Qandil short field manual for five chemical and biological agent

Nerve Agents
Organophosphate (organophosphorus) pesticides (insecticides) were developed in Germany in the mid of 1930s. Their mechanism of action is by inhibition of the aceylcholinesterase. They attack to the molecule of the enzyme and inactivate it. (See Basic Neurophysiology). This is true for small insects as well as for large animals and human beings.
Subsequently nerve agents were developed specifically for military purposes. The mechanism of action is the same as for insecticides, and in fact they are organophosphorus compound just the same. On by weight proportion they are just as lethal for insects as they are for human being. The Lethal Dose of, for instance, Sarin, is less then 0,1 mg/Kg. For a person of 60 kg weight this means that a drop containing less then 6 mg of Sarin in contact with the skin will result in death in at least 50% of the cases. Precursor of Sarin such as isopropyl alcohol and hydrogen fluoride are abundantly available in the international market. There are mainly four agents possibly available, their difference is on the physical rather than chemical properties. That is they are more or less persistent, which means remaining on the surfaces maintaining their toxicity, Vx is the most persistent, and least volatile. Sarin is the most volatile and the. least persistent. Tabun and Soman are intermediate between the two.
Tabun (O-ethyl dimethylamidophosphorylcyanide), also called GA, is the first that was synthesised, in 1936, at the IG Farben factory in Germany. It is also the easiest to produce. It was manufactured industrially in 1942, and in two years 12,000 tons were produced.
Sarin, (isopropyl methylphosphonofluoridate) also called GB, was also synthesised in Germany in 1938 and industrially produced in 1945 in small amount (only half a ton was made) Soman (pinacolyl methylphosphonofluoridate) also called GD, was first synthesised on 1944
Opposite to the first world war no chemical agents were used in the western battlefront during world war II (In 1936-37 the Italian army used "gas" in the invasion of Ethiopia, and the Japanese allegedly used "gas" in the invasion of China).
After the war, on the 1950s in USA a new class of agents was investigated, both in order to find more powerful insecticides (and conversely more toxic to human) and better defense against nerve agents. These were called collectively V-agents. In 1955 Amiton was industrially manufactured as a powerful insecticide. However it was soon taken off the market because was too toxic to human and animals. In 1961, in USA, industrial production for military use of an agent called Vx was started.
Vx (O-S-diisopropylaminomethyl-methylphosphonothiolate) is approximately ten fold more powerful than Sarin.
All the four agents described are moderately soluble in water with slow hydrolysis, highly soluble in lipids (oil) and rapidly inactivated by strong alkalis and chlorinated compounds. It is for these reasons that hypochlorite (bleach), water, and water and soap are useful decontaminating agents. Nerve agents are, in pure status, colorless liquid. Impure thy are yellowish brownish. Pure Sarin is odorless, but said to have a pungent odd smelling when in use. Pure Tabun has a faint smelling of fruits and might develop, when used, a faint odor of bitter almond because of its cyanide content. Pure Soman is also having a faint smelling of fruits and can have a smell of camphor when in use. Pure Vx is odorless.

Detection
All four agents may be detected by various mean. Paper three colors detectors can be used to test liquids. (None available presently in North Iraqi Kurdistan)

Protection
Normal clothing is penetrated by all these agents, as is the skin. This is true for liquid or vaporized agent. Fortunately the absorption of vapors through the skin is slow, a contaminated area can be passed by if respiratory and eye protection is available. Otherwise one has to hold the breath and run away. In a car close the window hold the breath and get as distant as possible before reopening the windows and breathing. Only full gear total body suit with hood and mask and overboots gives protection. For liquid form and contaminated wet surface non touch technique, such as holding the contaminated item by a plastic foil or bag while wearing surgical gloves, should be used, remembering persistence can last for weeks. For vapor contamination, as in case of Sarin, one has to wait for the agent to be dissipated by air motion.

Prevention
Carbamate pyridostigmine, if available, should be given at the dose of 30 mg every 8 hours. It would start being effective some two hours after the first dose, but full benefit is only after the third dose. The mechanism of action of pyridostigmine is by reversible binding to acetylcholinesterase. The enzyme bound to pyridostigmineis is therefore kept protected by the binding with the organophosphate (nerve agent). For reason related to the strength of the binding the enzyme can resume or keep its function after being bound with pyridostigmine, while the binding with the nerve agent is much more damaging because is stronger and longer lasting. Actually in the case of Soman the binding with acetylcholinesterase. hardly breaks down at all, is irreversible. So the mechanism of action of pyridostigmine is by competitive binding.
Pyridostigmine has been used extensively during the Gul War of 1991, The tablets were taken for a periods of 4 to 5 days by troops deemed at risk. Uncontrolled studies on some 42,000 troops have shown that the tolerance, at the given dosage, was good. About half of the soldiers had loose stools abdominal cramps and nausea. Other effects were rhinorrhea, sweating, headache, urinary urgency, tingling of the extremities. These symptoms were not requiring suspension of treatment of from duties. Symptoms would ameliorate taking the drug with food.
However other sources would see in the use of pyridostigmine a potential cause of the so called Gulf Syndrome, an ill defined series of disturbances common among Gulf War veterans.

Sings and symptoms
Sings and symptoms are basically of three types and cause by

the excessive amount of acetylcholine in the muscarinic receptors of neural junction in the smooth cell and glands of the Peripheral Nervous System, affecting salivation, sweating, gastrointestinal motion, urinary motion, pupil size, bronchial secretion and bronchial spasm.
the excessive amount of acetylcholine in the Central Nervous System interneuronal junctions of the type where transmission is done by this neurotransmitter, causing confuse behavior, depression of the respiratory center, and even convulsion
the excessive amount of acetylcholine in the neuromuscular junction of all skeletal muscles, causing twitching, fasciculation, weakness, and ultimately fatigue and non function. . There will be involuntary muscular twitching in all part of the body, scattered muscular fasciculations and occasional muscle cramps.

As is the case with all poisons and toxic substances, the intensity and severity of the symptoms vary with the amount of toxic substance absorbed and individual sensibility. Accordingly the timing of onset will vary. Intense exposure will cause convulsion and respiratory arrest. Death occurs rapidly without orderly progression of symptoms. The description of the clinical picture is therefore valid for minimal to mild to moderately severe cases. This are the ones which would benefit most from both decontamination and supportive treatment.
One has to expect a number of cases with headache, nausea, small pin pointed pupils, running nose (rhinorrhea), intense salivation and drooling, diffuse muscular twitching and fasciculations. Though muscarinic receptor stimulation will bring a picture of so called parasympathetic hyperactivity, and hence one would expect bradycardia, yet increase level of acetylcholine in the sympathetic ganglions can increase the sympathetic tone as well, and tachycardia could be present instead.
All the symptoms can progress to a worse picture of confusion (CNS effect), wheezing and difficulty in breathing (muscarinic effect on bronchi with increased secretion and bronchial constriction particularly the smallest bronchi), nausea and vomiting (muscarinic effect on the gastgrointestinal tract) severe muscular twitching and generalized muscle weakness (nicotinic effect on the skeletal muscles).
In a worse yet phase there will appear respiratory failure and hypoxia (caused by both respiratory muscle fatigue and obstruction of small bronchi by secretion plus constriction), convulsion and unconsciousness (by direct CNS effect compounded by hypoxia. Involuntary urination and defecation might come at this stage.

Treatment
The basic treatment will be postural drainage of secretion and Atropine injection, 2 mg IM. If suction available can be used for short times, two three seconds, then a long interval so the patient can breath. Excessive prolonged suction will suck air and oxygen out of the lung. Atropine to be repeated if necessary after half an hour, up to three times. Diazepam (Valium) should be given 10 mg per os. Diazepam IV slowly should be reserved for convulsion. Postural drainage of bronchi combined with Atropine will help the respiration and counteract all muscarinic symptoms and somewhat the CNS effects.
If possible -if available- Atropine will be givencombined with pralidoxime I.M. such as in the MARK I Kit –containig 600 mg of pralidoxime chloride-. This also can be repeated after half an hour, up to a total of three times. I.V. pralidoxime is reserved, if available, for hospital use (Adults 1-2 grams IV bolus over ten minutes initially, children 20-50 mg/Kg IV over thirty minutes, to be repeated after one to two hours, and then every twelve hours according to symptoms, or as continuous infusion IV at the dose of 10-50 mg/Kg/hour up to 500 mg per hour, for 24 hours).

Decontamination
Since prolonged exposure to small amount of agent on the skin will progress to cause severe symptoms, decontamination is necessary. Localized sweating on the skin areas affected is a sure sign of localization of here the agent has been in touch with the skin.
Fortunately, for the chemical nature of the agents the decontamination for the nerve agents is the same than for Mustard agent. It will be based on the use of chlorinated water and water and soap. Chlorination of water will be with 10 cc of bleach (which is about 4,5% hypochlorite) added to one liter of water. This will give a chlorination of water of about 0,05%, For eyes and mucosae and open wound one cc. f bleach per liter (concentration 0,005%) should be used.
Procedure will be the same as for mustard: use surgical gloves, undress the patients and place clothes in a plastic bag. This bag will be placed in a second bag to be closed by one other person. Bag will be given to relatives to bury it or wash it with chlorinated water. Caution must be used with water employed for it is to be assumed contaminated and potentially contaminating. Urines and feces of patients are not contaminating. Remember the gloves employed are themselves contaminated, fresh clothing should not be handle with gloves wearing hands which have done the decontamination. If appropriate ad hoc showers are available, one should add bleach to the water tank in the proportion given, which is 10 cc of 5% bleach per liter of water. The shower area should be decontaminated in between patients with higher concentration of bleach chlorinated water with common household detergent added using common floor cleaning swap.
Little protection if any is given by surgical mask, one should remember it always. However the risk of inhaling nerve agent while decontaminating is minimal if any at all.
(The NATO manual does not recommend wet method, as in the case of blistering agents it recommends use of "dry’ method with chlorinated cream and ointments, none of which is available in North Iraqi Kurdistan presently. Moreover is likely that new biological methods are presently available in NATO army, based on biological DNA recombinant technology production of enzymes attacking the organophoisphate molecules, such as Alteromonas Prolidase -Chem Biol Interact 1999 May 14; 119-120, 455-462).