The Risk Assessment Information System

Toxicity Profiles

Condensed Toxicity Summary for 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 Young, Ph.D., Chemical Hazard Evaluation Group in the Biomedical and Environmental Information Analysis Section, Health Sciences Research Division, Oak Ridge National Laboratory*.

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.

Mercury is a naturally occurring element existing in multiple forms and in various oxidation states. It is used in a wide variety of products and processes. In the environment, mercury may undergo transformations among its various forms and among its oxidation states. Exposure to mercury may occur in both occupational and environmental settings, the latter primarily involving dietary exposure (ATSDR 1989).

Absorption, distribution, metabolism, and excretion of mercury is dependent upon its form and oxidation state (ATSDR 1989, Goyer 1991). Organic mercurials are more readily absorbed than are inorganic forms. An oxidation-reduction cycle is involved in the metabolism of mercury and mercury compounds by both animals and humans (ATSDR 1989). The urine and feces are primary excretory routes. The elimination half-life is 35 to 90 days for elemental mercury and mercury vapor and about 40 days for inorganic salts (Goyer 1991).

Ingestion of mercury metal is usually without effect (Goldwater 1972). Ingestion of inorganic salts may cause severe gastrointestinal irritation, renal failure, and death with acute lethal doses in humans ranging from 1 to 4 g (ATSDR 1989). Mercuric (divalent) salts are usually more toxic than are mercurous (monovalent) salts (Goyer 1991). Mercury is also known to induce hypersensitivity reactions such as contact dermatitis and acrodynia (pink disease) (Mathesson et al. 1980). Inhalation of mercury vapor may cause irritation of the respiratory tract, renal disorders, central nervous system effects characterized by neurobehavioral changes, peripheral nervous system toxicity, renal toxicity (immunologic glomerular disease), and death (ATSDR 1989).

Toxicity resulting from subchronic and chronic exposure to mercury and mercury compounds usually involves the kidneys and/or nervous system, the specific target and effect being dependent on the form of mercury (ATSDR 1989). Organic mercury, especially methyl mercury, rapidly enters the central nervous system resulting in behavioral and neuromotor disorders (ATSDR 1989, Goyer 1991). The developing central nervous system is especially sensitive to this effect, as documented by the epidemiologic studies in Japan and Iraq where ingestion of methyl mercury-contaminated food resulted in severe toxicity and death in adults and severe central nervous system effects in infants (Bakir et al. 1973, Amin-Zaki et al. 1974, Harada 1978, Marsh et al. 1987). Blood mercury levels of <10 µg/dL and 300 µg/dL corresponded to mild effects and death, respectively (Bakir et al. 1973). Teratogenic effects due to organic or inorganic mercury exposure do not appear to be well documented for humans or animals, although some evidence exists for mercury-induced menstrual cycle disturbances and spontaneous abortions (Derobert and Tara 1950, Amin-Zaki et al. 1974, ATSDR 1989).

A subchronic and chronic oral RfD of 0.0001 mg/kg/day for methyl mercury is based on a benchmark dose of 1.1 µg/kg/day relative to neurologic developmental abnormalities in human infants (EPA 1995, 1996). A subchronic and chronic oral RfD of 0.0003 mg/kg/day for mercuric chloride is based on immunologic glomerulonephritis (EPA 1996). A Lowest Observed Adverse Effect Level (LOAEL) of 0.63 mg Hg/kg/day for mercuric chloride was identified (EPA 1987). No Observed Adverse Effect Levels (NOAELs) were not available for oral exposure to inorganic mercury or methyl mercury. A subchronic and chronic inhalation RfC of 0.0003 mg Hg/m3 for inorganic mercury (EPA 1995, 1996) is based on neurological disorders (increased frequency of intention tremors) following long-term occupational exposure to mercury vapor (Fawer et al. 1983). The LOAELs for subchronic and chronic inhalation exposures to inorganic mercury are 0.32 and 0.03 mg Hg/m3, respectively. NOAELs were unavailable. An inhalation RfC for methyl mercury has not been determined.

No data were available regarding the carcinogenicity of mercury in humans or animals. EPA has placed inorganic mercury in weight-of-evidence classification D, not classifiable as to human carcinogenicity (EPA 1996). Weight-of-evidence classifications of C (possible human carcinogen) have been assigned to mercuric chloride and methyl mercury by EPA (1996) based upon limited evidence of carcinogenicity in rodents. No slope factors have been calculated.

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Last Updated 2/13/98

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