Chlorine Toxicity 

Updated: May 13, 2019
Author: Gerald F O'Malley, DO; Chief Editor: Zygmunt F Dembek, PhD, MPH, MS, LHD 

Overview

Practice Essentials

Chlorine gas is a pulmonary irritant with intermediate water solubility that causes acute damage in the upper and lower respiratory tract. Occupational exposures constitute the highest risk for serious toxicity from high-concentration chlorine (see the image below). Mixing of chlorine bleach (sodium hypochlorite) with ammonia or acidic cleaning agents is a common source of household exposure. As with all poisons, the dose determines the toxicity. Exposure to low concentrations of chlorine for prolonged periods may have destructive effects, as might very short-term exposure to high concentrations.

Chest radiograph of a 36-year-old chemical worker Chest radiograph of a 36-year-old chemical worker 2 hours postexposure to chlorine inhalant. She had severe resting dyspnea during the second hour, diffuse crackles/rhonchi on auscultation, and a partial pressure of oxygen of 32 mm Hg breathing room air. The radiograph shows diffuse pulmonary edema without significant cardiomegaly. Used with permission from Medical Aspects of Chemical and Biological Warfare, Textbook of Military Medicine. 1997: 256.

Signs and symptoms

Symptoms may vary depending on the degree of exposure. Exposure possibilities include acute low levels, acute high levels, and chronic low levels.

Low-level (3-5%, 1-15 ppm) acute exposure

Most poisonings fall into this category and are caused by household exposure to low-concentration cleaning products. Manifestations are as follows:

  • Eye tearing, nose and throat irritation
  • Sneezing
  • Excess salivation
  • General excitement or restlessness

High-level (20%, >30 ppm) acute exposure

In addition to the symptoms seen with low-level exposure, high-level exposure may result in the following:

  • Dyspnea: Upper airway swelling and obstruction may occur
  • Violent cough
  • Nausea and vomiting (with the odor of chlorine in emesis)
  • Lightheadedness
  • Headache
  • Chest pain or retrosternal burning
  • Muscle weakness
  • Abdominal discomfort
  • Dermatitis (with liquid exposure): Corneal burns and ulcerations may occur from splash exposure to high-concentration chlorine products
  • Esophageal perforation

Chronic exposure

Manifestations of chronic exposure include the following:

  • Acne (chloracne)
  • Chest pain
  • Cough
  • Sore throat
  • Hemoptysis

Findings on physical examination may include the following:

  • Tachypnea
  • Cyanosis (most prevalent during exertion)
  • Tachycardia
  • Wheezing
  • Intercostal retractions
  • Decreased breath sounds
  • Rales (pulmonary edema)
  • Nasal flaring
  • Aphonia, stridor, or laryngeal edema
  • Ulceration or hemorrhage of the respiratory tract
  • Rhinorrhea
  • Lacrimation, salivation, and blepharospasm
  • Chloracne or tooth enamel corrosion (with chronic exposure)
  • Redness, erythema, and chemical burns to the skin from dose-dependent exposure to liquid

See Presentation for more detail.

Diagnosis

Studies in patients with significant exposure to chlorine gas may include the following:

  • Pulse oximetry
  • Serum electrolyte, blood urea nitrogen (BUN), and creatinine levels
  • Arterial blood gases
  • Chest radiography
  • Electrocardiogram 
  • CT scan of the chest
  • Ventilation-perfusion scan
  • Pulmonary function testing
  • Laryngoscopy or bronchoscopy

Abnormalities include hypoxia (from bronchospasm or pulmonary edema)[1] and metabolic acidosis. The metabolic acidosis may be hyperchloremic (nonanion gap). Chest radiograph findings are frequently normal initially but later may show nonspecific abnormalities, pulmonary edema, pneumonitis, mediastinal free air, myocardial depression,[2] or signs of ARDS.

See Workup for more detail.

Management

The most important aspect of treating patients exposed to chlorine gas is the provision of good supportive care, as follows:

  • Supplemental oxygen (humidified if possible) as necessary
  • Fluid restriction and diuretics for impending pulmonary edema
  • Positive end-expiratory pressure (PEEP) in patients with noncardiogenic pulmonary edema
  • Beta2 agonists and other bronchodilators as necessary for bronchospasm
  • Nebulized lidocaine for analgesia and reduction of cough
  • Consider nebulized sodium bicarbonate
  • Consider inhaled or parenteral corticosteroids
  • Copious saline irrigation for skin or eye exposures

Consider admission and observation for the following patients, even if they are initially asymptomatic, as they are at increased risk of progression to respiratory failure:

  • Patients exposed to large concentrations in an enclosed environment
  • Patients with underlying respiratory or cardiovascular disease
  • Children

See Treatment and Medication for more detail.

Educate patients on the risks associated with the improper handling of chlorine pool chemicals and the improper mixing of household cleaning chemicals. For patient education resources, see Chemical Warfare, Personal Protective Equipment, and Bronchoscopy.

Background

Chlorine gas is a pulmonary irritant with intermediate water solubility that causes acute damage in the upper and lower respiratory tract. Currently, occupational exposures constitute the highest risk for serious toxicity from high-concentration chlorine. Mixing of chlorine bleach (sodium hypochlorite) with ammonia or acidic cleaning agents is a common source of household exposure. See Etiology. 

Chlorine gas has also been used repeatedly as a chemical weapon.[3]  The respiratory and mucous membrane irritant effects of chlorine have been well known for many years. John Doughty, a New York City schoolteacher, first suggested use of chlorine gas as a chemical warfare agent during the American Civil War. This proposal was never acted upon during that war.[4]

Chlorine gas was officially introduced into the chemical warfare arsenal in 1915 at Ypres, Belgium. Accounts of chlorine attacks at Ypres describe an olive-green cloud rolling over the Allied positions, following the ground contours, and sinking into the trenches. Soldiers seeking safety in those trenches were overcome by the gas and experienced tearing eyes, vomiting, and difficulty breathing. They abandoned their trenches and suffered great losses from artillery and rifle fire.

An estimated 93,800 tons of chlorine gas was produced during World War I, with more than half produced by Germany. Total gas casualties in World War I were estimated at almost 1.3 million troops. Of the 70,552 American soldiers poisoned with various gases in World War I, 1843 were exposed to chlorine gas.[4] Chlorine was abandoned as a warfare agent when the use of gas masks was introduced and more effective compounds were created and deployed.

However, on at least three occasions in January and February 2007, insurgents in Iraq incorporated chlorine tanks in vehicle-borne improvised explosive device (VBIED) attacks. Most of the deaths from the attacks were caused by the explosion, but many people were treated and hospitalized for chlorine exposure.[5]  It has also been reported that Islamic State militants used chlorine gas when attacking the northern Iraq city of Kirkuk in 2016.[6]

The Organization for the Prohibition of Chemical Weapons (OPCW) has confirmed that since 2013, chlorine gas has been the agent used in numberous chemical attacks in Syria affecting thousands of civilians and resulting in hundreds of deaths.[3]  

Pathophysiology

Chlorine is a greenish-yellow, noncombustible gas at room temperature and atmospheric pressure. Prolonged exposure to chlorine gas may occur because its moderate water solubility delays onset of upper airway symptoms for several minutes. In addition, chlorine gas is heavier than air in its pure form, 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 develop. As the concentration of chlorine gas exposure increases, the severity of symptoms and rapidity of onset increase. The IDHL (immediately dangerous to life or health) is 10 ppm. Concentrations above 400 ppm are often fatal.[7]

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-]

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] Because of their high water solubility, chloramine exposures result in rapid symptom development. However, for mechanistic reasons that are not clear, chlorine 88 nitrogenous compounds result in less severe symptoms at onset. Because these initial symptoms are often mild, however, they may not prompt immediate retreat, thus resulting in prolonged exposure, with pulmonary and ocular symptoms predominating.[9]

Mechanism of activity

The mechanisms of 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.[10]

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,[11] this concept is now considered controversial.[12, 13]

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 mucous membranes.[14]

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 chlorine to the human body.[15]

Physiologic response

The early response to chlorine exposure depends on the following[1] :

  1. Concentration of chlorine gas
  2. Duration of exposure
  3. Water content of the tissues exposed
  4. Individual susceptibility

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 the following[16] :

  • Pulmonary edema
  • Pneumonia
  • Pneumonitis
  • Hyaline membrane formation
  • Multiple pulmonary thrombosis
  • Ulcerative tracheobronchitis

The hallmark of pulmonary injury associated with chlorine toxicity is pulmonary edema, manifested clinically as dyspnea, adventitious lung sounds, and 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.

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.[15] 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.[17]

Volunteers with hyperreactive airways were noted to experience an exaggerated airway response to exposure of 1 ppm chlorine gas.[18] 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.[19]

Eye injury

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 partially buffered by the tear film and the proteins present in tears. Consequently, acid burns to the eye are typically limited to the epithelial and basement membrane, rarely extending to the deep endothelial cells.

Acid burns to the periphery of the cornea and conjunctiva often heal uneventfully. Burns to the center of the cornea may lead to corneal ulcer formation and subsequent scarring.

Ingestion

Ingestion is unlikely to occur because chlorine is a gas at room temperature. Solutions that are able to generate chlorine (eg, sodium hypochlorite bleach) may cause corrosive injury if ingested.[7]

Etiology

Occupational exposures constitute the highest risk for serious exposure to high-concentration chlorine. Chlorine liquid is presently used in cleaning agents (eg, bleach, disinfectants), in water purification, and in the manufacture of items such as plastics. It is used in the following industries:

  • Pesticide
  • Refrigerant
  • Paper and pulp
  • Textile
  • Metallurgy
  • Pharmaceutical
  • Cosmetic
  • Battery
  • Water and sewage purification
  • Food processing

Other exposures occur during industrial or transportation accidents. More than 200 significant industrial accidents involving chlorine have occurred since World War I. In addition, chemical attacks on civilians have been reported in both Iraq and Syria.

Household exposure occurs with chlorination tablet accidents during swimming pool maintenance,[20, 21, 22] or with inappropriate mixing of sodium hypochlorite (bleach) cleaning agents with ammonia products, which produces chloramine gas. Typically, this occurs in an enclosed environment such as a restroom. Chlorine gas also may be released in the household by mixing sodium hypochlorite solutions with acidic cleaning agents (toilet bowl cleaners).

Epidemiology

In the United States, chlorine is the most common inhalational irritant. In 2017, the American Association of Poison Control Centers (AAPCC) reported 4039 single exposures to chlorine gas, 2166 single exposures to chlorine gas when household acid is mixed with hypochlorite, and 2115 single exposures to chloramine gas.[23]  

Chlorine is used in chemical, paper, and textile industries, along with sewage treatment. In each of these industries, the potential exists for accidental release. In addition, chlorine can be used in sabotage, warfare, and terrorist actions.[24, 25] For example, insurgents in Iraq incorporated chlorine tanks in vehicle-borne improvised explosive device attacks.[5]

Prognosis

Most individuals exposed to chlorine gas recover without significant sequelae. Even exposure to high-concentration chlorine gas is unlikely to result in significant, prolonged pulmonary disease.

Morbidity from moderate and severe exposures is typically caused by noncardiogenic pulmonary edema. This may occur within 2-4 hours of exposure to moderate chlorine concentrations (25-50 ppm) and within 30-60 minutes of severe exposures (>50 ppm).

In serious exposures, sloughing of the pulmonary mucosa occurs in 3-5 days, and oozing areas become covered with mucopurulent exudate. This chemical pneumonitis is often complicated by secondary bacterial invasion.

Resolution of pulmonary abnormalities in most individuals occurs over the course of 1 week to 1 month after the exposure. Smokers and persons with asthma are most likely to demonstrate persistence of obstructive pulmonary defects.[11] In a study of patients exposed to chlorine gas released after a train derailment, hypoxia on room air and the ratio of partial pressure of oxygen to fractional concentration of oxygen in inspired air (PO2/FiO2) predicted the duration of hospitalization and the need for intensive care support.[24]

Residual effects

Although no definite conclusion can be drawn concerning the long-term effects of an acute chlorine gas exposure, findings suggest increased risk of persistent nonspecific airway responsiveness. Furthermore, following an acute exposure, some patients with injured pulmonary epithelium have progressed to develop pulmonary fibrosis.[26]  Bronchiolitis obliterans and emphysema have also been described in patients following acute exposures.

Significant immedate reductions in lung function were reported in a study of 1807 millworkers exposed to chlorine gas after a train derailment led to an estimated 54,915-kg release of chlorine in Graniteville, South Carolina. Improvement was seen in the second year; but the proportion of mill workers experiencing accelerated annual decline in FEV1 significantly increased in the 18 months following the exposure. In addition, the study found that smokers experienced additional FEV1 and FVC loss in the years after the accident.[27]  

Irritant-induced asthma (formerly known as reactive airway dysfunction syndrome [RADS]), is a variant of occupational asthma that occurs after a single, high-dose exposure or after repeated low-level exposure.[28] Within minutes to hours, these individuals develop respiratory symptoms[29] followed by persistent bronchial hyperresponsiveness.[30]

Persistent anxiety after acute exposure to chlorine gas has been observed. In one large-scale accident, 37% of respondents had a positive posttraumatic stress screen 8-10 months post disaster, 44% of which were considered severe; 27% of all individuals had a positive indication for tendency to panic. Tendency to panic was significantly associated with acute injury and female sex.[31]

 

Presentation

History

Symptoms may vary depending on the degree of exposure. Exposure possibilities include acute low levels, acute high levels, and chronic low levels.

Acute exposure (low levels)

Most poisonings fall into this category and are caused by household exposure to low-concentration cleaning products. Manifestations are as follows:

  • Eye tearing, nose and throat irritation

  • Sneezing

  • Excess salivation

  • General excitement or restlessness

Acute exposure (high levels)

In addition to the symptoms seen with low-level exposure, high-level exposure may result in the following:

  • Dyspnea: Upper airway swelling and obstruction may occur

  • Violent cough

  • Nausea and vomiting (with the smell of chlorine in emesis)

  • Lightheadedness

  • Headache

  • Chest pain or retrosternal burning

  • Muscle weakness

  • Abdominal discomfort

  • Dermatitis (with liquid exposure): Corneal burns and ulcerations may occur from splash exposure to high-concentration chlorine products

Chronic exposure

Manifestations of chronic exposure include the following:

  • Acne (chloracne)

  • Chest pain

  • Cough

  • Sore throat

  • Hemoptysis

Physical Examination

Findings on physical examination may include the following:

  • Tachypnea

  • Cyanosis (most prevalent during exertion)

  • Tachycardia

  • Wheezing

  • Intercostal retractions

  • Decreased breath sounds

  • Rales (pulmonary edema)

  • Nasal flaring

  • Aphonia, stridor, or laryngeal edema

  • Ulceration or hemorrhage of the respiratory tract

  • Rhinorrhea

  • Lacrimation, salivation, and blepharospasm

  • Chloracne or tooth enamel corrosion (with chronic exposure)

  • Redness, erythema, and chemical burns to the skin from dose-dependent exposure to liquid

Superheated chlorine gas from an industrial fire or chemical warehouse explosion may carry the danger of direct thermal injury to the mucous membranes of the eyes, mouth, and respiratory tract in addition to the chemical effects.

 

DDx

Differential Diagnoses

 

Workup

Approach Considerations

The diagnosis of acute chlorine toxicity is primarily clinical, based on respiratory difficulties and irritation. However, laboratory testing is useful for monitoring the patient and evaluating complications. Studies in patients with significant exposure to chlorine gas may include the following:

  • Pulse oximetry
  • Serum electrolyte, blood urea nitrogen (BUN), and creatinine levels
  • Chest radiography
  • Electrocardiogram (ECG)
  • Ventilation-perfusion scan
  • Pulmonary function testing
  • Laryngoscopy or bronchoscopy

Abnormalities include hypoxia (from bronchospasm or pulmonary edema)[1] and metabolic acidosis, which may be a hyperchloremic (nonanion gap) acidosis.[7] It is postulated that this may be caused by the absorption of hydrochloric acid following the reaction of chlorine gas with mucosal water.[24, 32]

Handheld peak flow meters can be used to measure the degree of bronchospasm and follow the response to treatment. Pulmonary function tests may indicate obstructive or restrictive patterns and can provide measurements of the degree of limitation.

Biomarkers

In a study that screened for chlorinated biomolecules by the use of mass isotope ratio filters, two biomarkers present in bronchoalveolar lavage fluid (BALF) from chlorine gas exposed mice were identified. The potential chlorine specific markers were all chlorohydrins of unsaturated pulmonary surfactant phospholipids; phosphatidylglycerols, and phosphatidylcholines. The relevance of these markers for human exposure was verified by their presence in in vitro chlorinated human BALF. The biomarkers were detectable for 72 h after exposure and were absent in nonexposed control animals or in humans diagnosed with chronic respiratory diseases.[3]  

Chest Radiography

The chest radiograph findings are frequently normal initially but may exclude other causes of hypoxia in the differential. Abnormalities may nonspecific; however, pulmonary edema, pneumonitis,[33] and adult respiratory distress syndrome (ARDS) may be seen in some cases. The radiograph below shows diffuse pulmonary edema without significant cardiomegaly.

Chest radiograph of a 36-year-old chemical worker Chest radiograph of a 36-year-old chemical worker 2 hours postexposure to chlorine inhalant. She had severe resting dyspnea during the second hour, diffuse crackles/rhonchi on auscultation, and a partial pressure of oxygen of 32 mm Hg breathing room air. The radiograph shows diffuse pulmonary edema without significant cardiomegaly. Used with permission from Medical Aspects of Chemical and Biological Warfare, Textbook of Military Medicine. 1997: 256.

CT scan of the chest can reveal the extent of interstitial pulmonary edema.

A ventilation-perfusion scan showing abnormal retention of radiolabeled xenon gas at 90 seconds suggests lower airway injury.

Histologic Findings

The image below shows a sample of lung tissue obtained from biopsy of a patient with exposure to chlorine.

A section from a lung biopsy (hematoxylin and eosi A section from a lung biopsy (hematoxylin and eosin stain; original magnification X 100) from a 36-year-old chemical worker taken 6 weeks postexposure to chlorine. At that time, the patient had no clinical abnormalities and a partial pressure of oxygen of 80 mm Hg breathing room air. The section shows normal lung tissues without evidence of interstitial fibrosis and/or inflammation. Used with permission from Medical Aspects of Chemical and Biological Warfare, Textbook of Military Medicine. 1997: 256.
 

Treatment

Approach Considerations

The most important aspect of treating patients exposed to chlorine gas is the provision of good supportive care. No antidotes are available. Emergency department (ED) personnel are at low risk for cross-contamination in cases of exposure to chlorine gas. However, the patient’s clothing should be removed if it has been contaminated with liquid chlorine. Wear appropriate protective gear during decontamination, especially if the exact toxin is not identified.

Evaluate the airway, breathing, and circulation. Provide supplemental oxygen (humidified if possible) as necessary; depending on the patient’s oxygen requirements, it may be delivered by nasal cannula, face mask, nonrebreather mask, noninvasive positive pressure ventilation, or intubation. Severe respiratory distress indicates the need for endotracheal intubation. Because of the risk of laryngospasm, several back-up modalities should be available at the time of intubation (ie, fiberoptic laryngoscope, cricothyrotomy tray).

Positive pressure ventilation with positive end-expiratory pressure (PEEP) set at 5-10 mm Hg may improve oxygenation in patients with noncardiogenic pulmonary edema and allow for lower fraction of inspired oxygen (FIO2) settings. An FIO2 greater than 50% for longer than 24 hours may result in oxygen toxicity.

Closely monitor the patient's fluid input and output because of the potential of pulmonary edema. Fluid restriction may be required and diuretics may be used to treat impending pulmonary edema.

Treat initial bronchospasm with beta agonists such as albuterol. Ipratropium may be added. Poor responses may require terbutaline or aminophylline. Nebulized lidocaine (4% topical solution) may provide analgesia and reduce coughing.

Other medications that may be used in the treatment of chlorine gas exposure include nebulized sodium bicarbonate and inhaled or systemic corticosteroids; however, evidence of efficacy is mixed. No evidence supports the use of prophylactic antibiotics.

Patients with skin or eye exposure to chlorine require copious irrigation with saline. Consider ophthalmologic consultation for patients with significant ocular involvement.

Consider admission and observation for the following patients, even if they are initially asymptomatic, as they are at increased risk of progression to respiratory failure:

  • Patients exposed to large concentrations in an enclosed environment
  • Patients with underlying respiratory or cardiovascular disease
  • Children

Cases of chronic reactive airway disease after acute exposures to chlorine gas are described in the literature. Consider referring patients for pulmonary function testing.

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 Occupational Safety and Health Administration (OSHA) level A or level B personal protective equipment (PPE), with positive pressure self-contained breathing apparatuses with full face plates as well as protective overgarments.[25, 34]

Chemical-protective clothing should be worn because chlorine gas can condense on the skin and cause irritation and burns.[7] Staging areas should be situated upwind of the chlorine gas site.

Care at the site consists of the following:

  • Remove the individual from the toxic environment

  • Bring the container (double-bagged and sealed) or material safety data sheets (MSDS), if applicable, so medical personnel can identify the toxic agent; a digital photo of the product label (if possible) is preferred over the product itself to limit healthcare facility contamination

  • 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 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.

Hospital Admission

Patients who are asymptomatic on presentation and remain asymptomatic 6 hours after exposure may be discharged with appropriate instructions and in the presence of reliable family members. They should be advised that pulmonary edema may present in a delayed fashion after chlorine gas exposure.

Patients who present with symptoms that continue for 6 hours after exposure should be admitted for an observation period of at least 24 hours. If they are asymptomatic at 24 hours, they may be discharged with appropriate follow-up care.[35]

Consider admission and observation for the following patients, even if they are initially asymptomatic:

  • Patients exposed to large concentrations in an enclosed environment
  • Patients with underlying respiratory or cardiovascular disease
  • Children

Request critical care or pulmonary consultation for most admissions. Toxicology or poison control center consultation is recommended.

Skin and Eye Exposure

Skin exposures require copious irrigation with saline. Duration of skin irrigation, although not well studied, should probably be from 3-5 minutes.[7] If skin exposure is significant, wash with a mild soap and water.

In cases of suspected ocular injury, determine initial pH using a reagent strip capable of measuring the ranges 0-14. Irrigate the eye with normal saline until the pH returns to 7.4. Remove contact lenses (if present) prior to irrigation. Topical anesthetics help limit pain and improve patient cooperation during initial evaluation and management.[36]

After irrigation, evaluate the cornea with fluorescein staining under a slit lamp. Treat corneal abrasions with antibiotic ointment. Measure ocular pressures. Obtain ophthalmologic consultation for patients with significant ocular involvement.

Sodium Bicarbonate

In the past, several authors advocated nebulized sodium bicarbonate for treatment of chlorine gas exposure. The mechanism of action is believed to be the neutralization of hydrochloric acid formed in the airways. Most recommendations are based on anecdotal experience, and little supporting clinical data are available.[37, 38, 39] Theoretically, an exothermic reaction may occur when bicarbonate mixes with hydrochloric acid.[1, 40, 22] Animal studies suggest that nebulized sodium bicarbonate may cause chemical pneumonitis.

In a randomized, controlled trial in 44 patients with reactive airways dysfunction syndrome (RADS) due to chlorine inhalation, forced expiratory volume in 1 second (FEV1) values at 120 and 240 minutes were significantly higher in patients treated with nebulized sodium bicarbonate (4 mL of 4.20% NaHCO3 solution) than in those who received saline.[41] Treatment of all patients included corticosteroids and nebulized, short-acting β2-agonists. No significant difference in quality of life questionnaire scores was found between the two groups.

Corticosteroids

Inhaled and parenteral steroids have been used with many patients exposed to chlorine gas, but no strong clinical evidence supports their use except in patients with an exacerbation of underlying reactive airway disease.[39] Some animal studies demonstrate better lung compliance and arterial oxygen tension when inhaled steroids are initiated within 30 minutes of exposure.

Parenteral steroids are advocated by some authors to prevent short-term reactions and long-term sequelae.[42, 43] Other authors argue against this practice, because of insufficient clinical trials.[1]

Investigational Treatments

Studies in animal models have found benefit from postexposure treatment with N-acetylcysteine (NAC)[44] and a combination of ascorbate and deferoxamine.[45] Treated rats demonstrated favorable histopathological changes in pulmonary tissue compared with controls.

The role of transient receptor potential (TRP) channel inhibitors in acute lung injury secondary to chlorine and other toxic inhalational agents is becoming more clear, and TRP inhibitors have been shown to suppress pulmonary inflammation in this setting.[46]  However, caution should be used in interpreting these studies because these interventions have not been studied in humans for this condition.

 

Deterrence/Prevention

Proper labeling and avoiding mixing chemicals facilitate prevention. Household cleaning products should not be mixed. Using proper precautions when handling swimming pool chemicals reduces risks. Adequate ventilation is necessary when handling any potentially noxious chemical.

As accidental occupational exposures to chlorine gas comprise a significant percentage of severe exposures, proper methods of training and supervision are beneficial. Enforcement of existing work safety regulations may lead to fewer exposures. On a larger scale, chemical warfare treaties between countries and the safe transportation and handling of industrial chlorine compounds facilitate deterrence.

Training prehospital and hospital providers in the management of chemical casualties can improve the treatment provided to exposed personnel while minimizing personal risks. Hospitals can establish mass casualty plans and perform drills to ensure that preparations are adequate in the event of a large-scale industrial accident.

Long-term exposure to small amounts of chlorine gas may contribute to pulmonary disease.[47] 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 a 10-hour day or a 40-hour work week and a short-term exposure limit of 1 ppm.[48]

 

Medication

Medication Summary

No antidote for chlorine gas is available. Instead, the goal of pharmacotherapy is to reduce morbidity and prevent complications. 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.

Beta2 Agonists

Class Summary

Beta2 agonists act on beta2 receptors to relax bronchial smooth muscle and thereby increase airway diameter. These agents have little effect on cardiac muscle contractility.

Albuterol (Proventil HFA, Ventolin HFA, ProAir HFA, VoSpire ER)

Albuterol is a beta2-agonist useful for treatment of bronchospasm. It is the preferred choice for initial treatment because of its rapid onset of action.

Terbutaline

Terbutaline is a selective beta 2-agonist that relieves bronchospasm by acting on beta 2 receptors to relax bronchial smooth muscle.

Anticholinergics, Respiratory

Class Summary

Believed to work synergistically with bronchodilators.

Ipratropium (Atrovent)

Inhibits secretions from some respiratory mucosa; historically atropine was used in asthma, but ipratropium has fewer adverse effects.

Xanthine Derivatives

Class Summary

These agents were historically used to treat asthma but lost favor because of their toxic effects and narrow therapeutic windows. They have largely been displaced by newer agents.

Theophylline (Theo 24, Elixophyllin, Theochron SR)

Theophylline is believed to potentiate exogenous catecholamines, stimulate endogenous catecholamine release, and relax the diaphragmatic musculature.

Local Anesthetics, Amides

Class Summary

Inhaled topical anesthetics have been used to reduce cough and may reduce pain associated with chlorine inhalations.

Lidocaine (Xylocaine)

Lidocaine stabilizes neuronal membranes by inhibiting the ionic fluxes required for initiation and conduction of impulses. When administered by nebulizer, lidocaine acts in areas exposed to chlorine injury.

Corticosteroids, Inhalants

Class Summary

Corticosteroids have anti-inflammatory properties and cause profound and varied metabolic effects. These agents modify the body's immune response to diverse stimuli. In animal models of chlorine gas exposure, inhaled corticosteroids have been shown to improve respiratory function. Their exact mechanism of function in chlorine gas exposure is unclear.

Budesonide inhaled (Pulmicort Flexhaler)

Inhaled budesonide is a second-line agent for use in moderate-to-severe chlorine exposures.