Gaseous chlorine is poisonous and classified as a pulmonary irritant. It has intermediate water solubility with the capability of causing acute damage to the upper and lower respiratory tract. Chlorine gas has many industrial uses, but it was also once used as a chemical weapon in World War I. Today, most incidents of chlorine exposure are through accidental industrial or household exposures. As for industrial exposures, there have been several instances of train accidents carrying liquid chlorine that caused the release of chlorine gas to the surrounding environment. At home, a mixture of chlorine bleach with other household products that contain acid or ammonia is a common source of exposure to chlorine gas.
Toxicity to chlorine gas depends on the dose and duration of exposure. At concentrations of 1 to 3 ppm chlorine gas acts as an eye and oral mucous membrane irritant, at 15 ppm there is an onset of pulmonary symptoms, and it can be fatal at 430 ppm within 30 minutes.
Because of its strong odor, chlorine gas can be detected easily. Symptoms of chlorine gas exposure include burning of the conjunctiva, throat, and the bronchial tree. Higher concentrations can produce bronchospasm, lower pulmonary injury, and delayed pulmonary edema.
Chlorine gas can be used as a disinfecting agent at swimming pools, or it could form by mixing household agents. The combination of bleach (sodium hypochlorite) with acid produces chlorine gas, a heavy green-yellow gas with a strong odor. Chlorine gas has also been used as an industrial solvent and has other industrial uses such as the production of bulk materials, bleached paper products, plastics such as PVC, and solvents. Chlorine gas is also used to make dyes, textiles, paint, and even medications.
Chlorine gas is pressurized and cooled for easy storage in liquid form. When released, the liquid form of chlorine quickly turns into yellow-green colored gas with an irritating odor. Since chlorine is heavier than air, it accumulates in low-lying areas.
Chlorine gas has been used as an agent of war as recently as 2007 in Iraq.
In 2016, the American Association of Poison Control Centers reported over 6300 exposures to chlorine, making it the most common inhalational irritant in the United States. About 35% of exposures to chlorine gas were attributed to mixing of household acid with hypochlorite.
In addition to household exposure, there have been multiple episodes of incidents involving chlorine gas release. One of the worst was a 2007 collision of a railroad tanker carrying chlorine with another train causing rupture of the tank and release of 90 tons of chlorine gas into the surrounding area. Exposure to chlorine gas at the site of the accident resulted in 9 fatalities and 520 visits to local emergency departments in Graniteville, South Carolina.
Chlorine gas is also the most frequent cause of major toxic release incidents internationally. Because of its widespread industrial use, chlorine gas has substantial potential for accidental release.
Besides household and industrial accidental exposures, chlorine gas has also been used as an agent of war. Germany used chlorine gas in World War I as a chemical weapon. More recently in 2007 insurgents in Iraq executed multiple attacks by outfitting chlorine tankers with explosives and detonating them in multiple locations causing hundreds of civilian casualties.
Chlorine was thought to cause direct tissue damage by generating free oxygen species. However, more recent studies show that cellular injury may result from oxidation of functional groups in cell components from the reaction of chlorine gas with tissue water. This reaction forms hypochlorous and hydrochloric acid along with free oxygen radicals.
Hypochlorous and hydrochloric acid cause most of the toxic effects attributed to chlorine gas. These acids are produced by the reaction of chlorine (Cl2) with water.
Mild exposure may cause mucosal membrane irritation. More severe exposure will induce edema of both the upper airway and the lung parenchyma. Large acute exposure can induce wheezing, cough, and dyspnea. Acute lung injury and/or adult respiratory distress syndrome (ARDS) can also be seen in some severe cases. Chlorine gas is primarily reactive only at a local level, thus absorbed systemic effects are not commonly observed.
Acids formed by the reaction of chlorine gas with water can react with the conjunctival mucous membrane, and although rare due to buffering by the tear film, can cause burns and corneal abrasions. These acid burns are generally superficial, only affecting the epithelial and basement membrane.
Experimental studies using a low concentration of chlorine gas show that the upper airway absorbs the vast majority of inhaled chlorine. The lower respiratory tract absorbs only 5% of chlorine gas. Animal models suggest that chlorine gas absorbed in the lower respiratory tract causes much greater toxicity than similar amounts in the upper airway. Thus, the upper airway functions as a protective scrubber to the exposure of chlorine gas.
When exposed to low concentration chlorine gas (up to 2 ppm) mucous membrane irritation results. Higher concentration exposures between 9 ppm and 50 ppm may lead to chemical pneumonitis and bronchiolitis obliterans. In animal models, exposure to 200 ppm leads to extensive bronchial constriction. Exposure to levels of 800 ppm proves lethal to half of all exposed animals while concentrations of 2000 ppm lead to immediate respiratory arrest.
Symptoms of chlorine gas exposure are usually varied depending on the type of exposure. For acute exposure at low levels (less than 5 ppm), patients can have lacrimation, nose and throat irritation, and excess salivation. Acute exposure at high levels causes dyspnea, violent cough, nausea, vomiting, lightheadedness, headache, chest pain, abdominal discomfort, and corneal burns in addition to the same symptoms of low-level acute exposure. Chronic exposure to chlorine gas can lead to chest pain, cough, sore throat, and hemoptysis.
On physical exam, clinicians can discover respiratory findings such as tachypnea, cyanosis, wheezing, intercostal retractions, decreased breath sounds, rales, nasal flaring, stridor, hemorrhage of the respiratory tract, and rhinorrhea. Non-respiratory findings may include tachycardia, lacrimation, and salivation.
Most patients should have pulse oximetry performed if possible. Mass casualty exposures may require triage of resources to those with more obvious symptoms. Acutely, exposed patients with significant symptoms frequently will require a chest radiograph to determine the degree of lower respiratory tract involvement. Those with pronounced systemic symptoms (vomiting, altered mental status, acidosis, among others) will require laboratory evaluation which may include serum electrolytes, BUN and creatinine levels, arterial blood gas analysis, and electrocardiography. After stabilization pulmonary function testing, ventilation-perfusion testing, and laryngoscopy/bronchoscopy are occasionally used to determine the extent of the injury.
Treatment of chlorine gas exposure is mostly supportive. Removal of the individual from the contaminated environment is the first step of management. Clinicians will assess the patient’s airway, breathing, and circulation, and provide humidified oxygen as necessary. Severe exposures may require endotracheal intubation. In cases of non-cardiogenic pulmonary edema, positive end-expiratory pressure (PEEP), fluid restriction, and diuretics can be used. Bronchospasm is treated with beta-agonists such as albuterol. The management of ocular exposure requires irrigation with copious water or saline.
If irritation continues, clinicians should evaluate for corneal abrasion. Nebulized, 4% sodium bicarbonate may prove helpful as an adjunct treatment of chlorine gas exposure, although experience with this treatment is limited. Research has not yet proven any benefit to corticosteroids nor the administration of systemic nitrites as a treatment for chlorine gas exposure.
Most exposures to chlorine gas will present with a clear history of exposure obtained either from the patient themselves or first responders arriving from the scene. From prior exposures at chlorinated swimming pools, most patients will recognize the distinct odor of chlorine gas. Rarely a patient in respiratory distress and altered mental status may be found after the complete dispersal of chlorine gas making the history unclear. Salivation, lacrimation, rhinorrhea, and bronchospasm can occur in cholinergic toxicity as well as chlorine gas exposure.
Chlorine gas exposure usually has a good prognosis with most exposed individuals recovering without significant residual deficits. Pulmonary edema appears to be the most common cause of morbidity for moderate-to-severe exposures. This usually occurs within 2 to 4 hours of exposure to moderate chlorine concentration (25 to 50 ppm) or 30 to 60 minutes of severe exposure (greater than 50 ppm). Resolution of pulmonary abnormalities usually ensues in a week to a month after exposure. Smokers and patients with asthma are likely to have persistent obstructive pulmonary defects.
Studies on the long-term, adverse effects from acute chlorine exposure are inconclusive with some studies showing decreased vital capacity, diffusing capacity, and total lung capacity and others showing no consistent pattern of pulmonary function deficits.
Sloughing of the pulmonary mucosa can occur within 3 to 5 days in severe exposures leading to chemical pneumonitis that can often be complicated by secondary bacterial invasion and infection. Smoking and pre-existing respiratory conditions such as asthma and chronic obstructive pulmonary disease appear to increase the risk of long-term complication such as pulmonary fibrosis.
Attempts to reduce chlorine gas exposures focus on three strategies. First, improved transportation safety of a large volume liquid chlorine, typically transported by rail. Second, development and adherence to strict industrial protocols for the use of chlorine to prevent inadvertent industrial exposure. Third, consumer education about the risk of mixing cleaning chemicals. Providers will need to educate patients exposed to chlorine gas at their homes. Failure to understand the risks of mixing certain solutions may lead to repeated exposures.
Pulmonary or choking agents cause an inflammatory reaction when they come into direct contact with the eyes and upper airway. They can be life-threatening if inhaled. No specific antidote exists. Treatment is mainly supportive and consists of removal of the patient from the source, decontamination, airway maintenance, bronchodilator administration, and eye irrigation.
Chlorine gas poisoning is usually self-limited and mostly requires supportive treatment. Physicians and other health professionals including nurses, EMS workers, and physician assistants can play a vital role in educating the patient on prevention of a future episode in household cases of accidental exposure resulting from of mixing chlorine/bleach with other cleaning products. Although rare, if the poisoning was because of a suicide attempt, evaluation by a mental health professional should proceed discharge. an interprofessional team approach to decontamination and treatment is required for best patient outcomes. Specialty care nurses in emergency, prehospital, and flight are involved in triage, patient monitoring, and patient education. They monitor and provide updates to the team. Pharmacists review prescribed medication and drug-drug interactions. [Level V]
|||Chauhan S,Chauhan S,D'Cruz R,Faruqi S,Singh KK,Varma S,Singh M,Karthik V, Chemical warfare agents. Environmental toxicology and pharmacology. 2008 Sep [PubMed PMID: 21783898]|
|||Gummin DD,Mowry JB,Spyker DA,Brooks DE,Fraser MO,Banner W, 2016 Annual Report of the American Association of Poison Control Centers' National Poison Data System (NPDS): 34th Annual Report. Clinical toxicology (Philadelphia, Pa.). 2017 Dec [PubMed PMID: 29185815]|
|||Wenck MA,Van Sickle D,Drociuk D,Belflower A,Youngblood C,Whisnant MD,Taylor R,Rudnick V,Gibson JJ, Rapid assessment of exposure to chlorine released from a train derailment and resulting health impact. Public health reports (Washington, D.C. : 1974). 2007 Nov-Dec [PubMed PMID: 18051671]|
|||Das R,Blanc PD, Chlorine gas exposure and the lung: a review. Toxicology and industrial health. 1993 May-Jun [PubMed PMID: 8367885]|
|||White CW,Martin JG, Chlorine gas inhalation: human clinical evidence of toxicity and experience in animal models. Proceedings of the American Thoracic Society. 2010 Jul [PubMed PMID: 20601629]|
|||Schwartz DA, Acute inhalational injury. Occupational medicine (Philadelphia, Pa.). 1987 Apr-Jun [PubMed PMID: 3303382]|
|||Vajner JE 3rd,Lung D, Case files of the University of California San Francisco Medical Toxicology Fellowship: acute chlorine gas inhalation and the utility of nebulized sodium bicarbonate. Journal of medical toxicology : official journal of the American College of Medical Toxicology. 2013 Sep [PubMed PMID: 23719961]|
|||Brooks SM,Weiss MA,Bernstein IL, Reactive airways dysfunction syndrome (RADS). Persistent asthma syndrome after high level irritant exposures. Chest. 1985 Sep [PubMed PMID: 4028848]|
|||Francis HC,Prys-Picard CO,Fishwick D,Stenton C,Burge PS,Bradshaw LM,Ayres JG,Campbell SM,Niven RM, Defining and investigating occupational asthma: a consensus approach. Occupational and environmental medicine. 2007 Jun [PubMed PMID: 17130175]|
|||Jones RN,Hughes JM,Glindmeyer H,Weill H, Lung function after acute chlorine exposure. The American review of respiratory disease. 1986 Dec [PubMed PMID: 3789518]|