U.S. EPA Contaminated Site Cleanup Information (CLU-IN)

U.S. Environmental Protection Agency
U.S. EPA Technology Innovation and Field Services Division



Mercury (Hg) is a highly toxic element that is found both naturally and as an introduced contaminant in the environment. Although its potential for toxicity has been demonstrated dramatically in highly contaminated areas such as Minamata Bay, Japan, in the 1950s and 60s, research has shown that mercury can be a threat to the health of people and wildlife in many environments that are not obviously polluted. The risk is determined by the route of exposure, the form (species) of mercury present (some forms are more toxic or bioavailable than others), and the geochemical and ecological factors that influence how mercury moves and changes form in the environment.

There are many similarities in the toxic effects of the various mercury species, but also significant differences. The organic mercury compounds include methylmercury, methylmercuric chloride, dimethylmercury, and phenylmercuric acetate. Microorganisms in the environment can alter inorganic mercury to an organic form, such as methylmercury (MeHg, or CH3Hg), which is the most common organic form. It affects the immune system, alters genetic and enzyme systems, and damages the nervous system, including coordination and the senses of touch, taste, and sight. Exposure to methylmercury usually occurs through ingestion (i.e., eating contaminated fish and wildlife), and when ingested, it is absorbed more readily and excreted more slowly than other forms of mercury. Exposure to organic mercury from food results in an absorption six times greater than the same amount of inorganic mercury. Soluble organic mercury is absorbed readily from the gastrointestinal tract, while inorganic mercury is absorbed only very sparingly.

Metallic, or elemental, mercury and the inorganic salts, including mercurous chloride, mercuric chloride, mercuric acetate, and mercuric sulfide, are classified under the general heading of inorganic mercury. Elemental mercury (Hg0), the familiar silvery liquid form released from broken thermometers, and its accumulation in the body through inhalation of vapors can cause tremors, gingivitis, and excitability, and even death at high levels of accumulation or exposure. Elemental mercury can be found in higher concentrations in environments such as gold mine sites, where it is used to extract gold. If elemental mercury is ingested, it is absorbed relatively slowly (unlike inhaled elemental mercury) and may pass through the digestive system without causing damage.

Adapted from:

Mercury in the Environment
U.S. Geological Survey Fact Sheet 146-00, 2000.

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The Human Health Effects of Mercury | Ecotoxicity of Mercury

The Human Health Effects of Mercury

Elemental mercury is a metal, liquid at ambient temperatures, that generates vapor under standard conditions of temperature and atmospheric pressure. Mercury is present in ambient air from natural sources, but generally originates from human activity such as combustion of fossil fuels, domestic and medical waste, and various manufacturing and mining activities. Although mercury is present in the atmosphere and in some drinking waters, the most significant exposure for the general population is from the ingestion of organomercurial compounds in dietary sources (e.g., fish and shellfish). As organomercury compounds readily pass the placental barrier, the developing fetus is at risk if these are present in the mother's diet. Organomercurial compounds are also present in milk, thus providing a route of exposure for nursing infants. Pregnant women and children are a sensitive sub-population for mercury exposure.

Inhaled mercury vapor is efficiently absorbed by the lungs and moves into the bloodstream, and it is estimated that 70-80 percent of inhaled vapor is absorbed. In contrast, less than one percent of an oral dose of elemental mercury is absorbed by the gastrointestinal tract. Inorganic mercury salts are generally not well absorbed by the lungs or skin although some absorption may occur. The extent to which inorganic mercury is absorbed by the gastrointestinal tract is dependent on the solubility of the salt; the age, health, and nutritional status of the organism ingesting them. Approximately 2-38 percent of a dose of inorganic mercury may be absorbed. However, organomercurial compounds are completely absorbed from the gut and many are readily absorbed through the skin. The kidney is the organ with the highest levels of mercury bioaccumulation, no matter what route of exposure. Highly lipophilic elemental mercury and organomercury enter the brain and readily pass the placental barrier, and bioaccumulate in the brain and fetus. Inorganic mercury can both pass the placental barrier and into the brain, but to a much lesser extent than the elemental form. Once absorbed, elemental mercury and organomercurials undergo conversion to the inorganic divalent cation. This is a cyclical oxygenation/reduction (redox) process, and the divalent cation can be reconverted to elemental mercury.

It is suggested that mercury exerts toxicity through the binding of the divalent cation to the sulfur-containing thiol (sulfhydryl) functional group present in proteins. This functional group is common to the many proteins that comprise intra and extracellular structures, such as organelles. Once mercury is protein bound, the protein may lose its ability to either support cell structures, or to participate in cell transport processes, or to act as an enzyme.

Large doses of mercury are acutely poisonous, whether by inhalation (mercury vapor), ingestion (inorganic and organic forms of mercury), or dermal absorption (organomercury). Acute mercury poisoning causes severe gastrointestinal distress, shock, cardiovascular collapse, renal failure and may result in death. However, lower doses of mercury absorbed over extended periods of time, may also have deleterious toxic effects. The U.S. Environmental Protection Agency's Integrated Risk Information System (IRIS) Program has developed oral reference doses (RfDs) for mercuric chloride (inorganic mercury) and methylmercury (organic mercury). An RfC, an inhalation reference dose analogous to an RfD, has been developed for mercury vapor and is expressed in mg/m3, and is also based on a daily exposure. Human health epidemiological studies and peer reviewed toxicological investigations using laboratory animals are used to develop RfDs and RfCs, and the principal studies selected for this purpose are those chronic studies that have the most sensitive endpoints, e.g., the neurological impairment of the developing fetus. This enables a value to be developed for an RfD/RfC that is protective of sub-populations sensitive to the effects of mercury. However, each form of mercury has many other toxic effects, and these are fully discussed in the Agency for Toxic Substances and Disease Registry (ATSDR) Toxicological Profile for Mercury (1999).

The RfD developed by the IRIS Program for methylmercury is 1 E-4 mg/kg-day (0.0001 mg/kg-day). This value is based on human epidemiological studies that identified mercury-induced neuropsychological impairment as the critical effect.

The IRIS Program presents an RfD of 3 E-4 mg/kg-day for mercuric chloride. The most sensitive effect of mercuric chloride is the induction of autoimmune glomerulonephritis. In this disease, the body develops antibodies to the kidney's glomerular basement membrane (anti-GBM). As anti-GBM antibodies attack the glomerular membrane, protein leaks into the urine, and glomerular damage is caused that may progress to terminal renal failure.

Elemental mercury (as a vapor) has an RfC of 3 E-4 mg/m3. Six principal and supporting studies of the effects of occupational inhalation of mercury vapor were used to derive the RfC. Some of the critical effects investigated include the development of intention tremor in the subjects' hands, disturbances in memory and sleep disorders, changes in brain activity as measured by electro-encephalograms (EEGs) and alterations in the functioning of the autonomic nervous system.

One of the potential long-term effects of chemical exposure is the development of cancer. The IRIS Program examined the results of epidemiological investigations and toxicological studies and concluded that mercuric chloride and methylmercury can be considered possible human carcinogens, a "C" classification. The human data are inadequate to classify methylmercury as a carcinogen, and the C classification for this compound is based on the limited evidence of carcinogenicity from laboratory rodent studies. No quantitative estimate of carcinogenic risk has been calculated for methylmercury.

Mercuric chloride is also classified as a possible human carcinogen on the basis of laboratory rodent studies as no human data are available. There is no quantitative estimate of carcinogenic risk for mercuric chloride.

The data are inadequate to classify elemental mercury vapor as a human carcinogen, and the substance is rated "D" by the IRIS Program. Existing human epidemiological studies are confounded by concurrent worker exposure to other industrial chemicals, cigarette smoke, and in some studies, to radiation.


There are some genotoxicity data that suggest methylmercury can produce chromosomal damage, but other studies do not indicate the compound is genotoxic. Mercuric chloride has given both positive and negative results in a wide variety of in vivo and in vitro tests for genotoxicity. One investigation has provided some limited evidence for the genotoxicity of inhaled mercury vapor, but other investigations have not found it to be genotoxic.

Adapted from:

Mercuric Chloride (HgCl2) (CASRN 7487-94-7)
U.S. Environmental Protection Agency Integrated Risk Information System

Methylmercury (MeHg) (CASRN 22967-92-6)
U.S. Environmental Protection Agency Integrated Risk Information System

Mercury, elemental (CASRN 7439-97-6)
U.S. Environmental Protection Agency Integrated Risk Information System

Adobe PDF LogoElemental Mercury and Inorganic Mercury Compounds: Human Health Aspects
Concise International Chemical Assessment Document 50
World Health Organization 2003

Adobe PDF LogoAssessing Elemental Mercury Vapor Exposure from Cultural and Religious Practices
Riley D.M., Newby A., Leal-Almeraz T., and Thomas V.M
Environmental Health Perspectives Volume 109 Number 8 August 2001

Adobe PDF LogoEmergence of Delayed Methylmercury Toxicity after Perinatal Exposure in Metallothionein-Null and Wild-Type C57BL Mice
Yoshida N., Shimizu N., Suzuki M., Environmental Health Perspectives Vol 116 No. 6 June 2008

Evolution of Our Understanding of Methylmercury as a Health Threat
Environmental Health Perspectives Vol 104 No. 52 April 1996

Adobe PDF LogoGuidance for Implementing the January 2001 Methylmercury Water Quality Criterion
US EPA OST January 2009 EPA 823-F-09-002

Adobe PDF LogoInitial Risk-based Prioritization of Mercury in Certain Products November 2008

List of References for Methylmercury Human Health Affects
U.S. EPA Website.

Mercury, elemental (CASRN 7439-97-6)
U.S. EPA. Integrated Risk Information System (IRIS).

Adobe PDF LogoMercury Study Report to Congress Volume IV: An Assessment of Exposure to Mercury in the United States
U.S. EPA, Office of Air Quality Planning & Standards and Office of Research and Development.
EPA 452-R-97-006, 1997.
Contact: Kathryn R. Mahaffey, mahaffey.kate@epa.gov

Adobe PDF LogoMercury Study Report to Congress Volume V: Health Effects of Mercury and Mercury Compounds
U.S. EPA, Office of Air Quality Planning & Standards and Office of Research and Development.
EPA 452-R-97-007, 349 pp., 1997.
Contact: Kathryn R. Mahaffey, mahaffey.kate@epa.gov

Adobe PDF LogoMercury Study Report to Congress Volume VII: Characterization of Human Health and Wildlife Risks from Mercury Exposure in the United States
U.S. EPA, Office of Air Quality Planning & Standards and Office of Research and Development.
EPA 452-R-97-009, 152 pp., 1997.
Contact: Kathryn R. Mahaffey, mahaffey.kate@epa.gov

Adobe PDF LogoMetallic Mercury (Hg0): The Biological Effects of Long-Time, Low to Moderate Exposures
Efskind, J.
Euro Chlor Science Dossier 13, 50 pp, 2009

This report presents current knowledge of the effects of exposure to low levels of metallic mercury vapor and defines gaps in knowledge that need more research. For the purposes of this report, a "low" level of exposure is considered to be one that gives a kidney burden producing a mercury urine concentration below 30 µg Hg/g creatinine.

Methylmercury (MeHg) (CASRN 22967-92-6)
U.S. EPA. Integrated Risk Information System (IRIS).

New Jersey Mercury Task Force Report, Volume II: Exposure and Impacts
New Jersey Department of Environmental Protection, 2002.
Contact: Leslie McGeorge, 609-292-1623

Adobe PDF LogoPublic Health Goal for Inorganic Mercury In Drinking Water
California Environmental Protection Agency, Office of Environmental Health Hazard Assessment, 1999.
Contact: Lubow Jowa, 916-327-7327

Adobe PDF LogoComparative Toxicity of Ethyl and Methyl Mercury
Lucier, G.
Institute of Medicine of the National Academies, 17 slides, 2001

Adobe PDF LogoTask Force on Ritualistic Uses of Mercury Report
EPA 540-R-01-005, OSWER 9285.4-07, 111 pp., 2002.

The task force undertook an examination of human exposure to mercury due to the use of elemental mercury as part of certain spiritual practices and folk traditions.

Adobe PDF LogoThird National Report on Human Exposure to Environmental Chemicals
Department of Health and Human Services, Center for Disease Control, Atlanta, GA. NCEH Publication 05-0570, 475 pp, 2005.

This report series provides an ongoing assessment of the U.S. population's exposure to environmental chemicals by measuring the chemicals or their metabolites in human specimens, such as blood or urine. The report coverage includes metals (e.g., mercury), PCBs, dioxins, polycyclic aromatic hydrocarbons, pthalates, and numerous pesticides. The report is designed to allow users to determine public health information in the following areas: (1) which chemicals get into Americans and at what concentrations, (2) prevalence of people with chemical levels above those of chemicals with a known toxicity level, (3) reference ranges that can be used by physicians and scientists to determine whether a person or group has an unusually high exposure, (4) effectiveness of public health efforts to reduce exposure of Americans to specific chemicals, (5) exposure levels among minorities, children, women of childbearing age, or other potentially vulnerable groups, (6) trends in levels of exposure of the population, and (7) priorities for research on human health effects.

Toxicological Effects of Methylmercury
National Research Council, Committee on the Toxicological Effects of Methylmercury.
National Academies Press, Washington, DC. ISBN: 0-309-07140-2, 368 pp., 2000.

Toxicological Profile for Mercury
Agency for Toxic Substances and Disease Registry, 1999.
Contact: ATSDR Information Center, ATSDRIC@cdc.gov, 1-888-422-8737

National Library of Medicine Specialized Information Services.

This site contains a cluster of databases on toxicology, hazardous chemicals, and related areas, including the Hazardous Substances Data Bank (HSDB), Integrated Risk Information System (IRIS), and Toxics Release Inventory (TRI). The site supports simultaneous searching in multiple databases.

Workshop on the Scientific Issues Relevant to Assessment of Health Effects from Exposure to Methylmercury, November 18-20, 1998

A U.S. interagency committee organized this workshop to discuss and evaluate the major epidemiological studies associating methylmercury exposure with an array of developmental measures in children.

Ecotoxicity of Mercury

Mercury has the potential to both bioaccumulate and biomagnify as it moves up the food chain, and these aspects of the behavior of mercury in the environment add greatly to the risks it presents to both environmental and human receptors.

Bioaccumulation can be defined as the accumulation of a contaminant, such as mercury, in an animal or plant. The bioaccumulation of mercury requires the sequestration of the metal that enters the organism through diet, water intake, respiration, skin or for a plant, root contact. Mercury sequestration results in contaminant concentrations that are greater than those of the organism's environment.

The concentration of mercury achieved by bioaccumulation is governed by many factors, for example: rate of uptake, rate of elimination, metabolic transformation of the contaminant, the lipid content of the organism, and the integrity and health of the organism. Methylmercury, an extremely lipid-soluble organic form of mercury, is generated from inorganic mercury by microbial action in sediment, and the greatest proportion of mercury bioaccumulated in animal tissue is in this form. However, a small percentage of inorganic mercury may also be bioaccumulated.

Biomagnification occurs as a contaminant moves from one trophic level to the next higher level in the food chain. There is a progressive accumulation of the metal, so that the mercury concentration in a predator's tissues can exceed the levels in its prey by a large factor. As successive trophic levels require greater amounts of prey, great increases in contaminant concentration can be seen. Top tier predators, such as the mink, otter, bald eagle, and other raptor species are at particular risk from the effects of environmental mercury contamination.

Toxicity to Plants

Mercury is taken up by aquatic and terrestrial plants, with higher levels of mercury generally accumulating in the roots than in other parts of the plant, although the metal is distributed throughout the plant. This general pattern is found in both rooted and free floating aquatic plants.

Although phenyl mercury acetate and other mercury compounds have been used as seed dressings to combat fungal infections and damage to germinating seed, there is evidence to suggest that organic and inorganic forms of mercury are toxic to plants. The U.S. Department of Energy's Oak Ridge National Laboratory has developed phytotoxicity benchmarks for organic and inorganic mercury in solution and soil. These benchmarks are concentrations that may be used as a guide to determine whether a contaminant identified at a site merits further investigation. The benchmarks were derived from the results of investigations on the effect of mercury on plant growth in soils and solutions, that utilized many plant species and growth-related endpoints such as germination, root elongation weight of shoots and roots, chlorophyll content, and transpiration. Benchmark values of 0.002 parts per million (ppm) and 0.005 ppm respectively were developed for organic and inorganic mercury in solution, and a value of 0.3 ppm for inorganic mercury in soil (Efroymson et al. 1997).

Toxicity to Terrestrial and Aquatic Invertebrates

Mercury toxicity to both marine and freshwater invertebrates has been extensively investigated in the laboratory, using a wide variety of test organisms. Marine toxicity studies have employed starfish, clams, mussels, lobsters, crabs, shrimps, polychaete worms, and sandworms. Freshwater studies have used water fleas, stoneflies, mayflies, crayfish, midges, caddis flies, and bristle worms. Some general observations can be made about mercury toxicity to these diverse groups of animals as common factors emerge. Methyl mercury is more toxic to invertebrates than either aryl mercury, or inorganic mercury species, and that the larval stages of these organisms are the most sensitive to mercury toxicity. Concentrations of 1�10 micrograms per liter (µg/L) are acutely toxic to the larval stages of many species of aquatic invertebrates. Water quality conditions influence mercury toxicity toward aquatic invertebrates, for example, rising water temperature enhances mercury toxicity. Conversely, the toxic effects of mercury may be lessened by increasing water hardness. Some evidence suggests that mercury exerts behavioral effects on some invertebrates, making them more liable to predation.

Median lethal concentration (LC50) values for some terrestrial invertebrates have been developed. For the earthworm Octochaetus pattoni, LC50 values fall with continued exposure. A 10-day exposure to mercury gives an LC50 of 2.39 milligrams per kilogram (mg/kg), but 60 days exposure reduces the value to 0.79 mg/kg.

Toxicity to Fish

LC50 values have been experimentally determined for inorganic mercury for many freshwater fish species. The values for a 96-hour LC50 are between 33 and 400 µg/L. Saltwater species have higher LC50 values than freshwater species. Although inorganic mercury is acutely toxic to freshwater fish it is not as toxic as the organomercurial compounds. As previously noted for invertebrate species, water quality parameters such as dissolved oxygen content, dissolved organic carbon content, temperature, salinity, and water hardness influence the toxicity of mercury in the aquatic environment. However, concentrations of mercury that are not acutely toxic to fish may still adversely impact reproduction, and may also result in physiological, biochemical, and behavioral disturbance. The larval stages of fish are particularly sensitive to mercury toxicity. Mercury exposure to the larval stages of fish may result in reduced hatching success, deformities, and reduced survival.

Toxicity to Amphibians and Reptiles

Most investigations of the toxicity of mercury to amphibians have employed the egg and larval (tadpole) stages of these animals, and have determined acute toxicity. There appears to be considerable species variation in sensitivity of egg and larval stage amphibians to the effects of inorganic mercury. An LC50 value of 1.3 µg/L for mercuric chloride for the narrow-mouthed toad (Gastrophyne carolinensis) has been determined, and, out of a list of 14 American amphibians, 8 have LC50 (7 day exposure) values less than 10 µg/L. Some species appear to be less sensitive and 6 of the 14 have LC50 values within the range 36.8 to 107.5 µg/L. The marbled salamander (Ambystoma opacum) is at the upper end of the range at 107.5 µg/L.

No toxicological studies of mercury employing reptiles as test subjects are readily available. However, there is evidence to suggest that mercury is bioaccumulated by top-tier reptilian predators such as turtles and alligators.

Toxicity to Birds

Many investigations have addressed the toxicity of organomercurial compounds to birds, and organomercury has proved to be more toxic to birds than inorganic salts. Many laboratory toxicological studies have employed gallinaceous birds, the chicken (Gallus gallus domesticus), and other domestic fowl closely related to it. However, the domestic fowl may not adequately represent wild species, and caution should be taken when interpreting the studies that employ them. Some field reports suggest that wild waterfowl may be more sensitive to the toxic effects of mercury than the domestic waterfowl used in laboratory investigations. Organomercurial compounds cause reproductive impairment in birds, and numerous deleterious effects have variously been reported from the many investigations of this issue. These effects include a reduction in hatchability, reduction of egg production and egg volume, production of soft or thin-shelled eggs, and an increased mortality of young birds. The use of organomercury seed dressings led to the acute poisoning and death of grain eating birds. The species of birds, raptors (hawks, eagles, vultures, falcons, merlins etc.), that preyed on the dying birds or their carcasses were also killed.

As top-tier predators, the raptors are vulnerable to the effects of bioaccumulated mercury in their prey, and breeding failure has been observed in raptor species in North America and Europe. Although organochlorine pesticides also compromise the reproductive success of these birds, and pesticide residues may be present in raptors that are the subjects of field studies to determine the magnitude of the effects of dietary mercury, statistical analysis has shown an inverse relationship between mercury content of eggs and brood size. That is, a higher egg-mercury content was associated with a reduced number of successfully reared birds. The field study that identified an inverse relationship between egg-mercury content and reproductive productivity was conducted in Scotland, on merlins feeding on estuarine birds. A similar impact was observed on peregrine falcons, feeding in a coastal area. Loon populations have been adversely impacted by mercury accumulated in the tissues of the fish and aquatic invertebrates that comprise their diet. However, a recent report suggests the effects of bioaccumulated mercury may not be limited to raptors or piscivorous birds, and that elevated mercury levels are observable in insectivorous songbirds.

Toxicity to Mammals

Piscivorous mammals such as the otter and mink, and top-tier predators such as the Florida panther are vulnerable to the acute toxic effects of dietary mercury, and are also at risk from the sub-lethal effects that can impair behavior and reproduction. A toxicological dietary study of the mink (Mustela vison) showed organic mercury to be more toxic than mercuric chloride. Mink dosed with 5 mg/kg methylmercury in their diet developed anorexia, loss of weight, balance and coordination after 25 days. Ataxia, tremors, and paralysis developed 4 days after the onset of methylmercury related effects. These animals died, despite efforts to arrest the progress of mercury toxicosis by removing methylmercury from their diet and by chelation therapy to remove the metal. No outward clinical manifestations of mercury poisoning were seen in mink dosed with 10 mg/kg dietary mercuric chloride.

Adapted from:

Mercury Environmental Aspects Environmental Health Criteria 86
International Programme on Chemical Safety World Health Organization Geneva 1989

Adobe PDF LogoToxicological Benchmarks for Screening Contaminants of Potential Concern for Effects on Terrestrial Plants 1997 Revision
Efroymson R.A., Will M.E., Suter G.W., and Wooten
A.C. ES/ER/TM-85/R3

Adobe PDF LogoContaminants in Aquatic Habitats at Hazardous Waste Sites: Mercury
National Oceanic and Atmospheric Administration, NOAA Technical Memorandum NOS ORCA 100, 80 pp, 1996

Adobe PDF LogoDevelopment of an Ecological Risk Assessment Methodology for Assessing Wildlife Exposure Risk Associated with Mercury-Contaminated Sediments in Lake and River Systems
C.D. Knightes and R.B. Ambrose Jr.
EPA 600-R-06-073, 80 pp, 2006

ECOTOX Database
U.S. EPA Website.

The ECOTOX database provides single chemical toxicity information for aquatic and terrestrial life. Peer-reviewed literature is the primary information source, supplemented by data files provided by various government agencies.

Adobe PDF LogoEmergence of Delayed Methylmercury Toxicity after Perinatal Exposure in Metallothionein-Null and Wild-Type C57BL Mice
N. Yoshida, N. Shimizu, M. Suzuki
Environmental Health Perspectives Vol 116 No. 6 June 2008

Adobe PDF LogoEvolution of Our Understanding of Methylmercury as a Health Threat
Environmental Health Perspectives Vol 104 No. 52 April 1996

Impacts of Mercury Exposures on Free-Ranging Post-Fledged Piscivorous Birds

Mercury Contents in Aquatic Macrophytes from Two Reservoirs in the Paraíba do Sul: Guandú River System, SE Brazil
M.M. Molisani, R. Rocha, W. Macado, et al.
Brazilian Journal of Biology vol 66 No. 1a Sao Carlos Feb 2006

Mercury Environmental Aspects Environmental Health Criteria 86
International Programme on Chemical Safety World Health Organization Geneva 1989

Adobe PDF LogoMercury Hazards to Fish, Wildlife, and Invertebrates: a Synoptic Review
Eisler, Ronald, U.S. Fish and Wildlife Service, Patuxent Wildlife Research Center, Laurel, MD.
U.S. Fish and Wildlife Service, Biological Report 85(1.10), Contaminant Hazard Reviews #10, April 1987
Contact: Ronald Eisler, Ronald_Eisler@usgs.gov

Adobe PDF LogoMercury in Birds of San Francisco Bay Delta: Trophic Pathways, Bioaccumulation, Ecotoxicological Risk to Avian Reproduction. 2006 Annual Administrative Report.
J. Ackerman, C. Eagles-Smith, G. Heinz, et al.

Adobe PDF LogoMercury (Mercury in General, Hg, CAS number 7439-97-6)
Environmental Contaminants Encyclopedia, R.J. Irwin, M. VanMouwerik, L. Stevens, M.D. Seese, and W. Basham (compilers). National Park Service, Water Resources Division, Fort Collins, CO. 108 pp., 1997.
Contact: Roy Irwin, roy_irwin@nps.gov

Adobe PDF LogoMercury Poisoning in a Wild Mink
G. Wobeser
Journal of Wildlife Diseases July 1976

Methods/Indicators for Determining When Metals Are the Cause of Biological Impairments of Rivers and Streams: Species Sensitivity Distributions and Chronic Exposure-Response Relationships from Laboratory Data
P. Shaw-Allen and G.W. Suter II, U.S. EPA, Cincinnati, OH.
Report No: EPA 600-X-05-027, pp, July 2005

Provides information on the effects of the common aquatic metal contaminants (cadmium, chromium, copper, lead, mercury, nickel, and zinc, plus arsenic and selenium) on laboratory animals for use in the strength-of-evidence step of the stressor identification process to help determine whether metals contribute to biological impairments.

Adobe PDF LogoPoisoning Wildlife: The Reality of Mercury Pollution
L. Schweiger, F. Stadler, and C. Bowes
National Wildlife Federation September 2006

Adobe PDF LogoToxicological Benchmarks for Screening Contaminants of Potential Concern for Effects on Terrestrial Plants 1997 Revision
R.A. Efroymson, M.E. Will, G.W Suter, and A. Wooten
A.C. ES/ER/TM-85/R3, 123 pp, 1997

Toxicological Profile for Mercury
Agency for Toxic Substances and Disease Registry, 1999.
Contact: ATSDR Information Center, ATSDRIC@cdc.gov, 1-888-422-8737

This document provides data for bioaccumulation and biomagnification of inorganic and organic mercury.