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How sarin gas affects humans, symptoms of damage to the body. Effect on humans

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Sarin is an organic phosphorus-based poisonous substance. This isopropyl ester of methylfluorophosphonic acid is odorless and colorless.

Sarin is classified as a highly toxic substance with a nerve-paralytic effect. Under normal conditions, it is a liquid that evaporates quickly and has no odor. Therefore, when spraying it in the air, a person cannot smell it, but is discovered only after the first signs of poisoning of people appear. The lowest concentration of gas in the air for the appearance of the first symptoms of human poisoning is 0.0005 mg per cubic decimeter of atmosphere. If the concentration is increased 150 times, then a person in the zone of such infection will live only a minute.

Sarin gas has a detrimental effect on the human body even in liquid form. To do this, it is enough to get on the skin in a dosage equal to 24 mg per 1 kg of weight, which will lead to death.

The gas affects the body when it comes into contact with the mucous membrane of the mouth. For irreversible consequences to occur, 0.14 mg per 1 kg of weight is sufficient.

Thus, sarin gas: the effect on humans is deplorable; upon contact with this toxic substance, the chances of survival are low, since it is colorless and odorless.

All toxic substances intended for military purposes primarily affect nervous system of people. But sarin has its own peculiarity: it can come into contact with enzymes. When gas molecules enter the body, they bind to the cholinesterase protein. As a result, the protein is modified and cannot perform its main task - supporting the performance of nerve fibers.

The freezing temperature of sarin is - 57⁰ C. Frost resistance allows the use of poisonous gas in winter or in areas with a cold climate.

Symptoms of gas poisoning

In our unstable world, no one is safe from gas poisoning. No one can guarantee that someone, somewhere, for some reason, will use a toxic substance. Poisoning of the body occurs through the lungs, skin and through the oral mucosa. An attacker could poison food or water. Therefore, you should know the symptoms of poisoning.

Sarin is a gas, its effect is cumulative, that is, it is capable of accumulating inside the body over a certain period of time, this process leads to death. When a substance is ingested, the first symptoms of poisoning appear after a short period of latent phenomena, then poisoning develops quickly.

A longer prodromal segment (10–15 minutes) in case of poisoning of the body through the skin. But if the gas enters through the lungs or gastrointestinal tract, then the interval of hidden phenomena is almost always absent.

Symptoms of poisoning:

If a toxic substance enters the body through a wound on the skin, then the first sign of poisoning is a muscle spasm in the contact area. In case of poisoning through the gastrointestinal tract, the first symptoms are: development of salivation, nausea, vomiting, diarrhea, cramps in the abdominal area. Sarin can also enter the body through the lungs, then the eyes and the lungs themselves are the first to suffer.

Degrees of sarin poisoning

Sarin poisoning can be mild, moderate or severe. The degree of poisoning depends on the amount of the toxic substance that affected the person.

Easy degree: Toxicologists call this form of poisoning “mystical.” This is due to the symptoms that appear in the patient first. He complains of general weakness, headache in the eye area, and restless sleep. And also vision deteriorates, that is, it is difficult to see objects located in the distance, and “night blindness” appears in the dark. When examining the patient, toxicologists note the presence of a constricted pupil.

Average degree: this form is classified as bronchospastic. Here symptoms such as suffocation, severe pain in the abdomen, which are paroxysmal in nature, diarrhea. All other manifestations of intoxication are more pronounced than with mild poisoning. Toxicologists make the diagnosis based on the manifestation of bronchial asthma, sharp paroxysmal abdominal pain, and diarrhea.

A person with moderate sarin poisoning has only a 50% chance of recovery. But if medical assistance is not provided on time, then this indicator tends to 100%.

Severe degree of poisoning: It is called convulsive-paralytic. The patient experiences symptoms similar to those of moderate poisoning, only they are more fleeting and severe. Therefore, the patient falls into an unconscious state. In this case, the eyes remain open, the pupils are constricted. The skin and mucous membranes have a bluish color. Clonic-tonic convulsions appear, which turn into paralysis. After a few minutes, breathing stops and death occurs.

First aid

First aid is provided to people with mild to moderate poisoning. In severe cases, all processes proceed very quickly and death occurs.

First aid algorithm:

Remove the person from the contaminated area or provide protective equipment: protective suit, gas mask. Remove all contaminated clothing from the person. Wash your face and hands with liquid from an individual anti-chemical bag, if you don’t have one, then with a solution of tea soda.
Give an intramuscular injection of the antidote - atropine. It is administered every 10 minutes until the person feels relief. The dosage of atropine for a mild form is 2 cubes, for an average form 4.
Then praldoxime, diazepam, dipyroxime, etc. are added to the treatment. These drugs stop seizures and restore cholinesterase protein.

According to their chemical structure, nerve agents belong to the organophosphorus substances (OPS). These include sarin, soman, and V-gases.

In addition to toxic substances, it has been synthesized and continues to be synthesized a large number of organophosphorus substances for peaceful purposes. These are primarily organophosphorus insecticides (chlorophos, thiophos, metaphos, karbofos, fosamide, etc.), organophosphorus drugs (pyrophos, phosphakol, armin, fosarbine, fadaman, etc.), organophosphorus additives for lubricating oils, synthetic fibers, and organophosphorus polymers.

Organophosphorus toxic substances are esters of phosphoric acids (ortho- and pyrophosphoric). So, sarin is isopryl ether.

Sarin and soman are colorless (or slightly yellowish) liquids with a characteristic odor for each substance; the specific gravity of these substances is slightly higher than unity (1.02-1.1). They dissolve well in organic solvents, including fats and fat-like substances, are less soluble in water, and quickly create lethal concentrations of vapors in the air. In a droplet-liquid state they can contaminate the area in summer: sarin for up to 8 hours, soman for up to a day.

Sarin and soman are not stable in an alkaline environment: 8-10% solutions of caustic alkalis (caustic potassium and caustic sodium), as well as a 10% solution of ammonia in water, quickly destroy the toxic substance.

The chemical name of V-gases is phosphorylthiocholines. O-ethyl-3-dimetcan be cited as a representative of this subgroup of organophosphorus substances. This substance is a colorless liquid, poorly soluble in water, well soluble in organic solvents, flammable substances, and lubricants. Penetrates well into rubber products and is absorbed by paint and varnish coatings. Due to its low volatility (10-8 mg/l at a temperature of 20 ° C), it remains in place for a long time.

V-gases, soman, sarin are persistent toxic substances.

When using these gases, injuries will most often occur when a droplet-liquid substance gets on the skin or by inhalation of vapors of these agents.

Lethal concentrations and doses: sarin inhalation dose is 0.06; soman - 0.002; V-gases - 0.001.

All representatives of FOV have a pronounced cumulative effect.

Compounds found in nature and in production have been used as chemical weapons.

Entry and distribution in the body. The entrance gates for FOV are the skin, respiratory organs, conjunctiva, and digestive organs. Once in the body and in the blood, OPAs find themselves in unfavorable conditions, since they are unstable in an alkaline environment, and the blood has a slightly alkaline reaction.

That part of the agent that does not bind to biochemical structures is neutralized in the blood after some time. It is assumed that the process of destruction of OPA can be catalyzed by enzymes. The products of the transformation of OPA in the form of simple compounds (in particular, phosphorus) are removed by the kidneys.

Clinical picture

Clinic of acute lesions. The first symptoms of FOV damage appear, as a rule, after a certain period of latent phenomena; Then the clinic develops rapidly.

The prodromal period is more extended (10-15 minutes) when the agent enters the body through the skin. In case of inhalation damage and damage through gastrointestinal tract the period of latent phenomena may be practically absent. The first symptoms of the disease are a feeling of tightness in the chest and suffocation. The visible mucous membranes and skin become cyanotic, the neck veins are tense. Breathing is noisy, the patient is breathing open mouth, is fixed in the asthmatic pose (sitting, resting his hands to include auxiliary muscles in the act of breathing).

Noteworthy are the enlarged intercostal spaces and the barrel-shaped expanded chest. The lower border of the lungs is lowered. Percussion sound is boxed.

On auscultation, dry and coarse moist rales are heard diffusely. The pulse is frequent, well-filled at first, then becomes rare and easily compressed. Blood pressure, after a small short-term increase, decreases, sometimes falls catastrophically. At the same time, vision is impaired: the patient complains of pain in the eye sockets, he has difficulty distinguishing objects far away, he sees poorly in the twilight (like a patient with hemerolopia - “night blindness”), his eyelashes seem sharply thickened. Abdominal pain appears intermittently. Nausea, profuse salivation, vomiting, and diarrhea are noted. Twitching of muscle fibers and muscle groups occurs. Further, the twitching becomes generalized. The patient loses consciousness and falls. At the same time, clonic-tonic convulsions of the muscles of the face, neck, upper belt and finally total clonic-tonic convulsions appear. Sometimes convulsions occur continuously and end in paralysis, sometimes they occur in paroxysms: a cascade of convulsions is replaced by a period of relaxation, followed by a new attack of clonic-tonic convulsions. During the period of convulsions, cyanosis increases. Death occurs when breathing stops. Cardiac activity continues for several minutes.

Depending on the route of entry, some features may occur in the development of the disease. Thus, when an agent penetrates through the skin and wound surface, the first signs of damage will be muscle twitching in the area where the poison is absorbed. In case of poisoning through the gastrointestinal tract, drooling, vomiting, diarrhea, and cramping abdominal pain develop more quickly. Vision and breathing are quickly impaired in case of inhalation damage to FOV and somewhat more slowly in case of poisoning through the skin or gastrointestinal tract.

Damage from organophosphorus substances, depending on the dose of poison, can be mild, moderate or severe.

Easy defeat. Due to its predominant syndrome, some toxicologists call this form “mystical.” The patient complains of a state of “tension,” weakness, restless sleep, headache, which is localized in the eye sockets, poor vision of distant objects, absence or sharp deterioration of twilight vision, and excessive salivation. Some complain of a feeling of tightness behind the sternum and repeated loose stools.

On examination, one notices the narrowing of the pupil, sometimes to the size of a pinhead, and the injection of conjunctival vessels. A well-filled pulse is usually increased. Blood pressure is slightly elevated or normal. In the lungs, the percussion sound is pulmonary; wheezing is not audible. The tongue is clean and moist. The abdomen is soft and painless. In the descending colon, liquid contents are noted on palpation.

The diagnosis is made based on a combination of visual disturbances (such as deterioration of twilight vision, development of acute myopia, miosis), pain in the orbital area with sleep disorders and increased salivation.

Moderate damage. Moderate lesions are sometimes called the bronchospastic form of the disease. The patient complains of suffocation, paroxysmal abdominal pain, frequent loose stools, poor vision of distant objects, deterioration or absence of night vision. The patient is in the asthmatic position. The skin and visible mucous membranes are cyanotic, the neck veins are swollen, and breathing is noisy. Twitching of individual muscle groups is noted. The patient sweats profusely. The pupils are constricted, the conjunctival vessels are injected. The pulse is well filled and rare. Blood pressure is normal or slightly elevated. The chest is barrel-shaped expanded. Percussion sound is boxed. The lower border of the lung is lowered.

Auscultation reveals a large number of dry and moist coarse bubbling rales, a moist tongue, profuse salivation, vomiting, the abdomen is soft, the spleen is not palpable, the large intestine is palpated in the form of cords, the stool is liquid with an admixture of mucus.

The diagnosis is made on the basis of bronchial asthma syndrome, miosis, fibrillary twitching of individual muscle groups, cramping abdominal pain and diarrhea, and a decrease in blood cholinesterase activity (by 60-70%).

Heavy defeat. This form of damage is called convulsive-paralytic. After the appearance of symptoms of FOB damage, characteristic of a moderately severe disease, as a rule, the patient quickly falls into an unconscious state. The eyes are open, the pupils are sharply constricted. The skin and mucous membranes are cyanotic. Clonic-tonic convulsions are noted, which occur continuously, or periods of convulsions are replaced by periods of relaxation. The longer and longer the periods of relaxation, the more favorable the outcome of the lesion. Against the background of convulsions and during periods of relaxation, twitching of various muscle groups is observed. The pulse is weak, rare. Blood pressure is reduced, sometimes falling catastrophically. Breathing is noisy, the chest is barrel-shaped, the percussion sound is boxy, the lower border of the lungs is lowered. On auscultation, a mass of dry and coarse rales are heard. During the period of convulsions, pulmonary ventilation completely stops, and the cyanosis of the skin and mucous membranes sharply increases. There is profuse salivation and vomiting is possible. The abdomen is soft during the interconvulsive period, the liver and spleen are not palpable. The large intestine is palpated in the form of a cord. The rectal sphincter is gaping. There is involuntary separation of the contents of the intestines and bladder. Death usually occurs from primary respiratory arrest. The diagnosis is made on the basis of a combination of clonic-tonic convulsions with bronchial asthma syndrome, generalized fibrillations, miosis, diarrhea, bluish discoloration of the skin and mucous membranes, and a decrease in blood cholinesterase activity (by 80-90%).

Complications and consequences of acute injury. When a person affected by FOB combines convulsions with vomiting, due to the fact that the natural outlet for vomit is closed due to a spasm of the masticatory muscles, aspiration of vomit can occur and suffocation may develop due to blockage of the lumen of the bronchi. If the vomiting was not profuse and the vomit entered the lungs, then aspiration bronchopneumonia is possible, which is often suppurative in nature (abscess pneumonia).

Bronchopneumonia, which is a consequence of blockage of spasmodic bronchioles and bronchi with abundant secretion of the bronchial glands - mucus plugs, is quite common. Bruises, dislocations and even fractures are very likely, which can occur during convulsions. As a result of severe damage to FOB, paresis, paralysis, and mental disorders are noted. The nature of the patients' behavior changes sharply: they become uncooperative and their professional skills decline. Long-term polyneuritis with severe muscle atrophy was noted. Long-term consequences of FOB damage are vegetative neuroses from the cardiovascular system (vascular dystonia, angina pectoris), digestive organs (disorders of the secretory and motor functions of the gastrointestinal tract, which can simulate gastritis, gastroenteritis, enterocolitis, spastic colitis), respiratory organs (bronchial asthma).

Chronic Poisoning Clinic

With repeated exposure to OPA in small doses, as well as in case of violations of safety regulations during production, storage, transportation, or irrational use of organophosphorus compounds as insecticides and medicines, chronic poisoning can develop, since these poisons have a pronounced cumulative ability.

The clinical picture of chronic OPV poisoning is very diverse and depends on a number of reasons: the portal of entry, the duration of contact, the total dose, and the initial state of the autonomic nervous system. When organophosphate poisons enter the conjunctival sac, temporary myopia and deterioration of night vision may develop. When OPA enters the body through inhalation, attacks of suffocation are early manifestations of poisoning. Visual disturbances are also common in patients.

If poisoning occurs as a result of the intake of OPV through the gastrointestinal tract, the first signs of the disease are nausea, vomiting, diarrhea, and cramping abdominal pain. The selectivity of damage to various systems and organs largely depends on the ratio of the tone of the sympathetic and parasympathetic nerves in various organs: the prevalence of the tone of the parasympathetic nerves creates conditions for increased sensitivity of a given organ to FOB. Thus, in people with physiologically increased secretion and peristaltic activity of the gastrointestinal tract, the first manifestations of chronic FOB poisoning are nausea, cramping abdominal pain, and diarrhea. In people prone to hypotonic reactions and spasms of heart vessels, cardiovascular disorders primarily occur. With any route of admission, mental disorders are noted. Initially, patients complain of disturbing sleep with frightening dreams, a state of causeless anxiety, tension, decreased memory, and attention. They become difficult to communicate in a team, often lose professional skills - they degrade as specialists.

Thus, chronic poisoning with organophosphorus compounds can cause serious disorders in both the mental sphere and internal organs. The picture of chronic poisoning is very diverse, which can lead the patient to doctors of various profiles: a psychiatrist, a neurologist, a therapist, an ophthalmologist.

Pathogenesis

Organophosphorus substances, absorbed through the mucous membranes and skin, enter the blood and penetrate with it into all tissues of the body.

It is known that FOBs have the property of inhibiting the function of vital enzymes, such as cholinesterase, dehydrogenase, phosphatase, thrombin, trypsin, etc. The greatest consequences for the poisoned organism result from inhibition of the activity of cholinesterases.

Cholinesterases are enzymes that regulate in the body the amount of an active substance involved in the conduction of nerve impulses through synaptic formations - acetylcholine. Substances with such properties are called mediators. Acetylcholine is released at the ends of excited centrifugal nerves and causes excitation of the innervated cell. Nerves that excite the cell using acetylcholine are called cholinergic. As soon as the excitation of the cholinergic nerve stops, the excited cell must go into a resting state, for which acetylcholine must be destroyed. Acetylcholine, with the participation of cholinesterases, is broken down into choline and acetic acid.

When poisoning with OPA, as a result of their ability to inhibit the activity of cholinesterases, a large amount of acetylcholine accumulates in the body, which maintains cells sensitive to this mediator in a state of prolonged excitation. The mediator acetylcholine causes excitation of cells in various organs and tissues: in the central nervous system, autonomic ganglia, in all internal organs, as well as in motor muscles. With the accumulation and retention of acetylcholine in these organs, pathological excitation remains, and if exposed to a very large amount of the mediator, paralysis of their function may occur. Thus, an excess of acetylcholine in skeletal muscles initially leads to its tension and causes twitching of individual fibers (fibrillation). If the mediator continues to accumulate, muscle tone decreases - they relax and become unable to contract.

If these phenomena develop in the respiratory muscles, death occurs from cessation of external respiration. This phenomenon is called neuromuscular block, or relaxation of the respiratory muscles. The accumulation of acetylcholine in the bronchi and intestines leads to a reduction in the muscles of these organs - bronchial spasm, intestinal spasm or increased peristalsis develop. The muscles of the arterioles relax under the influence of acetylcholine, so arterial pressure decreases, the heart rate slows down. There is an indication that FOBs affect the cholinoreactive structures of the body not only indirectly (through acetylcholine), but also directly (by interacting with them).

Inhibition of FOB enzymes phosphoglucomutases and dehydrogenases, which are involved in the activation of oxidative processes occurring in cells and providing them with the necessary energy, leads to energy starvation of tissues. This exacerbates the harmful effects of excess acetylcholine.

Thus, inhibition of cholinesterase activity and the associated accumulation of acetylcholine in the body during FOB poisoning distorts the normal functioning of the central and peripheral nervous systems and, naturally, all organs.

The effectiveness of treatment of affected FOVs largely depends on the timely cessation of further entry of FOVs into the body. If chemical agents come into contact with the skin in a droplet-liquid state or in the form of drizzle, the exposed skin areas should be treated with the liquid of an individual anti-chemical package (IPP). If it is unavailable, you can use a 10% ammonia solution - ammonia. If the skin comes into contact with FOV, wipe it vigorously with a degasser, and then wash it with soap and water. If FOV gets into the eyes, the conjunctival sac is washed with a 2% solution of baking soda.

In case of poisoning through the gastrointestinal tract, give copious amounts of soda (2% solution of baking soda) and induce vomiting. If possible, wash the stomach with a 2% solution of baking soda, followed by the administration of a suspension of activated carbon (10-15 g of activated carbon is stirred in 3/4 cup of a 2% solution of baking soda). To treat affected FOBs, antidotes (antidotes), syndromic drugs and symptomatic drugs are used.

Cholinesterase reactivators have been proposed as antidotes, but acetylcholine antagonists - anticholinergics (atropine) and adrenergic agonists (adrenaline, ephedrine) are more common. Atropine is administered intramuscularly in a 0.1% solution of 1-3 ml repeatedly. The daily dose of atropine in the treatment of severe forms of FOV damage can reach 24-30 ml and more than 0.1% solution. The atropine prescription regimen is designed in such a way that the patient does not complain of difficulty breathing and notices mild dry mouth. The appearance of severe dryness of the mucous membranes, thirst, sharp dilation of the pupil, redness of the face indicate an overdose of atropine. In case of severe damage to FOV, anticholinergics are used in combination with cholinesterase reactivators: diperoxime, 1 ml of a 15% aqueous solution, is administered intramuscularly at intervals of 4-6 hours. Adrenaline in a 0.1% solution, 1 ml each, and ephedrine in a 5% solution 1 ml solution is administered intramuscularly.

If the administration of antidotes does not relieve seizures, then to relieve them, one of the medicinal substances of the barbituric acid group is used - barbiturates (sodium thiopental, hexenal, barbamyl). Sodium thiopental is administered intramuscularly in a 2.5% solution, 5 ml each, hexenal - 5 ml of a 10% solution, also intramuscularly. A reliable anticonvulsant effect is achieved by intramuscular injection of 2 ml of a 2.5% solution of aminazine, 2 ml of a 2% solution of diphenhydramine and 2 ml of a 2% solution of promedol. In case of severe respiratory distress, the affected FOV is given artificial respiration and oxygen is prescribed.

Due to the fact that one of the causes of respiratory distress is the narrowing of the lumen of the bronchi, conventional two-handed methods of artificial respiration are ineffective. Such affected people need active artificial respiration - instrumental (DP-3, GS-6, RPA-3, etc.) or using the mouth-to-mouth method. Symptomatic drugs are also used that increase blood pressure (10% solution of caffeine-sodium benzoate, 1 ml intramuscularly or subcutaneously, etc.), stimulating breathing while simultaneously administering oxygen (cytiton, 1 ml intramuscularly). Severely affected FOVs, as a rule (for the purpose of prevention and treatment of pneumonia), require antibiotics and sulfonamides. All manipulations should be as gentle as possible.

Such patients require constant monitoring by medical personnel. In addition, when vomiting occurs, severely affected patients should be promptly introduced with mouth dilators, and if vomit is aspirated, they should be sucked out.

Prevention

If there is a threat of contact with FOV, it is necessary to wear gas masks and use skin protection. If infected with droplet-liquid FOV, the skin and visible areas of clothing should be treated with IPP degassers, and personal weapons should be degassed with the liquid of an individual degassing package (IDP). If there is no PPI, the skin should be wiped with a 10% ammonia solution (V-gases are not destroyed). Mucous membranes should be protected from the IPP degasser and ammonia. The mucous membranes accessible to treatment are washed with a 2% soda solution. If you don’t have a PPI or ammonia on hand, then exposed skin should be washed with water and soap (preferably household soap). When infected with FOV, a prophylactic antidote is administered before symptoms of poisoning appear.

Currently, a number of prescriptions for a prophylactic antidote are used, one of which may consist of an aqueous solution of proserin and an aqueous solution of atropine sulfate.

In case of infection with FOV, a full dose is administered; in case of suspicion or threat of infection, a half dose of the prophylactic antidote is administered. As soon as possible, you need to take a shower, change your underwear and uniform.

First aid. Put on a gas mask, inject an antidote intramuscularly from a syringe tube, treat exposed skin and visible areas of contaminated clothing with PPI degassers, and degas personal weapons. In case of suffocation, perform artificial respiration without removing the gas mask. In case of convulsions, re-administer the antidote.

First aid. The exposed skin areas are re-treated with a PPI degasser and an antidote is administered. In case of suffocation, oxygen is given by connecting a gas mask helmet to an oxygen device. Carry out artificial respiration. Adrenaline (1 ml of 0.1% aqueous solution), ephedrine (1 ml of 5% aqueous solution), caffeine-sodium benzoate (1 ml of 10% aqueous solution), 1 ml of cititon are administered intramuscularly. In cold weather, the affected person should be wrapped warmly and covered with heating pads.

Sarin gas is practically unknown to the general public, but everyone needs to know its effect on humans and the signs of injury from this substance.

Sarin is one of the most dangerous substances on the entire planet, the use of which is not widespread. Many people remember this name exclusively from school safety lessons, but others also encounter it in the course of their work. Today gas is considered a weapon of mass destruction; it was recognized as dangerous at the end of the last century, but its spread throughout the world began much earlier.

The use of this substance has Negative influence on the central nervous system of humans and animals, has a paralytic effect, and at high concentrations is fatal. You can eliminate the danger only by completely avoiding contact with this substance, since sarin poisoning will cause great damage to the body and all vital systems.

Story

This chemical, which can almost instantly disrupt the functioning of the human central nervous system, was first discovered in 1938 during chemical experiments on the development of the most common insecticides.

Almost immediately after receiving the serial number, the scientists who received this mixture sent samples of it to the military, who, in turn, found widespread use of the dangerous substance and received the most powerful weapon of the century.

Note! Simplified name for this chemical mixture was obtained by adding the first letters of the scientists who first discovered this substance. To this day, their name is immortalized in history, and chemists are aware of the value and danger of the discovery.

The discovery of the chemical mixture occurred almost just before the start of World War II, but, oddly enough, it was never used during combat operations. It is believed that Hitler had a negative attitude towards such dubious and poorly understood gases, since during the previous war one of these substances had a negative effect on his eyesight. Perhaps it was this fact that significantly reduced the number of casualties and changed the outcome of the war.

By the end of World War II, the spread of gas had reached unprecedented proportions - it was adopted by such great states as Great Britain, the United States of America, and even Soviet Union.

Despite this, throughout the years of existence of the substance and many military and political conflicts, no dangerous gas was used, the toxic substance remained behind the scenes and did not harm ordinary citizens.

Victims

Sarin is a poisonous substance, and some people have experienced its effects. Tests of this chemical substance gained great activity, and already in 1953 caused a wide public outcry.

The fact is that during tests of the effects of gas on humans, the subject died, and this caused an immediate reaction from society. Trials regarding the dangers of sarin did not bring results, since the testers presented everything as an accident.

The main use of the dangerous poison began during the war between Iraq and Iran. One major sarin attack killed more than seven thousand people, most of them civilians. The danger of the poisoned gas was that none of the victims even had time to feel negative symptoms, and as a result of an overdose, death occurred in the shortest possible time.

Impact

Sarin gas, which has an extremely negative effect on humans, in its normal state poses virtually no danger. Typically, this substance is liquid and evaporates in the atmosphere and has absolutely no odor, which is what makes the toxic substance so dangerous.

The minimum concentration of a hazardous chemical in the air that can cause unpleasant symptoms of illness, and even serious poisoning, is considered to be only 0.0005 mg. If the gas concentration is increased one hundred and fifty times, then the death of the victim located in the affected area occurs no later than one minute after the toxin enters the body.

It is important to understand that not only the vapors of this substance have a poisonous effect on the human body, but also the liquid, which is considered the normal state of sarin. If it gets on the skin or in the oral cavity, a small concentration of the substance will cause a lot of unpleasant symptoms, and exceeding the permissible dose for a person leads to inevitable death.

Note! The use of sarin is possible even with low temperatures air, since the solidification temperature of the substance is minus 57 degrees Celsius. This suggests that when using gas in wartime, no one will be able to avoid serious poisoning.

Almost every combat unit that is based on chemical components is aimed at damaging the human nervous system as much as possible. Characteristic feature Sarin gas is believed to be due to its amazing ability to bind enzymes in the human body that can no longer perform their basic functions and are destroyed.

In this case, absolutely all systems of the body suffer, and the person either receives serious intoxication, leading to the development of many pathologies, or dies in a short time.

Symptoms

Since the toxic substance is colorless and odorless, serious intoxication with poison can be determined only after the appearance of primary symptoms. Unfortunately, after their appearance, few people have time to undergo rehabilitation, since household use of the poison is not observed, and the use mainly occurred during military operations.

You can be poisoned by this dangerous substance in several ways, each of which poses a serious danger to human health and life:

The poison is dangerous when inhaled; if its concentration in the air is high, then the likelihood of death increases, creating the possibility of mass destruction of everyone who is in the zone of exposure to the toxin.
Sarin poison is easily absorbed through human skin, and in this case, poisoning can be not only dangerous, but also fatal.
The poison that penetrates the mouth and stomach of a person kills him in a matter of minutes, in this case the chances of rehabilitation and recovery are almost zero.

Mild degree

With a mild degree of poison intoxication, the chances of survival are quite high; the main thing is to provide first aid in a timely manner and remove the victim from the affected area.

The symptoms that occur with this type of poisoning are often difficult to distinguish from intoxication of any other nature; this creates additional danger, since the gas, which is colorless and odorless, can increase its concentration, thereby killing the victim.

Symptoms of such intoxication of the body may include the following:

Noticeable shortness of breath.
Unpleasant sensations in the chest area.
General weakness throughout the whole body.
Foggy consciousness.

Average degree

Signs of moderate sarin damage are expressed much more clearly, so it is not difficult to notice them. This must be done in a timely manner, since even a small increase in the concentration of a substance in the air can become critical.

The main sign of moderate sarin gas poisoning is severe constriction of the pupil. In the victim, it narrows to such an extent that it more closely resembles a blackhead. Then a number of the following unpleasant signs are added:

A sudden feeling of fear appears, and unreasonable panic attacks are possible.
Cold sweat appears on the surface of the victim's skin.
The patient's larynx is seized by unpleasant spasms, leading to shortness of breath and even asthma attacks.
As a result of the gas's effect on the body, nausea and even severe vomiting occur.
The number of contractions of the heart muscle increases.
In some cases, the victim exhibits urinary and fecal incontinence.

Note! The probability of death with moderate sarin poisoning is fifty percent, so it is important to promptly provide first aid to the victim and administer an antidote that blocks the effect of the toxin on the body.

If help is not provided to the victim on time, the risk of death increases to one hundred percent. Therefore, it is important, when minimal signs of intoxication appear, to call a team of specialists who will administer an antidote and provide qualified treatment.

Severe degree

If sarin gas enters the human body in a critical concentration, severe poisoning with the substance occurs. It is almost always impossible to get rid of such intoxication using improvised means. The symptoms of such poisoning are the same as those of moderate severity, however, their appearance occurs much faster and can kill a person in a matter of minutes.

The patient experiences convulsions, severe vomiting, and a couple of minutes after these signs appear, the victim completely loses consciousness. If you do not provide qualified assistance in a timely manner and do not administer an antidote that blocks the effects of a harmful substance, you will not be able to avoid death.

Five to ten minutes after the substance enters the body, convulsions turn into paralysis, the respiratory center of the body can no longer perform its direct functions, and death occurs. You need to act immediately to save the patient; in the case of this poison, minutes count.

Safety

Poisoning with the dangerous gas sarin has caused a lot of harm in recent decades. human lives. It is difficult to predict in advance what will happen in the world in the near future, which is why it may often be simply impossible to get rid of possible poisoning.

Naturally, the main thing that every person needs to know, regardless of the political situation, education and lifestyle, is how to administer the antidote, how to act in the case of different stages of poisoning, and in what cases the life of a victim of harmful gas can be saved.

The risk group primarily includes people who work at military enterprises where chemical weapons are being developed. Although chemicals are practically not used in modern warfare due to agreement between states, the risk exists, and people who come into contact with the gas must take all safety precautions.

It is also worth paying attention to the safety rules for people who work with chemicals in various areas of industry. The gas is odorless and colorless, so it can only be detected in the air with special devices or when the permissible concentration is exceeded. It is important to understand that safety precautions regularly save thousands of lives.

In wartime and during hostilities of various types, each person must take care not only of his own safety, but also of the safety of his loved ones. In the event of a possible chemical attack, it is necessary to stock up on protective equipment that will significantly reduce the concentration of the substance in the body and reduce the risk of mortality.

To do this, all civilians must have gas masks, respirators, or at least protective bandages. Clothes should be tight and cover all parts of the body.

Only if you implement and observe all safety measures, you reduce the risk of mortality and increase your chances of salvation. In case of serious danger, first of all, try to get as far as possible from the place where the gas is spreading, this will greatly ease the situation.

Help

When poisoned by a dangerous chemical, helping the victim is what in many cases not only alleviates the patient’s condition, but also saves his life. If exposure to a toxin occurred in Peaceful time, you must first call a team of specialists, describe the situation in detail and say the name of the gas that caused the poisoning.

Effective first aid to a victim of sarin gas will only be if the poisoning is mild or moderate in nature. In case of severe poisoning, the victim has practically no chance of survival, however, it is necessary to try to help and call a doctor.

If at least one or more signs of gas poisoning appear, the following action algorithm should be followed:

The injured person must be removed from the affected area as soon as possible. If possible, the person must be provided with protective equipment, including a gas mask or respirator and protective clothing to prevent increased intoxication. If poisoning occurs indoors, it is necessary to open all doors and windows so that the gas reduces its concentration, and be sure to make sure that there are no people nearby, since in this case even passers-by are at risk.
Before protecting the victim with special clothing, it is necessary to remove all contaminated clothing as quickly as possible and clean the skin with a specialized individual solution from a bag or a solution of ordinary soda.
IN mandatory it is necessary to inject the antidote into the victim’s muscle. In the case of sarin, the antidote is atropine and similar substances. The injection of this drug into the muscle should be done every ten minutes until the victim’s pupils return to normal - his condition must be monitored.
The final step to getting rid of the symptoms of mild or moderate intoxication is specialized treatment. It should be provided by a doctor, if it is possible to contact him. Therapy is provided with drugs such as Toxagonin, Diazepam and others.

After rescue activities, the victim must be provided with complete rest and free access to fresh air. If possible, you must definitely call a doctor and go to the hospital to receive qualified treatment.

Only a physician, based on test results and examination of the patient, will determine the possible consequences of poisoning, prescribe subsequent treatment and get the victim back on his feet as quickly as possible.

Video: Sarin is a colorless, odorless and tasteless killer.

Possible consequences

Even if the necessary assistance is provided to the victim, it is possible to get rid of the consequences of poisoning in rare cases. The most terrible consequence occurs if the poisoning was severe, or assistance with moderate severity was not provided properly. In this case, inevitable death occurs.

With a mild degree of poisoning, the affected person’s performance is significantly reduced for several days. In this case, the victim needs complete rest and access to fresh air, as well as a doctor’s examination for consequences. A week after rehabilitation and removal of the toxin from the body, all vital functions begin to gradually recover.

Average severity of poisoning involves the inability to go about your business and live a normal life for two whole weeks. At the same time, the risk of death with qualified treatment is reduced to almost zero. A month after eliminating the serious condition and two weeks of treatment, the body begins to gradually recover, and a month and a half after intoxication, symptoms are practically not observed.

Every person should know how to behave in case of poisoning by a chemical substance. Even in peacetime you can get poisoned dangerous poison, as it is used in the chemical industry. It is necessary to protect yourself and your loved ones in advance, and then no problems with intoxication will arise.

Classification of toxic chemical compounds intended to destroy the manpower of a potential enemy. The history of the creation of the nerve gas sarin, its physiological effect on the human body. Reaction equations for sarin utilization.

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Federal State Budgetary Educational Institution of Higher Professional Education

"Irkutsk State University"

Chemical faculty

Essay

" Chemical warfare agents"

Completed by: 2nd year student

Gabdrashitova A.S.

Checked: Assoc. Mikhailenko V.L.

Irkutsk 2015

Introduction

1. History of the creation of sarin

2. General characteristics

3. Physiological action on the human body

4. Signs of sarin damage

5. Prevention

7. Treatment

8. Recycling reaction equations

8.1 Hydrolysis

8.2 Reactions with hypochlorites

8.3 Reactions with alcohols and phenols

Bibliography

Introduction

Toxic substances(OV) - toxic chemical compounds designed to destroy enemy personnel during military operations and at the same time preserve material assets during an attack in the city. They can enter the body through the respiratory system, skin and digestive tract. The combat properties (combat effectiveness) of agents are determined by their toxicity (due to the ability to inhibit enzymes or interact with receptors), physicochemical properties (volatility, solubility, resistance to hydrolysis, etc.), ability to penetrate the biobarriers of warm-blooded animals and overcome defenses.

The most effective way to use toxic substances is the aerosol method, in which the layer of air closest to the ground will become infected with tiny droplets (fog) and chemical vapors.

The damaging effect of toxic substances has a number of features.

Behind a short time they can cause mass lesions in the nature of acute intoxication (poisoning). Toxic substances are characterized by a volumetric effect, contaminating the ground layer of air over large areas. In a vapor (gaseous) state, as well as in the form of aerosols (fog, smoke), chemical agents can penetrate into unsealed protective structures (premises) and cause injury to people in them. In the air, on the ground and in various objects external environment OB more or less long time retain their damaging properties.

Human injury can occur when inhaling air contaminated with vapors and aerosols of toxic substances; in case of contact with drops and exposure to chemical vapors on the skin and mucous membranes; upon contact with objects and terrain contaminated with toxic substances, as well as upon consumption of food and water contaminated with chemical agents.

Criteria for the combat effectiveness of an agent: toxicity, speed of action (time from contact with the agent until the effect appears), durability.

Toxicity toxic substances is the ability of an agent to cause damage when it enters the body in certain doses. The concept of toxic dose is used as a quantitative characteristic of the damaging effect of chemical agents and other compounds toxic to humans and animals. When inhaled, toxodose is equal to the product of the concentration of agents in the air and the exposure time in minutes (mg * min/l); When the agent penetrates through the skin, gastrointestinal tract and bloodstream, toxodosis is measured by the amount of agent per kilogram of live weight (mg/kg).

Durability- this is the ability of an agent to maintain its destructive effects in the air or on the ground for a certain period of time. The transition to a combat state of agents and their action in the atmosphere and on the ground are influenced by physicochemical characteristics: volatility, viscosity, surface tension, melting and boiling points, resistance to environmental factors.

Classification of agents

1. First generation

1.1. Agents with blister action (persistent agents: sulfur and nitrogen mustards, lewisite)

1.2. General toxic agent (unstable agent hydrocyanic acid);

1.3. Asphyxiating agents (unstable agents phosgene, diphosgene);

1.4. Irritant agents (adamsite, diphenylchloroarsine, chloropicrin, diphenylcyanarsine)

2. Second generation

2.1. Nerve agent

3. Third generation

3.1. Psycho-chemical agents

Nerve agents - a group of lethal agents that are highly toxic phosphorus-containing agents (sarin, soman, Vi-X).

Soman - colorless liquid with a faint smell of camphor, density 1.01 g/cm3, boiling point 185-187 ° C, solidification temperature from -30 to -80 ° C, poorly soluble in water.

V-X - colorless liquid, odorless, density 1.07 g/cm; part of Vi-X - up to 5% - dissolves in water. Liquid Vi-X has the viscosity of motor oil, a boiling point of 237 °C, low volatility, and solidifies at approximately - 50 °C.

All phosphorus-containing substances are highly soluble in organic solvents and fats and easily penetrate intact skin. They act in droplet-liquid and aerosol (vapor, fog) states. Once in the body, phosphorus-containing chemical agents inhibit (suppress) enzymes that regulate the transmission of nerve impulses in the systems of the respiratory center, blood circulation, cardiac activity, etc. Poisoning develops quickly. At small toxic doses (mild lesions), constriction of the pupils of the eyes (miosis), salivation, chest pain, and difficulty breathing occur. In case of severe lesions immediately; then comes difficulty breathing, profuse sweating, stomach cramps, involuntary separation of urine, sometimes vomiting, convulsions and respiratory paralysis.

Common toxic substances actions - a group of fast-acting volatile agents (hydrocyanic acid, cyanogen chloride, carbon monoxide, arsenic and hydrogen phosphide) that affect the blood and nervous system. The most toxic are hydrocyanic acid and cyanogen chloride.

Hydrocyanic acid-colorless volatile liquid with the smell of bitter almonds, boiling point 26°C, freezing point - minus 14°C, density 0.7 g/cm3, soluble in water and organic solvents.

Chlorcyanide - colorless, heavy, volatile liquid, boiling point 19 ° C, freezing point - minus 6 ° C, density 1.2 g/cm3, poorly soluble in water, well soluble in organic solvents.

In case of severe poisoning with a generally toxic agent, a metallic taste in the mouth, tightness in the chest, a feeling of strong fear, severe shortness of breath, convulsions, and paralysis of the respiratory center are observed.

Asphyxiating agents, which, when inhaled, damage the upper respiratory tract and lung tissue. The main representatives: phosgene and diphosgene.

Phosgene - colorless liquid, boiling point 8.2 °C, freezing point - minus 118 °C, density 1.42 g/cm3. Under normal conditions it is a gas, 3.5 times heavier than air .

Diphosgene colorless oily liquid with the smell of rotten hay, boiling point 128 ° C, freezing point - minus 57 ° C, density 1.6 g/cm3.

When inhaling phosgene, you feel the smell of rotten hay and an unpleasant sweetish taste in the mouth, a burning sensation in the throat, cough, and tightness in the chest. Upon leaving the contaminated atmosphere, these signs disappear. After 4-6 hours, the condition of the affected person deteriorates sharply. A cough appears with copious discharge of foamy fluid, breathing becomes difficult.

Poisonous substances with blister action - mustard gas And nitrogen mustard. Chemically pure mustard gas is an oily, colorless liquid; technical mustard is an oily liquid of yellow-brown or brown-black color with the smell of mustard or garlic, 1.3 times heavier than water, boiling point 217°C; chemically pure mustard hardens at a temperature of about 14°C, and technical mustard at 8°C; it dissolves poorly in water, and well in fats and organic solvents. Mustard gas acts in droplet-liquid, aerosol and vapor states.

Mustard gas easily penetrates the skin and mucous membranes; Once in the blood and lymph, it spreads throughout the body, causing general poisoning of a person or animal. When drops of mustard gas come into contact with the skin, signs of damage are detected after 4-8 hours. In mild cases, redness of the skin appears, followed by the development of swelling and a feeling of itching. With more severe skin lesions, blisters form, which burst after 2-3 days and form ulcers. In the absence of infection, the affected area heals in 10-20 days. Damage to the skin by mustard vapors is possible, but less so than by drops.

Mustard fumes cause damage to the eyes and respiratory system. When the eyes are affected, there is a feeling of eye congestion, itching, inflammation of the conjunctiva, necrosis of the cornea, and the formation of ulcers. 4-6 hours after inhaling mustard gas vapor, you feel a dry and sore throat, a sharp painful cough, then hoarseness and loss of voice, inflammation of the bronchi and lungs.

Irritating toxic substances- a group of agents acting on the mucous membranes of the eyes (lacrimators, for example chloroacetophenone) and upper respiratory tract (sternites, for example adamsite). The most effective agents have a combined irritating effect of the type CC And C-Er, which are in service with the armies of imperialist states.

Psychogenic toxic substances- a group of agents that cause temporary psychoses due to disruption of chemical regulation in the central nervous system. Representatives of such agents are substances such as “LSD” (lesergic acid diethylamide) and Bi-Z. These are colorless crystalline substances, poorly soluble in water, and are used in an aerosol form. If they enter the body, they can cause movement disorders, visual and hearing impairments, hallucinations, mental disorders or completely change the normal pattern of human behavior; a state of psychosis similar to that observed in patients with schizophrenia.

PersistentOB- a group of high-boiling agents that retain their damaging effect from several hours to several days and even weeks after use. Persistent toxic substances (PTC) evaporate slowly and are resistant to air and moisture. The main 51 representatives are V-X (V-gases), soman, mustard gas.

UnstableOB- a group of low-boiling agents that contaminate the air for a relatively short period (from several minutes to 1-2 hours). Typical representatives of NO are phosgene, hydrocyanic acid, and cyanogen chloride.

1. History of the creation of sarin

Chemical name: methylphosphoric acid isopropyl ester fluoride; methylfluorophosphoric acid isopropyl ester; isopropyl methyl fluorophosphonate.

Conventional names and codes: sarin, GB (USA), Trilon 144, T 144, Trilon 46, T 46 (Germany).

Sarin was discovered in 1938 in Wuppertal-Elberfeld in Germany's Ruhr Valley by two German scientists trying to develop more powerful pesticides. Sarin is the second most powerful, after soman, of the four G-series toxic substances created in Germany. G-series is the first and oldest family of nerve agents: GA (tabun), GB (sarin), GD (soman) and GF (cyclosarin). Sarin, the discovery of which occurred after the herd, was named after its researchers: Schrader, Ambros, Rüdiger and Van der LINde.

2. General characteristics

Sarin (GВ) is a colorless or yellowish volatile liquid with a weak fruity odor, density 1.09 g/cm3, boiling point 147°C, solidification temperature from -30 to -50°C. Miscible with water and organic solvents in any ratio, soluble in fats. Resistant to water, which causes contamination of stagnant bodies of water for a long time, up to 2 months. When it comes into contact with human skin, uniforms, shoes and other porous materials, it is quickly absorbed into them.

Sarin is a nerve agent. When sarin is heated, vapors are formed. In its pure form, sarin has virtually no odor, so at high concentrations, which are easily created in the field, a lethal dose can quickly and unnoticeably accumulate inside the body.

This is a very important property of sarin, which increases the possibility of its sudden use, especially in cases where delivery vehicles are used that can quickly and relatively quietly create very high concentrations in the target area. Under such conditions, personnel subjected to a chemical attack will not detect the danger in time and will not be able to put on gas masks and use skin protection in a timely manner.

The main combat state of sarin is steam. Under average meteorological conditions, sarin vapors can spread downwind up to 20 km from the place of application. Durability of sarin (in funnels): in summer - several hours, in winter - up to 2 days.

GB is one of the main lethal chemical agents in service with the US Army. According to American official documents, it is designed to destroy enemy personnel by infecting the surface layer of the atmosphere with steam. The GB substance is used to equip service chemical ammunition of group A, including artillery shells of cannon and rocket artillery, including naval, aerial bombs and cassettes, warheads of operational-tactical missiles. Ammunition intended for use by GB is coded with three green rings and marked with the words "GB GAS".

3. Physiological effect on the human body

A characteristic physiological feature of GB, like other organophosphorus agents, is its ability to chemically bind and inactivate biological catalysts various reactions in the body (enzymes), among which cholinesterase plays an important role - a protein found in many organs and tissues of the body, but which performs its main function in the nervous system, regulating the process of transmission of nerve impulses.

When sarin vapor is inhaled, its damaging effect manifests itself very quickly, so it is possible to create such high concentrations in the field that they will be enough to receive a lethal dose into the body in a few breaths. In this case, death can occur within a few minutes.

At low concentrations of sarin in the air, if gas masks are not used, those affected will experience, first of all, a severe runny nose, heaviness in the chest, as well as constriction of the pupils, as a result of which vision deteriorates. These symptoms are sometimes mild. When a large dose of sarin is inhaled, symptoms of damage occur very quickly, they manifest themselves in the form of severe shortness of breath, nausea and vomiting, spontaneous discharge, severe headache, loss of consciousness and convulsions leading to death.

Sarin, being in a liquid or vapor state, can penetrate into the body and through the skin. In this case, the nature of its damaging effect will be the same as when entering through the respiratory system. However, damage to the body when sarin enters through the skin will occur somewhat more slowly. It takes a few drops of sarin or very high concentrations of its vapor to infect the body through the skin. It should be noted that when exposed both through the skin and through the respiratory tract, sarin has a cumulative effect, that is, it tends to accumulate in the body.

4. Signs of sarin damage

The first signs of exposure to sarin (and other nerve agents) on a person are nasal discharge, chest congestion and constriction of the pupils. Soon after this, the victim has difficulty breathing, nausea and increased salivation. Then the victim completely loses control over body functions, vomits, and involuntary urination and defecation occur. This phase is accompanied by convulsions. Ultimately, the victim falls into a comatose state and suffocates in a fit of convulsive spasms followed by cardiac arrest.

Relative toxicity of GB by inhalation LCt 50 0.075 mg. min/l. The first signs of damage are constriction of the pupils of the eyes (miosis) and difficulty breathing; they appear at GB concentrations in air of 0.0005 mg/l after 2 minutes. Skin resorptive toxodose GB is LD 50 24 mg/kg, oral - 0.14 mg/kg. When acting through the bare skin of a vaporous substance LCt 50 12 mg. min/l.

At exposure 0.1 LCt 50 or 0.1 LD 50 Mild lesions are usually observed, the signs of which are miosis, salivation, and sweating. Almost simultaneously, signs of poisoning develop, associated with the phenomena of spasm of blood vessels, bronchi, lungs and heart muscle. Shortness of breath, difficulty breathing, pain in the chest and forehead, general weakness and weakening of consciousness occur. Mild lesions lead to loss of performance for 1-5 days.

Moderate poisoning occurs at 0.2 LCt 50 or 0.2 LD 50 . Signs of damage occur faster and are more pronounced. Persistent miosis, pain in the eyes with strained vision, and lacrimation occur. Intensifying headache, there is a discharge of watery fluid from the nose. As the feeling of fear increases, an increase in cold sweat appears. The developing periodic spasm of the larynx and bronchi leads to difficulty breathing, asthmatic attacks, nausea and vomiting. Against the background of an increase in heart rate, small muscle twitches, loss of coordination of movements, and short-term convulsions are observed. Involuntary urination and stool loss occur. The affected person is incapacitated for 1-2 weeks, and if medical care is not provided in a timely manner, death is possible. Complete restoration of cholinesterase activity and recovery lasts for 4-6 weeks.

Severe poisoning is caused by 0.3-0.5 LCt 50 or 0.3-0.5 LD 50 . In this case, the period of hidden action is practically absent. The signs of damage are the same as for moderate poisoning, but develop very quickly. The affected person complains of loss of pupillary reflex, excruciating pressure in the eyes and severe headaches. Vomiting, urine and feces, and suffocation occur. After about 1 minute, loss of consciousness occurs and severe convulsions are observed, turning into paralysis. Death occurs within 5-15 minutes from paralysis of the respiratory center and heart muscle.

With the same toxodoses of GB, signs of damage appear most quickly (after 1 minute or even earlier) during inhalation, somewhat more slowly (after a few minutes) when entering the body through the gastrointestinal tract, and most slowly (after 15-20 minutes and later) through skin. At the site of liquid agent contact with the skin, small muscle twitches are observed.

5. Prevention

Prevention is based on the administration of a reversible anticholinesterase agent. Pyridostigmine is suggested in doses of 30 mg three times daily to inhibit approximately 30% of blood cholinesterase. In cases of severe poisoning, this 30% of the protected cholinesterase is spontaneously reactivated, and if the same phenomenon occurs at the cholinergic synapses, the victim will recover. (Re-inhibition of the enzyme may occur if the toxicant remains in the body and is available to bind to cholinesterases after pyridostigmine has been eliminated.)

6. Protection

When units operate military equipment in an atmosphere contaminated with sarin, gas masks and a combined arms comprehensive protective kit are used for protection. When operating in contaminated areas on foot, additionally wear protective stockings.

When staying for a long time in areas with high levels of sarin vapor, it is necessary to use a gas mask and a general protective kit in the form of overalls. Protection against sarin is also ensured by the use of sealed equipment and shelters equipped with filter-ventilation units. Sarin vapor can be absorbed by uniforms and, after leaving the contaminated atmosphere, evaporate, contaminating the air. Therefore, gas masks are removed only after special treatment of uniforms, equipment and control of air contamination.

7. Treatment

Treatment of a person affected by sarin should begin immediately after diagnosis. Immediate actions include urgent isolation of the victim from the damaging agent (contaminated area, contaminated air, clothing, etc.), as well as from all possible irritants (for example, bright light), treating the entire surface of the body with a weak alkali solution, or a standard chemical protective agent.

If a toxic substance enters the gastrointestinal tract, rinse the stomach with a large amount of slightly alkaline water.

Simultaneously with the above actions, the urgent use of the following antidotes is necessary:

· Atropine, an M-cholinergic receptor blocker, is used to relieve physiological signs of poisoning.

· Pralidoxime, dipyroxime, toxogonin, HI-6, HS-6, HGG-12, HGG-42, VDV-26, VDV-27 - acetylcholinesterase reactivators, specific antidotes of organophosphorus substances that can restore the activity of the acetylcholinesterase enzyme if used within the first hours after poisoning.

· Diazepam is a centrally acting anticonvulsant drug. Seizure reduction was markedly reduced when treatment initiation was delayed; 40 minutes after exposure the decrease is minimal. Most clinically effective antiepileptic drugs may not be able to stop sarin-induced seizures.

· In field conditions, it is necessary to immediately administer Afin or Budaxin from a syringe tube (included in the individual first aid kit AI-1, which is equipped with each mobilized soldier), if they are unavailable, you can use 1-2 tablets of Taren from the first aid kit AI-2.

Subsequently, pathogenetic and symptomatic treatment is carried out depending on the prevailing symptoms of the lesion in a given victim.

8. Recycling reaction equations

8.1 Hydrolysis

Methylphosphonic acid isopropyl ester fluoride hydrolyzes in neutral aqueous solutions to form two non-toxic products - isopropyl methylphosphonic acid hydrofluoric acid:

The rate of hydrolysis increases with increasing temperature and GB concentration, but changes especially strongly in the presence of acids, alkalis and various catalysts.

When the concentration of GB in an aqueous solution is less than 14 mg/l and a temperature of 25C, 50% of the product is hydrolyzed in 54 hours. At higher concentrations of GB, the rate of hydrolysis increases due to the catalytic influence of its products. Acid isopropyl ester of methylphosphonic acid easily dissociates into ions:

Hydrogen ions (protons) are known to be capable of forming hydrogen bonds with fluorine atoms, which leads to a weakening of the latter’s bond with phosphorus and to facilitating the attack of a positively polarized phosphorus atom by a water molecule:

In this regard, even without the addition of acids, the hydrolysis of GB is a self-accelerating (autocatalytic) process, since the acidic substances formed as a result of hydrolysis supply protons in ever-increasing quantities.

Naturally, adding any mineral or organic proton-donor acids to water will accelerate the hydrolysis of GB. Thus, at a concentration of GB in a solution of 140 mg/l and a temperature of 20-30C, the compound almost completely decomposes at pH = 3 in 100 hours, and at pH = 1 - in less than 2 hours.

Hydrolysis of GB in the presence of alkalis occurs much faster than in the presence of acids. This is explained by the greater nucleophilicity of the hydroxyl anion HO - compared to an undissociated water molecule:

The total hydrolysis of GB in an alkaline medium is described by the equation:

The rate of hydrolysis varies in proportion to the concentration of hydroxyl ions, increasing with its increase. The time for complete decomposition of GB with a concentration of 140 mg/l at a temperature of 20-30C and pH = 9.5 is 66 minutes, and at pH = 11.5 about 1.5 minutes. The approximate hydrolysis time of GB (h) for pH = 7-13 and temperature 25° C can be calculated using the formula:

t 1/2 =5.4* 10 8 * 10 - p n.

Thus, aqueous solutions of alkalis can be used to destroy methylphosphonic acid isopropyl ester fluoride.

When GB is boiled with solutions of acids and alkalis, the reaction does not stop at the replacement of the fluorine atom, but further hydrolysis occurs at the ester bond:

When there is an excess of alkalis, the reaction products are salts of methylphosphonic and hydrofluoric acids and isopropyl alcohol:

All products are non-toxic.

8.2 Reactions with hypochlorites

Hypochlorites of alkali and alkaline earth metals dissociate in aqueous-alkaline solutions into a metal cation and a hypochlorite anion, for example:

The hypochlorite anion determines the direction and rate of the reaction of hypochlorites with GB, since, on the one hand, like all anions, it is more nucleophilic than a water molecule, and on the other hand, the distribution of electron density in it along the bond between oxygen and chlorine is such that electrons slightly shifted towards oxygen. As a result, the anion has two reaction centers: a nucleophilic center on the oxygen atom and an electrophilic center on the chlorine atom. Taking into account the presence in the GB molecule of one electrophilic reaction center on the phosphorus atom and two nucleophilic ones - on the fluorine and phosphonyl oxygen atoms, we can imagine two options for the formation of the transition state:

The relatively high rate of this step suggests that the polar hypochlorite ion acts both as a nucleophilic reagent and as a polar catalyst for the decomposition of GB. In any case, the result of the first stage of the process is the easy replacement of fluorine in GB with a hypochlorite group:

The resulting compound is very unstable and decomposes with the regeneration (taking into account the alkaline environment) of the hypochlorite ion:

The catalytic effect of the decomposition of GB by hypochlorite ions is confirmed by the strong dependence of the reaction rate on the pH of the medium, with an increase in which the degree of dissociation of hypochlorite molecules into ions increases. Thus, when the substance GB is decomposed by chlorine in an aqueous solution, the reagent is essentially hypochlorous acid, which generates hypochlorite ions in an alkaline environment, i.e. in solution there is an equilibrium:

In an acidic environment, this equilibrium will shift to the left, towards the formation of molecular chlorine, and in an alkaline environment, to the right, towards the formation of ClO - ions. It has been experimentally shown that at pH = 7, hydrolysis of GB occurs at a concentration of molecular chlorine that is 8 times lower than at pH = 6, and at pH = 8 - three times lower than at pH = 7.

The rate of decomposition of GB by aqueous-alkaline solutions of hypochlorites is only 2-2.5 times lower than by aqueous solutions of alkalis, therefore hypochlorites can be used to create polydegassing formulations that make it possible to destroy, along with G-gases, also V-gases and mustard gases.

Catalysts for the decomposition of GB are also many other compounds, for example, sodium, potassium or calcium chromate, molybdate and tungsten acids, the dissociation products of which are the anions CrO 4 2-, MoO 4 2- or WoO 4 2-. The mechanism of their action is similar to hypochlorite ions, but the accelerating effect is significantly (according to some sources, 100 times or more) weaker. In some cases, aqueous or aqueous-alkaline solutions of these substances can be used to degas devices.

8.3 Reactions with alcohols and phenols

sarin toxic paralytic disposal

Isopropyl ester of methylfluorophosphonic acid reacts with alcohols and phenols only in the presence of hydrogen fluoride acceptors (for example, tertiary aliphatic amines, pyridine, etc.) to form medium esters of methylphosphonic acid:

Of practical importance for the purpose of degassing GB are reactions with alcoholates and phenolates of alkali metals in solvents, promoting the dissociation of these compounds, for example:

Nucleophilic RO ions attack the positively polarized phosphorus atom and easily replace fluorine. Since the reaction occurs even in a slightly alkaline environment (at pH 7.6), alcohol solutions of some phenolates, for example sodium cresolate, are used to degas GB on the skin, clothing and other surfaces:

The interaction of GB with phenolates occurs so easily that even dry alkali metal phenolates decompose vaporous GB. This can be used, in particular, to destroy GB adsorbed on clothing after leaving a contaminated atmosphere or upon entering ventilated shelters: clothing is “dusted” with a mixture of finely divided phenolates and talc.

Phenolates with two to three hydroxy groups, two of which are located in ortho position to each other (1,2-dioxybenzene, i.e. pyrocatechol, or even better 1,2,3-trioxybenzene, i.e. pyrogallol), react GB is even easier to handle than regular phenolates, especially if they form a monophenolate ion like:

The increase in the reaction rate is apparently associated with an increase in the electrophilicity of the phosphorus atom due to the transfer of the proton of the free hydroxy group of the bi-, tri-functional phenol to the phosphonyl oxygen GB or the formation of a hydrogen bond between them:

The rate of interaction of GB with di- or trifunctional phenols is comparable to the rate of alkaline hydrolysis.

Alcoholates of alkali metals interact very vigorously with GB (as well as with other known chemical agents) in anhydrous mixtures of even associated neutral and basic organic solvents, which makes it possible to prepare polydegassing formulations based on them. Alkaline alcoholates of amino alcohols or alkoxy alcohols are especially suitable for these purposes.

Conclusion

Nerve agents are a group of lethal agents that are highly toxic phosphorus-containing agents that cause damage to the central nervous system. Such agents are used to defeat unprotected enemy personnel or for a surprise attack on personnel equipped with gas masks. In the latter case, it is meant that the personnel will not have time to use gas masks in a timely manner. The main purpose of using nerve agents is the rapid and massive incapacitation of personnel with the greatest possible number of deaths.

Such substances can enter the human body through the respiratory system, wounds, skin, mucous membranes of the eyes, as well as the gastrointestinal tract (with contaminated food and water).

Bibliography

1. Atamanyuk V.G., Shirshev L.G., Akimov N.I. Civil defense. M., 1986, pp. 49-51

2. Aleksandrov V.N., Emelyanov V.I. Toxic substances M. Military Publishing House, 1990, pp. 65-73

3. Classification of chemical warfare agents - http://zabroha.ucoz.ru/blog/klassifikacija_boevykh_otravljajushhikh_veshhestv/2012-06-12-152

4. http://stvol8.narod.ru/ximorujie/zarin.htm

5. http://weaponsas.narod.ru/Ch_GB.htm

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