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 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.
View Image
Chemical structure of chloropicrin.
Detection
The odor is a distinctive warning property of this liquid compound.
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.
Ingestion
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.
Injection
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. Exposed persons reported the following signs and symptoms:
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%)
Mortality/Morbidity
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.
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).
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.
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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]
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.
Inhalation
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.
Ingestion
Do not induce vomiting.
Rinse mouth immediately with water.
Have the victim drink milk, egg whites, or large quantities of water if available.
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.
Inhalation
Continue assisted ventilation and initiate artificial ventilation as needed to support pulmonary function.
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]
Ingestion
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.
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]
Clinical Context:
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.
Clinical Context:
In reduced form, leukomethylene blue is an electron donor to reduce methemoglobin. Reduction of methylene blue is by NADPH generated by G-6-PD.
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]
Kermit D Huebner, MD, FACEP, Research Director, Carl R Darnall Army Medical Center
Disclosure: Nothing to disclose.
Coauthor(s)
David N Trickey, MD, Staff Physician, Department of Emergency Medicine, Martin Army Community Hospital
Disclosure: Nothing to disclose.
Specialty Editors
Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Received salary from Medscape for employment. for: Medscape.
Chief Editor
Zygmunt F Dembek, PhD, MPH, MS, LHD, Associate Professor, Department of Military and Emergency Medicine, Adjunct Assistant Professor, Department of Preventive Medicine and Biometrics, Uniformed Services University of the Health Sciences, F Edward Hebert School of Medicine
Disclosure: Nothing to disclose.
Additional Contributors
Mark Keim, MD, Founder, DisasterDoc, LLC; Adjunct Professor, Emory University Rollins School of Public Health; Adjunct Professor, Harvard Affiliated Disaster Medicine Fellowship
Disclosure: Nothing to disclose.
Acknowledgements
The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous author, Joanne Williams, MD, to the development and writing of this article.
Dow AgroSciences. Material Safety Data Sheet: Chloropicrin. Available at http://www.vikanemonitor.com/images/chloropicrin_msds.pdf. 7/22/99; Accessed: October 16, 2018.
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