Continuing Education Activity

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.
Most incidents of chlorine exposure are through accidental industrial or household exptoosures.
Toxicity to chlorine gas depends on the dose and duration of exposure. 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. This activity reviews the evaluation and
treatment of chlorine gas toxicity and highlights the role of the interprofessional team in
managing the patients affected by it.
Objectives:
 Describe the pathophysiology of chlorine gas toxicity.
 Summarize the epidemiology of chlorine gas toxicity.
 Outline the typical presentation of a patient with chlorine gas toxicity.
 Summarize the importance of improving care coordination among the interprofessional
team to enhance the delivery of care for patients affected by chlorine gas toxicity.
Earn continuing education credits (CME/CE) on this topic.
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Introduction
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.[1]
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.
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Etiology
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.
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Epidemiology
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.[2]
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.[3]
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.
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Pathophysiology
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.[4]
 Cl2+ H2O <--> HCl + HOCl <--> 2HCl + O-
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.[5][6]
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.
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Toxicokinetics
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.[4]
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History and Physical

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.[4]
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Evaluation
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.
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Treatment / Management
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.[7]
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Differential Diagnosis
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.
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Prognosis
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.[8]
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.[7][9]
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Complications
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.[10]
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Deterrence and Patient Education

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.
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Pearls and Other Issues

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.
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Enhancing Healthcare Team Outcomes

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]