CBRNE - Vesicants, Mustard - Hd, Hn1-3, H



Mustard agents are vesicants (blister agents) used in warfare to produce casualties, degrade fighting efficiency, and force opposing troops to wear full protective equipment. Mustard agents are cytotoxic alkylating compounds and include nitrogen mustards (HN-1, HN-2, HN-3), sulfur mustards (H, HD, HT), and mustard-lewisite (HL). Mustard agents are oily liquids ranging from colorless (in pure state) to pale yellow to dark brown, depending on the type and purity. They have a faint odor of mustard, onion, garlic, or horseradish, but because of olfactory fatigue, do not rely on odor for detection.

Volatility varies with the particular compound. Mustard agents are only slightly soluble in water and are heavier than water; thus, they may persist for long periods. HN-1 is more volatile and less persistent than HD, but it is only one fifth as potent a vesicant to the skin. HN-3 is less volatile and more persistent than HD and has equal vesicant effects.

Mustard agents rapidly penetrate clothing and skin. Chemical protective mask with charcoal filters, chemical protective overgarments with charcoal, and butyl rubber chemical protective gloves and boots afford full protection against mustard agents.

More than two dozen nations may have the capability to manufacture offensive chemical weapons. Mustard agents are simple to manufacture and therefore can be a first choice for countries or terrorists who decide to have a capacity for chemical warfare agents. Mustard agents may be delivered by artillery shell, mortar shell, rockets, bombs, or aircraft spray. Since World War I, mustard use in at least 12 conflicts has been supported by evidence or allegations. Historically, mustard agents are the most widely used type of chemical warfare agent.

Mustard agents constitute both a vapor and a liquid threat. Mustard agents cause tissue damage within several minutes of contact.[1] No immediate symptomatic or local reaction occurs to mustard vapor or liquid. Decontamination must be performed immediately after contact to prevent injury. A latent period occurs, ranging from 4-12 hours after mild exposure and 1-3 hours after severe exposure, prior to the onset of symptoms. More than 80% of mustard casualties are from vapor exposure, but more severe injuries are caused after contact with liquid mustard agents.

Mustards first were produced in 1822, but their harmful effects were not discovered until 1860. On July 12, 1917, the Germans delivered artillery shells containing HD on a World War I battlefield near Ypres, Belgium. More than 20,000 casualties resulted from this first use of mustard as a chemical warfare agent. Subsequently, mustard agents accounted for 80% of chemical casualties in World War I. Among 6980 cases of mustard burns during World War I, the location of the lesions were as follows: eyes, 86%; respiratory, 75%; scrotum, 42%; face, 27%; anus, 24%; legs, 11%; buttocks, 10%; hands, 4%; and feet, 1.5%. Fewer than 5% of casualties from mustard who reached medical treatment died. Mustard injuries were slow to heal and necessitated an average convalescent period of more than 6 weeks.

Italy allegedly used mustard against Abyssinia in the 1930s. Japan allegedly used mustard agents against the Chinese from 1937-1944.

Nitrogen mustard agents were synthesized in the late 1930s. Mechlorethamine (HN-2) became the prototypical mustard agent used as a cancer chemotherapeutic agent. Germans and Americans started the military production of nitrogen mustard agents in 1941 and 1943, respectively. They have not been used on the battlefield.

Toward the end of World War II, a German air attack on the Italian port of Bari struck a US ship loaded with mustard agent munitions. Large amounts of mustard agents were released to the atmosphere and into the harbor water. Many soldiers and sailors were exposed to the mustard-contaminated water. Of 617 US mustard casualties, 83 died.

During the Yemen War of 1963-1967, Egypt reportedly used mustard bombs against the royalist troops in North Yemen.

During the Iran-Iraq war from 1979-1988, approximately 5000 Iranian soldiers were reported killed by Iraqi chemical agents, 10-20% by mustard agents. Additionally, 40,000-50,000 individuals were injured resulting in many chronic medical problems.[2, 3]

After the February 1991 cease-fire ending the Persian Gulf War, United Nations inspection teams discovered mustard agents at Al Muthanna, Iraq.

Besides the threat of chemical attack, a larger concern may be the tons of mustard agents that were produced for war and then dumped at sea, buried in landfills, or left to decay in storage facilities.[4] In Sweden, recurring incidents of mustard agent exposures involve fisherman who encounter discarded chemical weapons that were dumped in the waters off the coast after World War II. Before the 1970s, the United States dumped obsolete chemical weapons at sea; three separate incidents of exposure to sulfur mustard munitions were reported.[5]

Developing nations and terrorist groups can easily obtain HD because of its low cost and availability. The US stockpile of mustard chemical warfare agents currently is undergoing destruction.


Mustard agents are lipophilic and are absorbed readily across intact skin and mucous membranes. The rapid penetration is enhanced by moisture, heat, and thin skin. The physical properties (low volatility and a freezing point of 14o C) of sulfur mustard (H, HD, HT) make it a better weapon for use in warm or hot environments due to a greater risk of vapor inhalation. Approximately 20% of HD is absorbed by the skin, the remainder evaporates. Of the absorbed HD, 10-50% of the mustard dose binds to the skin as reacted (fixed) mustard, and the remaining 50-90% is distributed in the circulation as unreacted (free) mustard to almost all organs and tissues. Because of dilutional effects, systemic effects are observed only at high doses. Mustard is eliminated from the body in the urine as a by-product of alkylation.

No single mechanism or clear understanding exists for the biological damage caused by mustard agents.[6] The toxic effects of mustards depend on their rapid covalent binding to a large number of biological molecules and in the formation of a reactive cyclic ethylene sulfonium ion. Mustard agent molecules contain 2 reactive binding groups. Mustards can bind to nucleophiles such as nitrogen in the base components of nucleic acids and sulfur in SH-groups in proteins and peptides. Mustards can destroy a large number of cellular substances by alkylation of DNA, which leads to DNA strand breaks and apoptosis.

Mustards also bind to cellular glutathione, a small peptide that is a major free radical scavenger. Glutathione depletion leads to inactivation of enzymes, loss of calcium homeostasis, lipid peroxidation, cellular membrane breakdown, and cell death. Pretreatment of cells with N -acetylcysteine has shown benefit in some studies.

Individual cell death within 2 hours of vapor exposure has been demonstrated in an animal model and general cell necrosis within 12 hours.



The concentration-time product capable of killing 50% of exposures (LCt50) of mustard vapor is 1500 mg·min/m3, and the lethal dose to 50% of exposures (LD50) of liquid mustard on the skin is 100 mg/kg.

Mustards are mutagenic resulting in a slight increased incidence of lung cancer, bladder cancer, and leukemia.


The clinical presentation of exposure to a vesicant depends on the route of administration and the agent used. Moderate-to-severe liquid cutaneous, inhalational, or gastrointestinal (GI) exposures cause systemic symptoms of nausea, vomiting, fever, malaise, and prostration. Other effects are as follows:

Ocular effects

The eyes are most sensitive and vulnerable to mustard. Ocular effects precede cutaneous manifestations and occur at lower concentrations (as low as one tenth) than that required to affect the airways. Nitrogen mustard (HN) causes more severe and earlier ocular lesions than sulfur mustard (HD).

Conjunctivitis follows an exposure time of approximately 1 hour to a concentration barely perceptible by odor that does not affect the skin or respiratory mucosa significantly. After mild exposure, a latent period of 4-12 hours is followed by lacrimation, a sensation of grit in the eyes, conjunctival injection, and edema (palpebral and bulbar).[20] Recovery requires 1-2 weeks.

In World War I, 75% of eye exposures were classified as mild conjunctivitis. In more modern times, conjunctivitides occurred in 85% of all Iranian casualties, with 8% sustaining long-term consequences[6] ; 15% of Iranian soldiers developed delayed keratitis.[4] Delayed ocular symptoms follow a latent period of 1-40 years, and reduced symptoms are reported in cold climates.[7]

After heavy exposure, eye signs and symptoms appear after 0.5-3 hours, and severe lesions may appear. Blepharospasm is common.[20]

A steamy haziness of the cornea or an orange-peel roughening of the cornea may occur. Spotty hemorrhagic discolorations of the iris may be observed. Temporary blindness is common, but permanent blindness is rare.

Mild corneal involvement demonstrates corneal erosions with fluorescein staining. Superficial corneal scarring and vascularization or iritis may occur.

With severe corneal involvement, dense corneal opacification with deep ulceration and vascularization occurs. Local necrosis of the cornea may rupture the globe. Panophthalmitis may occur and result in eye loss if appropriate therapy is not instituted.

Recovery from the ocular effects, especially with corneal involvement, may take months. Delayed ocular manifestations may occur abruptly from 1-40 years after exposure.[6] They exacerbate and remit in an unpredictable fashion.

Cutaneous effects

The severity of cutaneous effects of mustard and the rapidity with which they develop are influenced by the degree of exposure and the weather. Hot, humid weather results in more severe lesions. Warm, moist areas, such as the perineum, external genitalia, axillae, antecubital fossae, and neck, are most susceptible.

The latent period from contact with liquid or vapor exposures is usually 6-12 hours but may be as short as 1/2 hour when the weather is hot and humid. The effects appear more rapidly from liquid agent than from vapor.

The initial cutaneous effect is erythema, resembling sunburn. Slight skin edema may occur with mild exposures, but in severe burns, edema is greater. Vapor exposures may not cause skin lesions. Systemic symptoms such as malaise, vomiting, and fever may develop approximately at onset of erythema.

Intense cutaneous pruritus is common, may last for several days, and may persist after healing.

Erythema is followed by vesication as a result of liquefaction necrosis in the epidermal basal cell keratinocytes. The stratum corneum remains intact. Separation of the epidermis from the dermis occurs.[4] A liquid droplet with 10 mcg of mustard produces vesication. Vesicles are more concentrated in warm, moist areas such as the groin and axilla. Vesicles and bullae may be painful and are filled with yellow transudate that tends to coagulate. This fluid does not contain mustard and is not a risk to contacts.[6]

Reabsorption of the fluids takes place in approximately 1 week if the vesicles or bullae do not rupture. If rupture occurs, the burn is considered an open wound and is susceptible to secondary infection. Spontaneous healing occurs slowly with little scar formation.

Exposed areas of skin may (20% of patients) develop a persistent brown pigmentation except at the site of actual vesication, where a temporary depigmentation is seen.[6] The rate of healing typically is 1-2 weeks for facial lesions and up to 2-4 weeks or longer for other areas of the skin. Secondary infection may increase the severity of the lesions and delay healing. Skin lesions are more severe in light-skinned, younger, and female patients.[4]

Arsenical vesicants such as phenyldichloroarsine (PD) or chlorovinyldichloroarsine (L) often are mixed with mustard agents for chemical warfare weapons. When mixed as such, the resulting skin lesions are not more severe than either agent alone but tend to confuse and make the specific diagnosis difficult.

Respiratory effects

A longer latent period (4-24 h) may occur before the onset of respiratory symptoms. In patients with eye symptoms, expect the development of respiratory effects. Inhalation of mustard vapors may damage the laryngeal and tracheobronchial mucosa. Single exposure to a low concentration of vapor does not cause significant injury. Extreme, repeated, or chronic exposures may lead to the development of pulmonary fibrosis, chronic bronchitis, and bronchiectasis.

Respiratory effects develop slowly and reach maximal severity in several days. Symptoms begin in the upper airways and progress to the lower airways. Early symptoms begin with hoarseness, sneezing, rhinorrhea, sore throat, and loss of voice. This is followed by a cough, which subsequently becomes productive. Fever, dyspnea, chest tightness, rhonchi, and wet crackles may develop. Mild symptoms last 1-2 weeks. Recovery is slow, and coughing may persist for 1 or more months.

Moderate acute exposure leads to mucous membrane hyperemia, edema, and necrosis. Profuse, thin, mucopurulent rhinorrhea occurs; sinusitis may develop later. Mucosal findings range from small discrete ulcerations to extensive sloughing.

Pharyngitis usually appears 1-3 days after inhaling mustard vapors and may occur with nasal involvement in mouth breathers. The palate, uvula, tonsils, and pharynx are hyperemic and edematous. Multiple whitish ulcerations appear, varying in size according to severity of exposure. Laryngeal involvement resembles that of the pharynx. Edema and necrosis may lead to airway obstruction. Hoarseness, which almost always is present, may last 3-6 weeks or longer.

Severe inhalation exposures lead to a diphtherialike pseudomembrane, which may form a cast of the tracheobronchial tree. Mechanical obstruction from pseudomembrane formation and laryngospasm may cause death in the first 24 hours. Mild patchy pulmonary edema and focal atelectasis occur. Chemical pneumonitis may appear after the first 24 hours. Hemorrhagic pulmonary edema is not common and occurs only with severe damage. Symptoms resemble acute respiratory distress syndrome. Suppurative bacterial bronchitis and bronchopneumonia are frequent complications (particularly with Pseudomonas) 36-48 hours after exposure;[6] the latter is responsible for almost all deaths from vapor exposure.

In World War I, early mortality occurred in slightly more than 2% of US troops exposed to mustard and was caused almost entirely by pulmonary complications. Approximately 10% of the Iranian casualties treated in western European hospitals during the Iran-Iraq War developed progressive stenosis of the tracheobronchial tree.

Respiratory symptoms can occur 15 years after exposure in a previously asymptomatic individual.[6]

Gastrointestinal effects

Liquid mustard ingestion leads to GI mucosal necrosis and hemorrhage. Severe GI effects from mustard poisoning are relatively infrequent.

Initial symptoms include nausea, vomiting, painful diarrhea, and prostration. Vomiting and bloody diarrhea beginning days after a high-dose exposure imply a poor prognosis.

Hematopoietic and lymphatic effects

With systemic absorption of near lethal doses, hematopoietic and lymphatic tissue injuries occur, resulting in myelosuppression (leukopenia, thrombocytopenia, and anemia). Bone marrow suppression may be evident by 4 hours postexposure. High mortality rates were seen in Iran-Iraq war veterans who had an absolute neutrophil count < 200 cells/mm3.[4] See the Absolute Neutrophil Count calculator.

The thymus, spleen, and lymph nodes may involute rapidly. The development of shock, thrombocytopenia, leukopenia, and hemorrhagic diathesis are grave prognostic signs. Bone marrow failure resulting in fulminant sepsis and bleeding is the most frequent cause of late deaths from mustard exposure.

Neurologic effects

Neuropathic symptoms may persist years after exposure.[4] Chronic pain at the sites of cutaneous injury may be due to the destruction of nerve fibers and receptor.

Symptoms include allodynia, paresthesias, stinging, burning, and itching. These may be aggravated by sunlight exposure or shifts in ambient temperature.

Laboratory Studies

No hospital laboratory test exists to identify or quantify mustard exposures, since mustard is biotransformed and bound to tissues within minutes of adsorption.

Obtain a complete blood count, serum electrolytes, and coagulation studies; observe these periodically in all patients except those with isolated mild ocular or cutaneous involvement. Leukocytosis occurs during the first day. After large systemic adsorption, leukopenia may begin on day 3-5. A leukocyte count of 500/μL or less is an unfavorable prognostic sign.

Other Tests

The US military has the capability of detecting mustard agents in the environment with the use of the M256A1, M272 water testing kit, miniature chemical agent monitor (MINICAMS), individual chemical agent detector (ICAD), M18A2, M21 remote sensing alarm, M90, M93A1 Fox, Bubbler, chemical agent monitor (CAM), depot area air monitoring system (DAAMS), and M8 or M9 chemical detection paper.

Chest Radiography

Mustards may cause a chemical pneumonitis. Secondary infection may lead to lobular or lobar consolidation. Radiographic appearance follows the characteristics of the type of secondary pneumonia.

Prehospital Care

Patients contaminated with mustard agents endanger unprotected health care providers. Decontaminate patients exposed to mustard agents before transport and entry into medical treatment facilities to prevent vapor accumulation. Providers attending contaminated patients should have protective masks, butyl rubber gloves (latex gloves are NOT adequate), and chemical protective overgarments.

Unless carried out within 1-2 minutes, decontamination of victims exposed to mustard agents does not prevent subsequent blistering. After that brief window, decontamination still should be carried out as follows, to prevent secondary contamination:

Emergency Department Care

No specific treatment or antidote can reverse or prevent the cellular effects of mustard agents.[8] Symptomatic treatment is used to address affected organ systems.

Treatment of eye exposure

Measures for eye exposure are as follows:

Treatment of skin exposure

Mild mustard erythema requires no specific treatment. One animal study suggests rapid application of povidone-iodine ointment within 20 minutes of exposure may protect the skin from vesication. Topical steroid creams or sprays or calamine lotion may provide symptomatic relief of annoying pruritus. Address tetanus immunization in patients with cutaneous or ocular involvement.

Debride ruptured vesicles or bullae. Cleanse the underlying skin with sterile saline. Small areas of involvement can be dressed with petroleum gauze. Facial lesions are best covered with bacitracin ointment and left open.

Applying a 1/8-inch thick layer of mafenide acetate or silver sulfadiazine burn cream may treat larger areas of involvement best. Clean and redress these larger wounds twice a day. Multiple or large areas of vesication are cleansed easily with whirlpool bathing. HD-induced lesions heal slowly, often ulcerate, and vesicate repeatedly.

Culture wounds that become infected similar to thermal burns and administer appropriate parenteral antibiotics.

Avoid overhydration, since fluid losses generally are less than with thermal burns.

Liberal uses of narcotic analgesics are warranted to treat painful skin lesions.

Povidone-iodine applied to unbroken and unblistered skin may lessen the severity of dermal toxicity and reduce the incidence of blister formation.[4]

Treatment of respiratory exposure

Mild respiratory tract injury requires no specific treatment. Symptomatic treatment with antitussive medication and steam or cool mist inhalations may be tried.

Hospitalization is required for moderate or severe respiratory tract injuries. Inhaled beta-agonists may benefit patients with bronchospasm.

Patients with respiratory obstruction, hypoxia unresponsive to supplemental oxygen, or respiratory failure should undergo endotracheal intubation and mechanical ventilation. Direct antibiotic therapy for secondary bacterial pneumonia toward the specific organisms recovered and their antibiotic sensitivities.

Nebulized N -acetylcysteine (NAC) may possibly reduce lung injury.[4]

Treatment of systemic toxicity

Treatment of systemic toxicity from mustard is supportive, as follows:


Seek ophthalmologic consultation as soon as possible when eye involvement is present. Admit patients with corneal findings to the hospital.

Involve plastic surgeons in the care of those with cutaneous injuries admitted to the hospital.

Consult hematology and/or oncology specialists for patients with aplastic anemia, which is much more common after HN exposure.

Medication Summary

The goals of pharmacotherapy are to neutralize toxicity, reduce morbidity, and prevent complications.

Homatropine (AK-Homatropine, Isopto-Homatropine)

Clinical Context:  Contains homatropine hydrobromide, which blocks action of certain parasympathetic nerves and cholinergic drugs; used in ophthalmology for mydriatic and cycloplegic effects; peripheral effects are much weaker than those of atropine; preferred to atropine for diagnostic purposes because its action is more rapid, less prolonged, and is controlled readily by physostigmine; effect is exerted in 15-30 min and passes off in 12-24 h; usually does not produce complete paralysis of accommodation in children.

Atropine ophthalmic (Isopto, Atropair, Atropisol)

Clinical Context:  For use as long-acting mydriatic and cycloplegic; most potent ophthalmic parasympatholytic available; by paralyzing sphincter pupillae muscle, helps dilate pupil; also paralyzes ciliary muscle; effect lasts 7-10 d; also indicated to decrease GI motility.

Class Summary

Instillation of long-acting cycloplegic agents can relax any ciliary muscle spasm that can cause a deep aching pain and photophobia.

Atropine IV/IM (Atropair, Isopto, Atropisol)

Clinical Context:  Acts at parasympathetic sites in smooth muscle and decreases GI motility.

Dosage may require reduction in elderly patients due to possible occurrence of cardiovascular and CNS adverse effects.

Class Summary

Thought to work centrally by suppressing conduction in vestibular cerebellar pathways. They may have an inhibitory effect on the parasympathetic nervous system.

Morphine sulfate (Duramorph, Astramorph, MS Contin)

Clinical Context:  DOC for narcotic analgesia because of its reliable and predictable effects, safety profile, and ease of reversibility with naloxone; morphine sulfate administered IV may be dosed in a number of ways and commonly is titrated until desired effect is obtained.

Meperidine (Demerol)

Clinical Context:  Narcotic analgesic with multiple actions similar to those of morphine; may produce less constipation, smooth muscle spasm, and depression of cough reflex than similar analgesic doses of morphine.

Hydrocodone bitartrate and acetaminophen (Vicodin ES)

Clinical Context:  Drug combination indicated for relief of moderate to severe pain.

Class Summary

Pain control is essential to quality patient care. Analgesics ensure patient comfort, promote pulmonary toilet, and have sedating properties, which are beneficial for patients who have sustained burns.

Albuterol (Proventil, Ventolin)

Clinical Context:  Bronchodilator in reversible airway obstruction due to asthma; relaxes bronchial smooth muscle by action on beta 2-receptors with little effect on heart rate.

Class Summary

Primary action is to decrease muscle tone in both small and large airways in the lungs, thus increasing airflow and ventilation. This category includes beta-adrenergic, methylxanthine, and anticholinergic medications.

Silver sulfadiazine (Silvadene)

Clinical Context:  Used topically for dermal burns and useful in prevention of infections from second-degree or third-degree burns; has bactericidal activity against many gram-positive and gram-negative bacteria, including yeast.

Class Summary

Topical and ophthalmic antibiotics routinely are used for dermal and ocular burns, respectively. Injured tissues lose many of their protective mechanisms and are at increased risk of infection.

Tetanus toxoid adsorbed or fluid

Clinical Context:  Immunizing agents of choice for most adults and children >7 y are tetanus and diphtheria toxoids. Necessary to administer booster doses to maintain tetanus immunity throughout life.

Pregnant patients should receive only tetanus toxoid, not a diphtheria antigen-containing product.

In children and adults, may administer into deltoid or midlateral thigh muscles. In infants, preferred site of administration is mid thigh laterally.

Class Summary

Used to induce active immunity against tetanus in selected patients.

Codeine/guaifenesin (Robitussin AC, Guiatuss AC, Mytussin AC, Brontex liq)

Clinical Context:  Treats minor cough resulting from bronchial and throat irritation.

Class Summary

Indicated for control of excessive cough.

Hydrocortisone 1% (Cortaid, Dermacort, Westcort)

Clinical Context:  Adrenocorticosteroid derivative suitable for application to skin or external mucous membranes. Has mineralocorticoid and glucocorticoid effects resulting in anti-inflammatory activity.

Class Summary

Indicated for inflammation of skin.

Further Outpatient Care

For 12 hours prior to discharge, observe patients who are exposed to mustard and who are initially asymptomatic.

Chronic health problems may develop after mustard exposure including respiratory diseases (asthma, pulmonary fibrosis, bronchiectasis), skin lesions (dermal scarring), neoplasms (gastrointestinal cancers, chronic myelocytic leukemia, respiratory cancers, and skin cancers), and ocular problems (keratitis, corneal ulcers, conjunctivitis).

Further Inpatient Care

Patients with moderate-to-severe cutaneous effects are best managed in a hospital burn unit. The period of recuperation is much longer than that for thermal burns. Patients with significant pulmonary involvement usually require ICU admission.

Topical combination therapy with zinc desferrioxamine and dexamethasone resulted in faster corneal reepithelization and less severe neovascularization in an animal model. Keratoplasty may be necessary to recover visual function.

Adequate nutrition and fluid and electrolyte replacement are mandatory for patients with severe poisonings who have vomiting, diarrhea, leukopenia, hemoconcentration, and shock.

Patients with severe leukopenia require isolation and may require appropriate antibiotics. Colony-stimulating factors, such as filgrastim and pegfilgrastim, may help reduce the incidence of life-threatening infections associated with neutropenia.[4, 6]


The Israel Defense Force is developing a topical skin protectant (IB1) that is a passive protective lotion and, when applied before exposure, may significantly reduce the toxicity of sulfur mustard chemical warfare agents.[9]

Patient Education

For patient education information, see Chemical Warfare and Personal Protective Equipment.


Daniel J Dire, MD, FACEP, FAAP, FAAEM, Clinical Professor, Department of Emergency Medicine, University of Texas Medical School at Houston; Clinical Professor, Department of Pediatrics, University of Texas Health Sciences Center San Antonio

Disclosure: Nothing to disclose.

Specialty Editors

Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Chief Editor

Zygmunt F Dembek, PhD, MPH, MS, LHD, Associate Professor, Department of Military and Emergency Medicine, Adjunct Assistant Professor, Department of Preventive Medicine and Biometrics, Uniformed Services University of the Health Sciences, F Edward Hebert School of Medicine

Disclosure: Nothing to disclose.

Additional Contributors

Fred Henretig, MD, Director, Section of Clinical Toxicology, Professor, Medical Director, Delaware Valley Regional Poison Control Center, Departments of Emergency Medicine and Pediatrics, University of Pennsylvania School of Medicine, Children's Hospital

Disclosure: Nothing to disclose.


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