The symptoms of exposure during and after exposure include coughing, choking, tightness in the chest, nausea, and sometimes vomiting and headache.
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A symptom-free period will then follow, usually lasting from 2 to 24 hours. Thus, the symptoms of lung damage often do not manifest themselves until a few hours have passed and they are aggravated by physical exertion. Rest and medical observation are therefore essential.
As the pulmonary edema progresses, a frothing sputum develops. In these cases, the patient usually recovers with little or no residual damage. All contact with these agents should be avoided, specifically through the use of protective clothing, and breathing and eye protection. Blister agents, also referred to as vesicants, are some of the most common chemical weapons; they include mustard agents, Lewisite and phosgene oxime.
When inhaled, vesicants harm the respiratory tract; when ingested, they can cause vomiting and diarrhea. Blister agents can be dispersed as a liquid, aerosol, vapour or dust. Mustard agents are characterized by a latent symptom-free period, which usually lasts several hours, depending on the quantity of agent involved, the mode of exposure and environmental conditions.
In contrast, Lewisite and phosgene oxime both work quickly; symptoms, such as coughing and burning, appear almost immediately. Dispersed as a gas, blood agents enter the body by inhalation and are then distributed through the body via blood. They act to inhibit blood cells from using and transferring oxygen, thereby depriving the body of oxygen and essentially causing the victim to suffocate.
The emergence of symptoms of infection by blood agents may be delayed.
For example, exposure to arsine or cyanogen chloride can lead to severe lung, eye and skin damage, but these may not manifest themselves for several hours. Nerve agents may be dispersed as a liquid, vapour, aerosol or dust. For example, when the agent is inhaled, respiratory symptoms emerge first; when ingested, the first symptoms will be gastrointestinal.
Antidotes to nerve agents do exist and are stocked by some ambulance teams and hospitals, but because nerve agents work so quickly, these are only effective if introduced immediately after exposure. The use of chemical weapons is generally associated with the technological advances that created modern warfare in the 20th century. The U. Chemical weapons had been used extensively, and a new convention was being negotiated to reduce its use and development. However, the use of poison and disease in war, against soldiers and civilians alike, dates back much further. Below is a timeline of some key points in the history of chemical warfare.
Use of arsenical smokes by the Chinese.
Chemical Warfare Agents: Toxicity at Low Levels
The Assyrians poison enemy wells with rye ergot, and the Athenian magistrate Solon uses the purgative herb hellebore during the siege of Krissa. Spartans are reported to have used arsenic smoke during the Peloponnesian War. In , Germany uses gas warfare near Ypres in France. German troops used 6, cylinders, releasing tonnes of chlorine gas on both soldiers and civilians. Soon after, Britain and France also start to use gas.
By , one in every four artillery shells fired contains gas of one type or another. The use of chemical weapons during World War I causes 1 million casualties, more than 90, of which are fatal. It includes an article reaffirming the previous agreements regarding chemical weapons, and prohibiting the manufacture or importation of such weapons as well as their means of production by Germany. The protocol was broadly ratified with the exception of the United States and Japan.
This is the first open breach of the Geneva Protocol. Over the same period, Japan produces 8, tonnes and the United States produces , tonnes. These substances are more persistent than their forerunners, and are about ten times more poisonous than sarin. Late s Planes and helicopters delivering aerosols of several colours attack Laos and Kampuchea.
Some of these clouds are thought to be comprised of trichothecene toxins in particular, T2 mycotoxin. He died several days later. To date, States have signed the Convention; States have ratified it. The Convention enters into force on 29 April Due to the poor quality of the sarin agent and an ineffective dispersal system, casualties are lower than expected.
Later, the group is found to have been experimenting with anthrax and other biological agents. Durham Chair , Colin R. McArthur and Kenneth L. The lower the number, the more lethal the agent. Basic Facts about Tabun GA. Basic Facts about Soman GD. Basic Facts about Sarin GB. ABC News. Jeffrey K. Sidell, E. Takafuji and D. Such weapons might be: purchased from legitimate industrial suppliers; stolen from military installations; stolen from medical or scientific research facilities; or obtained from state sponsors which support terrorist activities.
Summary Table Causative agents.
Means of exposure. Lethal dosage Rate of action. Mode of action. Examples of commercial uses of chemicals or precursors. Choking agents.
Handbook of Toxicology of Chemical Warfare Agents - 2nd Edition
Delayed to rapid. Damages respiratory tract, causing extensive fluid build-up in the lungs. Shortness of breath; irritation of mucous membranes; coughing; tightness of chest Culminates in fluid build-up in lungs leading to fatal choking Vomiting, fluid build-up in lungs. Disinfectants, plastics, pesticides, solvents, chemical synthesis, dyes and herbicides. Blister agents. Rapid delayed symptoms for sulphur mustard.
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Causes blisters on skin and damages the respiratory tract, mucous membranes, and eyes. Skin blistering, respiratory tract damage, burning of the eyes. Paper and rubber manufacturing, pharmaceuticals, insecticides, plastics, detergents, cosmetics, lubricants, ceramics, toiletries, waxes and polishes. Blood agents. Interferes with the absorption of oxygen into the bloodstream.
Agents inhibit cell respiration; heart and central nervous system are susceptible Cyanogen chloride also greatly irritates eyes and lungs In moderate cases: vomiting dizziness deeper, more rapid breathing In severe cases: convulsions respiratory failure sudden loss of consciousness leading to death. Agents are highly volatile; flush eyes with water; remove contaminated clothing; rinse exposed skin with water Antidotes: intravenous administration of sodium nitrite and sodium thiosulfate for detoxification purposes Pretreatment under development in the UK.
Pesticides, fumigating, electroplating, gold and silver extraction, dyes, pigments and nylon production. The intraocular pressure IOP may increase and remain elevated for a few days. After several hours, the corneal epithelium begins to form vesicles and slough. In severely injured eyes, there is constriction of the pupils, dilatation of blood vessels within the iris, hemorrhages, and necrosis.
Pulmonary Chemical-Warfare Agents
Chemical anterior uveitis develops, leading to adhesions of the iris to the lens capsule with ensuing cataract formation. Late sequelae include corneal scarring and neovascularization as well as severe and chronic elevation of IOP due to neovascular glaucoma. Strong evidence indicates that mustard injury is mediated, at least in part, by the formation and action of reactive oxygen species ROS , in addition to its action as an alkylating agent. This notion is supported by the findings of a dramatic increase fold in copper levels 7 and a decrease in ascorbic acid within the anterior chamber 8 after ocular exposure to mustard compounds, both being indicators of oxidative stress.
Free radicals have also been shown to play a role in corneal inflammation after exposure to other ocular irritants, such as alkali substances. These reduced metal ions, in turn, can react with H 2 O 2 to produce the hydroxyl radical, which causes further damage. If indeed the formation of ROS is part of the pathogenesis of mustard-induced injury, curbing their formation could be highly beneficial.
Seventy-six New Zealand Albino rabbits weighing 2. Local anesthetic drops benoxinate HCl 0. The vacuum trephine was used to limit the area of application to a circle 4 mm in diameter in the center of the cornea. Immediately after application, NM was quickly absorbed from within the trephine, with small sponges Weck-Cel; Medtronicsolan, Jacksonville, FL , followed by washing of the eye within the trephine with copious amounts of normal saline.
The trephine was then removed, and the eye was again washed intensively with additional normal saline.
Local treatment was immediately initiated according to the protocol described below. In control eyes four additional animals, eight eyes , saline solution instead of NM was applied to the cornea for 5 minutes within the trephine. In control treatment, the vehicle saline was used as eye drops after exposure to NM.
This was necessary mainly during the first 5 to 10 days after injury.