Diphosgene Exposure 

  • Author: Paul P Rega, MD, FACEP; Chief Editor: Robert G Darling, MD, FACEP   more...
 
Updated: Jun 3, 2011
 

Background

Diphosgene (DP, trichloromethylchloroformate) was a product of the chemical weapons race in World War I. It belongs to a class of chemicals termed lung-damaging agents or choking agents. These agents attack lung tissue directly, causing pulmonary edema. Diphosgene is described not only as a respiratory irritant but also as a lacrimator. The lacrimatory effect makes diphosgene more easily detected than phosgene (CG). The mechanism of action is not well understood, but the chemical is believed to react directly upon the alveolar and capillary walls. The production of leukotrienes and the excessive accumulation of neutrophils may affect the alveolar sites sufficiently to cause pulmonary edema.

The Germans staged the first major successful chemical attack of the war using chlorine. Chlorine then was replaced by phosgene, which caused greater casualties. Gas masks of the era were designed to filter out phosgene. Diphosgene was created by combining phosgene with chloroform, which destroyed the gas filters, and it was first utilized in the field in May 1916. Blistering and nerve agents largely have replaced the pulmonary agents chlorine, phosgene, and diphosgene.

In the field, diphosgene (DP) rapidly vaporizes and breaks down into phosgene and chloroform. It is a colorless gas under standard temperatures and pressures, but it can also be found as an oily, colorless liquid. It emits an odor reminiscent of green corn or new mown hay. Its lethal dose is 3000 mg ⋅ min/cubic meter for 50% of exposed resting adults. Clinically, DP behaves in essentially the same manner as phosgene. The chloroform does not reach levels sufficient to cause toxicity, even of the liver, during tactical employment. DP is heavier than air and remains in low-lying areas for longer periods. Therefore, children are at increased risk for a greater absorption of the agent. Doses are cumulative, since DP is not detoxified in the body. Symptoms may be delayed for more than 3 hours after exposure with minimal contact, but in the presence of high concentrations, the effects will be immediate, especially with its strong lacrimator action.[1]

Diphosgene deployment almost surely indicates a purposeful, not an accidental, event. Industrial accidents have occurred with both chlorine and phosgene but not with diphosgene, which is not a normal product of manufacturing processes. It also is relatively unstable and degrades easily into phosgene and chloroform. Diphosgene must be transported in glass (instead of metal) containers. No automatic detectors are available for use in the field.

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Pathophysiology

Like phosgene, the principal feature of diphosgene (DP) is delayed pulmonary edema. Although the mechanism is not entirely clear, edema may be caused by direct alveolar damage when diphosgene breaks down into hydrochloric acid and carbon dioxide in the presence of water. DP also causes irritation of the upper respiratory tract and rarely can cause airway obstruction. Respiratory effects occur at doses of 1-10 ppm. Doses greater than 25 ppm can be rapidly fatal. Toxicity varies with both the concentration of vapor and the length of exposure. Because of the low water solubility of diphosgene, patients often inhale significant amounts of vapor before symptoms appear.

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Contributor Information and Disclosures
Author

Paul P Rega, MD, FACEP  Assistant Professor, Department of Public Health and Preventive Medicine, The University of Toledo College of Medicine; Assistant Professor, Department of Emergency Medicine, The University of Toledo College of Medicine; Director of Emergency Medicine Education and Disaster Management, OMNI Health Services

Paul P Rega, MD, FACEP is a member of the following medical societies: American College of Emergency Physicians and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

Mark Keim, MD  Senior Science Advisor, Office of the Director, National Center for Environmental Health, Centers for Disease Control and Prevention

Mark Keim, MD is a member of the following medical societies: American College of Emergency Physicians

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Rick Kulkarni, MD 

Rick Kulkarni, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine

Disclosure: WebMD Salary Employment

John D Halamka, MD, MS  Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center

John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Chief Editor

Robert G Darling, MD, FACEP  Adjunct Clinical Assistant Professor of Military and Emergency Medicine, Uniformed Services University of the Health Sciences, F Edward Hebert School of Medicine; Associate Director, Center for Disaster and Humanitarian Assistance Medicine

Robert G Darling, MD, FACEP is a member of the following medical societies: American College of Emergency Physicians, American Medical Association, American Telemedicine Association, and Association of Military Surgeons of the US

Disclosure: Nothing to disclose.

Acknowledgments

The authors and editors of eMedicine gratefully acknowledge the contributions of previous authors, Eric Mowatt-Larssen, MD, and Timothy Vollmer, MD, to the development and writing of this article.

References
  1. American Academy of Orthopedic Surgeons, Stewart CE. Pulmonary Agents. In: Stewart CE. Weapons of Mass Casualties and Terrorism Response Handbook. Boston: Jones & Bartlett; 2006:42 (Ch.4).

  2. Chemical Casualty Care Division USAMRICD. Medical Response to Chemical Warfare and Terrorism. 3rd ed. 1997:i-xiv, 1-8.

  3. Choking Agents. Defense Treaty Inspection Readiness Program. Available at http://dtirp.dtra.mil/tic/treatyinfo/vd_comp05.htm. Accessed June 13, 2007.

  4. Compton JAF. Diphosgene. In: Military Chemical and Biological Agents. 1987:124-134.

  5. Givens M. Phosgene and toxic gases. In: Keyes DC, Burstein LJ, et al, eds. Medical Response to Terrorism, Preparedness and Clinical Practice. Philadelphia, Pa: Lippincott Williams & Wilkins; 2005.

  6. Lillie SH, Hanlon E, Kelly JM, eds. Potential Military Chemical/Biological Agents and Compounds (FM3-11.9). Jan 2005.

  7. Micromedex. PoisinDex [Web site]. Phosgene. Accessed September 8, 2000.

  8. Nelson LS. Simple asphyxiants and pulmonary irritants. In: Goldfrank's Toxicologic Emergencies. 6th ed. 1998:1523-1538.

  9. Traub SJ. Respiratory agent attack (toxic inhalational injury). In: Ciottone GR, Anderson PD, Auf Der Heide E, Darling RG, Jacoby I, Noji E, Suner S, eds. Disaster Medicine. 3rd ed. Philadelphia, PA: Mosby/Elsevier; 2006:chap 93; 573-575.

  10. Urbanetti JS. Toxic inhalation injury. In: Textbook of Military Medicine. Part 1. 1997:247-270.

  11. US Army. Diphosgene. General Reimer Digital Library [Web site]. Accessed September 27, 2000.

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