The Risk Assessment Information System

Toxicity Profiles

Condensed Toxicity Summary for METHYL MERCURY

NOTE: Although the toxicity values presented in these toxicity profiles were correct at the time they were produced, these values are subject to change. Users should always refer to the Toxicity Value Database for the current toxicity values.


Prepared by: Robert A. Young, Ph.D., D.A.B.T., Chemical Hazard Evaluation and Communication Group Biomedical and Environmental Information Analysis Section, Health and Safety Research Division, *, Oak Ridge, Tennessee.

Prepared for: Oak Ridge Reservation Environmental Restoration Program.

*Managed by Martin Marietta Energy Systems, Inc., for the U.S. Department of Energy under Contract No. DE-AC05-84OR21400.

Methyl mercury is formed by biotic and abiotic methylation of mercury (McComish and Ong, 1985). Methyl mercury has been used as a fungicide, disinfectant, and in industrial processes (Singer and Nowak, 1980; Berlin et al., 1983).

Methyl mercury is highly toxic and is readily absorbed by the body following ingestion or inhalation (Aberg et al., 1969; Meittenen, 1973; Berlin et al., 1983). Methyl mercury may be metabolized to inorganic mercury by the liver and kidneys, with further transformation occurring to form the divalent cation (ATSDR, 1989). Methyl mercury is excreted as inorganic mercury, primarily in the feces (Norseth and Clarkson, 1971).

The target organ for methyl mercury toxicity is the central nervous system (CNS), especially the brain, and may occur at doses as low as 3 µg/kg in humans (WHO, 1976). Methyl mercury is neurotoxic to several species of experimental animal and to humans. The LD50 values for various rodent species range from 21 to 57.6 mg/kg (RTECS, 1986). Manifestation of toxic effects (neurobehavioral alterations and degenerative changes in the central and peripheral nervous system) is probably a function of accumulation of critical levels of mercury (Goyer, 1991). Histopathologic correlates have been identified in the brains of humans and animals prenatally exposed to methyl mercury (Choi et al., 1987; Hughes and Annua, 1976).

Exposure to methyl mercury in the diet (fish and contaminated grain) has caused epidemic poisonings in Iraq and Japan, characterized by severe developmental effects (impaired motor and cognitive functions) in infants of exposed mothers (Bakir et al., 1973; Amin-Zaki et al., 1974; WHO, 1976). The primary target organ for oral exposure to methyl mercury is the brain; the effects on this organ accounting for the developmental toxicity of the chemical (Magos, 1980; Goyer, 1991). Data on the effects of inhalation exposure to methyl mercury are lacking for both humans and animals.

A reference dose (RfD) of 3E-04 mg/kg/day has been calculated by the U.S. EPA and is based on the intake that would be required to produce a blood mercury level of 200 µg/mL, which is a level associated with minimal health effects in humans (U.S. EPA, 1991; U.S. EPA, 1990). In deriving the RfD, an uncertainty factor of 10 was applied for extrapolation from a LOAEL to NOAEL. Confidence in the RfD is medium.

An inhalation reference concentration (RfC) for methyl mercury is not available.

No data were available for assessing the carcinogenic potential of methyl mercury.

Retrieve Toxicity Profiles Formal Version

Last Updated 2/13/98

Join the RAIS User's Group for Updates