociate in the lumen (Endo et al.
1990). Absorption of mercurous compounds is less likely, probably because of solubility (Friberg and
Nordberg 1973) or its conversion into the divalent cation in the gastrointestinal tract.
The divalent cation exists in both a nondiffusible form (tissues) and a diffusible form (blood) (Halbach and
Clarkson 1978; Magos 1967) (see Section 2.3.2). The mechanism for the distribution of mercury and its
compounds probably depends on the extent of uptake of the diffusible forms into different tissues or on the
mercury-binding to protein-binding sites (sulfhydryl groups) in red cells and plasma proteins (Clarkson
1972b).
Mechanisms for the toxic effects of inorganic and organic mercury are believed to be similar. It has been
suggested that the relative toxicities of the different forms of mercury (e.g., metallic, monovalent, and
divalent cations and methyl- and phenylmercury compounds) are related, in part, to its differential
accumulation in sensitive tissues. This theory is supported by the observation that mercury rapidly
accumulates in the kidneys and specific areas of the central nervous system (Rothstein and Hayes 1960;
Somjen et al. 1973).
The accumulation of methylmercury and inorganic mercury in the brain of female monkeys (Macaca
fascicularis) was studied by Vahter et al. (1994). In this study, animals received oral doses of
50 µg/kg/day for either 6, 12, or 18 months. In normal-weight monkeys (2.4–4.1 kg), a steady-state blood
concentration for total mercury was attained in approximately 4 months. The elimination half-life in the
blood was found to be 26 days. Accumulation in the brain appeared to be biphasic, with an elimination
half-life of 35 days for brain methylmercury in those monkeys exposed for 12 months. The elimination
half-life of inorganic mercury, on the other hand, was reported be on the order of years. It was also found
that inorganic mercury accounted for approximately 9% of the total brain mercury at 6–12 months, 18% at