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eMedicine Specialties > Emergency Medicine > Toxicology
Toxicity, Chlorine Gas
Eli Segal, MD, CM, Assistant Professor, Department of Family Medicine, McGill University; Attending Physician, Department of
Emergency Medicine, The Sir Mortimer B Davis-Jewish General Hospital
Eddy Lang, MDCM, CCFP (EM), CSPQ, Assistant Professor, Department of Family Medicine, McGill University; Consulting Staff,
Department of Emergency Medicine, The Sir Mortimer B Davis-Jewish General Hospital
Updated: Jan 11, 2010
Introduction
Background
Chlorine gas is a pulmonary irritant with intermediate water solubility that causes acute damage in the upper and
lower respiratory tract. Chlorine gas was first used as a chemical weapon at Ypres, France, in 1915. Of the 70,552
American soldiers poisoned with various gases in World War I, 1843 were exposed to chlorine gas.[1 ]
Pathophysiology
Chlorine is a greenish-yellow, noncombustible gas at room temperature and atmospheric pressure. The
intermediate water solubility of chlorine accounts for its effect on the upper airway and the lower respiratory tract.[2 ]
Exposure to chlorine gas may be prolonged because its moderate water solubility may not cause upper airway
symptoms for several minutes. In addition, the density of the gas is greater than that of air, causing it to remain
near ground level and increasing exposure time. The odor threshold for chlorine is approximately 0.3-0.5 parts per
million (ppm); however, distinguishing toxic air levels from permissible air levels may be difficult until irritative
symptoms are present.
Chlorine is moderately soluble in water and reacts in combination to form hypochlorous (HOCl) and hydrochloric
(HCl) acids. Elemental chlorine and its derivatives, hydrochloric and hypochlorous acids, may cause biological
injury. The chemical reactions of chlorine combining with water and the subsequent derivative reactions with HOCl
and HCl are as follows:
a1) Cl2 + H2 O ⇔ HCl (hydrochloric acid) + HOCL (hypochlorous acid) or
a2) Cl2 + H2 O ⇔ 2 HCl + [O-] (nascent oxygen)
b) HOCl ⇔ HCl + [O-]
Mechanism of activity
The mechanisms of the above biological activity are poorly understood and the predominant anatomic site of injury
may vary, depending on the chemical species produced. Because of its intermediate water solubility and deeper
penetration, elemental chlorine frequently causes acute damage throughout the respiratory tract.[2 ]Cellular injury is
believed to result from the oxidation of functional groups in cell components, from reactions with tissue water to
form hypochlorous and hydrochloric acid, and from the generation of free oxygen radicals. Although the idea that
chlorine causes direct tissue damage by generating free oxygen radicals was once accepted,[3 ]this idea is now
controversial.[4,5 ]
Solubility effects
Hydrochloric acid is highly soluble in water. The predominant targets of the acid are the epithelia of the ocular
conjunctivae and upper respiratory mucus membranes.[6 ]
Hypochlorous acid is also highly water soluble with an injury pattern similar to hydrochloric acid. Hypochlorous acid
may account for the toxicity of elemental chlorine and hydrochloric acid to the human body.[7 ]
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Early response to chlorine gas
Chlorine gas, when mixed with ammonia, reacts to form chloramine gas. In the presence of water, chloramines
decompose to ammonia and hypochlorous acid or hydrochloric acid.[8 ]The early response to chlorine exposure
depends on the (1) concentration of chlorine gas, (2) duration of exposure, (3) water content of the tissues
exposed, and (4) individual susceptibility.[9 ]
Immediate effects
The immediate effects of chlorine gas toxicity include acute inflammation of the conjunctivae, nose, pharynx,
larynx, trachea, and bronchi. Irritation of the airway mucosa leads to local edema secondary to active arterial and
capillary hyperemia. Plasma exudation results in filling the alveoli with edema fluid, resulting in pulmonary
congestion.
Pathologic findings
Pathologic findings are nonspecific. They include severe pulmonary edema, pneumonia, hyaline membrane
formation, multiple pulmonary thromboses, and ulcerative tracheobronchitis.[10 ]
The hallmark of pulmonary injury associated with chlorine toxicity is pulmonary edema, manifested as hypoxia.
Noncardiogenic pulmonary edema is thought to occur when there is a loss of pulmonary capillary integrity, and
subsequent transudation of fluid into the alveolus is present. The onset can occur within minutes or hours,
depending upon severity of exposure. Persistent hypoxemia is associated with a higher mortality rate.
The eye seldom is damaged severely by chlorine gas toxicity; however, burns and corneal abrasions have
occurred. Acids formed by the chlorine gas reaction with the conjunctival mucous membranes are buffered, in part,
by the tear film and the proteins present in tears. Consequently, acid burns to the eye typically cause epithelial and
basement membrane damage but rarely damage deep endothelial cells. Acid burns to the periphery of the cornea
and conjunctiva often heal uneventfully, while burns to the center of the cornea may lead to corneal ulcer formation
and subsequent scarring.
In animal models of chlorine gas toxicity, immediate respiratory arrest occurs at 2000 ppm, with the lethal
concentration for 50% of exposed animals in the range of 800-1000 ppm.[7 ]Bronchial constriction occurs in the
200-ppm range with evidence of effects on ciliary activity at exposure levels as low as 18 ppm. With acute
exposures of 50 ppm and subacute inhalation as low as 9 ppm, chemical pneumonitis and bronchiolitis obliterans
have been noted. Mild focal irritation of the nose and trachea without lower respiratory effects occur at 2 ppm.
In one study of chlorine gas toxicity conducted on human volunteers, 4 hours of exposure to chlorine at 1 ppm
produced significant decreases in forced vital capacity (FVC), forced expiratory volume in one second (FEV1), and
peak expiratory flow rate.[11 ]An increase in airway resistance was demonstrated. In a controlled volunteer study,
patients with hyperreactive airways demonstrated an exaggerated airway response to exposure of 1 ppm chlorine
gas.[12 ]While in another study, patients with rhinitis and advanced age demonstrated a significantly greater nasal
mucosal congestive response to chlorine gas challenge than patients who did not have rhinitis or those of younger
age.[13 ]However, the mechanism of response to chlorine in nasal tissue does not appear to include mast cell
degranulation.
Frequency
United States
Chlorine gas is one of the most common single, irritant, inhalation exposures, occupationally and environmentally.
In 1983, an estimated 191,000 US workers were at risk of exposure to chlorine in various forms.[14 ]In a recent
study of 323 cases of inhalation exposures reported to poison control centers, the largest single source of
exposure (21%) was caused by mixing bleach with other products.[15 ]The greatest number of victims were injured
in manufacturing and the entertainment and recreation services sectors.
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International
Internationally, chlorine gas accounts for the largest single cause of major toxic release incidents.[16 ]Use of chlorine
internationally is parallel to use by the US in chemical, paper, and textile industries and in sewage treatment.
Mortality/Morbidity
Five-year cumulative data (1988-1992) from the American Association of Poison Controls Centers' National Data
Collection System revealed 27,788 exposures to chlorine. Of these exposures, the outcome was categorized in
21,437 cases; 40 resulted in a major effect, 2091 resulted in a moderate effect, 17,024 resulted in a minor effect,
and 2099 had no effect. Three fatalities occurred.[17,18,19,20,21 ]Another case series associated worse outcomes with
advanced age, initial low peak expiratory flow rate (PEFR), exposure in an enclosed space, and prolonged shortand long-term exposure.
Minor effects include signs or symptoms that are minimally bothersome and quickly resolved.
Moderate effects include signs or symptoms that are more pronounced or more prolonged than minor
effects. These may have a systemic nature and usually require some form of treatment.
Major effects include signs or symptoms that are life-threatening or result in significant residual disability or
disfigurement.
Clinical
History
Cough (52-80%)
Shortness of breath (20-51%)
Chest pain (33%)
Burning sensation in the throat and substernal area (14%)
Nausea or vomiting (8%)
Ocular and nasal irritation (4-6%)
Choking
Muscle weakness
Dizziness
Abdominal discomfort
Headache
Physical
Decreased breath sounds
Tachypnea
Tachycardia
Wheezing
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Nasal flaring
Intercostal and subcostal retractions
Cyanosis
Rhinorrhea
Lacrimation
Hoarseness of the voice or stridor
Rales (acute respiratory distress syndrome [ARDS]/noncardiogenic pulmonary edema)
Crepitus (associated with pneumomediastinum)[22 ]
Causes
Chlorine gas is one of the most common single, irritant, inhalation exposures, occupationally and
environmentally. Possible sources of exposure are as follows:
Industrial bleaching operations
Sewage treatment
Household accidents involving the inappropriate mixing of hypochlorite cleaning solutions with acidic
agents
Transportation releases
Swimming pool chlorination tablet accidents[23 ]
Storage tank failure
Chemical warfare
Adverse effects of inappropriate mixtures of household cleaners usually are caused by prolonged exposure
to an irritant gas in a poorly ventilated area. The most common mixtures of cleaning agents are sodium
hypochlorite (bleach) with acids or ammonia. Potential irritants released from such mixtures are chlorine
gas, chloramines, and ammonia gas.
Differential Diagnoses
Acute Respiratory Distress Syndrome
Toxicity, Ammonia
Asthma
Toxicity, Carbon Monoxide
Burns, Chemical
Toxicity, Caustic Ingestions
Burns, Ocular
Toxicity, Cyanide
Burns, Thermal
Toxicity, Hydrogen Sulfide
CBRNE - Chemical Warfare Agents
Toxicity, Phosgene
Chronic Obstructive Pulmonary Disease and Emphysema
Pneumonia, Bacterial
Pneumonia, Viral
Other Problems to Be Considered
Sulfur dioxide toxicity
Nitrogen dioxide toxicity
Hydrogen fluoride toxicity
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Metal fume fever
Workup
Laboratory Studies
Arterial blood gas
Abnormalities include hypoxia[9 ]and metabolic acidosis.
The metabolic acidosis may be hyperchloremic (nonanion gap). A postulated mechanism for the
production of this acidosis is the absorption of hydrochloric acid following the reaction of chlorine gas
with water.[24,25 ]
Imaging Studies
Chest x-ray (CXR) findings often are normal, but a CXR may be indicated to rule out pulmonary edema,
pneumonitis,[26 ]and acute ARDS.
Ventilation perfusion scan
Abnormal retention of radiolabeled xenon gas at 90 seconds suggests lower airway injury.
Ventilation perfusion scans have been used to determine lung damage in smoke inhalation.
Other Tests
Monitor oxygen saturation.
Obtain an electrocardiogram (ECG).
Pulmonary function tests may indicate obstructive or restrictive patterns.
PEFRs may reveal obstructive airway disease and response to therapy.
Procedures
Perform a fiberoptic laryngoscopy or bronchoscopy with intubation, as necessary, if laryngospasm is
suspected or clinically evident.
Treatment
Prehospital Care
Prehospital care providers should take necessary precautions to prevent contamination. The use of a chemical
cartridge respirator or self-contained breathing apparatus with full face mask should protect against the effects of
chlorine gas. However, in the setting where other potential chemical exposures exist, higher levels of protection
should be considered.
Remove the individual from the toxic environment.
Bring container, if applicable, so medical personnel can identify toxic agent.
Commence primary decontamination of the eye and skin, if necessary.
Real-time measurement of chlorine gas, both quantitative and qualitative, is possible through the use of
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mobile equipment.
Chlorine gas is denser than air and accumulates close to the ground. Therefore, during chlorine-related accidents,
people should be instructed to seek higher altitudes to avoid excessive exposure.
For related information, see Medscape's Disaster Preparedness and Aftermath Resource Center.
Emergency Department Care
Decontamination
Eye and skin exposures require copious irrigation with saline. In cases of suspected ocular injury,
determine initial pH using a reagent strip. Continue irrigation with 0.9% saline until the pH returns to
7.4.
Topical anesthetics help limit pain and improve patient cooperation.
Following irrigation, perform slit lamp examination, including fluorescein staining.
Measure ocular pressures.
Treat corneal abrasions with antibiotic ointment.
Supplemental oxygen
Maintain a PaO2 of 60 mm Hg or greater.[27 ]
Long-term (>24 h) elevated fraction of inspired oxygen (FIO2) greater than 50% may result in oxygen
toxicity.
Fluid restriction in patients with ARDS
Treatment of bronchospasm
Bronchodilators (inhaled albuterol or other beta-agonists) have been used frequently for the
management of respiratory symptoms. Animal models have demonstrated improvements in blood
gas parameters, airway pressure, and lung compliance with the administration of aerosolized
terbutaline.
The role of inhaled ipratropium is not well defined.
Lidocaine (1% solution) added to nebulized albuterol results in both analgesic and coughsuppressant actions.
Intubation for laryngospasm
Fiberoptic aid may be required if significant edema is present.
Consider using the largest size endotracheal tube possible to optimize pulmonary toilet.
Hypoxemic respiratory failure
Treat with positive-pressure ventilation.
High positive end-expiratory pressure (PEEP) (8-10 mm Hg) and inverse ratio ventilation may be
beneficial in ARDS.
In an animal model, prone positioning immediately following exposure to chlorine gas improved
pulmonary function, whereas treatment in the supine position was associated with further
compromise of pulmonary gas exchange.
Sodium bicarbonate
Use of nebulized solution of sodium bicarbonate, while recommended by some authors,[28,29 ]lacks
sufficient clinical evidence.
The mechanism of action is thought to be through the neutralizing of the hydrochloric acid formed
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when chlorine gas comes into contact with water. Lack of clinical trials and the theoretical possibility
that an exothermic reaction may be produced when bicarbonate mixes with hydrochloric acid have
led some authors to question its use.[9,30,31 ]Nonetheless, several pediatric and adult case reports did
describe a clinical improvement in patients with chlorine gas induced pulmonary injury who are
treated with inhaled sodium bicarbonate.
In a randomized, controlled trial 44 patients received either nebulized sodium bicarbonate (4 mL of
4.20% NaHCO3 solution) or saline treatment following chlorine gas exposure.[32 ]Treatment of all
patients included corticosteroids and nebulized, short-acting β2-agonists. Compared to the placebo
group, the NaHCO 3 group had significantly higher FEV1 values at 120 and 240 min.
Steroids
Parenteral steroids, while advocated by some authors to prevent short-term reactions and long-term
sequelae,[33,34 ]are not recommended by others[9 ]because of insufficient clinical trials.
Animal studies suggest improvements in pulmonary function and lung compliance with treatment of
inhaled steroids, alone and in conjunction with aerosolized beta-agonists. Earlier administration of
inhaled steroids in animal studies was associated with more beneficial effects.
Prophylactic antibiotics are not recommended.
Consultations
Consult critical care personnel if patient exhibits severe and protracted respiratory distress.
Consult an ophthalmologist for patient with ocular burns.
Consult a medical toxicologist if one is available in the area.
Medication
Beta-agonists, although not well studied in humans, have been widely used for the management of respiratory
symptoms in chlorine gas exposure, and they have demonstrated efficacy in animal models. They should be
considered a first-line agent in the setting of chlorine gas exposure and respiratory symptoms or signs.
Bronchodilators
Bronchodilatation through respiratory smooth muscle relaxation improves the respiratory status of the person who
is exposed to chlorine gas.
Albuterol (Proventil, Ventolin)
Beta-agonist for bronchospasm. Relaxes bronchial smooth muscle by action on beta2-receptors with little effect on
cardiac muscle contractility.
Dosing
Adult
5 mg in 2.5 mL NS for nebulization prn
Pediatric
0.2 mg/kg/dose PO prn
Interactions
Beta-adrenergic blockers antagonize effects; inhaled ipratropium may increase duration of bronchodilatation by
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albuterol; cardiovascular effects may increase with MAOIs, inhaled anesthetics, TCAs, and sympathomimetic
agents
Contraindications
Documented hypersensitivity
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits
outweigh risk to fetus
Precautions
Caution in hyperthyroidism, diabetes mellitus, and cardiovascular disorders; promotes tachycardia, especially in
children; may cause or exacerbate tachydysrhythmias
Inhaled corticosteroids
Anti-inflammatory inhaled corticosteroids have been shown in animal models to improve respiratory function
following experimental chlorine gas exposure. Exact mechanism of function in chlorine gas exposure unclear.
Budesonide (Pulmicort, Rhinocort)
Second-line agent for use in moderate-to-severe exposures.
Dosing
Adult
200-400 mcg, via oral inhalation, twice initially; may increase to 800 mcg bid
Pediatric
200 mcg, via oral inhalation, twice initially; may increase to 400 mcg bid
Interactions
None reported
Contraindications
Documented hypersensitivity
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits
outweigh risk to fetus
Precautions
Prolonged use, application over large surface areas, application of potent steroids, and occlusive dressings may
increase systemic absorption of corticosteroids and may cause Cushing syndrome, reversible HPA axis
suppression, hyperglycemia, and glycosuria; adverse effects include oral thrush, hoarseness, adrenal suppression,
glaucoma, skin bruising, and alteration in bone metabolism
Aerosolized sodium bicarbonate
When inhaled, these agents may neutralize (if administered early) or counteract the effects of inhaled chlorine.
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Sodium bicarbonate (Neut)
Theoretical reason for use is to reduce tissue injury caused by the acidic agent in airway. May not be useful if
patient does not present immediately postexposure. Route of administration is inhalation via nebulizer.
Dosing
Adult
4 mL of a 3.75% solution made by diluting 2 mL of a standard 7.5% solution with 2 mL NS inhaled via nebulizer;
administer once; repeat prn
Pediatric
Administer as in adults
Interactions
Theoretical exothermic reaction by an interaction with acidic inhalant
Contraindications
Documented hypersensitivity
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits
outweigh risk to fetus
Precautions
Use not well established; monitor for complications while administering
Follow-up
Further Inpatient Care
Consider hospitalization to observe and treat the patient with chlorine gas exposure in a highly monitored
setting in any of the following cases:
Symptoms persist after 6 hours.
Patient was severely exposed.
Child was exposed.
Patient has a history of underlying respiratory or cardiovascular disease.
Some authors suggest observation for a minimum of 24 hours because pulmonary edema may occur for 24
hours after exposure. Pulmonary edema occasionally may induce severe hypoxemia in minutes.
Patients who are asymptomatic 24 hours after exposure may be discharged from hospital.[35 ]
For a severe reaction, follow up with a pulmonologist.
Further Outpatient Care
No hospitalization is required for mild chlorine exposure or for patients who remain asymptomatic.
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Transfer
Transfer, as necessary, if local resources (eg, critical care, toxicologist, pulmonologist) are not available.
Deterrence/Prevention
Deterrence may decrease the number of accidental exposures to chlorine gas. Proper descriptions on
swimming pool chlorinator solutions with detailed warnings to avoid mixing solutions would prevent a great
number of accidents.
As accidental occupational exposures to chlorine gas comprise a significant percentage of severe
exposures, proper methods of training and supervision are beneficial. Proper enforcement of regulations
covering these work situations should be helpful.
Long-term exposure to smaller amounts of chlorine gas may contribute to pulmonary disease.
The current US legal limit for occupational exposure to chlorine gas enforceable by the Occupational Safety
and Health Administration (OSHA) is 0.5 ppm averaged over an 8-hour day, not to exceed 1.0 ppm for more
than 15 minutes at a time.[36 ]
Complications
Short-term effects of acute exposures of chlorine gas
Smokers and those with asthma are most likely to demonstrate persistence of obstructive pulmonary
defects.[3 ]
Within 3-5 days, after the sloughing off of the mucosa, oozing areas become covered with
mucopurulent exudate. This can result in chemical pneumonitis, often complicated by secondary
bacterial invasion.
Residual effects following acute exposures of chlorine gas
Long-term follow-up studies of acute human exposures to chlorine gas provide conflicting data on
the potential for long-term adverse effects from short-term chlorine exposure.
In one study, after 2 years of follow-up, research subjects displayed decreased vital capacity,
diffusing capacity, and total lung capacity with a trend towards higher airway resistance.[37 ]This
suggests that persistent dose-related lung function deficits may occur following acute chlorine gas
exposure.
Other studies demonstrated no consistent pattern of pulmonary function deficits following acute
exposure.[38,26,39,40 ]
Jones et al found that long-term sequelae after acute chlorine gas exposure were more affected by
cigarette smoking than by the chlorine gas exposure.[3 ]
Although no definite conclusion can be drawn concerning the long-term effects of an acute chlorine
gas exposure, findings point to an increased nonspecific airway responsiveness that may persist.
Following an acute exposure, some patients displayed eventual repair of injured pulmonary
epithelium with fibrosis.[41 ] Bronchiolitis obliterans and emphysema have been described in patients
following acute exposures.
Reactive airway dysfunction syndrome (RADS), or irritant-induced asthma, is a variant of occupational
asthma that occurs in individuals who are acutely exposed to high concentrations of an irritant product and
develop respiratory symptoms in the minutes or hours that follow. They develop persistent bronchial
hyperresponsiveness after the inhalational incident.[42 ]A similar pathology may occur with repeated
exposures.[43 ]
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Prognosis
Resolution of pulmonary abnormalities in most individuals occurs over the course of one week to one month
following exposure.
Patient Education
For excellent patient education resources, visit eMedicine's Bioterrorism and Warfare Center. Also, see
eMedicine's patient education articles Chemical Warfare and Personal Protective Equipment.
Miscellaneous
Medicolegal Pitfalls
Early discharge (Pulmonary edema may present after several hours.)
Failure to consider co-inhalants
Failure to manage the airway aggressively in a patient with laryngospasm
Special Concerns
The following populations are at higher risk of severe reaction and progression to respiratory failure than
other populations.
Children and elderly individuals
Those with underlying respiratory or cardiovascular disease
Smokers
Multimedia
Media file 1: Chemical Terrorism Agents and Syndromes. Signs and symptoms. Chart courtesy
of North Carolina Statewide Program for Infection Control and Epidemiology (SPICE), copyright
University of North Carolina at Chapel Hill, www.unc.edu/depts/spice/chemical.html.
PDF available at http://img.medscape.com/pi/emed/ckb/emergency_medicine/756148-812410-820779820881.pdf.
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Keywords
chlorine gas exposure, chlorine gas inhalation, chlorine gas toxicity, pulmonary irritant, hypochlorous acid, HOCl,
hydrochloric acid, HCl, elemental chlorine, chlorine exposure, inhalation of chlorine gas, chemical weapon
Contributor Information and Disclosures
Author
Eli Segal, MD, CM, Assistant Professor, Department of Family Medicine, McGill University; Attending Physician,
Department of Emergency Medicine, The Sir Mortimer B Davis-Jewish General Hospital
Eli Segal, MD, CM is a member of the following medical societies: American College of Emergency Physicians and
Royal College of Physicians and Surgeons of Canada
Disclosure: Nothing to disclose.
Coauthor(s)
Eddy Lang, MDCM, CCFP (EM), CSPQ, Assistant Professor, Department of Family Medicine, McGill University;
Consulting Staff, Department of Emergency Medicine, The Sir Mortimer B Davis-Jewish General Hospital
Eddy Lang, MDCM, CCFP (EM), CSPQ is a member of the following medical societies: American College of
Emergency Physicians
Disclosure: Nothing to disclose.
Medical Editor
Peter MC DeBlieux, MD, Professor of Clinical Medicine and Pediatrics, Section of Pulmonary and Critical Care
Medicine, Program Director, Department of Emergency Medicine, Louisiana State University Health Sciences
Center
Peter MC DeBlieux, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy
of Emergency Medicine, American College of Emergency Physicians, American Medical Association, Radiological
Society of North America, and Society of Critical Care Medicine
Disclosure: Nothing to disclose.
Pharmacy Editor
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.
Managing Editor
John G Benitez, MD, MPH, FACMT, FACPM, FAAEM, Associate Professor, Department of Medicine, Clinical
Pharmacology Division, Vanderbilt University; Managing Director, Tennessee Poison Center
John G Benitez, MD, MPH, FACMT, FACPM, FAAEM is a member of the following medical societies: American
Academy of Emergency Medicine, American College of Medical Toxicology, American College of Preventive
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Medicine, Society for Academic Emergency Medicine, Undersea and Hyperbaric Medical Society, and Wilderness
Medical Society
Disclosure: Nothing to disclose.
CME Editor
John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess
Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending
Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency
Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency
Medicine
Disclosure: Nothing to disclose.
Chief Editor
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.
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