To access the remainder of this piece of premium content, you must be registered with Firehouse. Already have an account? Login
Register in seconds by connecting with your preferred Social Network.
Complete the registration form.
The lethal dose of liquid mustard applied to the skin is about seven grams spread over 25 percent of the body surface area. The threshold for skin erythema and blistering is 10 micrograms (a microgram is one millionth of a gram) per square centimeter deposited on the skin. The median lethal dose (LD50, or lethal dose for 50 percent of the population) for ingestion of mustard is estimated as 0.7 mg/kg of body weight. Damage occurs primarily to the skin, eyes and respiratory tract.
Vapor threshold doses of mustard that cause effects to the eyes are 0.1 Mg/M3 over 10 to 30 minutes of continuous exposure. Doses of 200 mg-min/m3 may cause corneal edema (swelling and fluid buildup within the cornea), keratitis (inflammation of the cornea) and blepharospasm (uncontrolled winking), leading to temporary blindness.
Irritation of the nasal mucous membranes and hoarseness first occur at doses ranging from 12 to 70 mg-min/m3. Lower respiratory effects, such as tracheobronchitis (bronchitis or inflammation of the trachea), tachypnea (excessively rapid respirations), cough and bronchopneumonia (inflammation of the lungs), begin to occur with doses exceeding 200 mg-min/m3.
Mild skin erythema may be seen with doses of 50 mg-min/m3. Severe erythema, followed by blistering, may begin at concentration-time profiles exceeding 300 mg-min/m3. Warm, humid environments may cause the earlier development of erythema and blistering at lower doses. The maximum safe doses for mustard have been established as 5 mg-min/m3 for skin exposure and 2 mg-min /m3 for eye exposure. The threshold limit value-time weighted average (TLV-TWA) for mustard is 0.003 mg/m3.
The Immediately Dangerous to Life and Health (IDLH) measure for mustard is recommended at 1.67 mg/m3. There is no known antidote for mustard agent. Mustard has been established as a human carcinogen.
Unless decontamination occurs within seconds after exposure to mustard, the results will be minimal. Hypochlorite solutions or large volumes of water are used to attempt to flush the agent from affected tissues. If decontamination is begun after symptoms start, it will have no effect.
Mustard enters the body through the cells of the skin or mucous membranes and produces biochemical damage within seconds ; no known procedure can reverse the process. Treatment of mustard exposure is much the same as for thermal burns and involves managing the symptoms and lesions (blisters). Mustard is rapidly transformed when it contacts the tissues in the body but is not found to be present in the blood, blister fluid, tissue, or urine.
Photo by Robert Burke
A powered air-purifying respirator (PAPR) uses a battery-operated blower designed to deliver decontaminated air at a slight positive pressure into a full facepiece.
Mustard exposures are rarely fatal and patients recover over a period of months. In World War I, one third of all U.S. casualties were the result of chemical exposure (sulfur mustard) but the fatality rate was only 5 percent.
Lewisite is a vesicant believed to have been used by Japan against China in the 1930s. It has no other known battlefield uses. Phosgene oxime is also a vesicant which has not been used on the battlefield.
Mustard is found in artillery shells, mortar shells, land mines and ton containers, which are similar to the ton containers used to ship and store chlorine. It is not likely that mustard would be used in terrorist activity because of the time it takes for mustard to act and its low volatility; however, if it were to be used, many hours would pass before the symptoms began to surface. This time delay would make diagnosis and determination of the incident source difficult.
Nerve agents are the most toxic of all chemical agents used in weapons. Nerve agents are nothing more than close relatives of organophosphate pesticides; however, military nerve agents are much more toxic. In fact, many of the nerve agents were discovered by chemists trying to make new pesticides.
Pesticides generally work by interfering with the functions of the central nervous system, and nerve agents act by the same means. Some common organophosphate pesticides include Malathione and Parathion. Another group of pesticides called carbamates cause the same type of central nervous system damage as the nerve agents although they are not related chemically. A common carbamate is the pesticide Sevin. Nerve agents were discovered in the 1800s but their toxicity was not realized until the early 1900s.