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Overview

Background

Heavy metal toxicity is an uncommon diagnosis. With the possible exceptions of acute iron toxicity from intentional or unintentional ingestion and suspected lead toxicity, emergency physicians will rarely be alerted to the possibility of metal exposure. Yet, if unrecognized or inappropriately treated, heavy metal exposure can result in significant morbidity and mortality.

Many of the elements that can be considered heavy metals have no known benefit for human physiology. Lead, mercury, and cadmium are prime examples of such toxic metals.

The toxicity of heavy metals depends on a number of factors. Specific clinical manifestations vary according to the metal in question, the total dose absorbed, and whether the exposure was acute or chronic. The age of the person can also influence toxicity. For example, young children are more susceptible to the effects of lead exposure because they absorb several times the percent ingested compared with adults and because their brains are more plastic, and even brief exposures may influence developmental processes. The route of exposure is also important. Elemental mercury is relatively inert in the gastrointestinal tract and also poorly absorbed through intact skin, yet inhaled or injected elemental mercury may have disastrous effects.^[1]

Some elements may have very different toxic profiles, depending on their chemical form. For example, barium sulfate is basically nontoxic, whereas other, more water-soluble barium salts are rapidly absorbed and cause profound, potentially fatal hypokalemia. The toxicity of radioactive metals like polonium relates more to their ability to emit particles than to their ability to bind cell proteins.

Exposure to metals may occur through the diet, from medications, from the environment, or in the course of work or play. Where heavy metal toxicity is suspected, time taken to perform a thorough dietary, occupational, and recreational history is time well spent, since identification and removal of the source of exposure is frequently the only therapy required.

A full dietary and lifestyle history may reveal hidden sources of metal exposure. Metals may be contaminants in dietary supplements, or they may leach into food and drink stores in metal containers such as lead decanters. Persons intentionally taking colloidal metals for their purported health benefits may ultimately develop toxicity. Metal toxicity may complicate some forms of drug abuse. Beer drinker’s cardiomyopathy was diagnosed in alcoholics in Quebec, and later Minnesota, during a brief period in the 1970s when cobalt was added to beer on tap to stabilize the head. A parkinsonian syndrome among Latvian injection drug users of methcathinone was linked to manganese toxicity.

Classic examples of environmental contamination include the Minamata Bay disaster and the current epidemic of arsenic poisoning in Southeast Asia. In the 1950s, industrial effluent was consistently dumped into Japan’s Minamata Bay, and methylmercury bioaccumulated to exceedingly high concentrations in local fish. Although some adults did develop signs and symptoms of toxicity, the greatest impact was on the next generation, into which many children were born with severe neurologic deficits.

Currently, millions of people living in and around Bangladesh are at risk for organ dysfunction and cancer from chronic arsenic poisoning from the water supply. In an effort to bypass water sources rife with bacterial contamination, tube wells were sunk throughout that area, deep into the water table.^[2] Unfortunately, the bedrock in that part of the world is rich in arsenic, giving these deeper water stores—and the crops they irrigate—a high concentration of arsenic, and toxicity is epidemic throughout the area. Childhood lead poisoning linked to the ingestion of old paint chips in North America is another good example of environmental contamination.

In total, however, occupational exposure has probably accounted for the vast majority of heavy metal poisonings throughout human history.

The classic acute occupational heavy metal toxicity is metal fume fever (MFF), a self-limiting inhalation syndrome seen in workers exposed to metal oxide fumes. MFF, or "brass founder’s ague," "zinc shakes," or "Monday morning fever," as it is variously known, is characterized by fever, headache, fatigue, dyspnea, cough, and a metallic taste occurring within 3-10 hours after exposure. The usual culprit is zinc oxide, but MFF may occur with magnesium, cobalt, and copper oxide fumes as well.

Chronic occupational exposure to metal dusts has also been linked to the development of pneumoconioses, neuropathies, hepatorenal degeneration and a variety of cancers. These syndromes develop slowly over time and may be difficult to recognize clinically. In the United States, Occupational Safety and Health Administration (OSHA) regulations guide the surveillance of workers at risk and suggest exposure limits for metals of industrial importance.

The first antidote to heavy metal poisoning, and the basis for chelation therapy today, was British Anti-Lewisite (BAL, or dimercaprol), a large molecule with sulfhydryl groups that bind arsenic, as well as other metals, to form stable covalent bonds that can then be excreted by the body. BAL was developed by the British during World War II in anticipation of a reinitiation of chemical warfare as had been waged earlier in the century.

This article provides a brief overview of general principles in the diagnosis and management of metal toxicity. The table below reviews the typical presentation of the most commonly encountered metals and their treatment, in summary form. It is not intended to guide clinical decision-making in specific cases.^{[3, 4, 5, 6, 7]}

Table. Typical Presentation of the Most Commonly Encountered Metals and Their Treatment (Open Table in a new window)

Metal	Acute	Chronic	Toxic Concentration	Treatment
Arsenic	Nausea, vomiting, "rice-water" diarrhea, encephalopathy, MODS, LoQTS, painful neuropathy	Diabetes; hypopigmentation/hyperkeratosis; cancer: lung, bladder, skin; encephalopathy	24-h urine: ≥50 µg/L urine, or 100 µg/g creatinine	BAL (acute, symptomatic) DMSA (succimer) DMPS (Europe)
Bismuth	Acute kidney injury, acute tubular necrosis	Diffuse myoclonic encephalopathy	No clear reference standard	*
Cadmium	Pneumonitis (oxide fumes)	Proteinuria, lung cancer, osteomalacia	Proteinuria and/or ≥15 µg/g creatinine	*
Chromium	Gastrointestinal hemorrhage, hemolysis, acute renal failure (Cr⁶⁺ ingestion)	Pulmonary fibrosis, lung cancer (inhalation)	No clear reference standard	NAC (experimental)
Cobalt	Beer drinker’s (dilated) cardiomyopathy	Pneumoconiosis (inhaled), goiter	Normal excretion: 0.1-1.2 µg/L (serum) 0.1-2.2 µg/L (urine)	NAC CaNa₂ EDTA
Copper	Blue vomitus, gastrointestinal irritation/hemorrhage, hemolysis, MODS (ingested); MFF (inhaled)	Vineyard sprayer’s lung (inhaled), Wilson disease (hepatic and basal ganglia degeneration)	Normal excretion: 25 µg/24 h (urine)	BAL D-Penicillamine DMSA (succimer)
Iron	Vomiting, gastrointestinal hemorrhage, cardiac depression, metabolic acidosis	Hepatic cirrhosis	Nontoxic: < 300 µg/dL Severe: >500 µg/dL	Deferoxamine
Lead	Nausea, vomiting, encephalopathy (headache, seizures, ataxia, obtundation)	Encephalopathy, anemia, abdominal pain, nephropathy, foot-drop/ wrist-drop	Pediatric: symptoms or [Pb] ≥45 µ/dL (blood); Adult: symptoms or [Pb] ≥70 µ/dL	BAL CaNa₂ EDTA DMSA (succimer)
Manganese	MFF (inhaled)	Parkinson-like syndrome, respiratory, neuropsychiatric	No clear reference standard	*
Mercury	Elemental (inhaled): fever, vomiting, diarrhea, ALI; Inorganic salts (ingestion): caustic gastroenteritis	Nausea, metallic taste, gingivo-stomatitis, tremor, neurasthenia, nephrotic syndrome; hypersensitivity (Pink disease)	Background exposure "normal" limits: 10 µg/L (whole blood); 20 µg/L (24-h urine)	BAL DMSA (succimer) DMPS (Europe)
Nickel	Dermatitis; nickel carbonyl: myocarditis, ALI, encephalopathy	Occupational (inhaled): pulmonary fibrosis, reduced sperm count, nasopharyngeal tumors	Excessive exposure: ≥8 µg/L (blood) Severe poisoning: ≥500 µg/L (8-h urine)	*
Selenium	Caustic burns, pneumonitis, hypotension	Brittle hair and nails, red skin, paresthesia, hemiplegia	Mild toxicity: [Se] >1 mg/L (serum); Serious: >2 mg/L	*
Silver	Very high doses: hemorrhage, bone marrow suppression, pulmonary edema, hepatorenal necrosis	Argyria: blue-gray discoloration of skin, nails, mucosae	Asymptomatic workers have mean [Ag] of 11 µg/L (serum) and 2.6 µg/L (spot urine)	Selenium, vitamin E (experimental)
Thallium	Early: Vomiting, diarrhea, painful neuropathy, coma, autonomic instability, MODS Late: Alopecia, Mees lines, residual neurologic symptoms	Alopecia, neuropathy	Toxic: >3 µg/L (blood)	MDAC Prussian blue
Zinc	MFF (oxide fumes); vomiting, diarrhea, abdominal pain (ingestion)	Copper deficiency: anemia, neurologic degeneration, osteoporosis	Normal range: 0.6-1.1 mg/L (plasma) 10-14 mg/L (red cells)	*
*No accepted chelation regimen; contact a medical toxicologist regarding treatment plan. MODS, multi-organ dysfunction syndrome; LoQTS, long QT syndrome; ALI, acute lung injury; ATN, acute tubular necrosis; ARF, acute renal failure; DMPS, 2,3-dimercapto-1-propane-sulfonic acid; CaNa₂ EDTA, edetate calcium disodium; MDAC, multi-dose activated charcoal; NAC, N-acetylcysteine; DMSA (succimer), dimercaptosuccinic acid.

Next: Pathophysiology

Pathophysiology

The pathophysiology of the heavy metal toxidromes remains relatively constant. For the most part, heavy metals bind to oxygen, nitrogen, and sulfhydryl groups in proteins, resulting in alterations of enzymatic activity. This affinity of metal species for sulfhydryl groups serves a protective role in heavy metal homeostasis as well.

Increased synthesis of metal-binding proteins in response to elevated levels of a number of metals is the body's primary defense against poisoning. For example, the metalloproteins are induced by many metals. These molecules are rich in thiol ligands, which allow high-affinity binding with cadmium, copper, silver, and zinc, among other elements. Other proteins involved in heavy metal transport and excretion through the formation of ligands are ferritin, transferrin, albumin, and hemoglobin.

Although ligand formation is the basis for much of the transport of heavy metals throughout the body, some metals may compete with ionized species such as calcium and zinc to move through membrane channels in the free ionic form. For example, lead follows calcium pathways in the body, so hence its deposition in bone and gingivae. Thallium is taken up into cells like potassium because of their similar ionic radii.

Nearly all organ systems are involved in heavy metal toxicity; however, the most commonly involved organ systems include the central nervous system (CNS), peripheral nervous system (PNS), and the gastrointestinal, hematopoietic, renal, and cardiovascular (CV) systems. To a lesser extent, lead toxicity involves the musculoskeletal and reproductive systems. The organ systems affected and the severity of the toxicity vary with the particular heavy metal involved, the chronicity and extent of the exposure, and the age of the individual.

A literature review by Giulioni et al indicated that heavy metal exposure is strongly associated with male infertility. According to the evidence, sperm concentration, motility, and morphology are negatively impacted by lead exposure, for the most part via oxidative stress and enzymatic inhibition. Cadmium exposure can produce sperm abnormalities through disruption of the blood-testis barrier and acrosomal function, while oxidative stress, apoptosis, and damage to sperm motility have been associated with arsenic exposure.^[8]

Next: Pathophysiology

Epidemiology

Frequency

United States

In 2023, according to the 41st Annual Report of the National Poison Data System (NPDS) from America's Poison Centers, there were 7905 single-substance exposures to heavy metals (not including iron or arsenic-including pesticides). Of those, 2348 were reported in children aged 5 years or younger, 1013 were reported in children aged 6-19, and 3599 were reported in persons aged 20 years or older.^[9]

Lead

Within the United States, lead remains the most frequently encountered toxic metal, owing to long-term exposure. In children, exposure has been shown to be a result of living in houses that contain lead paint. Between 1998 and 1999, “either an interior lead dust hazard or an interior deteriorated lead-based paint hazard” occurred in the homes of 22% of US children aged 0-5 years, with this proportion having declined to 15% in 2005-2006.^[10]

Evidence has shown that lead blood levels of less than 10 μg/dL have adverse neurodevelopmental outcomes in children younger than 5 years.^[11]According to the US Centers for Disease Control and Prevention (CDC), an estimated 500,000 US children aged 1-5 years have blood lead levels of 3.5 μg/dL or higher, with 3.5 μg/dL being the level at which the CDC recommends that public health actions be initiated for youngsters in this age group.^{[12, 13]}

In children aged 1-5 years, the median blood lead level fell from 15 µg/dL in 1976-1980 to 0.6 µg/dL in 2017 to March 2020, a 96% reduction. The largest declines in blood lead levels corresponded with the US Environmental Protection Agency phasing out leaded gasoline from 1973-1995.^[10]

Lead exposure in the adult population is more commonly occupational, namely in mining, manufacturing, and construction. Overall, the national prevalence rate of blood lead levels of 10 μg/dL or greater in employed adults declined from 26.6 per 100,000 in 2010 (among 37 states) to 20.4 in 2013 (among 29 reporting states). In 2013, of the 4547 adults with blood lead levels of 25 μg/dL or greater who had a known lead exposure history, 93.7% had occupational exposure^[14]

In 2023, according to the NPDS, there were 2349 single-substance exposures to lead. This included 1214 reported in children aged 5 years or younger, 283 reported in children aged 6-19 years, and 653 in persons aged 20 years or older.^[9]

Arsenic

Exposure to arsenic within the United States can occur through many routes. It has been used with both criminal and suicidal intent as an agent to poison individuals or groups.^[15]Medications used to treat disease, such as the chemotherapeutic agent arsenic trioxide, are iatrogenic sources. Industrial exposure to the waste products of smelting plants is another potential source. Arsenic-containing pesticides are still used in some areas of the country, with its use mostly found in cotton fields.^[16]

In 2023, according to the NPDS, there were 749 single-substance exposures to arsenic (excluding pesticides), including 557 reported in persons aged 20 years or older. There were also 12 single-substance exposures to arsenic-containing pesticides.^[9]

Iron

Iron toxicity in the United states is largely the result of ingestion of iron tablets or multivitamins but can also be a result of blood transfusions. Iron ingestion is particularly hazardous for children who unintentionally ingest iron-containing tablets.^[17]In adults, ingestion is largely intentional.

In 2023, according to the NPDS, there were 5780 single-substance exposures to iron and iron salts (not including iron-supplemented multivitamins). Of those, 2380 were reported in children aged 5 years or younger, 1017 were reported in children aged 6-19 years, and 2105 were reported in persons aged 20 years or older.^[9]

Mercury

Mercury toxicity can occur through exposure to mercury in its pure elemental form, as an inorganic salt, or through organic mercury compounds. Toxicity to the pure elemental form stems largely from inhalation of mercury vapor as a result of occupational exposure, for example melting mercury-containing dental amalgam. Another common route is vacuuming spilled mercury from a broken thermometer. Exposure to the inorganic salts and organic compounds stems largely from ingestion.^[18]

Industrial emissions of mercury have polluted fresh and coastal waters, leading to contamination of fish. This has raised public concerns about long-term exposure to mercury through the consumption of wild fish.^[19]

In 2023, according to the NPDS, there were 872 single-substance exposures to elemental mercury (excluding thermometers). This included 49 reported in children aged 5 years or younger, 109 reported in children aged 6-19 years, and 530 reported in persons aged 20 years or older. Also that year there were 793 single-substance exposures to mercury-containing thermometers, including 117 reported in children aged 5 years or younger, 90 reported in children aged 6-19 years, and 390 reported in persons aged 20 years or older. In addition, there were 275 other single-substance mercury exposures in 2023, including 201 reported in persons aged 20 years or older.^[9]

International

Heavy metal toxicity has emerged as a significant occupational hazard associated with electronics recycling in China and Southeast Asia. Much of the recycling industry there takes place within the informal sector, and the use of personal protective equipment (eg, respirators) is poorly regulated and uncommon.

Large-scale epidemics of lead poisoning were reported in China in 2009, involving more than 2000 children living near smelting plants and sparking riots.^{[20, 21]}The true prevalence of lead poisoning in childhood worldwide is not well understood. Availability of leaded gasoline, paint, cosmetics, and piping in many lower income countries suggests that there is a significant if under-recognized burden of toxicity.

Studies of street dust in Chinese cities have found elevated levels of heavy metals in street dust. These have included cadmium, chromium, and arsenic posing potential risk of carcinogenicity.^[22]

Chronic arsenic toxicity is epidemic in Bangladesh and contiguous areas of the Indian subcontinent, where arsenic is an important component of bedrock. As previously discussed, deep tube wells constructed to provide an alternative water source to bacteriologically suspect surface deposits frequently supply water with a high arsenic content, with major public health consequences for the region.

Race- and sex-related demographics

In the United States, a higher incidence of lead toxicity occurs in the African-American population because of delays in removing lead sources from the environment in lower socioeconomic areas.

Little or no difference in prevalence exists between the sexes. Occupations with heavy metal exposure that predominantly involve a particular sex are associated with higher rates of exposure in that sex.

Age

Several points are of concern in heavy metal toxicity with respect to age. Generally, children are more susceptible to the toxic effects of the heavy metals and are more prone to unintentional exposures.

Inorganic lead salts enter the body by way of ingestion or inhalation. For adults, only about 10% of the ingested dose is absorbed. In contrast, children may absorb as much as 50% of an ingested dose.

The percentage of absorbed lead is increased with deficiencies of iron, calcium, and zinc. It is also increased with a predominantly milk diet, possibly due to the high lipid content.

Children and infants are prone to developmental delays secondary to lead toxicity. One study found that blood lead concentrations obtained in children aged 6 years are more strongly associated with cognitive and behavior development than are blood lead concentrations measured in children aged 2 years.^[23]

Next: Pathophysiology

Prognosis

Metal toxicity is rarely encountered clinically and may be challenging to recognize. If untreated, acute exposures may progress to multiorgan failure and death or permanent organ damage. Chronic exposure to metals may present with nonspecific symptoms, but if it is not identified and the exposure is allowed to continue, permanent neurologic damage, organ failure, or cancer may develop.

Studies of a possible association of toxic metals and autism have yielded inconsistent results. Adams et al reported significantly higher average excretion levels of lead, tin, thallium, and antimony in 67 patients with autism spectrum disorder, compared with 50 neurotypical controls.^[24]

Encephalopathy is a leading cause of mortality in patients with either acute or chronic heavy metal toxicity.

Clinical Presentation

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Rathnayake IV, Megharaj M, Krishnamurti GS, Bolan NS, Naidu R. Heavy metal toxicity to bacteria - are the existing growth media accurate enough to determine heavy metal toxicity?. Chemosphere. 2013 Jan. 90(3):1195-200. [QxMD MEDLINE Link].
Schwartz BS, Hu H. Adult lead exposure: time for change. Environ Health Perspect. 2007 Mar. 115(3):451-4. [QxMD MEDLINE Link].
Bowler RM, Roels HA, Nakagawa S, et al. Dose-effect relationships between manganese exposure and neurological, neuropsychological and pulmonary function in confined space bridge welders. Occup Environ Med. 2007 Mar. 64(3):167-77. [QxMD MEDLINE Link].
Agency for Toxic Substances and Disease Registry. Toxicological Profile for Zinc. ATSDR. September 30, 2020; Accessed: January 22, 2023.
Munday SW. Arsenic. Hoffman RS, Howland MA, Lewin NA, Nelson LS, Goldfrank LR, eds. Goldfrank's Toxicologic Emergencies. 10th ed. New York: McGraw-Hill Education; 2015.
Calello DP, Henretig FM. Lead. Hoffman RS, Howland MA, Lewin NA, Nelson LS, Goldfrank LR, eds. Goldfrank's Toxicologic Emergencies. 10th ed. New York: McGraw-Hill Education; 2015.
Giulioni C, Falsetti F, Maurizi V, et al. The impact of heavy metals exposure on male fertility: a scoping review of human studies. J Basic Clin Physiol Pharmacol. 2025 Apr 22. [QxMD MEDLINE Link].
Gummin DD, Mowry JB, Beuhler MC, et al. 2023 Annual Report of the National Poison Data System® (NPDS) from America's Poison Centers®: 41st Annual Report. Clin Toxicol (Phila). 2024 Dec. 62 (12):793-1027. [QxMD MEDLINE Link]. [Full Text].
US Environmental Protection Agency. Key Findings of America’s Children and the Environment. EPA. Available at https://www.epa.gov/americaschildrenenvironment/key-findings-americas-children-and-environment. Accessed: April 21, 2025.
Canfield RL, Henderson CR Jr, Cory-Slechta DA, Cox C, Jusko TA, Lanphear BP. Intellectual impairment in children with blood lead concentrations below 10 microg per deciliter. N Engl J Med. 2003 Apr 17. 348(16):1517-26. [QxMD MEDLINE Link].
Ruckart PZ, Jones RL, Courtney JG, et al. Update of the Blood Lead Reference Value - United States, 2021. MMWR Morb Mortal Wkly Rep. 2021 Oct 29. 70 (43):1509-12. [QxMD MEDLINE Link]. [Full Text].
US Centers for Disease Control and Prevention. About Childhood Lead Poisoning Prevention. CDC. Available at https://www.cdc.gov/lead-prevention/about/index.html. March 13, 2025; Accessed: April 21, 2025.
Alarcon WA, State Adult Blood Lead Epidemiology and Surveillance (ABLES) Program Investigators. Elevated Blood Lead Levels Among Employed Adults - United States, 1994-2013. MMWR Morb Mortal Wkly Rep. 2016 Oct 14. 63 (55):59-65. [QxMD MEDLINE Link]. [Full Text].
Sharp D. In Maine, pains linger for arsenic poisoning survivors. LA Times. June 15, 2008. Available at https://articles.latimes.com/2008/jun/15/news/adna-arsenic15.
Hughes MF, Beck BD, Chen Y, Lewis AS, Thomas DJ. Arsenic exposure and toxicology: a historical perspective. Toxicol Sci. 2011 Oct. 123(2):305-32. [QxMD MEDLINE Link].
Chang TP, Rangan C. Iron poisoning: a literature-based review of epidemiology, diagnosis, and management. Pediatr Emerg Care. 2011 Oct. 27(10):978-85. [QxMD MEDLINE Link].
Clarkson TW, Magos L. The toxicology of mercury and its chemical compounds. Crit Rev Toxicol. 2006 Sep. 36(8):609-62. [QxMD MEDLINE Link].
Chalmers AT, Argue DM, Gay DA, Brigham ME, Schmitt CJ, Lorenz DL. Mercury trends in fish from rivers and lakes in the United States, 1969-2005. Environ Monit Assess. 2011 Apr. 175(1-4):175-91. [QxMD MEDLINE Link].
Parry J. Metal smelting plants poison hundreds of Chinese children. BMJ. 2009 Aug 24. 339:b3433. [QxMD MEDLINE Link].
Watts J. Lead poisoning cases spark riots in China. Lancet. 2009 Sep 12. 374(9693):868. [QxMD MEDLINE Link].
Zhang WC, Lü SL, Liu DY, Liu PW, Yonmochi S, Wang XJ, et al. [Distribution Characteristics of Heavy Metals in the Street Dusts in Xuanwei and Their Health Risk Assessment]. Huan Jing Ke Xue. 2015 May. 36 (5):1810-7. [QxMD MEDLINE Link].
Hornung RW, Lanphear BP, Dietrich KN. Age of greatest susceptibility to childhood lead exposure: a new statistical approach. Environ Health Perspect. 2009 Aug. 117(8):1309-12. [QxMD MEDLINE Link]. [Full Text].
Adams J, Howsmon DP, Kruger U, Geis E, Gehn E, Fimbres V, et al. Significant Association of Urinary Toxic Metals and Autism-Related Symptoms-A Nonlinear Statistical Analysis with Cross Validation. PLoS One. 2017. 12 (1):e0169526. [QxMD MEDLINE Link]. [Full Text].
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Table. Typical Presentation of the Most Commonly Encountered Metals and Their Treatment

Table. Typical Presentation of the Most Commonly Encountered Metals and Their Treatment

Metal	Acute	Chronic	Toxic Concentration	Treatment
Arsenic	Nausea, vomiting, "rice-water" diarrhea, encephalopathy, MODS, LoQTS, painful neuropathy	Diabetes; hypopigmentation/hyperkeratosis; cancer: lung, bladder, skin; encephalopathy	24-h urine: ≥50 µg/L urine, or 100 µg/g creatinine	BAL (acute, symptomatic) DMSA (succimer) DMPS (Europe)
Bismuth	Acute kidney injury, acute tubular necrosis	Diffuse myoclonic encephalopathy	No clear reference standard	*
Cadmium	Pneumonitis (oxide fumes)	Proteinuria, lung cancer, osteomalacia	Proteinuria and/or ≥15 µg/g creatinine	*
Chromium	Gastrointestinal hemorrhage, hemolysis, acute renal failure (Cr⁶⁺ ingestion)	Pulmonary fibrosis, lung cancer (inhalation)	No clear reference standard	NAC (experimental)
Cobalt	Beer drinker’s (dilated) cardiomyopathy	Pneumoconiosis (inhaled), goiter	Normal excretion: 0.1-1.2 µg/L (serum) 0.1-2.2 µg/L (urine)	NAC CaNa₂ EDTA
Copper	Blue vomitus, gastrointestinal irritation/hemorrhage, hemolysis, MODS (ingested); MFF (inhaled)	Vineyard sprayer’s lung (inhaled), Wilson disease (hepatic and basal ganglia degeneration)	Normal excretion: 25 µg/24 h (urine)	BAL D-Penicillamine DMSA (succimer)
Iron	Vomiting, gastrointestinal hemorrhage, cardiac depression, metabolic acidosis	Hepatic cirrhosis	Nontoxic: < 300 µg/dL Severe: >500 µg/dL	Deferoxamine
Lead	Nausea, vomiting, encephalopathy (headache, seizures, ataxia, obtundation)	Encephalopathy, anemia, abdominal pain, nephropathy, foot-drop/ wrist-drop	Pediatric: symptoms or [Pb] ≥45 µ/dL (blood); Adult: symptoms or [Pb] ≥70 µ/dL	BAL CaNa₂ EDTA DMSA (succimer)
Manganese	MFF (inhaled)	Parkinson-like syndrome, respiratory, neuropsychiatric	No clear reference standard	*
Mercury	Elemental (inhaled): fever, vomiting, diarrhea, ALI; Inorganic salts (ingestion): caustic gastroenteritis	Nausea, metallic taste, gingivo-stomatitis, tremor, neurasthenia, nephrotic syndrome; hypersensitivity (Pink disease)	Background exposure "normal" limits: 10 µg/L (whole blood); 20 µg/L (24-h urine)	BAL DMSA (succimer) DMPS (Europe)
Nickel	Dermatitis; nickel carbonyl: myocarditis, ALI, encephalopathy	Occupational (inhaled): pulmonary fibrosis, reduced sperm count, nasopharyngeal tumors	Excessive exposure: ≥8 µg/L (blood) Severe poisoning: ≥500 µg/L (8-h urine)	*
Selenium	Caustic burns, pneumonitis, hypotension	Brittle hair and nails, red skin, paresthesia, hemiplegia	Mild toxicity: [Se] >1 mg/L (serum); Serious: >2 mg/L	*
Silver	Very high doses: hemorrhage, bone marrow suppression, pulmonary edema, hepatorenal necrosis	Argyria: blue-gray discoloration of skin, nails, mucosae	Asymptomatic workers have mean [Ag] of 11 µg/L (serum) and 2.6 µg/L (spot urine)	Selenium, vitamin E (experimental)
Thallium	Early: Vomiting, diarrhea, painful neuropathy, coma, autonomic instability, MODS Late: Alopecia, Mees lines, residual neurologic symptoms	Alopecia, neuropathy	Toxic: >3 µg/L (blood)	MDAC Prussian blue
Zinc	MFF (oxide fumes); vomiting, diarrhea, abdominal pain (ingestion)	Copper deficiency: anemia, neurologic degeneration, osteoporosis	Normal range: 0.6-1.1 mg/L (plasma) 10-14 mg/L (red cells)	*
*No accepted chelation regimen; contact a medical toxicologist regarding treatment plan. MODS, multi-organ dysfunction syndrome; LoQTS, long QT syndrome; ALI, acute lung injury; ATN, acute tubular necrosis; ARF, acute renal failure; DMPS, 2,3-dimercapto-1-propane-sulfonic acid; CaNa₂ EDTA, edetate calcium disodium; MDAC, multi-dose activated charcoal; NAC, N-acetylcysteine; DMSA (succimer), dimercaptosuccinic acid.

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Author

Adefris Adal, MD, MS Clinical Assistant Instructor, Resident Physician, Department of Emergency Medicine, Kings County Hospital Center, State University of New York Downstate Medical Center

Disclosure: Nothing to disclose.

Coauthor(s)

Sage W Wiener, MD Assistant Professor, Department of Emergency Medicine, State University of New York Downstate Medical Center; Director of Medical Toxicology, Department of Emergency Medicine, Kings County Hospital Center

Sage W Wiener, MD is a member of the following medical societies: American Academy of Clinical Toxicology, American Academy of Emergency Medicine, American College of Medical Toxicology, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

John T VanDeVoort, PharmD Regional Director of Pharmacy, Sacred Heart and St Joseph's Hospitals

John T VanDeVoort, PharmD is a member of the following medical societies: American Society of Health-System Pharmacists

Disclosure: Nothing to disclose.

John G Benitez, MD, MPH Associate Professor, Department of Medicine, Medical Toxicology, Vanderbilt University Medical Center; Managing Director, Tennessee Poison Center

John G Benitez, MD, MPH is a member of the following medical societies: American Academy of Clinical Toxicology, American Academy of Emergency Medicine, American College of Medical Toxicology, American College of Preventive Medicine, Undersea and Hyperbaric Medical Society, Wilderness Medical Society, American College of Occupational and Environmental Medicine

Disclosure: Nothing to disclose.

Chief Editor

Additional Contributors

Mark Louden, MD Assistant Professor of Clinical Medicine, Division of Emergency Medicine, Department of Medicine, University of Miami, Leonard M Miller School of Medicine

Mark Louden, MD is a member of the following medical societies: American College of Emergency Physicians

Disclosure: Nothing to disclose.

Robert A Schwartz, MD, MPH Professor and Head of Dermatology, Professor of Pathology, Professor of Pediatrics, Professor of Medicine, Rutgers New Jersey Medical School

Robert A Schwartz, MD, MPH is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, New York Academy of Medicine, Royal College of Physicians of Edinburgh, Sigma Xi, The Scientific Research Honor Society

Disclosure: Nothing to disclose.

Kamila K Padlewska, MD, PhD Professor, Warsaw Academy of Cosmetics and Health Care; Chief Executive, Cosmetic-Medical Cooperative Izis, Poland

Disclosure: Nothing to disclose.

Acknowledgements

Richard H Sinert, DO Associate Professor of Emergency Medicine, Clinical Assistant Professor of Medicine, Research Director, State University of New York College of Medicine; Consulting Staff, Department of Emergency Medicine, Kings County Hospital Center

Richard H Sinert, DO is a member of the following medical societies: American College of Physicians and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Samara Soghoian, MD, MA Clinical Assistant Professor of Emergency Medicine, New York University School of Medicine, Bellevue Hospital Center

Samara Soghoian, MD, MA is a member of the following medical societies: American Academy of Clinical Toxicology, American College of Medical Toxicology, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Heavy Metal Toxicity

Background

Pathophysiology

Epidemiology

Frequency

Race- and sex-related demographics

Age

Prognosis

References

Tables

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