Chlorine Gas Toxicity



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]


Chlorine is a greenish-yellow, noncombustible gas at room temperature and atmospheric pressure. Its intermediate water solubility accounts for the effect on the upper airway and lower respiratory tract.[2] Prolonged exposure to chlorine gas may occur because its moderate water solubility delays onset of 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. As the concentration of chlorine gas exposure increases, the severity of symptoms and rapidity of onset increase. Concentrations above 400 ppm are often fatal.[3]

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 chlorine was at one time thought to cause direct tissue damage by generating free oxygen radicals,[4] this concept is now considered controversial.[5, 6]

Solubility effects

While chlorine gas is only moderately soluble in water, hydrochloric acid is highly soluble. The predominant targets of the acid are the epithelia of the ocular conjunctivae and upper respiratory mucus membranes.[7]

Hypochlorous acid is also highly water soluble with an injury pattern similar to hydrochloric acid. Hypochlorous acid may account for most of the toxic effects of elemental chlorine and hydrochloric acid to the human body.[8]

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.[9] 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.[10]

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 into the alveoli results in pulmonary congestion and edema.

Pathologic findings

Pathologic findings are nonspecific. They include pulmonary edema, pneumonia, hyaline membrane formation, multiple pulmonary thromboses, and ulcerative tracheobronchitis.[11]

The hallmark of pulmonary injury associated with chlorine toxicity is pulmonary edema, manifested clinically 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. The onset can occur within minutes or hours, depending upon severity of exposure. Persistent hypoxemia is associated with a higher mortality rate.

The eye is rarely 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.[8] 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.

The extent of tissue response varies with both the concentration of exposure as well as underlying tissue sensitivity. 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, as well as an increase in airway resistance.[12] Volunteers with hyperreactive airways were noted to experience an exaggerated airway response to exposure of 1 ppm chlorine gas.[13] 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.[14]



United States

Chlorine gas is one of the most common single irritant inhalation exposures, both occupationally and environmentally. In 1983, an estimated 191,000 US workers were at risk of exposure to chlorine in various forms.[15] 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.[16] The greatest number of victims were injured in manufacturing and the entertainment and recreation services sectors.


Internationally, chlorine gas accounts for the largest single cause of major toxic release incidents.[17] Use of chlorine internationally is parallel to use by the US in chemical, paper, and textile industries and in sewage treatment.

Chlorine gas has been used as a mechanism of injury in intentional exposures due to its availability and potential for mass casualty injury. First used in World War I, it has been used more recently in attacks in Iraq[18] and is considered a potential cause of serious mass casualty terrorist activity at home and abroad.[19]


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.[20, 21, 22, 23, 24] Another case series associated worse outcomes with advanced age, initial low peak expiratory flow rate (PEFR), exposure in an enclosed space, and prolonged short- and long-term exposure.




Laboratory Studies

Imaging Studies

Other Tests


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 on the upper and lower airways.. This, corresponds to an OSHA level A or level B PPE with positive pressure self-contained breathing apparatuses with full face plates as well as protective over garments.[19] ,[30] Chemical-protective clothing should be worn because chlorine gas can condense on the skin and cause irritation and burns.[3] Staging areas should be situated upwind of the chlorine gas site.

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

Eye and skin exposures require copious irrigation with saline. Duration of skin irrigation, although not well studied, should probably be from 3-5 minutes.[3]

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.

ED healthcare worker protection

Chlorine gas exposure, as opposed to liquid chlorine exposure, is unlikely to result in off-gassing.

Supplemental humidified oxygen

Maintain a PaO2 of 60 mm Hg or greater.[31]

Long-term (>24 h) elevated fraction of inspired oxygen (FIO2) greater than 50% may result in oxygen toxicity.

Fluid restriction

Fluid restriction is indicated 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 analgesia and cough-suppression.

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.[32]

Sodium bicarbonate

Use of nebulized solution of sodium bicarbonate, although recommended by some authors,[33, 34, 35] lacks sufficient evidence that demonstrates clinically relevant outcomes.

The mechanism of action is thought to be due to neutralization of hydrochloric acid formed 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.[10, 36, 37] Nonetheless, several pediatric and adult case reports describe clinical improvement in patients with chlorine gas induced pulmonary injury 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.[38] Treatment of all patients included corticosteroids and nebulized, short-acting β2-agonists. Compared to the placebo group, the NaHCO3 group had significantly higher FEV1 values at 120 and 240 min but no significant difference in quality of life questionnaire scores.


Parenteral steroids, while advocated by some authors to prevent short-term reactions and long-term sequelae,[39, 40] are not recommended by others[10] 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. Inhaled corticosteroid use, although reported,[35] has not been subjected to rigorous human study.

Ocular exposures

Topical anesthetics help limit pain and improve patient cooperation during initial evaluation and management.

Following irrigation, perform slit lamp examination, including fluorescein staining.

Measure ocular pressures.

Treat corneal abrasions with antibiotic ointment.

Prophylactic antibiotics are not recommended.


Medication Summary

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.

Albuterol (Proventil, Ventolin)

Clinical Context:  Beta-agonist for bronchospasm. Relaxes bronchial smooth muscle by action on beta2-receptors with little effect on cardiac muscle contractility.

Class Summary

Bronchodilatation through respiratory smooth muscle relaxation improves the respiratory status in chlorine gas exposure.

Budesonide inhaled (Pulmicort, Rhinocort)

Clinical Context:  Second-line agent for use in moderate-to-severe exposures.

Class Summary

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.

Sodium bicarbonate (Neut)

Clinical Context:  Theoretical reason for use is to reduce tissue injury caused by the acidic agent in airway. Potential decreased benefit if not administered immediately postexposure. Route of administration is inhalation via nebulizer.

Class Summary

When inhaled, these agents may neutralize (if administered early) or counteract the effects of inhaled chlorine.

Further Inpatient Care

Further Outpatient Care






Eli Segal, MD, CM, FRCP, Assistant Professor, Department of Family Medicine, McGill University; Attending Physician, Department of Emergency Medicine, Jewish General Hospital

Disclosure: Nothing to disclose.


Eddy S Lang, MDCM, CCFP(EM), CSPQ, Associate Professor, Senior Researcher, Division of Emergency Medicine, Department of Family Medicine, University of Calgary Faculty of Medicine; Assistant Professor, Department of Family Medicine, McGill University Faculty of Medicine, Canada

Disclosure: Nothing to disclose.

Specialty Editors

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 School of Medicine in New Orleans

Disclosure: Nothing to disclose.

John T VanDeVoort, PharmD, Regional Director of Pharmacy, Sacred Heart and St Joseph's Hospitals

Disclosure: Nothing to disclose.

John G Benitez, MD, MPH, Associate Professor, Department of Medicine, Medical Toxicology, Vanderbilt University Medical Center; Managing Director, Tennessee Poison Center

Disclosure: Nothing to disclose.

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

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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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,