Mercury in any form is poisonous, with mercury toxicity most commonly affecting the neurologic, gastrointestinal (GI) and renal organ systems. Poisoning can result from mercury vapor inhalation, mercury ingestion, mercury injection, and absorption of mercury through the skin. (See Etiology and Prognosis.)
Mercury has 3 forms: (1) elemental mercury, (2) inorganic salts, and (3) organic compounds. Perhaps the most deadly form of mercury is methylmercury. Only 2–10% of the ingested mercury is absorbed from the gut, and ingested elemental mercury is not absorbed at all; however, 90% of any methylmercury ingested is absorbed into the bloodstream from the GI tract. (See the images below.)
Organic mercury compounds, specifically methylmercury, are concentrated in the food chain. Fish from contaminated waters are the most common culprits. Industrial mercury pollution is often in the inorganic form, but aquatic organisms and vegetation in waterways such as rivers, lakes, and bays convert it to deadly methylmercury. Fish eat contaminated vegetation, and the mercury becomes biomagnified in the fish. Fish protein binds more than 90% of the consumed methylmercury so tightly that even the most vigorous cooking methods (eg, deep-frying, boiling, baking, pan-frying) cannot remove it. (See Etiology.)
For centuries, mercury was an essential part of many different medicines, such as diuretics, antibacterial agents, antiseptics, and laxatives. In the late 18th century, antisyphilitic agents contained mercury. It was during the 1800s that the phrase “mad as a hatter” was coined, owing to the effects of chronic mercury exposure in the hat-making industry, where the metal was used in the manufacturing process.
In 1889, Charcot, in his Clinical Lectures on Diseases of the Nervous System, attributed some rapid oscillatory tremors to mercury exposure. 
In Wilson’s classic textbook of neurology, published in 1940, Wilson concurred with Charcot’s attribution of tremors to mercury poisoning, but also described mercury-induced cognitive impairments, such as inattention, excitement, and hallucinosis. 
In 1961, researchers in Japan correlated elevated urinary mercury levels with the features of the previously mysterious Minamata disease. Before the etiology of Minamata disease was discovered, it plagued the residents around Minamata Bay in Japan with tremors, sensory loss, ataxia, and visual field constriction. (See Presentation.) 
Minamata disease is an example of organic toxicity. In Minamata Bay, a factory discharged inorganic mercury into the water. The mercury was methylated by bacteria and subsequently ingested by fish. Local villagers ate the fish and began to exhibit signs of neurologic damage, such as visual loss, extremity numbness, hearing loss, and ataxia. Babies exposed to the methylmercury in utero were the most severely affected. Furthermore, because mercury was also discovered in the breast milk of the mothers, the babies’ exposure continued after birth. 
On January 19, 2013, The Minamata Convention on Mercury was agreed upon at the fifth session of the Intergovernmental Negotiating Committee in Geneva, Switzerland. It is a global treaty to protect human health and the environment from the adverse effects of mercury. The major highlights of the convention included a ban on new mercury mines, the phase-out of existing ones, control measures on air emissions, and the international regulation of the informal sector for artisanal and small-scale gold mining. 
Mercury is still found in many industries, including in battery, thermometer, and barometer manufacturing. Mercury can also be found in fungicides used in the agricultural industry. Before 1990, paints contained mercury as an antimildew agent. In medicine, mercury is used in dental amalgams and various antiseptic agents. (See Etiology and Prognosis.)
Mercury may also be contained in some cosmetics, such as skin-lightening products. One study measured international skin-lightening products for their mercury content, focusing on products available to US consumers either online or in stores. The products were screened for mercury content using a portable x-ray fluorescence spectrometer. Of the 549 products tested, 6% contained mercury levels above 1000 ppm, and 45% contained mercury levels that exceeded 10,000 ppm. Of lightening products purchased in the United States, 3.3% were found to contain mercury in excess of 1000 ppm. According to the authors, the Food and Drug Administration limits the amount of mercury in most cosmetic products to 1 ppm. 
Minamata disease has devastating neurologic consequences as a primary outcome of methyl mercury intoxication; unfortunately, these are relatively resistant to treatment. Complications include the following (see Presentation):
Acute perioral and facial paresthesias
Respiratory distress and nonspecific dermatitis
Extremity numbness eventually appears, along with headache, fatigue, and tremor
Ataxia and dysarthria can also be observed
Severe poisoning eventually causes the patient to lie in a mute, semirigid posture that is broken only by episodes of crying or primitive reflexive movements. (See Presentation.)
Babies exposed in utero are the most severely affected. They are affected by low birth weight, seizure disorders, profound developmental delay, incomplete visual loss (including tunnel vision) or total blindness, and hearing loss.
Neurologic damage in the form of diffuse and widespread neuronal atrophy is most severe in patients exposed in utero. Long-term studies may indicate that even prenatal exposure at low concentrations can cause subtle, but detectable, decrements in the areas of motor function, language, and memory.
Children so affected may have long-term stigmata, including motor impairment, visual loss, hearing loss, developmental delay, and seizure disorders.
Several members of the Plenary Panel on Human Health in the 12th International Conference on Mercury as a Global Pollutant held in Korea in June 2015 wrote an excellent summary article on this meeting. 
Organic methylmercury toxicity and inorganic mercury toxicity show different pathologic effects. Organic methylmercury toxicity causes prominent neuronal loss and gliosis in the calcarine and parietal cortices and cerebellar folia, as seen in cases of classic Minamata disease. 
Inorganic mercury causes cerebral infarctions, as well as systemic features, such as pneumonia, renal cortical necrosis, and disseminated intravascular coagulopathy. A more diffuse, direct neuronal toxicity may also exist with organic mercury, as the brain weights of patients with Minamata disease are substantially lower than those of controls. 
Nevertheless, both types of exposure may blur. In monkey models of methylmercury intoxication, demethylation resulted in inorganic mercury deposition in brain cells. 
Elemental mercury (Hg) is found in liquid form, which easily vaporizes at room temperature and is well absorbed (80%) through inhalation. Its lipid-soluble property allows for easy passage through the alveoli into the bloodstream and red blood cells (RBCs). Once inhaled, elemental mercury is mostly converted to an inorganic divalent or mercuric form by catalase in the erythrocytes. This inorganic form has similar properties to inorganic mercury (eg, poor lipid solubility, limited permeability to the blood-brain barrier, and excretion in feces). Small amounts of nonoxidized elemental mercury continue to persist and account for central nervous system toxicity.
Elemental mercury as a vapor has the ability to penetrate the central nervous system (CNS), where it is ionized and trapped, attributing to its significant toxic effects. Elemental mercury is not well absorbed by the GI tract; therefore, when it is ingested (eg, thermometers), it is only mildly toxic.
Inorganic mercury toxicity occurs in several forms: metallic mercury (Hg), mercurous mercury (Hg1+), or mercuric mercury (Hg2+). Found mostly in the mercuric salt form (eg, batteries), inorganic mercury is highly toxic and corrosive. It gains access to the body orally or dermally and is absorbed at a rate of 10% of that ingested. It has a nonuniform mode of distribution secondary to poor lipid solubility and accumulates mostly in the kidney, causing significant renal damage. Although poor lipid-solubility characteristics limit CNS penetration, slow elimination and chronic exposure allow for significant CNS accumulation of mercuric ions and subsequent toxicity. Long-term dermal exposure to inorganic mercury may also lead to toxicity.
Excretion of inorganic mercury, as with organic mercury, is mostly through feces. Renal excretion of mercury is considered insufficient and contributes to its chronic exposure and accumulation within the brain, causing CNS effects.
Organic mercury can be found in 3 forms: aryl and short- and long-chain alkyl compounds. Organic mercurials are absorbed more completely from the GI tract than inorganic salts are; this is because of intrinsic properties, such as lipid solubility and mild corrosiveness (although organic mercury is much less corrosive than inorganic mercury).
Once absorbed, the aryl and long-chain alkyl compounds are converted to their inorganic forms and possess similar toxic properties to inorganic mercury. The short-chain alkyl mercurials (methylmercury) are readily absorbed in the GI tract (90–95%) and remain stable in their initial forms. Alkyl organic mercury has high lipid solubility and is distributed uniformly throughout the body, accumulating in the brain, kidney, liver, hair, and skin. Organic mercurials also cross the blood-brain barrier and placenta and penetrate erythrocytes, producing neurologic symptoms, teratogenic effects, and high blood to plasma ratio, respectively.
Methyl mercury exerts its most devastating effect on the CNS by causing psychiatric disturbances, ataxia, visual loss, hearing loss, and neuropathy. Neurologic damage in the form of diffuse and widespread neuronal atrophy is most severe in patients exposed in utero.
Excretion of alkyl mercury occurs mostly in the form of feces (90%), secondary to significant enterohepatic circulation. The biological half-life of methylmercury is approximately 65 days.
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.  Methylmercury disrupts the muscarinic cholinergic systems in the brainstem and occipital cortices as well. 
Methylmercury also inactivates sodium-potassium adenosine triphosphatase (Na+/K+-ATPase), which leads to membrane depolarization, calcium entry, and eventual cell death.  Several pathways may be simultaneously activated converging in apoptosis. 
Researchers have also identified excessive excitotoxins and dysregulation of the nitric oxide system in rodents exposed to methylmercury.  Methylmercury can also induce brain edema, and this may produce sulcal artery compression and consequent ischemia, which may account, at least in part, for the calcarine and parietal cell loss and gliosis.
Furthermore, methylmercury may sequester the element selenium and thereby disrupt cellular biochemical pathways that use selenium as an enzymatic cofactor. Substantial evidence suggests that supplementing selenium ameliorates or even reverses mercury toxicity in laboratory animals. 
Finally, the effects of mercury may be modified by a person’s genetic milieu. For example, the interaction between mercury exposure and a genetic polymorphism in heme biosynthesis (coproporphyrinogen oxidase) yielded additive impairments on a test of visual-motor skills in dental workers,  and, more recently, additive impairments were documented between urinary mercury levels and a serotonin transporter polymorphism on motor control tasks in a similar population.  Furthermore, certain heat shock protein polymorphisms have been associated with symptomatic mercury toxicity compared with asymptomatic, but, similarly exposed, controls,  in particular single-nucleotide polymorphisms of metallothionein (a group of heavy metal-binding proteins), have been associated with reduced hair mercury levels among dental professionals. 
Necrosis of the proximal tubules is a common direct renal toxic effect. Unexplained renal abnormalities with neuropsychiatric disturbances should prompt the physician to consider mercury toxicity.
Causes of elemental mercury toxicity include the following:
Fluorescent and mercury lamps
Paper pulp production
Silver and gold production
In the United States, exposure to organic mercury is primarily through ingestion of contaminated fish. Persons who consume large amounts of seafood from contaminated waters have an increased risk of toxicity. Surveys indicate that public awareness of the risks of mercury-contaminated fish is limited.
The causes of organic mercury toxicity also include the following:
The causes of inorganic mercury toxicity include the following:
Chemical laboratory work
Fur hat processing
Mercury vapor lamps
Vinyl chloride production
Newer compact, energy-efficient fluorescent lights contain substantial mercury concentrations, making breakages with subsequent release a concerning source of exposure. 
Products from mercury cell chlor-akali plants used in the production of high-fructose corn syrup have been shown to contain detectable levels of mercury. 
Mercury-containing disk batteries are a concern because of their ability to cause corrosion and ulceration of the GI mucosa. With battery ingestion, one would expect signs of inorganic mercury exposure, such as hypersalivation and vomiting, rather than signs of organic mercury poisoning.
One major risk factor for mercury toxicity is industrial contamination. Workers employed in the manufacturing of mirrors, thermometers, fluorescent lights, and radiography machines, as well as in gold mining, are at risk for inorganic mercury poisoning. Organic mercury poisoning can occur among exposed workers in the paper and pulp industries.
New York City public health officials traced potentially toxic urinary mercury levels in residents to contaminated skin-lightening creams, which were subsequently removed from stores and embargoed.  More recently, a similar exposure occurred in a Mexican-American family in California and Virginia.  Others have identified renal disease secondary to mercury toxicity from such putative beautifying topicals. 
Traditional religious and healing practices are risk factors for mercury exposure. Mercury has been identified as a contaminant in Chinese herbal balls,  and it has been used in the Santeria religion, as well as in Tibetan medicine.  Indeed, spectrophotometric measurements of mercury vapor concentrations were elevated in New Jersey buildings located near “botanicas” in a primarily Latino community, compared with a control community.  Furthermore, of herbal Ayurvedic preparations, 20% were found to contain high levels of mercury. 
Even the mercury vapors from dental amalgam have been of concern as a possible, although controversial, source of exposure among dental workers and the general population. A study of 1663 veterans used a wide battery of noncognitive tests and found no clinically evident deficits associated with amalgam exposure. However, a subclinical decrement in vibration as measured by an automated device correlated with amalgam exposure and accounted for 15% of the variance in a multiple regression model. [29, 30] Furthermore, no consistent correlation could be established between urinary mercury levels and nerve conduction parameters among dental professionals. 
Two randomized studies of a total of 1041 children aged 6–10 years whose dental caries were treated with either amalgam or resin composite fillings showed no group differences on extensive batteries of neuropsychological tests after 5–7 years of follow-up. [32, 33] After an exhaustive investigation and review of the evidence, including the form of mercury in question, the route of exposure, and the dose, the Public Health Service concluded that dental amalgams do not pose a serious health risk. [30, 34]
Intentional self-poisoning with oral or injected inorganic mercury has been described, with outcomes varying from coma and death despite heroic efforts  to surprisingly scant clinical sequelae in the setting of persistently elevated blood mercury levels 5 years after the attempt. 
A very controversial source of organic mercury exposure is thimerosal, a preservative used in vaccines to prevent bacterial contamination. The most commonly used vaccines that contain thimerosal are for diphtheria-tetanus-whole cell pertussis (DTP), Haemophilus influenzae (HIB), and hepatitis B. However, no definite link between this small amount of mercury and any known disease has been found. Nonetheless, concerns over mercury content in vaccine have led to the increased availability of mercury-free vaccines. [37, 38, 39]
The 2013 Annual Report of the American Association of Poison Control Centers’ National Poison Data System documented about 1300 single exposures to mercury or compounds containing mercury. Of these, 109 were in children younger than 6 years and 673 were in persons older than 19 years. Overall, 19 individuals were reported to have moderate effects, 5 had major effects, and none died as a result of mercury exposure. 
Worldwide, outbreaks of methylmercury intoxication are sporadic. Minamata Bay in Japan was involved in the first and most famous epidemic, but not the largest. In the early 1970s, one of the most severe mass poisonings in history occurred in Iraq, when nearly 95,000 tons of seed grains treated with a methylmercury-based fungicide were accidentally baked into bread for human consumption.  More than 6000 individuals were hospitalized, and hundreds died. Many were hospitalized for weeks before methylmercury intoxication was correctly diagnosed.
Mercury mining areas in China have also contributed to cases of methylmercury poisoning through the ingestion of rice grown in contaminated soil.  Small-scale gold mining in developing countries has also produced mercury toxicity. 
Toxicity probably affects developing fetuses and children preferentially compared with other age groups, but even on this point, the data are incomplete. Prenatal exposure through maternal consumption of predominantly fish and whale meat has been shown to impair development among children in the Faroe Islands, while maternal mercury exposure from fish consumption alone in the Seychelles did not result in significant developmental problems among children prenatally exposed. [44, 45] The protective effects of the naturally selenium-enriched fish diet of the Seychelles population has been proposed to explain this effect. 
In a case of a family exposed to methylmercury through the ingestion of contaminated pork, the more severe clinical manifestations were found in the younger children. 
Recovery from mercury poisoning is variable. Acute fulminant intoxication with methylmercury resulted in coma and death in the Minamata catastrophe. Delayed toxicity can also occur, as in a fatal case in which symptoms developed only several months following absorption of dimethylmercury through the skin.  Mercury vapors also can result in acute neurologic and generalized symptoms.
While the cognitive and emotional sequelae of mercury exposure, at least in adults, may diminish with time, tremors and neuropathic changes have been reported to persist for decades after inorganic mercury exposure. For example, among 104 workers examined 30 years following inorganic mercury exposure, the presence of resting tremors correlated significantly with prior cumulative mercury exposure. [48, 49]
Outcome in mercury toxicity depends on the form of the mercury compound and the severity of exposure. Mild exposure to inorganic (ie, elemental, mercuric salt) and organic compounds can result in a complete recovery. Fatality is usually the result of severe exposure to mercuric salt. Most organic mercury exposures leave a neurologic sequela. Minimal dermal exposure to dimethylmercury has resulted in progressive neurologic deterioration and death, with initial symptoms delayed for several months.
All forms of mercury are toxic to a fetus, but methylmercury most readily passes through the placenta. Even with an asymptomatic patient, maternal exposure can lead to spontaneous abortion or retardation.
Individuals who need to be admitted to the hospital include the following:
Individuals who ingested (or are thought to have ingested) mercury salts
Individuals thought to have elemental mercury inhalation and have pulmonary injury
Individuals who require intensive chelating therapy
Once the neurologic sequelae of Minamata disease are evident, the damage is irreversible, and severe intoxications have been fatal. However, the damage may be minimized if detected early enough. Effects of long-term exposure are only now being fully recognized. Most survivors of Minamata disease have chronic neuropathologic conditions such as the following:
Compared with other patients, babies exposed to Minamata disease in utero have a more dismal prognosis. Their sequelae include the following:
Severe developmental delay
Low birth weight
Persistent cognitive impairment
Of the original 121 individuals from Minamata Bay who were affected, nearly one third died shortly after their initial presentation. Subsequent investigations since the late 20th century resulted in the identification of more than 2000 additional patients who were affected by chronic sequelae of Minamata disease.
The primary source of environmental exposure to mercury in the general population is through the consumption of contaminated fish.  Fish consumption has clear health benefits, and the risk posed by mercury exposure is currently speculative. The fetal brain is more susceptible to mercury-induced damage than that of an adult. As a result of this data, the Environmental Protection Agency (EPA) reduced the allowable intake of methylmercury from 0.5 mcg to 0.1 mcg of mercury per kilogram per day, which is lower than the amount allowable according to other regulatory agencies. 
The EPA guideline is derived from reports of subtle and small neuropsychological changes in children in a study in the Faeroe Islands; the children’s exposure was mainly from whale consumption.  A similar study in the Seychelles found no adverse effects from fish consumption alone. 
The Food and Drug Administration (FDA) has recommended that pregnant women, breastfeeding mothers, and young children avoid eating fish with a high mercury content (>1 ppm), such as shark, swordfish, tilefish, and king mackerel. This also includes fresh and frozen tuna (mercury content between 0.5 ppm and 1.5 ppm). Canned tuna has exhibited variable mercury concentrations, with one study finding that 55% of cans contained mercury levels greater than 1 ppm, with white tuna demonstrating higher levels than light tuna. 
From a nonprofessional perspective, this translates into a weekly consumption of 1 can (198g, or 7oz) of tuna for an adult.  Rather than ban the sale of these species, Health Canada recommends that they be consumed no more than once per week or once per month by children and by women of childbearing age.  Mercury levels in freshwater fish vary, but, in general, bass, pike, muskellunge, and walleye have high levels of mercury and should be eaten in moderation. Provincial guidelines for sport fish often mirror federal seafood recommendations. 
Acute exposure caused by inhaled elemental mercury can lead to pulmonary symptoms. Initial signs and symptoms, such as fever, chills, shortness of breath, metallic taste, and pleuritic chest pain. Other possible symptoms include stomatitis, lethargy, confusion, and vomiting. In addition, elemental mercury can also be injected, causing a life-threatening pulmonary embolism.
Recovery is usually without sequela, but pulmonary complications of inhaled toxicity may include interstitial emphysema, pneumatocele, pneumothorax, pneumomediastinum, and interstitial fibrosis. Fatal acute respiratory distress syndrome (ARDS) has been reported following elemental mercury inhalation.
Thimerosal is a mercury-containing preservative used in some vaccines and other products since the 1930s. No harmful effects have been reported from thimerosal at doses used in vaccines, except for minor reactions, such as redness and swelling at the injection site. However, in July 1999, the Public Health Service agencies, the American Academy of Pediatrics, and vaccine manufacturers agreed that thimerosal should be reduced or eliminated in vaccines as a precautionary measure. Today, with the exception of some influenza vaccines, none of the vaccines used in the United States to protect preschool children against 12 infectious diseases contain thimerosal as a preservative. 
Exposure to mercury has been suggested to contribute to the development of autism in children. Although the mechanism for this disorder has many hypotheses, no evidence has confirmed a causal relationship between mercury exposure and the development of autism. In fact, in one study, the discontinuation of thimerosal-containing vaccines in Denmark seemed to be followed by an increase in incidence of autism. 
In 2004, Immunization Safety Review Committee of the US Institute of Medicine (IOM) shifted from the position of neutrality to the conclusion that “the evidence favors rejection of a causal relationship between thimerosal-containing vaccines and autism.”  Since 2004, 2 cohort studies from the United Kingdom examined the relationship between thimerosal contained within vaccines and autism, and their conclusions were in agreement with the IOM that there is no causal relationship between the two.
A recommendation from the American Academy of Pediatrics and the US Public Health Service states that the use of products containing thimerosal is preferable to withholding vaccinations, which protect against diseases that represent immediate threats to infants (ie, pertussis, H influenzae). For the hepatitis B vaccine, adjustments in timing within the ranges proposed in the immunization schedule provide additional opportunities to minimize thimerosal exposure to infants. If thimerosal-free vaccine is not available, the hepatitis B virus vaccination should be initiated in infants aged 6 months.
Unfortunately, a clinician can do little to prevent mercury toxicity. Public education can raise awareness about the risks associated with easily preventable sources of toxicity, such as contaminated herbal preparations or mercury thermometers.
Publicizing the amount of mercury contained in frequently eaten fish can help to reduce toxicity on a local level.
Mercury is being found more often in our household items such as fluorescent bulbs and the risk of potential exposure has increased. The need to understand proper procedure for disposing of potential exposure is critical. The EPA has outlined a clear process to dispose of accidental spill. For complete details on mercury spills with specifics related to a broken thermometer or fluorescent bulb, visit the EPA Web site. 
Minamata disease typically occurs in areas in which the population depends on seafood as a dietary staple and in areas in which industrial wastes contaminate the drinking water. Educate patients about alternative food sources and about eliminating their intake of contaminated fish.
Outbreaks of methylmercury poisoning also have occurred after the introduction of fungicide-treated grain into the food supply. Neither humans nor livestock should eat seed grain treated with mercurial fungicides.
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David A Olson, MD Clinical Neurologist, Dekalb Neurology Group, Decatur, Georgia
David A Olson, MD is a member of the following medical societies: American Academy of Neurology
Disclosure: Nothing to disclose.
Nicholas Lorenzo, MD, MHA, CPE Co-Founder and Former Chief Publishing Officer, eMedicine and eMedicine Health, Founding Editor-in-Chief, eMedicine Neurology; Founder and Former Chairman and CEO, Pearlsreview; Founder and CEO/CMO, PHLT Consultants; Chief Medical Officer, MeMD Inc
Disclosure: Nothing to disclose.
Tarakad S Ramachandran, MBBS, MBA, MPH, FAAN, FACP, FAHA, FRCP, FRCPC, FRS, LRCP, MRCP, MRCS Professor Emeritus of Neurology and Psychiatry, Clinical Professor of Medicine, Clinical Professor of Family Medicine, Clinical Professor of Neurosurgery, State University of New York Upstate Medical University; Neuroscience Director, Department of Neurology, Crouse Irving Memorial Hospital
Tarakad S Ramachandran, MBBS, MBA, MPH, FAAN, FACP, FAHA, FRCP, FRCPC, FRS, LRCP, MRCP, MRCS is a member of the following medical societies: American College of International Physicians, American Heart Association, American Stroke Association, American Academy of Neurology, American Academy of Pain Medicine, American College of Forensic Examiners Institute, National Association of Managed Care Physicians, American College of Physicians, Royal College of Physicians, Royal College of Physicians and Surgeons of Canada, Royal College of Surgeons of England, Royal Society of Medicine
Disclosure: Nothing to disclose.
Barry E Brenner, MD, PhD, FACEP Professor of Emergency Medicine, Professor of Internal Medicine, Program Director, Emergency Medicine, University Hospitals, Case Medical Center
Barry E Brenner, MD, PhD, FACEP is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Chest Physicians, American College of Emergency Physicians, American College of Physicians, American Heart Association, American Thoracic Society, Arkansas Medical Society, New York Academy of Medicine, New York AcademyofSciences, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.
Timothy E Corden, MD Associate Professor of Pediatrics, Co-Director, Policy Core, Injury Research Center, Medical College of Wisconsin; Associate Director, PICU, Children’s Hospital of Wisconsin
Disclosure: Nothing to disclose.
Barry M Diner, MD, MPH, FACEP Assistant Clinical Professor, Department of Emergency Medicine, Emory University School of Medicine; Attending Physician, St Luke’s Episcopal Hospital, Houston, Texas
Barry M Diner, MD, MPH, FACEP is a member of the following medical societies: American College of Emergency Physicians
Disclosure: Nothing to disclose.
Fred Harchelroad, MD, FACMT, FAAEM, FACEP Chair, Department of Emergency Medicine, Director of Medical Toxicology, Allegheny General Hospital; Associate Professor, Department of Emergency Medicine, Drexel University College of Medicine
Disclosure: Nothing to disclose.
Michael E Mullins, MD Assistant Professor, Department of Emergency Medicine, Washington University School of Medicine
Disclosure: Johnson & Johnson stock ownership None; Savient Pharmaceuticals stock ownership None
Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Medscape Salary Employment
David K Tan, MD, EMT-T, FAAEM Assistant Professor and Chief, EMS Section, Division of Emergency Medicine, Medical Director, Washington University EMS, Washington University in St Louis School of Medicine
Disclosure: Nothing to disclose.
Asim Tarabar, MD Assistant Professor, Director, Medical Toxicology, Department of Emergency Medicine, Yale University School of Medicine; Consulting Staff, Department of Emergency Medicine, Yale-New Haven Hospital
Disclosure: Nothing to disclose.
Jeffrey R Tucker, MD Assistant Professor, Department of Pediatrics, Division of Emergency Medicine, University of Connecticut and Connecticut Children’s Medical Center
Disclosure: Merck Salary Employment
John T VanDeVoort, PharmD Regional Director of Pharmacy, Sacred Heart & 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.
Mary L Windle, PharmD, Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Nothing to disclose.
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