Mercury Poisoning in Animals - Toxicology - MSD Veterinary Manual (2023)

Poisoning associated with various forms of mercury has decreased in recent years. Chronic exposure in fish and wildlife species associated with the bioaccumulation of mercury in the environment continues to be a problem. In domestic animal species, clinical signs of involvement of the nervous, gastrointestinal, respiratory, and reproductive systems are typical and are influenced by the form, dose, and duration of exposure. The diagnosis can be confirmed on the basis of the clinical picture, histopathological findings, and the results of tissue analysis analysis for mercury concentration. Because tissue damage is permanent and food safety implications are major factors, treatment options may be limited and often discouraged.

Historically, mercury poisoning was a common occurrence in humans and animals. The replacement of mercury-based products used for medicinal, agricultural or industrial purposes with alternative products has resulted in a reduction in cases of acute and chronic poisoning; although many wild species remain endangered. Predator species considered near the top of the food chain, such as fish, seals, polar bears, and several species of birds, bioaccumulate considerable amounts of mercury from food sources. Commercial fish foods, such as tuna, have been linked to chronic poisoning in humans and cats.

Mercury exists in a variety of chemical forms, including elemental mercury (eg, thermometers, light bulbs), inorganic mercury (mercuric or mercuric) salts (eg, batteries, latex paints), and organic mercury ( aryl, methyl or ethyl). Fossil fuels represent a significant environmental source of mercury. In the environment, inorganic forms of mercury are converted to methylmercury under anaerobic conditions in the sediments of most bodies of water. Similar conversions can also occur in the body.

Pathogenesis of mercury poisoning in animals

The physical, chemical, and kinetic properties of the various forms of mercury play an important role in influencing clinical manifestations, the extent and nature of lesions, and the distribution of mercury in tissues. Organic forms of mercury, mainly methylmercury, are lipid soluble and well absorbed orally. Consequently, bioaccumulation is extensive in tissues such as the brain, kidney, and fetus. Methylmercury interferes with metabolic activity, causing degeneration and necrosis in many tissues, although the brain and fetus are most susceptible.

In the brain, histologically, neuronal degeneration and perivascular cuffing are evident in the cerebrocortical gray matter. Cerebellar atrophy or hypoplasia and Purkinje cell degeneration are seen. Encephalomalacia, myelin loss, and axonal necrosis may also be evident.

Methylmercury is mutagenic, carcinogenic, embryotoxic, and highly teratogenic. Inorganic forms of mercury, including elemental mercury, are absorbed shortly after dermal exposure. Elemental mercury vapors are inhaled and rapidly absorbed. This highly toxic form of mercury causes corrosive bronchitis and interstitial pneumonia. All forms of mercury cross the placenta. Inorganic forms of mercury bind to sulfhydryl groups in enzymes and other thiol-containing molecules, such as cysteine ​​and glutathione. Tissues rich in these components, such as the renal cortex, accumulate notable concentrations of mercury. Inorganic forms of mercury are cytotoxic and highly corrosive. Consequently, these forms of mercury cause severe inflammation, ulcers, and tissue necrosis in the gastrointestinal tract. Pale, swollen kidneys manifesting histologically as tubular necrosis and interstitial nephritis are consistent findings.

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Clinical Findings of Mercury Poisoning in Animals

Inhalation of corrosive elemental mercury vapors in high concentrations causes severe dyspnea and impaired respiratory function, often fatal. Neurological manifestations may eventually develop at lower levels of exposure. Due to its corrosive nature, inorganic mercury mainly produces gastrointestinal symptoms, including anorexia, stomatitis, pharyngitis, vomiting, diarrhea, pain; as well as shock, dyspnea and dehydration. Death generally occurs within hours at high exposure levels. Surviving animals may have eczema, keratinization of the skin, anuria, polydipsia, hematuria, or melena. Neurological manifestations, including CNS depression or arousal similar to that seen in cases of organic mercury poisoning, may develop after chronic exposure. Depending on the level of exposure to organic mercury compounds such as methylmercury, clinical manifestations can take days to develop. Since these compounds are not corrosive, gastrointestinal signs do not occur.

Common neurologic manifestations include blindness, ataxia, incoordination, tremors, abnormal behavior, hypermetria, nystagmus (cats), and tonic-clonic seizures. Advanced cases can be characterized by depression, anorexia, proprioceptive defects, total blindness, paralysis, with high mortality.

The developing nervous system of young animals is particularly susceptible to organic mercury exposure and often manifests as cerebellar ataxia associated with cerebellar hypoplasia and death.

Diagnosis of mercury poisoning in animals

  • The tentative diagnosis is based on clinical signs; confirmed by analysis of tissue samples (eg kidney) for mercury content

  • Measurement of mercury concentration in urine can confirm exposure to inorganic mercury compounds

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The considerable variation associated with the clinical manifestations related to the different forms of mercury and the exposure time underscores the need for repeat tissue analyses. Because inorganic forms of mercury are excreted in the urine, urinary mercury concentrations are the most reliable indicator of exposure. In contrast, organic mercury compounds, which bioaccumulate in soft tissue, are best evaluated in liver, kidney, or brain tissue.

In most species, mercury concentrations in the blood, kidneys, brain, and food < 0.1 mg/kg (ww) are considered normal. When poisoning is suspected, concentrations >6 mg/kg (blood), 10 mg/kg (kidney), 0.5 mg/kg (brain), and 4 mg/kg (food, dry weight) are consistent with a diagnosis of mercury poisoning. . The kidney is generally considered the most useful tissue for diagnosis. Concentrations in all tissues can be substantially higher after chronic exposure. Marine mammals and fish generally contain substantially higher concentrations of mercury that may not be associated with clinical disease (compared to ruminants or companion animal species); however, they can be a potential source of exposure for the most susceptible species, particularly the fetus or younger animals.

Other tests, including those that detect proteinuria, azotemia, or nonregenerative anemia, may provide useful evidence to support a diagnosis of mercury poisoning. Diagnosis can be made based on analysis of tissue samples with appropriate histopathologic and clinical evidence, history, and clinical signs.

differential diagnosesThey may include conditions that cause gastrointestinal upset, renal disease, or neurological dysfunction manifested by tremors, ataxia, or seizures. metals likelead Lead poisoning in animals Lead poisoning in mammals and birds is characterized by neurological disorders, gastrointestinal disorders, hematological abnormalities, immunosuppression, infertility and renal disease... read more ,arsenic Overview of Arsenic Poisoning in Animals The chemical element arsenic (symbol As, atomic number 33) is a nonmetal or metalloid in group V of the periodic table. It is often referred to as metallic arsenic and for toxicological purposes... read more , such as cadmium;insecticides General description of insecticidal and acaricidal (organic) toxicosis in animals Insecticides are any substance or mixture of substances intended to prevent, destroy, repel or mitigate insects. Similarly, acaricides are substances that can destroy mites. A chemist can... read more , Includingorganophosphorus Organophosphate toxicosis in animals Organophosphates (OP) are derivatives of phosphoric or phosphonic acid. There are currently hundreds of OP compounds in use, and they have replaced the banned organochlorine compounds... read more ,carbamato Carbamate toxicosis in animals Carbamates are esters of carbamic acid. Unlike organophosphates (OPs), carbamates are not structurally complex. The volume of carbamates used now exceeds that of the OPs because carbamates are... read more , or organochlorine compounds; oxalates; Vitamin D; Ismycotoxins Summary of Mycotoxicosis in Animals For a discussion of mycotoxicosis in birds, see Mycotoxicosis in Poultry. Acute or chronic toxicosis in animals can result from exposure to food or bedding contaminated with toxins produced... read more such as T-2 toxin or thiamine deficiency should be considered. infectious diseases, includinghog cholera Classic Swine Fever ,erysipelas Erysipelothrix rhusiopathiae infection , miparvovirus felino Panleucopenia Felina , can resemble mercury poisoning.

Treatment and control of mercury poisoning in animals

  • As the degenerative changes are permanent and there are serious food safety concerns associated with mercury poisoning, treatment is strongly discouraged.

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  • Efforts to reduce exposure through food or water sources are important

Because the neurological and kidney damage resulting from mercury poisoning is irreversible, treatment may be ineffective. Consequently, the prognosis for a full recovery is very poor. In food-producing animals, the considerable accumulation of mercury in food-producing tissues and its profound effects on reproduction limit treatment options. Euthanasia and proper disposal is recommended, in consultation with regulatory officials.

In veterinary patients where treatment is indicated, oral administration of activated charcoal (1 to 3 g/kg) and sodium thiosulfate (0.5 to 1 g/kg) will bind mercury and limit absorption. Vitamin E and selenium, which are antioxidants, can limit oxidative damage. Chelation therapy may be helpful if treatment is started soon after exposure, before nephrotoxic effects become severe. The fat-soluble chelating dimercaprol (3 mg/kg body weight IM every 4 hours for 2 days, followed by four times on day 3 and twice daily treatment for 10 days) may be beneficial. For organic mercury poisoning, 2,3-dimercaptosuccinic acid (10 mg/kg orally three times daily for 10 days) has been helpful in dogs. If decontamination of the gastrointestinal tract is successful, administration of penicillamine (50 to 100 mg/kg per day orally for 2 weeks) may reduce clinical signs. Limiting consumption of mercury-contaminated foods, such as fish products or water, will reduce exposure.

The World Health Organization and many countries have established comprehensive guidelines that reflect the serious nature of mercury poisoning internationally for humans and animals. The water guidelines in most countries for mercury are 0.001 mg/L and 0.003 mg/L for humans and animals, respectively.

key points

  • Although cases of mercury poisoning in animals have decreased, bioaccumulation and food safety concerns related to mercury ingestion remain a priority worldwide.

  • The poor prognosis and the lack of universally effective treatment options remain concerns around the world.

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  • Due to the potential for human exposure, treatment in food-producing animals is not recommended.

For more information


What is the effect of mercury toxicity in animals? ›

Clinical Findings of Mercury Poisoning in Animals

Due to the its corrosive nature, inorganic mercury produces primarily gastrointestinal signs, including anorexia, stomatitis, pharyngitis, vomiting, diarrhea, pain; as well as shock, dyspnea, and dehydration. Death often occurs within hours at high levels of exposure.

What is the LD50 of mercury? ›

Inorganic Mercury salts (such as mercuric chloride) are toxic and corrosive. Toxicity ranges from high to moderate, depending on the form (LD50 from 6-200 mg/kg). They accumulate mainly in the kidney causing renal damage.

What are the toxicological properties of mercury? ›

The inhalation of mercury vapour can produce harmful effects on the nervous, digestive and immune systems, lungs and kidneys, and may be fatal. The inorganic salts of mercury are corrosive to the skin, eyes and gastrointestinal tract, and may induce kidney toxicity if ingested.

What is the best way to test for mercury toxicity? ›

The most commonly accepted methods of assessing mercury exposure are to test urine or blood. Both tests usually measure levels of total mercury (elemental, inorganic and organic). Elevated mercury in urine usually indicates exposure to an elemental or inorganic source of mercury, such as from a job that uses mercury.

What are the two harmful effects of mercury? ›

All Mercury is Toxic

Depending on the type and amount, exposures to mercury can damage the nervous system, kidneys, liver and immune system. Breathing mercury vapors can harm the nervous system, lungs and kidneys. Mercury vapors can pass easily from the lungs to the bloodstream.

What is the mechanism of action of mercury toxicity? ›

Mercury damages the nervous system through several potential mechanisms. Mercury binds to sulfhydryl groups and incapacitates key enzymes involved in the cellular stress response, protein repair, and oxidative damage prevention.

How many mg of mercury is toxic? ›

The lethal dose of methyl mercury is estimated to be 200 mg, with paresthesia of the hands, feet, and mouth occurring at a total body burden of 40 mg [Bakir et al.

What is the most toxic form of mercury? ›

The toxic effects of mercury depend on its chemical form and the route of exposure. Methylmercury [CH3Hg] is the most toxic 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.

What is the minimum mercury exposure? ›

The mercury concentration in whole blood is usually lower than 10 μg/L, but the value of 20 μg/L or below is considered normal.

What kind of toxin is mercury? ›

Inorganic mercury poisoning symptoms

Inorganic mercury is poisonous when swallowed. When the chemical enters your body, it travels through your bloodstream and attacks your brain and kidneys. Symptoms of inorganic mercury poisoning include: Burning sensation in your stomach and/or throat.

What is antidote for mercury? ›

Selenium as an antidote in the treatment of mercury intoxication.

What type of poisoning is mercury? ›

Mercury is a neurotoxin neurotoxin A substance that is known or suspected to be poisonous to nerve tissue.. How someone's health may be affected by an exposure to mercury depends on a number of factors: The form of mercury (for example, methylmercury or elemental (metallic) mercury);

What is the best mercury chelator? ›

Dimercaprol (BAL)

This is the drug of choice for the treatment of acute inorganic mercury toxicity. It is the preferred chelator for mercury salts. Dimercaprol is administered intramuscularly every 4 hours, mixed in a peanut oil base. It is excreted in urine and bile.

What is the OSHA standard for mercury? ›

OSHA: The legal airborne permissible exposure limit (PEL) is 0.1 mg/m3 averaged over an 8-hour workshift. NIOSH: The recommended airborne exposure limit (REL) is 0.05 mg/m3 (as Mercury vapor) averaged over a 10-hour workshift and 0.1 mg/m3 (as Mercury), not to be exceeded at any time.

What color tube for mercury? ›

Specimen Requirements

Royal blue-top (EDTA) tube; submit original tube.

How long does mercury stay in the body? ›

Once in your body, metallic mercury can stay for weeks or months. When metallic mercury enters the brain, it is readily converted to an inorganic form and is “trapped” in the brain for a long time.

What are the two most common sources of mercury exposure in humans? ›

Mercury exists in various forms, and people are exposed to each in different ways. The most common way people in the U.S. are exposed to mercury is by eating fish containing methylmercury. Other exposures may result from using or breaking products containing mercury.

What PPE is needed for handling mercury? ›

What Personal Protective Equipment (PPE) is needed when working with mercury? Eye/Face Protection: Wear chemical safety goggles. A face shield (with safety goggles) may also be necessary. Skin Protection: Wear chemical protective clothing e.g. gloves, aprons, boots.

What is the etiology of mercury toxicity? ›

The most common cause of mercury poisoning is from consuming too much methylmercury or organic mercury, which is linked to eating seafood. Mercury itself is naturally occurring, but the amounts in the environment have been on the rise due to industrialization.

What are the main contents of mercury poisoning treatment? ›

Treatment of acute mercury exposure generally consists of removal of the patient from further exposure followed by support of respiratory and cardiovascular function. There is no antidote for mercury, but chelation therapy is warranted in some cases.

Which enzyme would be blocked by mercury? ›

Mercury targets the enzymes uroporphyrinogen decarboxylase (UROD), and especially coproporphyrinogen oxidase (CPOX), thus leading to accumulation and excretion of 4 and 5 carboxyl porphyrines (Woods, 1995; Woods et al., 2005).

What is the target organ for methylmercury? ›

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.

What is the difference between mercury and methylmercury? ›

Organic mercury compounds are formed when mercury combines with carbon. Microscopic organisms in water and soil can convert elemental and inorganic mercury into an organic mercury compound, methylmercury, which accumulates in the food chain.

Who is most sensitive to mercury poisoning? ›

People at higher risk from mercury exposure include:
  • unborn babies.
  • infants.
  • children up to six years of age.
  • workers in industrial settings where mercury is used or produced.
  • people with kidney disease.
  • people born before the 1950s who were exposed to mercury in baby products and contracted pink disease.

Which form of mercury is least toxic? ›

RISK: Inorganic mercury is the least toxic of the three forms of mercury. It can damage the GI tract, as well as the kidneys and nervous system.

What is the formula for methylmercury? ›

Methyl mercury | CH3Hg - PubChem.

What is the TLV for mercury? ›

The ACGIH recommends a TLV-TWA of 0.05 mg/m3 for mercury vapor, measured as mercury, and a skin notation. NIOSH has a REL of 0.05 mg/m3 as an 8-hour TWA. The Agency proposed a PEL of 0.05 mg/m3 TWA for mercury and its vapor, measured as Hg, and the final rule establishes this limit, also with a skin notation.

How does mercury affect the brain? ›

Many studies show that high exposure to mercury induces changes in the central nervous system, potentially resulting in irritability, fatigue, behavioral changes, tremors, headaches, hearing and cognitive loss, dysarthria, incoordination, hallucinations, and death.

What is the chelating agent for mercury poisoning? ›

DMPS (unithiol) and DMSA (succimer), dithiol water-soluble analogs of BAL, were developed in the Soviet Union and China in the late 1950s. These three agents have remained the mainstay of chelation treatment of arsenic and mercury intoxication for more than half a century.

What are chelating agents for mercury? ›

Chelating drugs used to treat mercury poisoning may include succimer, edetate calcium disodium, BAL, or penicillamine. Whether a chelator is indicated or not will depend on the form of mercury involved, the person's mercury level, and if the person is having symptoms. Arsenic is a naturally occurring substance.

Is mercury a drug or toxin? ›

Mercury is a toxic heavy metal which is widely dispersed in nature. Most human exposure results from fish consumption or dental amalgam. Mercury occurs in several chemical forms, with complex pharmacokinetics.

Why is EDTA not used in mercury poisoning? ›

The lethality of mercury was tested in female Bufo regularis species (Amphibia) which were given EDTA immediately after the Hg2+ injection. The results show that the inherent toxicity of the EDTA-mercury complex is sufficiently high for it to be ineffective as an antidote.

How do you remove mercury from organs? ›

A diet rich in various nutrients and vitamins has been shown to promote mercury elimination from the body. Some of these nutrients include selenium, glutathione, and vitamins, including vitamins C and E. Besides, green algae called chlorella is also helpful in removing mercury from the body.

Does chelation remove mercury? ›

Metals that can be removed with chelation therapy include lead, mercury, and arsenic.

What are the 4 OSHA standards? ›

There are four groups of OSHA standards: General Industry, Construction, Maritime, and Agriculture. (General Industry is the set that applies to the largest number of workers and worksites). These standards are designed to protect workers from a wide range of hazards.

Is mercury considered a biohazard? ›

Elemental mercury and wastes containing mercury salts are regulated as toxic hazardous waste when the mercury is present in concentrations greater than 0.2 mg/L. Under no circumstances should any waste containing mercury be disposed of in the trash, put down the drain, or placed in biohazard bags or sharps containers.

What are 5 OSHA standards? ›

Examples of OSHA standards include require- ments to provide fall protection, prevent trenching cave-ins, prevent exposure to some infectious diseases, ensure the safety of workers who enter confined spaces, prevent exposure to such harmful substances as asbestos and lead, put guards on machines, provide respirators or ...

Is there a blood test for mercury toxicity? ›

The mercury blood test is used to detect an excess of mercury. It is ordered to determine if there has been an acute or chronic exposure to high levels of mercury. Specifically, the mercury blood test detects the level of methyl mercury in the blood.

What color is mercury as a gas? ›

At room temperature, exposed elemental mercury can evaporate to become an invisible, odorless toxic vapor. If heated, it is a colorless, odorless gas.

What is a purple top tube used for? ›

The purple top tube provides blood for infectious disease tests and ascertaining important data such as ABO/Rh (blood type), as well as whether the blood is positive or negative for cytomegalovirus (CMV), HIV, hepatitis, and West Nile virus, to name a few.

What are the consequences of mercury to wildlife and the environment? ›

When released into the environment, it accumulates in water laid sediments where it converts into toxic methylmercury and enters the food chain. Mercury contamination is a significant public health and environmental problem because methylmercury easily enters the bloodstream and affects the brain.

How does mercury in retrograde affect animals? ›

Your Pets Are Going to Want to Fight, Too

So Mercury in retrograde actually affects them more directly than us. Additionally, they will reflect our own anxious energy more readily. This manifests as fighting with each other and not following instructions.

How does mercury affect marine mammals? ›

Abstract. Marine mammals are more exposed to mercury (Hg) than any others animals in the world. As many trace elements, Hg it is able to impair the brain function, which could be a cause of population decline. Nevertheless, these issues have been scarcely studied because of the technical and ethical difficulties.

What is the most toxic form of mercury in the environment? ›

Toxic Effects

Methylmercury [CH3Hg] is the most toxic 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.

What are sources of mercury poisoning? ›

Mercury exists in various forms, and people are exposed to each in different ways. The most common way people in the U.S. are exposed to mercury is by eating fish containing methylmercury. Other exposures may result from using or breaking products containing mercury.

What is the level of mercury in animals? ›

In most species, blood, kidney, brain, and feed concentrations of mercury < 0.1 mg/kg (wet wt) are considered normal. When poisoning is suspected, concentrations >6 mg/kg (blood), 10 mg/kg (kidney), 0.5 mg/kg (brain), and 4 mg/kg (feed, dry wt) are consistent with a diagnosis of mercury poisoning.

What animals are affected by Mercury? ›

Mercury poisoning can also adversely affect wildlife species, such as wading birds, alligators, raccoons, and otters, that consume fish. In the late 1980s, there was great concern for Florida panthers that ate raccoons in the Everglades.

Can animals survive on Mercury? ›

Given that Mercury's surface can experience temperatures as low as -330 °F and as high as 800 °F, it is clear that no living organism could survive there.

How does Mercury impact on animals and plants where it is found? ›

Mercury, which can adversely alter the neurological and reproductive systems of humans and wildlife, has long been known to contaminate fresh-water lakes, fish and fish-eating birds, including loons and eagles.

Which types of animals have the highest levels of mercury? ›

Avoid a few key species.

King mackerel, marlin, orange roughy, shark, swordfish, tilefish, ahi tuna, and bigeye tuna all contain high levels of mercury. Women who are pregnant or nursing or who plan to become pregnant within a year should avoid eating these fish.

What animal has the most mercury? ›

Species of fish that are long-lived and high on the food chain, such as marlin, tuna, shark, swordfish, king mackerel and tilefish contain higher concentrations of mercury than others.

What sea animal has the most mercury? ›

Long-lived predators like tuna and swordfish tend to contain the most, because they also absorb mercury from their prey and they've had a long time to accumulate it. The lowest levels are found in short-lived species lower down the food chain, such as oysters and shrimp.


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