Poisoning with organochlorine compounds (hos). Poisoning with organochlorine pesticides and paraquat

OCs are resistant to environmental factors, they all belong to the group of persistent or very persistent drugs. OCs are concentrated in biological food chains, and also have a pronounced material cumulation.

COP is well absorbed by the mucous membranes of the gastrointestinal tract. This is facilitated by their property of lipotropy - CHOS are concentrated in fat-rich tissues. Usually, the greatest amount of these compounds is found in the internal fat, liver, brain and spinal cord, testes and endocrine glands (especially in the adrenal glands).

All CHOS are excreted in the milk of lactating animals. Even with an insignificant content of residues of these substances in the feed, a certain part of them is found in milk (about 20% of the pesticide). Isolation of CHOS in milk may continue after acute poisoning for a year or even more.

All CHOS are excreted with the egg, and almost all of them are associated with the yolk of the egg. Organochlorine pesticides are found in protein only in trace amounts.

Toxicodynamics

Different animal species have different sensitivity to these compounds. Of the laboratory animals, cats are the most sensitive to organochlorine preparations, followed by rats, mice and rabbits. Among farm animals, pigs show the highest sensitivity to organochlorine pesticides, followed by sheep, horses, cattle and chickens.

OCPs are poisons of polytropic action with a predominant violation of the function of the central nervous system and damage to parenchymal organs. With their toxic effect on the organism of animals, there is mainly the same type of hematological, biochemical and immunobiological changes.

In relation to the nervous system, organochlorine preparations manifest themselves mainly as convulsive poisons of central action, stimulating M- and N-cholinergic structures of the central nervous system and its peripheral parts. Damage to the respiratory center, laryngospasm and convulsive contractions of the respiratory muscles lead to the development of asphyxia. The dysfunction of the central nervous system is aggravated by developing tissue hypoxia due to inhibition of tissue respiration due to inhibition of cytochrome oxidase activity. There is a violation of redox processes occurring in mitochondria, and a decrease in the concentration of glycogen in the liver.

Clinical signs

COS poisoning can occur in acute and chronic forms.

OCP poisoning in different animal species proceeds the same way, with a characteristic symptom complex of dysfunction of the central nervous system, increased excitability, increased salivation, impaired coordination of movements and respiratory rhythm, convulsions of the clonic-tonic type, and tremor. Death occurs from paralysis of the respiratory center. The first signs of poisoning appear 15 minutes - 2 hours after the drugs enter the stomach. With a weak or moderate degree of poisoning, nervous phenomena quickly disappear and the animals recover. In severe poisoning, attacks of clonic-tonic convulsions intensify, paresis and paralysis gradually develop, and then a coma.

In acute intoxication, short-term general excitation and an increase in reflex sensitivity, tremor of individual muscle groups, especially the neck and limbs, increased and difficult breathing, impaired cardiac activity, and activation of intestinal motility are noted in animals. Then the excitation is replaced by depression, disorder of coordination of movements, periodic attacks of clonic-tonic convulsions, swimming movements.

In severe cases, with prolonged seizures, the body temperature slightly rises, severe shortness of breath, cyanosis, and a decline in cardiac activity appear. Death, as a rule, occurs as a result of paralysis of the respiratory center.

For cattle in the clinical picture of toxicosis, tongue prolapse, atony of the proventriculus, pain in the scar area, severe thirst, paresis of the hind limbs are characteristic.

In sheep with OCP poisoning, exophthalmia, dilated pupils, blurred vision, and tympania were noted.

Clinically, pigs show loss of appetite, severe depression, and uncoordinated movements. In severe cases, muscle tremors, playpen movements, clonic-tonic convulsions, intense salivation and vomiting, during which part of the poison is excreted with food masses.

Rabbits with poisoning are characterized by a sudden onset of a sharp increase in motor activity (sudden throws, bouncing, throwing around the cage), then clonic-tonic convulsions, paralysis (especially of the pelvic limbs).

In dogs, as well as in pigs, in addition to the nervous syndrome, increased salivation and vomiting are characteristic.

A bird that has received large amounts of OCPs has anorexia, tremors, asphyxia, paresis, paralysis, sudden convulsive throws, shortness of breath with an open beak.

All animals that have undergone OCP poisoning lose a lot of weight.

Pathological picture.

On autopsy of the corpses of dead animals in acute poisoning, no typical changes are found. Usually, the pathoanatomical picture of acute intoxication is characterized by a pronounced blood filling of the internal organs and vessels of the brain, small-focal and diffuse hemorrhages in the lungs, under the epi- and endocardium. In the lungs, congestion, edema, focal emphysema and atelectasis are noted. The mucous membranes are hyperemic. Hemorrhages are possible in the stomach and small intestine. With severe poisoning, edema and a sharp blood filling of the cerebral vessels, multiple hemorrhages in the medulla oblongata and gray matter of the spinal cord were noted. The liver is plethoric, often unevenly colored, the gallbladder is enlarged. In the endocrine glands (adrenals, thyroid and pancreas), hyperemia and small hemorrhages are noted. The spleen is usually enlarged.

Most COP cause serous, fibrinous or hemorrhagic nephritis, purulent myocarditis. Most OCPs at toxic doses cause damage to the walls of blood vessels. In the endocrine glands, pronounced hyperemia and small hemorrhages, in severe cases, dystrophic and necrotic changes (adrenals, thyroid, pancreas, testes).

Treatment.

1. Stopping the convulsive action of pesticides by combining anticonvulsants and sedatives (seduxen, phenobarbital), which provide a quick and prolonged blocking of the motor areas of the central nervous system.

2. Prevention of paralysis of the respiratory center during the development of intoxication (use of ephedrine hydrochloride).

3. Prevention of hepatotoxic action by introducing hepatoprotectors and donators of sulfhydryl groups (glutathione, metathion).

4. Blocking the pro-oxidant action of pesticides by using antioxidants (tocopherol acetate, sodium selenite).

5. Increasing the antitoxic function of the liver and normalizing the exchange of blood electrolytes (glucose-salt solution).

A good therapeutic effect is achieved with intravenous or intramuscular administration of chlorpromazine at a dose of 2 mg/kg at the onset of clinical symptoms of intoxication.

Then phenobarbital is applied at a dose of 50 mg / kg (in the form of a 10% solution on dimethyl sulfoxide), both intramuscularly and subcutaneously. The combination of these drugs allows you to quickly and effectively stop convulsions and transfer animals to a state of deep sleep. This condition in small animals is maintained by repeated administration of sodium barbital (at a dose of 100 mg/kg, subcutaneously or intramuscularly).

In order to reduce the negative prooxidant effect of pesticides and provide a hepatoprotective effect, sodium selenite is administered (0.2 mg/kg or tocopherol acetate intramuscularly at a dose of 1–2 ml of a 10% solution). A medicinal mixture is administered intravenously, containing: 1.0 g of methionine, 5.0 g of glucose, 0.2 g of ascorbic acid in 20 ml of isotonic sodium chloride solution.

The functional state of the central nervous and cardiovascular systems, as well as respiration is maintained by the administration of caffeine and ephedrine hydrochloride in the usual therapeutic doses.

To prevent acidosis and restore the composition of electrolytes, a glucose-saline solution is administered intravenously (glucose - 5.0 g; calcium chloride - 1.0 g; sodium chloride - 0.6 g; magnesium chloride - 0.2 g; water for injection - 100 ml) and sodium bicarbonate (4% solution, 1-2 ml/kg).

At the same time, enhanced vitamin therapy (thiamine bromide, pyridoxine and cyanocobalamin) is carried out in higher therapeutic doses.

To maintain cardiac activity, a 10% solution of calcium chloride or gluconate (0.5-1 ml / kg), 20-40% glucose solution (2 ml / kg), subcutaneously - a 20% solution of caffeine or cordiamine in usual doses are administered intravenously.

Anticonvulsants and sedatives: chlorpromazine (2 mg / kg), alcohol - for ruminants, chloral hydrate - for horses (in subnarcotic doses), phenobarbital (50 mg / kg), medinal (100 mg / kg) - for small animals.

Specific pathogenetic hepatoprotective action is provided by repeated administrations of methionine (25 mg/kg or glutathione (100 mg/kg) and ascorbic acid (5 mg/kg) in combination with glucose and vitamin E (5-10 mg/kg).

A good effect is given by intravenous or subcutaneous administration of unitiol at a dose of 10-20 mg/kg of body weight, since it restores thiol enzymes blocked by lipid peroxides.

Prevention

All agricultural enterprises must strictly comply with the established rules for the storage, transportation and use of organochlorine pesticides.

Feeding to animals seed grain treated with organochlorine preparations, as well as green mass from cultivated lands, grazing animals on them earlier than the established "waiting periods" is prohibited. Plants collected from areas treated with organochlorine pesticides should be examined for the presence of residues of the respective preparations.

Organochlorine compounds (OCs), as a rule, are used in agriculture to control pests of cereals, fruit trees, vegetables and field crops. Apply in the form of aerosols, dusts, emulsions and solutions. Of the entire group of COS, chlorindane, heptachlor, chlorthene, polychlorocamphene, and hexachlorobenzene are of the greatest practical importance. They are poorly soluble in water and well in organic solvents, including fats. All have pronounced cumulative properties and can persist in the external environment for a long time (for many years). Thus, the pesticide DDT is found in the soil even 8-12 years after application, so it is not currently used. COS is heat-resistant and can accumulate in foods of plant and animal origin.
COS enter the human body mainly through the respiratory system, the digestive tract and intact skin. Excreted by the kidneys, through the gastrointestinal tract and mammary glands.
Pathogenesis. COS have a general toxic and polytropic effect on the body. They are able to penetrate into nerve cells rich in lipoids, and also accumulate in lipoids of parenchymal organs. This explains the formation of symptoms of damage to the central nervous system and liver during intoxication with them. The accumulation of CHOS in the lipoids of parenchymal organs affects the processes of oxidation and phosphorylation occurring in them. In this regard, disturbances in carbohydrate metabolism, as well as changes in protein biosynthesis, are possible. The biochemical mechanism of action of COS, in all likelihood, is associated with the blockade of the respiratory enzymes of cells - cytochrome oxidase. Some of them, such as chlorindan, heptachlor, are capable of inhibiting, blocking the SH-groups of thioenzymes and proteins.
Many pesticides accumulate in the body, so when they enter, even in a small amount, the danger of poisoning is not excluded. They are sensitizers and can lead to the development of allergic reactions. There is an individual and age sensitivity to the action of HOS. Some people are hypersensitive to their action. Depending on the nature and duration of the action of the pesticide, its concentration, as well as the reactivity of the organism, acute or chronic poisoning may develop.
Pathological picture. In experiments it was found that in acute poisoning, a pronounced plethora of internal organs and the brain, small-focal and diffuse hemorrhages in the lungs are observed. Histologically, loosening and swelling of the walls of the vessels are noted, in the cerebral cortex - dystrophic changes in nerve cells, in the muscle of the heart - single small-focal infiltrates from cells of the lymphoid type and histiocytes; cloudy swelling of the liver and kidney cells, in some cases - the phenomenon of extra-capillary serous-desquamative glomerulonephritis.
Pathomorphological studies in chronic poisoning also indicate perivascular and pericellular edema with degenerative changes in the nerve cells of the brain. Foci of hemorrhages and degenerative-inflammatory changes in the lungs, liver, kidneys, and myocardium are revealed. In the nervous system, changes are in the nature of a diffuse dystrophic process.
clinical picture. The symptomatology is peculiar, depending on the form of intoxication and the route of intake of COS. So, when they enter through the respiratory organs, the greatest manifestations are noted in the upper respiratory tract and bronchi. In such cases, the first signs of intoxication may be redness of the mucous membranes of the eyes and throat, runny nose, nosebleeds, cough. If HOS entered the body through the gastrointestinal tract (more often observed in case of poisoning at home), nausea, vomiting, abdominal pain, and stool disorders appear. When the skin is contaminated, dermatitis, eczema, more often of an allergic nature, are noted.
Acute intoxication. Immediately after the poison enters the body or after some time, clinical symptoms of poisoning are detected: severe weakness in the legs, headache, dizziness, nausea, vomiting, fever up to 39 ° C. Sometimes there is general lethargy, twitching in the arms and legs, tremor. In the future, shortness of breath, cyanosis, and cardiac weakness are noted. As the disease progresses, symptoms of damage to the liver, kidneys and lungs are revealed. All this is accompanied by severe acidosis. The greatest changes are noted in the central nervous system.
The clinical picture of acute poisoning resembles that of toxic encephalitis with a predominant lesion of the subcortical region. In severe cases, ataxia, attacks of clonic-tonic convulsions, mental disorders, visual impairment are observed. Sometimes asthmatic bronchitis, tracheitis develop. In the peripheral blood - leukopenia, relative lymphocytosis, elevated ESR. Protein is found in the urine.
chronic intoxication. The disease develops gradually. Headaches, dizziness, insomnia appear, appetite decreases, mental and physical fatigue, increased irritability are noted. In the future, symptoms of trembling of the limbs, pain in them, especially along the nerve trunks, emotional lability, and increased sweating develop. Often, patients are concerned about dry cough, palpitations, pain in the region of the heart. In such cases, there is neurocirculatory dystonia, more often of a hypotonic type. The borders of the heart are enlarged with a shift to the left, the tones are muffled. On the ECG diffuse changes in the myocardium are determined. All this fits into the picture of myocardiopathy. Functional disorders of the central nervous system are characteristic, most often proceeding according to the type of asthenovegetative syndrome. Symptoms of diencephalic insufficiency may also develop. Observe a perversion of skin sensitivity, a change in vision. Chronic poisoning is accompanied by bronchitis, gastritis, hepatitis, impaired renal function (in the urine - protein, erythrocytes, cylinders). Some patients develop eczema, pyoderma. In the blood, leukocytosis, elevated ESR, reduced amount of hemoglobin and red blood cells.
In the clinical course, the following syndromes are conditionally distinguished: asthenovegetative, polyneuritic, cardiovascular, hepatic. Usually the disease proceeds in a compensated manner. However, complications are possible in the form of the development of pulmonary heart failure, bronchiectasis and bronchial asthma.
Treatment. In case of acute intoxication, the victim is removed from the polluted atmosphere, the skin is cleaned and the mucous membranes are washed with 2% sodium bicarbonate solution or isotonic sodium chloride solution. In case of irritation of the nasal mucosa (runny nose, sneezing), a 2-3% solution of ephedrine is instilled into the nose. In case of irritation of the trachea, bronchi (persistent painful cough), warm milk is used with the addition of 2% sodium bicarbonate solution (U4 teaspoon per 1 glass) or in half with alkaline mineral water, mustard plasters on the chest, inside codeine, dionine. Oxygen inhalations are shown. 20 ml of a 40% glucose solution and 500 mg of ascorbic acid are administered intravenously, vitamin B intramuscularly! (30-50 mg). When excited, barbiturates are used (carefully), phenobarbital, hexenal is administered intravenously. Intramuscularly - cocarboxylase (0.05 g), pyridoxine (1 ml of a 5% solution), calcium gluconate (5 ml of a 10% solution). Morphine preparations are contraindicated.
Treatment for chronic intoxication should be symptomatic. Shown are vitamin therapy (C, B^, Wb, B12)> the introduction of glucose with ascorbic and nicotinic acids intravenously, biogenic stimulants (aloe, plasmol, etc.), lipotropic agents and lipocaine in the presence of signs of liver damage. In cases of allergic manifestations, desensitizing therapy is prescribed (calcium chloride, ascorbic acid, diphenhydramine, suprastin). Persons who have undergone intoxication should receive a diet rich in lipotropic substances, calcium salts, and vitamins for a long time. Showing subsequent dispensary observation, treatment in sanatorium conditions.

According to their physical and technical properties, most of them are neurotropic and parenchymal poisons, many of them have irritating properties and cause reactions from the gastrointestinal tract, upper respiratory tract and skin. Due to the pronounced ability to cumulate, the intake of even small amounts can lead to chronic poisoning. They enter the human body through the respiratory system, the gastrointestinal tract, intact skin. Excreted by the kidneys, intestines.

The mechanism of action of organochlorine compounds is not well understood. It is believed that when they get into the blood and then into the cells, they block the respiratory enzymes of cells, inhibit oxygen consumption, disrupting the processes of phosphorylation oxidation and inhibit the cytochrome oxidase activity of tissues. The picture of acute poisoning, despite the similarity of clinical syndromes, can be very diverse, depending on the specific product. A pronounced difference in individual sensitivity is characteristic. The symptom complex of acute poisoning depends only on the route of entry and on the dose or concentration. When it enters the digestive tract, gastrointestinal disorders are first observed, then dysfunction of the central nervous system. With inhalation poisoning, there is a cough, runny nose, sometimes with fetid secretions, nosebleeds. The intake of certain products through the skin is accompanied by redness, rashes, dermatitis.

DDT (dichloro-diphenyl-trichlorothane) and hexochlorane (the product of the addition of 6 chlorine atoms to the benzene ring) is a white crystalline powder with a specific odor. The maximum allowable concentration is 0.1 mg/m. Enter through the respiratory system, gastrointestinal tract, can be absorbed through the skin (in organic solvents). They have a cumulative effect, accumulating in the liver and kidneys. They come out slowly. They can cross the placenta, be excreted in the milk of a nursing mother (contact between pregnant and lactating women is unacceptable). Both drugs inhibit the activity of a number of cellular enzymes, in particular the cytochrome system, as well as esterases, in particular cholinesterase.

Acute intoxication. The first signs of the disease appear a few hours after poisoning and develop gradually. The earliest symptoms of irritation of the mucous membranes of the oral cavity and upper respiratory tract will be: salivation, sneezing, a feeling of soreness in the throat, coughing, conjunctivitis. Then join the headache, dizziness, nausea, general weakness, lowering the temperature to 38-40, palpitations, pain in the epigastric region and in the right hypochondrium. Within a few days, the phenomena from the upper respiratory tract increase - tracheitis-bronchitis - bronchopneumonia with characteristic subjective symptoms is possible. The manifestations of damage to the nervous system are increasing. In mild cases, these are disorders of the type of asthenic-vegetative syndrome - fatigue, irritability, emotional instability, increased tendon reflexes, decreased sensitivity, and muscle weakness increase. In more severe cases, hand tremors, convulsions, paresis and paralysis join. In severe poisoning, the phenomena of toxic encephalitis develop - severe headaches, hyperkinesis (choreic movements), sweeping tremor of the hands, with a tendency to generalize and move to the body and head, convulsions and paralysis, visual impairment, death from respiratory paralysis. In parallel, liver damage and kidneys. The liver is enlarged, painful on palpation. In the urine albuminuria, gross hematuria, casts. In contact with the skin in mild cases - erythema and swelling with moderate itching and burning, in neglected cases - acute dermatitis.

Treatment. In case of acute poisoning with DDT and hexochlorane, the victim should be taken out of the area contaminated with the drug, and clothing should be changed. Oxygen inhalations are prescribed. In case of ingestion, gastric lavage with a solution of bicarbonate of soda or warm water, then an adsorbent, saline laxatives (magnesium) are given. 405 glucose solution with ascorbic acid (300 mg), 10% CaCL2 solution IV due to developing hypocalcemia, vitamin B1 -30-50 mg are intravenously injected. In order to prevent liver damage, large amounts (up to 2 liters) of glucose 5% in enemas and / in. Subcutaneous insulin - 5-10 units. In case of respiratory and circulatory disorders - lobelin 15 - 1.0 s / c, cordiamin - 25% - 2.0 s / c, camphor. In case of contact with the eyes, rinsing (with saline or water. In case of contact with the skin, pour over with soap and water. Excitation phenomena are stopped by the appointment of sedatives - camphor bromide, luminal. For convulsions - chloral hydrate in enemas.

In cases of chronic poisoning, nutrition is of great importance - limit the amount of fat, a diet rich in vitamins and carbohydrates. Prohibit drinking alcohol. Pay special attention to the state of the nervous system and liver. Shown in / in the introduction of glucose with ascorbic acid, insulin subcutaneously. Calcium gluconate intramuscularly. Vitamins LK, P, B1, lipocaine, cottage cheese. Rational employment is of great importance.

Prevention: The main principles of prevention are: observance of safety regulations, sanitary supervision of storage and use of pesticides, proper organization of preliminary and periodic examinations of workers. Persons who work with poisons. They are supplied with gas masks, protective clothing and footwear, safety goggles and respirators. Each person involved in the work with pesticides is given special food (0.5 liters of milk per day) and soap (400g per month). When working with powdered poisons and spraying drugs, the volatility of which is low, be sure to wear anti-dust valve respirators, goggles and gloves. When carrying out works on fumigation with strong acid, chloropicrin, dichlorates, metal bromide, a gas mask should be used. When working on pollination, spraying and pickling with highly toxic volatile preparations, it is necessary to use respirators with gas mask cartridges.

Every day after the end of the work, the outer clothing should be carefully calculated, and the underwear should be changed every 2-3 days. It is forbidden to take overalls home and store them in residential premises; they must be stored in warehouses in a specially designated place. After work, it is daily shaken out and knocked out in the open air (persons performing this work must wear gas masks or respirators) and regularly (once every ten days) are washed in a hot soapy soda solution.

The unused poisons remaining after the end of the work should be taken into account and immediately sent to the place of permanent storage. Places of preparation of working compositions after completion of work must be plowed or dug up.

When preparing poisonous working compositions, it is necessary to be careful not to get the poison into the eyes, lips and other parts of the body, especially wet from sweat. Cattle should not be allowed close to the place of preparation of poisonous working compounds and the latter should not be left unguarded in the field. Warning signs should be posted at work sites and especially on logs passing through cultivated areas. Grazing. Mowing grass, picking mushrooms and berries on the territory treated with poisons is not allowed.

While working with poisons, it is not allowed to eat, smoke, drink. For smoking, drinking and eating, special places should be set aside where it is forbidden to walk in overalls. Before eating, drinking and smoking, be sure to wash your hands with soap and water, and after work, face. The duration of the working day when working with poisons should not exceed 6 hours, and with potent substances 4 hours, and the completion of 2 hours is carried out on other processes not related to pesticides.

Block

During a periodic medical examination of the workers of the phosphorus plant, one of the workers complained of fatigue, sleep disturbance, pain in the muscles of the upper limbs, slight swelling of the joints of the hands, periodic pain in the right hypochondrium, bitterness in the mouth, nausea, and belching. Equipment repair worker. For 26 years it has been in contact with phosphorus and its inorganic compounds exceeding the MPC by 3 times. On examination, the hand is cyanotic, cold to the touch, hyperhidrosis of the palms. The terminal phalanges are edematous……..

Exercise: 1. Based on the examination data, make a diagnosis. Intoxication with phosphorus and its compounds. Chronic intoxication, because the history of work experience is 26 years of work in conditions where the MPC of phosphorus exceeds 3 times. 2. Make a decision about the patient's ability to work.

Option number 7

1. What effect does phosphorus have on the body:

a) + general resorptive and cauterizing

2. What indicates the severity of poisoning in case of lead intoxication:

a) +hypochromic anemia

3. Of the group of mercury-containing compounds, the following are of greatest practical importance: granosan and mercuran

4. In severe intoxication with amino and nitro compounds of benzene, erythrocytes form:

a) +Heinz bodies

5. Select the number of periodic inspections when working with manganese:

d) + once every 12 months

6. Name the broad-spectrum pesticides:

c)+insectofungicides

7. Where is phosphorus deposited:

a) + in bones and liver

8. In case of intoxication with amino and nitro compounds of benzene, the blood becomes chocolate-brown in color due to the high content in it of:

a) + methemoglobin

9. Violation of porphyrin biosynthesis and gemma-pathogenetic mechanism of intoxication:

b) + lead

10. Choose an antidote:

e) + vitamin B

Organochlorine pesticides are most widely used in various sectors of agriculture as insecticides, acaricides for pre-sowing seed treatment, soil fumigation, dusting and spraying of grain, vegetable, fruit and industrial crops. This group of pesticides combines compounds of various chemical structures: chlorine derivatives of cycloparaffins (hexachlorocyclohexane), benzene (chlorobenzene), terpenes (polychloropinene), diene series compounds (aldrin, heptachlor, thiodan), etc. A feature of these compounds is resistance to the environment, they dissolve well in fats and lipids and are able to accumulate in body tissues.

Pathogenesis. The toxic effect of organochlorine compounds is associated with a change in a number of enzyme systems and a violation of tissue respiration. GV Kurchatov considers pesticides of this chemical group as lipid-soluble non-electrolytes capable of passing through all the protective barriers of the body. Clinical symptoms of acute and chronic intoxication with organochlorine compounds are characterized by a wide variety of symptoms and symptom complexes, confirming the polytropic nature of their action.

Clinic. Features of clinical manifestations in acute intoxication largely depend on the route of entry of the poison into the body. When pesticides come into contact with inhaled air, signs of irritation of the upper respiratory tract and bronchi (acute bronchitis) appear first of all; Following local manifestations of toxic effects, when large amounts of pesticides enter the body, signs of damage to the central nervous system appear: headache, dizziness, tinnitus, which is accompanied by cyanosis, and skin hemorrhages may appear. The main form of manifestation of acute intoxication on the part of the nervous system is toxic encephalitis with damage to the subcortical parts of the brain. In severe cases, attacks of generalized convulsions occur, sometimes of an epileptiform nature, collaptoid and coma.

When large amounts of poison enter the body, the development of toxic-allergic myocarditis, toxic liver damage (before the development of liver cirrhosis), and nephropathy is possible. Sometimes, with repeated contact after suffering acute intoxication, damage to the blood system occurs (hypo- and aplastic anemia, panmyelophthisis, etc.). In the late period after acute intoxication with hexachlorane and other compounds, signs of damage to the peripheral nervous system may appear with the development of vegetative-sensory polyneuritis (polyneuropathy). The pathological process in these cases is characterized by a diffuse lesion of the nervous system by the type of encephalopolyneuritis or encephalomyelopolyneuritis.

Clinical picture of chronic intoxication organochlorine pesticides is characterized by the consistent development of toxic asthenia, asthenovegetative or asthenoorganic syndrome. In the latter, microorganic symptoms are observed, indicating the predominant localization of the pathological process in the brain stem. At the same time, hyposthenic manifestations of asthenia predominate and cerebral angiodistonic paroxysms occasionally occur: an intense headache suddenly appears, accompanied by nausea, general weakness, hyperhidrosis, paroxysmal dizziness, pallor of the skin, bradycardia. In the later stages of chronic intoxication, the peripheral nervous system is involved in the pathological process, vegetative-sensory polyneuritis or a mixed form of polyneuritis is observed.

In severe chronic intoxication, diffuse damage to the nervous system (encephalopolyneuritis) is possible with scattered small-focal organic symptoms, static-coordinating disorders and involvement in the toxic process of the extrapyramidal and hypothalamic regions, auditory nerves, and cervical autonomic nodes. Disorders of the nervous system are accompanied by endocrine disorders (inhibition of the activity of the adrenal cortex and insular apparatus of the pancreas, hyperfunction of the thyroid gland); in severe forms of intoxication, pluriglandular insufficiency may develop with leading hypothalamic disorders (hyperglycemia, arterial hypertension, obesity).

A certain place in the clinical picture of chronic intoxication is occupied by changes in the cardiovascular system (vegetative-vascular dystonia of hypo- or hypertonic type, myocardial dystrophy, toxic-allergic myocarditis).

The initial stages of chronic intoxication with organochlorine compounds are characterized by dysfunctions of the stomach, liver, kidneys; in later stages, signs of chronic gastritis with a hypoacid orientation, hepatitis, and nephropathy may appear. These disorders are more benign than in acute intoxications.

Significant changes in chronic intoxication occur in the blood, the main of them are hypochromic anemia, leukopenia due to granulocytes, thrombocytopenia; ESR tends to slow down.

Organochlorine compounds are widely used in agriculture to control pests of fruit trees, cereals, vegetables and field crops. Organochlorine pesticides include substances of various chemical origins:

chlorine derivatives of aromatic hydrocarbons (hexachlorane, hexachlorobenzene, hexachlorobutadiene, pentachlorophenol, etc.);

chlorine derivatives of terpenes (polychloropinene, chlorthene, polychlorocamphene, etc.);

diene chlorine derivatives (chlorindan, heptachlor, aldrin, dieldrin, endrin);

chlorinated hydrocarbons (dichloroethane, chlorecrin), ethersulfonate, etc.

As insecticides, COS are used in the form of dust, aqueous suspensions, mineral oil emulsions, solutions, aerosols. All CHOS are insoluble in water and highly soluble in organic solvents and fats. As a result, they can enter the body not only through the respiratory tract and digestive tract, but also through intact skin. Most COSs are characterized by significant stability in the external environment and thermal stability, due to which they retain their insecticidal activity and toxic properties for humans and animals for a long time after application. COS intensively accumulate (material cumulation) in the organs and tissues of the body rich in lipids (subcutaneous adipose tissue, liver, brain, kidneys). The processes of their metabolism and detoxification occur in the liver. COS are excreted with feces and urine, it is also possible to excrete them with breast milk (in women who are breastfeeding).

MACs for COS range from 0.001 mg/m3 (chlorindan, heptachlor), 0.1 mg/m3 (DDT, hexachloran) to 2 mg/m3 (ethersulfonate).

Due to the unequal chemical structure and physico-chemical properties, the toxicity of COS is different. Thus, the greatest toxicity is inherent in the group of compounds of the diene series (heptachlor, chlorindan), other pesticides are classified as moderately toxic and low toxic substances (ethersulfonate).

Pathogenesis

HOS have a general toxic polytropic effect on the body. Due to their ability to selectively accumulate in lipid-rich tissues, they are predominantly neurotoxic and hepatotoxic poisons. The accumulation of cholesterol in parenchymal organs leads to disruption of metabolic processes, primarily the processes of oxidation and phosphorylation, which is associated with inhibition of the activity of respiratory enzymes: cytochrome oxidase, a number of dehydrogenases. Some HOS (chlorindan, heptachlor) are able to block sulfhydryl groups, reduce the activity of thiol enzymes and structural proteins. Under the influence of CHOS, significant disturbances in carbohydrate metabolism and protein synthesis occur. They are also classified as sensitizing substances that can cause the development of allergic reactions. Occupational bronchial asthma, urticaria, allergic rhinitis, dermatitis, eczema may occur as a result of contact with HOS. In addition, COS have gonadotoxic and embryotoxic effects. In the experiment, under the influence of low concentrations, the duration and number of ovarian cycles, the number of fetuses decrease. The teratogenic effect of COS is also known: a decrease in the viability of newborn animals, a relatively shorter body length, a slower increase in body weight, and a lag in physical development.

Pathological picture

In acute poisoning with COS, a pronounced plethora of internal organs and the brain, small-focal and diffuse hemorrhages in the lungs are observed. Histologically, loosening and swelling of the vessel walls, degenerative changes in brain neurons are detected, in the myocardium - single small-focal infiltrates from lymphocytes and histiocytes, cloudy swelling of liver and kidney cells, signs of extracapillary serous-desquamative glomerulonephritis.

In the case of chronic poisoning, pathomorphological examination reveals perivascular and pericellular edema with degenerative changes in brain neurons. They detect foci of hemorrhages and degenerative-inflammatory changes in the lungs, liver, kidneys, and myocardium. In the nervous system, changes are in the nature of a diffuse dystrophic process.

Clinical picture

Acute intoxication.

Acute poisoning occurs as a result of a short-term effect of significant concentrations of CHOS on the body of workers during one work shift. COS is characterized by a polytropic effect with a predominant lesion of the nervous system, parenchymal and hematopoietic organs. Along with the general toxic resorptive effect, they have a local irritating effect. The clinical picture of acute COS poisoning depends on how pesticides enter the body. So, with inhalation intake, the highest intensity of signs of poisoning is observed in the upper respiratory tract and bronchi. If CHOS entered the body through the digestive tract, dyspeptic symptoms predominate: vomiting, diarrhea, intense abdominal pain, etc. An allergic component is often present in the clinical picture of acute poisoning. So, when the skin comes into contact with COS, dermatitis, eczema of allergic origin develop.

In acute poisoning of mild and moderate severity, patients complain of a feeling of fatigue, general weakness, intense headache, dizziness, pain, paresthesia and weakness in the limbs, increased salivation and sweating, lack of appetite, nausea, vomiting, a feeling of constriction in the projection of the esophagus, pain in the epigastric region and right hypochondrium, in the region of the heart, dry cough, shortness of breath, fever, fever, diarrhea. An objective examination reveals conjunctivitis, blepharospasm, trembling of the eyelids and facial muscles, nystagmus, visual impairment, fever up to 38-39 ° C, red dermographism, hyperhidrosis. Signs of acute toxic rhinitis, laryngitis, tracheobronchitis develop (runny nose, cough, shortness of breath). Characteristic symptoms of the cardiovascular system are arterial hypotension, tachycardia, tachypnea.

In severe poisoning with CHOS

In patients, the abdomen is tense, painful on palpation in the epigastric region and right hypochondrium, the liver is enlarged, painful on palpation. With an increase in the severity of poisoning, lethargy, trembling and cramps of the muscles of the limbs increase. Later, muscle hypotension, hyporeflexia, nosebleeds occur as a sign of hemorrhagic diathesis, dysuric manifestations, symptoms of kidney damage (albuminuria, microhematuria, cylindruria), acidosis.

In severe poisoning with COS, clouding of consciousness, stupor, coma, general tonic and clonic convulsions, flaccid or spastic paresis (paralysis) of the limbs, severe shortness of breath, turning into suffocation (acute toxic pulmonary edema, acute toxic pneumonitis), arterial hypotension, tachycardia, arrhythmias are observed. , blurred vision, a significant increase in body temperature (up to 40 ° C). In peripheral blood, leukocytosis, eosinophilia, a decrease in the number of erythrocytes, hemoglobin content per unit volume of blood, and an increase in ESR are determined. In the case of extremely severe acute poisoning with CHOS, the victim may die within 1-2 hours.

chronic intoxication.

COS have pronounced cumulative properties, so for some time intoxication occurs latently, asymptomatically. The initial signs of intoxication are general weakness, fatigue, insomnia, irritability, excessive sweating, numbness of the limbs, aching pain in the heart, cough, shortness of breath and palpitations with little physical exertion, loss of appetite, bitter taste in the mouth, nausea, periodic pain in epigastric region and right hypochondrium, not associated with eating, a tendency to frequent and prolonged acute respiratory infections. Over time, there are trembling of the limbs, pain and paresthesia in them, especially in the projection of the nerve trunks, emotional lability. The described symptoms of chronic COS intoxication fit into the clinical syndromes of lesions of the nervous (asthenovegetative syndrome, polyneuropathy), cardiovascular systems (toxic cardiomyopathy, arterial hypotension, autonomic dysfunction), respiratory organs (chronic toxic bronchitis), digestive organs (atrophic gastritis, toxic hepatitis) .

In the initial stages of chronic intoxication, the secretory function of the stomach is disturbed, for stages II-III, the development of chronic atrophic gastritis with insufficiency of the secretory function of the stomach, up to histamine-resistant achylia, is characteristic. There is also some phase in the development of renal dysfunction: at the initial stage, functional activity slightly increases due to increased renal circulation and glomerular filtration, and at later stages, as a result of the development of toxic nephropathy, kidney function is significantly impaired, signs of azotemia appear. In rare cases, hemorrhagic vasculitis may develop. The characteristic signs of chronic COS intoxication include disturbances in the activity of the endocrine glands (decreased activity of the adrenal cortex, islets of Langerhans, hyperthyroidism). In severe stages of intoxication, diencephalic syndrome sometimes occurs, occurring in the form of vegetovascular crises or vegetative-endocrine disorders. Some patients develop eczema, pyoderma, occupational bronchial asthma as a result of COS sensitization. Most often there is a combination of functional disorders of many systems as a result of the polytropic action of COS. In the blood, leukopenia is detected due to a decrease in the number of granulocytes, relative lymphocytosis, thrombocytopenia, mild hypochromic anemia.

Diagnostics

Diagnosis of COS intoxication is based on the data of the sanitary and hygienic characteristics of working conditions, clinical symptoms of poisoning. Early diagnosis of chronic intoxication with COS is difficult, since the initial signs are in the form of functional disorders of the central nervous system. They gradually progress, become more pronounced and proceed according to the type of toxic encephalomyelopolyneuropathy. Of the visceral syndromes, toxic hepatitis, toxic cardiomyopathy, chronic toxic bronchitis, COPD of toxic origin are most often observed. Determining the level of organochlorine pesticides in the blood and urine is of particular importance in the diagnosis of intoxication.

Diagnosis example: chronic intoxication as a result of prolonged exposure to a complex of pesticides, mainly organochlorine compounds, stage II, asthenovegetative syndrome, toxic hepatitis with a predominance of cytolytic and hepatodepressive syndromes, moderately severe hypochromic anemia. Occupational disease.

Treatment

To provide emergency assistance in case of acute poisoning with COS, the victims must be taken out of the premises contaminated with pesticides. If HOS gets on the skin, they must be removed with a swab and the skin washed with an alcohol-alkaline solution, or warm water and soap, or a 2-5% solution of sodium bicarbonate. If eye damage occurs, they should be immediately rinsed with clean running water for 10-15 minutes and 2-3 drops of a 30% solution of sulfacyl sodium should be instilled. If the poison enters the body through the mouth, it is urgent to induce vomiting (1 ml of a 1% solution of apomorphine hydrochloride) and rinse the stomach (through a tube) with water (10-15 l) with an adsorbent (activated carbon), 2% sodium bicarbonate solution, 2% solution magnesium sulfate or 1-2% sodium thiosulfate solution. After 10-15 minutes, the victim should take a saline laxative (30 g of magnesium sulfate in 300 ml of water with 30 g of activated charcoal), after 30 minutes, a siphon enema should be done.

When COS enters the body through the respiratory tract and there are symptoms of acute toxic rhinitis, 2 drops of a 2-3% solution of ephedrine or sofradex should be instilled into each nostril. If there are symptoms of irritation of the larynx, trachea, bronchi (cough), inhalations of a 2% sodium bicarbonate solution with a 0.5% solution of novocaine, bronchodilators (salbutamol, asthmapent, berotek) and mast cell membrane stabilizers (intal, cromolyn sodium) are indicated. In addition, antihistamines are prescribed (1 ml of a 1% diphenhydramine solution intramuscularly), corticosteroids (1-2 ml of a 3% solution of prednisolone) for the prevention of acute toxic pulmonary edema, and oxygen therapy is also carried out.

Patients with acute COS poisoning are shown active infusion therapy: intravenous drip injection of 500-800 ml of 5% glucose solution and isotonic sodium chloride solution with the addition of 5-10 ml of 5% ascorbic acid solution, 4 ml of 5% thiamine bromide solution, 2 ml of 1% riboflavin solution and 2 ml of 2% pyridoxine solution; neohemodesis is also shown. The daily volume of infusion therapy is 6-8 liters. It is advisable to carry out forced diuresis (60-120 mg of lasix or 100 g of mannitol intravenously). In the presence of hypocalcemia, calcium gluconate (10 ml of a 10% solution) or calcium chloride is administered intravenously.

With significant psychomotor agitation, chlorpromazine, sibazon, haloperidol are prescribed. In the case of seizures, 40-60 ml of a 20% solution of sodium hydroxybutyrate is used intravenously or 10 ml of a 25% solution of magnesium sulfate intramuscularly. With arterial hypotension, collapse, sulfocamphocaine, caffeine, cordiamine are indicated. The introduction of adrenaline (analogues) is contraindicated, since COS increase the sensitivity of myocardial receptors to it (sudden cardiac arrest is possible). In case of sudden respiratory arrest, 1 ml of a 1% solution of lobelin hydrochloride is administered intravenously. Morphine is contraindicated.

For the prevention and treatment of toxic hepatitis, lipotropic agents (a-lipoic acid), parenteral vitamins of group B and vitamin C, hepatoprotectors (glutargin, essential phospholipids (livovin), heptral, hepadif) are used.

The most effective in the treatment of acute poisoning with COS is the early use of efferent methods of extracorporeal detoxification: plasmapheresis, plasma sorption, lymphosorption, in case of impaired renal function - hemodialysis.

Treatment of chronic intoxication with CHOS is symptomatic. For functional disorders of the nervous system, citicoline (ceraxon), nootropil (piracetam, lucetam, fezam), vitamin therapy (milgamma, neurovitan), glutamic acid, trioxazine, bellaspon, adaptol, physiotherapy are recommended. In case of damage to the peripheral nervous system, vitamins of group B, vitamin C, biogenic stimulants (aloe, plasmol, phosphobion, ATP), balneotherapy, low-frequency electromagnetic (bioresonance) therapy, acupuncture, therapeutic exercises are prescribed.

With anemia, iron preparations, cyanocobalamin, folic acid, sodium nucleinate, pentoxyl are prescribed. Symptoms of hemorrhagic diathesis are stopped by rutin, vitamin P, ascorbic acid. It is necessary to carry out desensitizing therapy (antihistamines, calcium gluconate, UVI blood). Persons who have undergone COS intoxication should follow a diet enriched with lipotropic substances, proteins, calcium salts, and vitamins for a long time. Constant dispensary observation, periodic sanatorium-and-spa treatment is shown.

Working capacity examination

In case of acute poisoning with COS, temporary suspension from work associated with exposure to toxic substances is recommended. In the presence of chronic intoxication, the patient is transferred to work without contact with pesticides; work with significant physical exertion and under conditions of intense solar radiation is also contraindicated. In addition, further contact with COS is excluded in case of recurrent dermatitis, organic lesions of the nervous system, toxic hepatitis.

Prevention

To prevent COS poisoning, careful preliminary and periodic medical examinations, sanitary supervision of the storage and use of pesticides, the use of personal protective equipment when working with them, limiting the time of contact with chemicals (duration of the working day - 6 hours for work associated with the influence of hexachlorane, heptachlorane ).