Practice Essentials
Diphosgene (DP, trichloromethylchloroformate), which was created by combining phosgene with chloroform, 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. 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 first major successful chemical attack of World War I, which was staged by the Germans, used chlorine. Chlorine then was replaced by phosgene, which caused greater casualties. Gas masks of the era were designed to filter out phosgene. Diphosgene 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 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, diphosgene 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. Diphosgene 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 diphosgene 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. [2] Diphosgene must be transported in glass (instead of metal) containers.
Research is ongoing with regard to developing a sensitive, cost-effective, easy-to-use environmental sensing instrument that could detect a diphosgene release efficaciously. One device that shows promise is a high-resolution proton-transfer-reaction time-of-flight mass spectrometry (PTR-TOFMS) instrument. [3, 4]
Pathophysiology
As with phosgene, the principal feature of diphosgene (DP) exposure 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, exposed persons often inhale significant amounts of vapor before developing symptoms.
DP vapor is heavier than air. It decomposes on heating and produces toxic and corrosive fumes including chlorine and phosgene. DP also reacts with water to produce toxic and corrosive fumes. [5]
Patient Education
Alert patients about returning to the emergency department or contacting 911 if they develop respiratory changes, such coughing, wheezing, or shortness of breath. For patient education information, see Biological and Chemical Weapons.
