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

MERCURY 221
2. HEALTH EFFECTS
typically the first effect noted in all forms of mercury exposure, it can be an ultimate effect of either low-
dose chronic intake or high-dose acute mercury exposure.
The most sensitive end point following oral exposure of any duration to inorganic salts of mercury appears
to be the kidneys. Liquid metallic mercury can volatilize at ambient temperatures. The absorption of
metallic mercury vapors from lungs is high (about 80%) (Hursh et al. 1976), and the most sensitive target
following inhalation exposure to metallic mercury is the central nervous system. Absorbed metallic
mercury crosses the placenta, and the fetal blood may concentrate mercury to levels 10 or more times the
levels found in the maternal blood. Therefore, the developing fetal nervous system may be quite sensitive
to maternal exposures to mercury vapors.
Salts of mercury and organic mercury compounds are far less volatile than liquid mercury under most
conditions. Inhalation of mercury vapors from these forms is not considered a major source of exposure.
While inhalation of particulate matter containing mercury salts and/or organic compounds is possible,
intestinal absorption is a more likely route of exposure. The most sensitive end point for oral exposure to
alkyl mercury compounds (e.g., methylmercuric chloride or ethylmercurials) is the developing nervous
system, but toxicity to the adult nervous system may also result from prolonged low-dose exposures.
Mercury may adversely affect a wide range of other organ systems, if exposures are sufficiently high.
These effects may result from the mercuric ion’s affinity for sulfhydryl groups, which are ubiquitous in
animal tissue.
Pharmacokinetic studies indicate that repeated or continuous exposure to any form of mercury can result in
the accumulation of mercury in the body. Numerous studies using laboratory animals have shown that
retention of mercury in the brain may persist long after cessation of short- and long-term exposures.
Mercury is unusual in its ability to induce delayed neurological effects. This is especially prevalent with
exposure to alkyl mercury compounds. In such cases, the onset of adverse effects may be delayed for
months after the initial exposure. The delayed effects of methyl- and dimethylmercury reported in human
poisonings are thought, in part, to result from binding to red blood cells, and subsequent slow release.
Methylmercury also forms a complex in plasma with the amino acid cysteine, which is structurally similar
to the essential amino acid methionine (Aschner and Clarkson 1988). Clarkson (1995) proposed that
methylmercury can cross the blood-brain barrier "disguised" as an amino acid via a carrier-mediated
system (i.e., transport is not solely the result of methylmercury’s lipid solubility).