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Chlorine - Prehospital Management

Acute Management Overview

Agent Identification

  • Chlorine is a yellow-green, noncombustible gas with a pungent, irritating odor. Chlorine's odor or irritant properties are discernible by most individuals at 0.32 ppm, which is less than the OSHA permissible exposure limit (PEL) of 1 ppm. Chlorine's odor or irritant properties generally provide adequate warning of hazardous concentrations. It is a strong oxidizing agent and can react explosively or form explosive compounds with many common substances. Chlorine is heavier than air and may collect in low-lying areas.
  • Responders should obtain assistance in identifying the chemical(s) from container shapes, placards, labels, shipping papers, and analytical tests. General information on these identification technicques is located in Emergency Response Guidebook.
  • Identification Tools - CHEMM-IST, WISER, Chlorine Chemical Properties
  • Devices - Chemical Agent Detector C2 Kit (liquid and vapor), Draeger CDS Kit (vapor and aerosol), Hazmat Smart Strips (qualitative)
  • A comprehensive source for the selection of chemical identification equipment is the Guide for the Selection of Chemical Detection Equipment for Emergency First Responders, Guide 100-06, January 2007, 3rd Edition, published by the Department of Homeland Security to assist with this process.

Rescuer Protection

Chlorine Specific Triage

  • In a mass casualty situation, asymptomatic patients who are reliable historians and those who experienced only minor sensations of burning of the nose, throat, eyes, and respiratory tract (with perhaps a slight cough) may be released. In most instances these patients will be free of symptoms in an hour or less. They should be advised to seek medical care promptly if symptoms develop or recur. If the incident involved a small number of patients, or the victims included young children (especially infants or patients with special needs), they should be monitored in an ED "extended care" area for 6-12 hrs.
  • Victims exposed only to chlorine gas who have no skin or eye irritation do not need decontamination. They may be transferred immediately to the Support Zone. All others require decontamination.
  • Symptomatic patients complaining of persistent shortness of breath, severe cough, or chest tightness should be admitted to the hospital and observed until symptom-free (pulmonary injury may progress for several hours).
  • If the treater feels that the patient has been exposed to a significant amount of chlorine, despite a relatively a benign clinical appearance he/she should be admitted for observation.
  • Clinical signs of pulmonary edema will typically present 2-4 hours following a moderate exposure and 30 - 60 minutes following a severe exposure.


  • Rescue personnel are at low risk of secondary contamination from victims who have been exposed only to chlorine gas.
  • However, clothing or skin soaked with industrial-strength bleach or similar solutions may be corrosive to rescuers and may release harmful chlorine gas.
  • Victims exposed only to chlorine gas who have no skin or eye irritation do not need decontamination. They may be transferred immediately to the Support Zone. All others require decontamination.
  • Link to prehospital management section

Route of Exposure

  • Inhalation - most exposures to chlorine occur by inhalation. However, prolonged, low-level exposures, such as those that occur in the workplace, can lead to olfactory fatigue and tolerance of chlorine's irritant effects. Chlorine is heavier than air and may cause asphyxiation in poorly ventilated, enclosed, or low-lying areas.
  • Skin/Eye Contact - direct contact with liquid chlorine or concentrated vapor causes severe chemical burns, leading to cell death and ulceration.
  • Ingestion - ingestion is unlikely to occur because chlorine is a gas at room temperature. Solutions that are able to generate chlorine (e.g., sodium hypochlorite solutions) may cause corrosive injury if ingested.

Clinical Signs and Symptoms

  • Respiratory - being water soluble, chlorine is primarily absorbed by the upper airway. Exposure to low concentrations (1-10ppm) may cause eye and nasal irritation, sore throat and cough. Inhalation of higher concentrations (>15 ppm) can very rapidly lead to respiratory distress. This can occur almost immediately with initial symptoms of stridor, followed shortly by wheezing, rales, hemoptysis, and subsequent pulmonary edema. Clinical signs of pulmonary edema will present 2-4 hours following a moderate exposure and 30 - 60 minutes following a severe exposure. Immediate onset of laryngospasm with respiratory arrest can occur.
  • Cardiovascular - initial tachycardia and hypertension followed by hypotension may occur.
  • Gastrointestinal - ingestion of chlorine can cause significant esophageal and stomach injury. Esophageal pain with swallowing, drooling and refusal of food suggest a more significant injury. Substernal chest pain, abdominal pain and rigidity suggest profound injury and potential perforation of the esophagus and/or stomach.
  • Dermal - chlorine causes skin irritation and with sufficient concentration can cause burning pain, inflammation, and blisters. Liquefied chlorine can cause frostbite injury.
  • Ocular - low vapor concentrations can cause burning, redness, conjunctivitis, and tearing. Higher concentrations may result in corneal burns.
  • Link to Toxic Syndromes
  • Link to Primary and Secondary Survey

Differential Diagnosis

  • Phosgene is distinguished by its smell in high concentrations and delayed onset of pulmonary edema.
  • Chlorine has a characteristic odor even in low concentrations, immediate onset of respiratory distress, bronchospasm, eye, skin, and upper airway irritation.
  • Riot agents cause an acute onset of burning sensation in the eyes and upper airway without progression of symptoms. Riot agents do not cause laryngospasm except in high doses and patients never develop symptoms of peripheral pulmonary edema.
  • Nerve agents induce watery secretions as well as respiratory distress, but have a host of other symptoms, such as miosis, seizures, rapidity of onset, that can distinguish them from pulmonary agents.
  • The respiratory toxicity of vesicants (i.e. mustard) is usually delayed, but affects the central rather than the peripheral airway. Vesicant toxicity severe enough to cause dyspnea typically causes airway necrosis often with upper airway obstruction.
  • Link to Chemical Hazards Emergency Medical Management Intelligent Syndromes Tool (CHEMM-IST)


Acute Patient Care Guidelines References