Chloropicrin Poisoning

Updated: Mar 15, 2022
Author: Kermit D Huebner, MD, FACEP; Chief Editor: Zygmunt F Dembek, PhD, MS, MPH, LHD 


Practice Essentials

Chloropicrin is a soil fumigant used for its broad biocidal and fungicidal properties, primarily in high-value crops such as strawberries, peppers, onions, tobacco, flowers, tomatoes, and nursery crops.[1]  John Stenhouse, a Scottish chemist and inventor, synthesized chloropicrin in 1848. Because chloropicrin is toxic by all routes of entry, it has the potential for widespread destruction as a chemical warfare agent.

For patient education information, see Chemical Burns, Chemical Warfare and Personal Protective Equipment.

Properties, stability, and reactivity

Chloropicrin is a colorless–to–light green oily liquid with an intense and penetrating odor. Even though chloropicrin is not flammable, it poses a significant explosion hazard if involved in a fire. Bulk containers of this liquid are shock sensitive and can detonate. Chloropicrin is an irritant to all body surfaces. This liquid decomposes in the environment. Photochemical reactions with chloropicrin produce phosgene; other decomposition products include nitrogen oxides and chlorine compounds.

Chloropicrin photodegrades, with a half-life of 20 days. It is known to undergo violent reactions with aniline, 3-bromopropyne, sodium hydroxide/alcohol solutions, sodium methoxide, and propargyl bromide. Hazardous polymerization does not occur with chloropicrin. The chemical structure of chloropicrin is portrayed in the image below.

Chemical structure of chloropicrin. Chemical structure of chloropicrin.


The odor is a distinctive warning property of this liquid compound.

Table. Symptoms According to Concentrations (Open Table in a new window)

1 ppm*

Irritation with pain in the eyes

4 ppm

Incapacitates exposed individuals

20 ppm

Causes definite bronchial or pulmonary lesions

*Concentrations expressed in parts of material per million parts of air or water.



Overexposure leads to irritation of the nose and throat. Chloropicrin is a lacrimator. Exposure to vapors leads to coughing, labored breathing, sore throat, dizziness, bluish skin, vomiting, and in some instances, chemical pneumonitis and pulmonary edema.[2]

Contact with skin or eyes

Contact with chloropicrin can lead to chemical burns or dermatitis manifested by red, cracked, irritated skin. The extent of skin injury depends on the concentration and duration of exposure. Contact with the eyes can cause pain, redness, and tearing. Prolonged eye exposure to chloropicrin can cause blindness. Entrance through damaged skin causes similar symptoms as those seen in overexposure through inhalation.


If ingested, chloropicrin can cause burns to the mouth, throat, and esophagus. Other symptoms are similar to those of overexposure through inhalation. Ingestion of large quantities of chloropicrin liquid can be fatal.


Overexposure to chloropicrin by injection can lead to redness and irritation of surrounding tissues. Other symptoms are similar to those of overexposure through inhalation.

Chronic exposure

Dermatitis may result from repeated exposure to chloropicrin.


Chloropicrin is commonly used as a soil fumigant for agricultural pest control.[3] Human exposures have occurred in the United States, usually in residential areas in close proximity to agricultural areas.

The most recently reported large-scale exposure occurred in Kern County, California, in 2003.[4] One hundred sixty-five people developed symptoms as a result of off-site drift of chloropicrin from a nearby agricultural site. Peak concentrations of chloropicrin were estimated to exceed 1 part per million. 



Fatal chloropicrin exposures have been reported. An intentional ingestion of 100 mL of chloropicrin sodium solution resulted in death from metabolic acidosis and acute heart failure approximately 7 hours after ingestion.[5]  Homicidal intoxication has also been reported, in which an 18-year-old female died approximately 4 hours after being sprayed with a liquid that was later determined to be chloropicrin. Postmortem examination demonstrated severe pulmonary edema.[6]

Elevations of creatine phosphokinase levels have been described in the setting of chloropicrin exposure and may represent some degree of rhabdomyolysis.[7]  Chloropicrin may cause methemoglobinemia.[8]




Clinicians should attempt to elicit an accurate history to involve the setting of exposure. This may occur as an occupational exposure, as an intentional and unintentional industrial release, or as a terrorist attack.


Physical manifestations depend on the route of exposure.

  • Skin - Evidence of chemical burns or dermatitis manifested by red, cracked, irritated, or bluish skin
  • Eyes - Pain, redness, and tearing
  • Respiratory - Coughing, labored breathing, rales, and rhonchi

In the large-scale exposure that occurred in Kern County, California, exposed persons reported the following signs and symptoms[4] :

  • Eye pain, burning, or lacrimation (in 99% of cases)
  • Respiratory symptoms, including cough, dyspnea, or upper respiratory irritation (51%)
  • Gastrointestinal complaints such as nausea, vomiting, abdominal pain, or diarrhea (47%)
  • Headache (25%)




Laboratory Studies

Laboratory testing should be dictated by clinical presentation and condition of the patient. The provider may consider addition of creatine kinase (CK) and blood gases with co-oximetry. Chloropicrin may be detected by gas chromatography/mass spectrometry (GC/MS).



Prehospital Care

General considerations

The rescuer's protective equipment should be Level A (eg, triple gloves [polyethylene gloves and nitrile gloves over latex gloves], fully encapsulating chemical resistant suit and boots, hard hat, self-contained breathing apparatus). See the image below.

Level A suit (DuPont Tychem 10,000). Level A suit (DuPont Tychem 10,000).

Standard organic vapor filters used with gas masks or air-purifying respirators do not remove chloropicrin effectively.[9]

Initial treatment is primarily supportive. It includes symptomatic treatment of early adverse health effects and support of respiratory function. Patients should be kept warm and quiet to minimize the effects of accumulation of fluid in the lungs/pulmonary edema that may occur with severe exposures.[10]

Skin exposure

Immediately begin decontamination with running water. Flush for a minimum of 15 minutes. Remove contaminated clothing, taking care not to contaminate eyes further.

Eye exposure

If possible, open victim's eyes while under gentle running water. Use sufficient force to open the eyelids. The victim must "roll" the eyes. Flush for a minimum of 15 minutes.


Remove the victim to fresh air. Provide assisted ventilation as needed to support pulmonary function. Cover or remove gross contamination to avoid exposure to rescuers. Monitor for spasmodic narrowing of the large airways, and treat bronchospasms with beta2 agonists and corticosteroids. Monitor for laryngospasm, and treat it if it occurs.  Examine the mucous membranes for corrosive effects.[10]


Do not induce vomiting or administer charcoal.[10]   Rinse mouth immediately with water. Have the victim drink milk, egg whites, or large quantities of water if available.

Emergency Department Care

Skin exposure

If not completed in the field, continue decontamination with running water for at least 15 minutes.

Eye exposure

If not completed in the field, continue flushing for at least 15 minutes.


Continue assisted ventilation and initiate artificial ventilation as needed to support pulmonary function. Obtain a baseline chest x-ray and monitor respiratory function for 24 hours.[10]

In severe respiratory compromise, ventilatory support is mandatory. If a PaO2 cannot be maintained above 60 mm Hg with a fraction of inspired oxygen (FIO2) of 0.6 or less, then add positive end-expiratory pressure in an attempt to open previously closed alveoli.

For methemoglobinemia greater than 10-20%, consider administration of methylene blue 1-2 mg/kg as a 1% solution intravenously over 5 minutes, followed by a 15-30 mL flush.[8]

Signs of pulmonary edema may not be evident early after exposure. Observation for 24-48 hours for progression or worsening of symptoms is recommended.[8]


Contact poison control for the most current information.  Do not induce vomiting. Administer large quantities of water. Do not give diluents to a patient who is convulsing, unconscious, or unable to swallow.

Following ingestion exposure, gastric aspiration and endoscopic examination of the esophagus and stomach are recommended within 24 hours of exposure.[10]




Medication Summary

Albuterol and aminophylline may be beneficial in cases involving signs of bronchoconstriction. Use supplemental humidified oxygen in cases of respiratory compromise. For methemoglobinemia greater than 10-20%, consider the use of methylene blue.[8]

Sympathomimetic (adrenergic) agents

Class Summary

These agents relieve reversible bronchospasm by relaxing smooth muscles of the bronchi.

Albuterol (Ventolin)

Stimulates beta-adrenergic receptors. Main effect following oral inhalation is bronchodilation resulting from smooth muscles of bronchial tree. In event of chloropicrin intoxication, use nebulizer route of administration.

Respiratory smooth muscle relaxant

Class Summary

Aminophylline relieves bronchospasm through smooth muscle relaxation of respiratory tract, thereby increasing flow rates and vital capacity.

Aminophylline (Aminophyllin)

Theophylline compound with ethylenediamine; structurally classified as xanthine derivative. Directly relaxes smooth muscle of respiratory tract.


Class Summary

This agent is used to reduce methemoglobin.

Methylene blue (Urolene blue)

In reduced form, leukomethylene blue is an electron donor to reduce methemoglobin. Reduction of methylene blue is by NADPH generated by G-6-PD.