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Toxicity, Chlorine Gas

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
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
Contributor Information and Disclosures

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 Û HCl (hydrochloric acid) + HOCL (hypochlorous acid) or

a2) Cl2 + H2 O Û 2 HCl + [O-] (nascent oxygen)

b) HOCl Û 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

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.

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 short- and 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
  • 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 accidents23
    • 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.

More on Toxicity, Chlorine Gas

Overview: Toxicity, Chlorine Gas
Differential Diagnoses & Workup: Toxicity, Chlorine Gas
Treatment & Medication: Toxicity, Chlorine Gas
Follow-up: Toxicity, Chlorine Gas
Multimedia: Toxicity, Chlorine Gas
References
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References

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Further Reading

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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

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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 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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