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Some debate exists as to exactly what constitutes a "heavy metal" and which elements should properly be classified as such. Some authors have based the definition on atomic weight; others, on a specific gravity of greater than 4.0, or greater than 5.0. The actinides (the chemical elements with atomic numbers from 89 to 103, actinium through lawrencium; eg, uranium) may or may not be included. Most recently, the term heavy metal has been used as a general term for those metals and semimetals with potential human or environmental toxicity.^{[1, 2]} This definition includes a broad section of the periodic table under the rubric of interest.

Regardless of how one chooses to define the category, 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."

Yet, other metals are essential to human biochemical processes. For example, zinc is an important cofactor for several enzymatic reactions in the human body, vitamin B-12 has a cobalt atom at its core, and hemoglobin contains iron. Likewise, copper, manganese, selenium, chromium, and molybdenum are all trace elements that are important in the human diet. Another subset of metals includes those used therapeutically in medicine; aluminum, bismuth, gold, gallium, lithium, and silver are all part of the medical armamentarium. Any of these elements may have pernicious effects if taken in quantity or if the usual mechanisms of elimination are impaired.

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.^[3]

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, which was discovered by Marie Curie but only recently brought to public attention after the 2006 murder of Russian dissident Alexander Litvinenko, 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. More recently, a parkinsonian syndrome among Latvian injection drug users of methcathinone was linked to manganese toxicity.

Classic examples of environmental contamination include the Minimata Bay disaster and the current epidemic of arsenic poisoning in South East Asia. In the 1950s, industrial effluent was consistently dumped into Japan’s Minimata 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 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 ground water sources rife with bacterial contamination, tube wells were sunk throughout that area, deep into the water table.^[4] 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.

Metals have been used with malicious intent as poisons. Arsenic is perhaps more rightly classified as a metalloid, but it is consistently the single substance most commonly thought of as a poison. Metals have also been used in warfare as chemical weapons. Again, arsenic was the primary component of the spray known as Lewisite that was used by the British during trench warfare in World War I. Exposure produced severe edema of the eyelids, gastrointestinal irritation, and both central and peripheral neuropathies.

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.

In total, however, occupational exposure has probably accounted for the vast majority of heavy metal poisonings throughout human history. Hippocrates described abdominal colic in a man who extracted metals, and the pernicious effects of arsenic and mercury among smelters were known even to Theophrastus of Erebus (370-287 BC).

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.

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.^{[5, 6, 7, 8, 9]}

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	GI 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, GI 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, GI 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-grey 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.

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 both 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, 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 CNS, PNS, GI, hematopoietic, renal, and cardiovascular (CV). 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.

Frequency

United States

In 2021, the National Poisoning Data System (NPDS) of the American Association of Poison Control Centers (AAPCC) reported 8884 single exposures to heavy metals. Of those exposures, 2787 were in children younger than 6 years, and 4014 were in patients older than 19 years.^[10]

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. It is currently estimated that approximately 4 million households within the United States have children living within them that are being exposed to lead.^[11]

Evidence has shown that lead blood levels less than 10 μg/dL have been shown to have adverse neurodevelopmental outcomes in children younger than 5 years.^[12]The US Centers for Disease Control and Prevention (CDC) Advisory Committee on Childhood Lead Poisoning Prevention estimates that approximately 74,110 children aged < 5 years had a blood lead level of 5–9 µg/dL in 2013 (5 μg/dL is the level at which the CDC recommends that public health actions be initiated). In the US in 2013, 8,230 new cases of blood lead levels ≥10 µg/dLwere reported in children aged < 5 years.^[11]

The median concentration of lead in the blood of children age 1 to 5 years dropped from 15 µg/dL in 1976–1980 to 0.7 µg/dL in 2013–2014, a 95% decrease. The largest declines in blood lead levels corresponded with the US Environmental Protection Agency phasing out leaded gasoline from 1973-1995.^[13]

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 ≥10 μg/dL 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 4,547 adults with blood lead levels ≥25 μg/dL who had a known lead exposure history, 93.7% had occupational exposure^[14]

In 2021, the National Poisoning Data System (NPDS) of the American Association of Poison Control Centers (AAPCC) reported 2079 single exposures to lead. Of those exposures, 957 were in children younger than 6 years, and 683 were in patients older than 19 years.^[10]

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]

According to the AAPCC, in 2021, there were 610 single exposures related to arsenic (excluding pesticides) and 22 exposures to arsenic-containing pesticides.^[10]

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 2021, the AAPCC reported 5311 single exposures to iron and iron salts (not including iron-supplemented multivitamins). Of those, 2154 were in children younger than 6 years and 1528 were in adults older than 19 years. There were 7635 reported single exposures to multivitamins that contained iron. Of these exposures, 5973 were in children younger than 6 years.^[10]

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 2021 the AAPCC reported 612 single exposures to elemental mercury (excluding thermometers). Of these exposures, 49 were in children aged 5 years or younger and 360 were in adults aged 20 years or older. There were 1048 exposures to mercury-containing thermometers, 154 of them in children aged 5 years or younger and 467 in adults aged 20 years and older. There were 336 other mercury exposures, 28 in children aged 5 years or younger and 210 in adults aged 20 years and older.^[10]

International

Heavy metal toxicity has emerged as a significant occupational hazard associated with electronics recycling in China and South East 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. 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, possible 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 is more strongly associated with cognitive and behavior development than blood lead concentrations measured in 2-year-olds.^[23]

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 both acute and chronic heavy metal toxicity.

Clinical Presentation

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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	GI 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, GI 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, GI 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-grey 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.

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.