AUTHOR AND EDITOR INFORMATION

Section 1 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

INTRODUCTION

Section 2 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

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.

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. 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 + H₂O « HCl (hydrochloric acid) + HOCL (hypochlorous acid) or

a2) Cl₂ + H₂O « 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. 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, this idea is now controversial.

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.

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.

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. 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.

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.

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. 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. 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. 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. 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. 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. 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. 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. 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

Section 3 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

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)

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
  • 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.

DIFFERENTIALS

Section 4 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Other Problems to be Considered

Sulfur dioxide toxicity
Nitrogen dioxide toxicity
Hydrogen fluoride toxicity
Metal fume fever

WORKUP

Section 5 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Lab Studies

• Arterial blood gas
• • Abnormalities include hypoxia 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.

Imaging Studies

• Chest x-ray (CXR) findings often are normal, but a CXR may be indicated to rule out pulmonary edema, pneumonitis, 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

Section 6 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

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 mobile equipment.

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.
  • 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 cough-suppressant 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, lacks sufficient clinical evidence.
  • The mechanism of action is thought to be through the neutralizing of the 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. 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.
• Steroids
  • Parenteral steroids, while advocated by some authors to prevent short-term reactions and long-term sequelae, are not recommended by others 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

Section 7 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

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.

Drug Category: Bronchodilators

Bronchodilatation through respiratory smooth muscle relaxation improves the respiratory status of the person who is exposed to chlorine gas.

Drug Category: 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.

Drug Category: Aerosolized sodium bicarbonate

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

FOLLOW-UP

Section 8 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Further Inpatient Care

• Consider hospitalization to observe and treat patient 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.
• 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.

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.

Complications

• Short-term effects of acute exposures
• • Smokers and those with asthma are most likely to demonstrate persistence of obstructive pulmonary defects.
  • 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
• • 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. 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.
  • 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.
  • 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. 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. A similar pathology may occur with repeated exposures.

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

Section 9 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Medical/Legal 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

Section 10 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

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.
	View Full Size Image
Media type:  Image

REFERENCES

Section 11 of 11

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

• Academy of Health Sciences, US Army. First aid in toxic environments. In: First Aid for Soldiers, Virtual Naval Hospital. 1988. Available at: http://www.vnh.org/FirstAidForSoldiers/fm2111.html. Accessed November 8, 2004. [Full Text].
• Adelson L, Kaufman J. Fatal chlorine poisoning: report of two cases with clinicopathologic correlation. Am J Clin Pathol. Oct 1971;56(4):430-42. [Medline].
• Barrow CS, Alarie Y, Warrick JC, Stock MF. Comparison of the sensory irritation response in mice to chlorine and hydrogen chloride. Arch Environ Health. Mar-Apr 1977;32(2):68-76. [Medline].
• Blanc PD, Galbo M, Hiatt P, Olson KR. Morbidity following acute irritant inhalation in a population based study. JAMA. 1991;266:664-9. [Medline].
• Bosse GM. Nebulized sodium bicarbonate in the treatment of chlorine gas inhalation. J Toxicol Clin Toxicol. 1994;32(3):233-41. [Medline].
• Brooks SM, Weiss MA, Bernstein IL. Reactive airways dysfunction syndrome (RADS). Persistent asthma syndrome after high level irritant exposures. Chest. Sep 1985;88(3):376-84. [Medline].
• Chester EH, Kaimal J, Payne CB Jr, Kohn PM. Pulmonary injury following exposure to chlorine gas. Possible beneficial effects of steroid treatment. Chest. Aug 1977;72(2):247-50. [Medline].
• Chisholm CD, Singleton EM, Okerberg CV. Inhaled sodium bicarbonate therapy for chlorine inhalation injuries. Ann Emerg Med. 1989;18:466.
• D''Alessandro A, Kuschner W, Wong H, et al. Exaggerated responses to chlorine inhalation among persons with nonspecific airway hyperreactivity. Chest. Feb 1996;109(2):331-7. [Medline].
• Das R, Blanc PD. Chlorine gas exposure and the lung: a review. Toxicol Ind Health. May-Jun 1993;9(3):439-55. [Medline].
• Douidar SM. Nebulized sodium bicarbonate in acute chlorine inhalation. Pediatr Emerg Care. Dec 1997;13(6):406-7. [Medline].
• Gorguner M, Aslan S, Inandi T, Cakir Z. Reactive airways dysfunction syndrome in housewives due to a bleach-hydrochloric acid mixture. Inhal Toxicol. Feb 2004;16(2):87-91. [Medline].
• Guloglu C, Kara IH, Erten PG. Acute accidental exposure to chlorine gas in the Southeast of Turkey: a study of 106 cases. Environ Res. Feb 2002;88(2):89-93. [Medline].
• Gunnarsson M, Walther SM, Seidal T, Lennquist S. Effects of inhalation of corticosteroids immediately after experimental chlorine gas lung injury. J Trauma. Jan 2000;48(1):101-7. [Medline].
• Hedges JR, Morrissey WL. Acute chlorine gas exposure. JACEP. Feb 1979;8(2):59-63. [Medline].
• Heidemann SM, Goetting MG. Treatment of acute hypoxemic respiratory failure caused by chlorine exposure. Pediatr Emerg Care. Apr 1991;7(2):87-8. [Medline].
• Horton DK, Berkowitz Z, Kaye WE. The public health consequences from acute chlorine releases, 1993-2000. J Occup Environ Med. Oct 2002;44(10):906-13. [Medline].
• Jones RN, Hughes JM, Glindmeyer H, Weill H. Lung function after acute chlorine exposure. Am Rev Respir Dis. Dec 1986;134(6):1190-5. [Medline].
• Karellas NS, Chen QF, De Brou GB, Milburn RK. Real time air monitoring of hydrogen chloride and chlorine gas during a chemical fire. J Hazard Mater. Aug 15 2003;102(1):105-20. [Medline].
• Kaufman J, Burkons D. Clinical, roentgenologic, and physiologic effects of acute chlorine exposure. Arch Environ Health. Jul 1971;23(1):29-34. [Medline].
• Martinez TT, Long C. Explosion risk from swimming pool chlorinators and review of chlorine toxicity. J Toxicol Clin Toxicol. 1995;33(4):349-54. [Medline].
• Nelson LS. Simple asphyxiants and pulmonary irritants. In: Goldfrank LR, ed. Goldfrank's Toxicologic Emergencies. 6th ed. Stanford, Conn: Appleton & Lange;1998:1523-38.
• Parimon T, Kanne JP, Pierson DJ. Acute inhalation injury with evidence of diffuse bronchiolitis following chlorine gas exposure at a swimming pool. Respir Care. Mar 2004;49(3):291-4. [Medline].
• Roberge RJ, Martin TP. Relief of cough. Postgrad Med. 1997;101:46.
• Schwartz DA. Acute inhalational injury. Occup Med. Apr-Jun 1987;2(2):297-318. [Medline].
• Sexton JD, Pronchik DJ. Chlorine inhalation: the big picture. J Toxicol Clin Toxicol. 1998;36(1-2):87-93. [Medline].
• Shusterman D, Balmes J, Avila PC, et al. Chlorine inhalation produces nasal congestion in allergic rhinitics without mast cell degranulation. Eur Respir J. Apr 2003;21(4):652-7. [Medline].
• Shusterman D, Murphy MA, Balmes J. Influence of age, gender, and allergy status on nasal reactivity to inhaled chlorine. Inhal Toxicol. Oct 2003;15(12):1179-89. [Medline].
• Szerlip HM, Singer I. Hyperchloremic metabolic acidosis after chlorine inhalation. Am J Med. Sep 1984;77(3):581-2. [Medline].
• Tarlo SM, Broder I. Irritant-induced occupational asthma. Chest. Aug 1989;96(2):297-300. [Medline].
• Traub SJ, Hoffman RS, Nelson LS. Case report and literature review of chlorine gas toxicity. Vet Hum Toxicol. Aug 2002;44(4):235-9. [Medline].
• United States Army Medical Research Institute of Chemical Defense. Introduction, Pulmonary Agents. In: Medical Management of Chemical Casualties Handbook. 3rd ed.
• Vinsel PJ. Treatment of acute chlorine gas inhalation with nebulized sodium bicarbonate. J Emerg Med. May-Jun 1990;8(3):327-9. [Medline].
• Wang J, Zhang L, Walther SM. Inhaled budesonide in experimental chlorine gas lung injury: influence of time interval between injury and treatment. Intensive Care Med. Mar 2002;28(3):352-7. [Medline].
• Wang J, Abu-Zidan FM, Walther SM. Effects of prone and supine posture on cardiopulmonary function after experimental chlorine gas lung injury. Acta Anaesthesiol Scand. Oct 2002;46(9):1094-102. [Medline].
• Wang J, Zhang L, Walther SM. Administration of aerosolized terbutaline and budesonide reduces chlorine gas-induced acute lung injury. J Trauma. Apr 2004;56(4):850-62. [Medline].

Article Last Updated: Oct 10, 2006