Occupational diseases caused by exposure to chemical factors. In the national economy of the country, chemical substances, which are diverse in structure and physicochemical properties, are used. In production conditions, toxic substances enter the human body through the respiratory tract, skin, and gastrointestinal tract. After resorption into the blood and distribution to the organs, poisons undergo transformations, as well as deposition in various organs and tissues (lungs, brain, bones, parenchymal organs, etc.). Isolation of toxic substances that have entered the body occurs by the lungs, kidneys, through the gastrointestinal tract, by the skin.

Depending on the set of manifestations of the action of a chemical substance and from the organs and systems that are predominantly affected by it, industrial poisons can be combined into the following groups: irritating action; Neurotropic action; Hepatotropic action; Poisons of blood; Kidney poisons; Industrial allergens; Industrial carcinogens. Such a division is highly arbitrary, characterizes only the basic direction of the action of poisons and does not exclude the manifold nature of their influence.

Diseases caused by exposure to irritants. The main groups of irritant toxic substances are:

-chlorine and its compounds (hydrogen chloride, hydrochloric acid, chloric lime, chloropicrin, phosgene, chlorine-phosphorus oxide, phosphorus trichloride, silicon tetrachloride);

• Sulfur compounds (sulfur dioxide, sulfur dioxide, hydrogen sulphide, dimethyl sulfate, sulfuric acid);
• Nitrogen compounds (nitrogases, nitric acid, ammonia, hydrazine);
• Fluorine compounds (hydrogen fluoride, hydrofluoric acid and its salts, perfluoroisobutylene);
• Chromium compounds (chromic anhydride, chromium oxide, potassium and sodium dichromate, chromic alum);
• Carbonyl compounds of metals (nickel carbonyl, iron pentacarbonyl);
• Soluble beryllium compounds (beryllium fluoride, beryllium fluoride, beryllium chloride, beryllium sulphate).

All these compounds, penetrating the body by inhalation, cause predominantly the defeat of the respiratory system; Some of them can irritate the mucous membranes of the eyes. In acute intoxications, the severity of the damage to the respiratory tract is determined not only by the concentration of the chemical in the air and the duration of its action, but also by the degree of solubility of the poison in the water. Toxic substances, easily soluble in water (chlorine, sulfur dioxide, ammonia), act mainly on the mucous membranes of the upper respiratory tract, trachea and major bronchi. The action of these substances occurs immediately after contact with them. Substances that are difficult or almost insoluble in water (oxides of nitrogen, phosgene, dimethyl sulfate) affect mainly the deep parts of the respiratory system. Clinical signs, when exposed to these substances, usually develop after a latent period of varying duration. When exposed to tissues, toxic substances cause an inflammatory response, and in more severe cases, tissue destruction and necrosis.

Acute toxic damage to the respiratory system. The following clinical syndromes can be observed: acute damage to the upper respiratory tract, acute toxic bronchitis, acute toxic bronchiolitis, acute toxic pulmonary edema, acute toxic pneumonia.

With acute damage to the upper respiratory tract develops acute toxic laryngopharyngotracheitis. In mild cases, the victims complain of difficulty nasal breathing, perspiration and a feeling of scarring in the throat, burning behind the sternum, dry coughing, hoarseness. On examination, there is hyperemia of the mucous membranes of the nasal cavity, mouth, pharynx, larynx and trachea. The mucous secretions accumulate in the nasal cavity, nasal conchae and vocal folds swell. The process is usually easily reversible and ends with recovery within a few days.

When exposure to high concentrations of irritants develop more pronounced changes: against a background of severe hyperemia of the mucous membrane of the upper respiratory tract, areas of necrosis at the site of burns, an abundance of mucopurulent discharge in the nasal cavity and trachea. In such cases, the process can be delayed and recovery occurs in 10-15 days or more. In a number of cases, especially when an infection is attached, the process acquires a protracted course and chronic catarrhal inflammation of the nasal cavity, larynx and trachea can develop.

When exposed to very high concentrations of irritants, reflex reactions may predominate with spasm of the glottis; Marked hiccup, accompanied by whistling (stridoroznoe breath), and in some cases, lightning death due to asphyxiation. All these phenomena develop before the onset of inflammatory changes in the mucous membranes of the respiratory tract and require the provision of emergency care.

Acute toxic bronchitis is characterized by a diffuse lesion of the bronchial tree. The first signs of the disease, as a rule, appear immediately after exposure to a toxic substance. The clinical picture is determined by the depth of the bronchial wall and its prevalence. In mild cases, the victims complain of a dry painful cough, pain and sore throat, constriction and burning in the chest, shortness of breath. Simultaneously, signs of irritation of the upper respiratory tract, often conjunctiva of the eyes (lacrimation, photophobia) are noted. Objectively, hard breathing is sometimes determined with a bronchial shade, against which dry dry rales are heard. Mild cases of the disease, as a rule, have a short course, end in recovery after 3-7 days.

In more severe cases, patients experience burning, stinging and chest pain. Cough agonizing, suffocating, dry, often with attacks, after 2-3 days can be accompanied by the separation of a small amount of sputum, often with a trace of blood. Breathing is often difficult, breathing is noisy. There are some cyanosis of the lips and skin, tachycardia. Breathing is increased to 26-30 in 1 min; The respiratory musculature is involved in respiration. Against the background of hard breathing, dry scattered whistling and coarse buzzing rattles are heard. The phenomenon of acute emphysema is more or less pronounced. Signs of inflammation in toxic bronchitis are less pronounced compared to infectious bronchitis: patients may have fever to subfebrile, in blood-moderate neutrophilic leukocytosis, a slight increase in ESR. Radiologically, as a rule, changes are not determined. Only sometimes there is a slight increase in pulmonary pattern and an expansion of the roots of the lungs. With appropriate care and treatment, the disease after 2-6 weeks may result in complete recovery. However, often acute toxic bronchitis is complicated by infection, it becomes chronic, periodically exacerbated, slowly progresses and leads to the development of peribronchitis and pneumosclerosis.

Acute toxic bronchiolitis. The initial signs of the disease appear after a few hours, and in some cases after 1 -2 days after staying in a zone of high concentrations of toxic substances. The victim has a sharp shortness of breath, a painful cough - dry or with the discharge of thick mucous sputum, often with an admixture of blood. There are attacks of suffocation, stitching pain in the chest, profuse sweating, headache, loss of appetite, general weakness. The body temperature rises to 38-39 "C. During examination, pronounced cyanosis of the skin and mucous membranes is noted, breathing is increased to 36-40 per 1 minute. Box light is detected above the lungs, the edges of the lungs are lowered, their mobility is limited. Small bubbling wet wheezing.The disease is accompanied by severe tachycardia, a drop in blood pressure, deafness of heart sounds, often the liver becomes involved, which increases and becomes painful, there may be signs of nephropathy (proteinuria, cylindruria) .In peripheral blood - increased hemoglobin, erythrocytes, Leukocytosis with a stab, a relative lymphopenia, sometimes eosinophilia and an increase in ESR up to 50 mm / h. Radiographically, against the background of reduced transparency of pulmonary fields in the middle and lower regions, small focal formations are observed), sometimes merging with one another, expanding the roots of the lungs. For 2-3 nights. The outcome can be a complete recovery or transition to a chronic form with the development of obliterating bronchiolitis and pneumosclerosis.

Acute toxic pulmonary edema is the most severe form of lesion; Most often caused by nitrogen oxides. Leading importance in its development belongs to an increase in the permeability of the alveolar and capillary walls of the lungs. During the disease, several stages are conventionally distinguished: the stage of initial phenomena (reflex), hidden phenomena, clinical manifestations, reverse development. In the stage of the initial phenomena, which immediately develops after the action of a toxic substance, the victim has a slight irritation of the mucous membranes of the respiratory tract and eyes: a small cough, a swelling in the nasopharynx, tightness in the chest, and pain in the eyes. After 15-30 minutes, these symptoms disappear and a latent stage occurs, lasting 2-24 hours (an average of 4-b h). Gradually, the period of relative well-being is replaced by the stage of clinical manifestations. The victim gets more breathing, there is a cough with phlegm, cyanosis; The auxiliary muscles begin to take part in the respiratory act; The lower border of the lungs drops, the percussion sound acquires a boxy tint. In the lower parts of the lungs there appear sonorous small bubble moist wheezing, the number of which increases with the development of the disease. Serious and large bubbling wet rales appear. Breathing becomes bubbling. A large amount of foamy sputum is often separated from the blood. Tachycardia develops. Blood pressure remains normal or slightly increases. Blood clotting is determined: the amount of hemoglobin is increased to 100-120 g / l, erythrocytes up to 6-8 ¬10 (in the twelfth degree) / l, leukocytes up to 10-15 € 10 ^ l. Increase the viscosity and coagulability of blood. X-ray - a decrease in the transparency of lung tissue, blurred and blurred vascular-bronchial pattern, focal spotted darkening, reminiscent of "melting snow flakes." The oxygen content in the arterial blood drops sharply, and carbon dioxide increases. Developed widespread cyanosis and acrocyanosis pale violet hue ("blue hypoxemia").

At this stage, a symptom complex of "gray hypoxemia" can also be observed, in which the leading cause is a fall in cardiovascular activity (collapse). The patient's face becomes ashy-gray, covered with a cold sweat. Mucous membranes acquire a peculiar earthy shade. The limbs are cold and wet to the touch. The pulse becomes frequent, threadlike, difficult to palpate. Blood pressure drops sharply. In addition to arterial and venous hypoxemia, hypocapnia appears.

Severe forms of the disease can lead to death 24-48 hours after poisoning. A particularly unfavorable prognostic attitude is "gray hypoxemia." In more mild cases and timely treatment, the stage of reverse development occurs, usually on the third day after poisoning. Becomes less pronounced dyspnea and cyanosis, the amount of sputum is reduced. Decrease, and then damp rales disappear. The composition of peripheral blood is normalized. Recovering occurs within a few days or weeks.

With toxic pulmonary edema, neuropsychic disorders are often observed: the victims complain of a headache, dizziness; Emotional instability, irritability, a sense of anxiety, a depressive hypochondriacal state, sometimes arousal and convulsions are noted, and in severe cases, stupor, drowsiness, adynamia, loss of consciousness. At the height of toxic edema, there may be a decrease in diuresis up to anuria. In the urine - traces of protein, hyaline and granular cylinders, red blood cells. These changes are associated with the possibility of developing toxic nephrosis, caused by general vascular changes.

Toxic edema of the lungs is much more severe and is accompanied by a greater lethality than the pulmonary edema of another etiology. The most common complications of toxic pulmonary edema are secondary infection and the development of pneumonia.

Acute toxic pneumonia occurs in the first two days after exposure to toxic substances. At the same time, the symptoms of toxic laryngopharyngotracheitis or bronchitis may first dominate. Then the temperature rises, weakness, weakness, headache. When you cough, sputum is separated, often with an admixture of blood. In the lungs, against the background of hard breathing and dry wheezing, there are areas of small bubble voiced and wet wheezing and (or) crepitus. In the blood, leukocytosis increases. Radiologic examination reveals focal infiltrative changes of a greater or lesser extent. Primary toxic pneumonia, not complicated by infection, usually has a favorable course. At the end of the 5-7th day the process ends with recovery.

In the case of intoxication by some substances of irritating action, the lesions of the respiratory organs are combined with the general toxic effect, which is manifested by a violation of the functions of other systems and organs, primarily the nervous system. Of the irritating substances, hydrogen sulphide is considered the most powerful nerve poison, which, suppressing the enzymes of tissue respiration, leads to the development of histotoxic hypoxia. In this regard, with severe forms of poisoning in the clinical picture, signs of central nervous system lesions predominate (up to the comatose state). The most unfavorable lightning-fast form of poisoning, in which as a result of paralysis of the respiration and the vascular center, death immediately occurs.

The prognosis of acute respiratory tract infections is determined by the degree of severity of poisoning and the initial state of the organism. In some cases, even very severe lesions with appropriate care and treatment can result in complete recovery. Some of the patients who have experienced acute poisonings have been suffering from bronchitis for many months and even years, often exacerbating, taking a chronic course and combining with peribronchitis. The development of fibrotic process leads to pneumosclerosis, emphysema, bronchoectatic changes, cardiopulmonary insufficiency.

Treatment. First aid consists primarily in the immediate cessation of contact with the toxic substance. The victim is taken out of the gassed atmosphere, is released from clothing, and when the poison gets on the skin, it is washed abundantly with water and soap; Urgently hospitalized. Knowing the existence of a latent period when poisoning substances irritating action, even in the absence of signs of intoxication for the victim should be observed for at least 24 hours, creating him complete peace. Only after this, in the absence of any manifestations of intoxication, the rest regime is abolished. When the mucous membranes of the eyes are irritated, they are thoroughly rinsed with water or with 2% sodium hydrogen carbonate solution, with acute pain in the eyes instilled with a 0.1-0.2% solution of dicaine, and to prevent infection, an ophthalmic ointment (0.5% sintomycin, 10 % Sulfacyl) or 30% solution of sulfacyl sodium is instilled. When irritating the mucous membranes of the upper respiratory tract, rinsing with a 2% sodium bicarbonate solution or warm-moist inhalation of this solution is effective. With difficulty in nasal breathing, a 2% solution of ephedrine with addition of adrenaline (1: 1000) is buried in the nose.

When the larynx is affected, a silence regime is necessary; Recommended warm milk with sodium hydrocarbonate, borzhom. With a strong cough appoint codeine and dionine, distractions - mustard, cans. To prevent infection, prescribe sulfonamides and antibiotics. When a secret is accumulated, it must be removed (aspirated) through the catheter. When the phenomena of reflex spasm show antispasmodics (subcutaneous injection of atropine or ephedrine). In cases of severe laryngospasm, tracheotomy and intubation are necessary.

Respiratory disorders of respiration and cardiac activity can be inhaled with a so-called anti-smoke mixture (chloroform 40 ml, ethyl alcohol 40 ml, sulfuric ether 20 ml, ammonia 5 drops), which reduces the reflex receptivity of the receptors. Artificial respiration is indicated only when breathing is stopped, as in other cases it is fraught with the danger of developing pulmonary edema.

With bronchitis and bronchiolitis, complete rest, prolonged inhalation of oxygen, antitussive drugs, inhalation of corticosteroid preparations are shown. To prevent infection, antibacterial therapy is used, a combination of antibiotics and sulfonamides. In asthmatic conditions, bronchodilators and spasmolytics (euphyllin, adrenaline, isadrin), antihistamines (dimedrol, suprastin, pipolfen) are used.

With toxic pulmonary edema, one of the main methods of pathogenetic therapy is the use of urea, which has a powerful dehydrating effect on lung tissue. Sapuretics (furosemide) administered intravenously in a dose of at least 200 mg / day have a similar effect. With the purpose of unloading the small circle of blood circulation, ganglion blockers are used: arfonade, hexonium, pentamine, etc., as well as euphyllin. With a lowered arterial pressure, these drugs should be administered intravenously slowly (with caution and necessarily in combination with pressor amines). To reduce the permeability of the vascular wall, glucocorticoids (prednisolone up to 160-200 mg or hydrocortisone up to 150-300 mg / day), antihistamines (pipolphen), calcium chloride, vitamins of the P and C group, hypertonic glucose solution are used. Among the methods of symptomatic therapy, an important place is occupied by oxygen therapy combined with inhalation of antifoams (ethyl alcohol, antifosilan), under the influence of which the edematous exudate from the foamy state passes into the liquid, which reduces its volume and releases the respiratory surface of the lungs for the diffusion of gases. Effective regular inhalation of oxygen with the addition of bronchodilators (ephedrine), hormones and antibiotics. With the aim of removing the state of emotional stress and motor anxiety, the introduction of a lytic mixture (morphine 10 mg, 25 mg aminazine, 25 mg pylpolene) or neuroleptics (droperidol, etc.) is shown. In cases of vascular tone or cardiac failure, cardiovascular agents (camphor, caffeine, cordyamine, mezaton) or cardiac glycosides (korglikon, strophanthin) are prescribed. The introduction of epinephrine is not indicated because of the possible increase in the phenomena of edema. To stimulate breathing, subcutaneously injected lobeline or cititon. To prevent infection, antibiotics and sulfonamide preparations are prescribed.

Chronic toxic lesions of the respiratory system may be the result of long (10-15 or more years) exposure to relatively small concentrations of irritant substances or single or repeated acute intoxications.

When the upper respiratory tract is affected, chronic rhinitis, pharyngitis and laryngitis can develop, but the combined lesions of the nasal, pharyngeal and laryngeal mucosa are most common. Changes in the mucosa may be catarrhal, subatrophic, atrophic, rarely hypertrophic. Symptomatics and clinical manifestations of toxic lesions of the upper respiratory tract do not differ from those of other etiology.

Chronic toxic bronchitis is characterized by a recurrent and progressive course; The symptomatology of it does not differ from that of chronic bronchitis of another etiology. However, characterized by a large depth of damage to the bronchial tree, toxic bronchitis predisposes to an earlier formation of pneumosclerosis. Progression of pneumosclerosis can occur through the development of bronchiectasis or an increase in pulmonary and cardiac failure, which, however, can often occur simultaneously.

Diseases caused by the action of neurotropic substances. The poisons, which act mainly on the nervous system, include metallic mercury, manganese, arsenic compounds, carbon disulphide, tetraethyl lead, many narcotic substances, including hydrocarbons of the ultimate, unsaturated and cyclic series. In addition, involvement in the pathological process of the nervous system can also occur with intoxication with other chemicals that cause impairments in the functions of various organs and systems (lead, benzene, phthalate and phosphate plasticizers, vinyl chloride, carbon monoxide, diisocyanates and many other chemicals).

In acute and chronic intoxication with neurotropic poisons, various parts of the central and peripheral nervous system are involved in the pathological process. Light acute poisonings are characterized by nonspecific general toxicity: general weakness, headache, dizziness, nausea, etc. In more severe cases, nervous system disorders are observed in the form of acute excitation or oppression, fainting, collapse, coma, convulsions, psychotic disorders. The most severe consequences of acute poisoning are toxic coma or acute intoxication psychosis. With chronic intoxications, the conditions of vegetative dystonia, asthenovegetative, asthenoneurotic phenomena, polyneuropathies are more often noted. As for toxic encephalopathy, now its erased forms predominate, which denote as an astheno-organic syndrome - the appearance against a background of toxic asthenia of neurological microorganic symptoms. With encephalopathy, the brain stem divisions are more likely to suffer, therefore, the cerebellocovestobular, hypothalamic, extrapyramidal and other syndromes are isolated.

Manganese intoxication is encountered in the extraction and processing of manganese ores, in steelmaking and in the production of ferroalloys, in the manufacture and use of manganese-containing electrodes. The disease is caused by the defeat of the nerve cells and the vascular system of the brain and spinal cord, the predominant localization of the degenerative-dystrophic process in the subcortical nodes (the striatum body). The synthesis and deposition of dopamine, adrenergic and cholinergic mediation systems suffer.

In the clinical course, there are 3 stages. Stage I is characterized by asthenia, increased drowsiness, paresthesia and dull pain in the extremities, decreased activity, poor complaints, mild hypomia, muscle hypotension, revitalization of tendon reflexes, distal hypeesthesia. In the second stage of the disease symptoms of toxic encephalopathy increase: apathy, drowsiness, memory loss, a mock-intellectual defect is revealed. Pathognomonic features of extrapyramidal insufficiency: hypomymia, bradykinesia, pro- and retropasia, muscular dystonia. There are manifestations of polyneuropathy. For the III stage (manganese parkinsonism), severe extrapyramidal disorders are characteristic: masculinity of the face, dysarthria, bradykinesia, spastic-parietal, or cock, gait. Criticism to the disease is reduced, violent crying, laughter, a significant mnestic-intellectual defect are noted. Differentiate is necessary from Parkinsonism of a different etiology. The course of the disease is chronic progressive, organic changes are irreversible. If even the initial symptoms of intoxication are detected, further contact with manganese is prohibited.

Treatment is carried out in a hospital. In the 1st stage - injections of vitamins B1, B6, C, novocain IV, inside aminalon; 2-3 courses per year of antidote therapy (calcium-disodium EDTA salt according to the generally accepted scheme). In the II-III stages and in the long-term period, repeated courses of levodopa, midantana, central anticholinergics, drugs that improve blood supply and brain metabolism are shown. The prognosis for work capacity in the 1st stage is favorable, in II and III - unfavorable; In Stage III patients often need care.

Arsenic intoxication is possible in chemical, tannery, fur production, in the dressing of grains, the use of pesticides. Diffusive dystrophic changes in the central and peripheral nervous system are more pronounced in the anterior and lateral horns of the spinal cord, in the peripheral nerves. In production conditions, only chronic forms of intoxication are observed-fluke, rarely of moderate severity, occurring in the form of sensitive (less often mixed) forms of polyneuropathy. The initial hyperesthesia or hyperpathy is replaced by hypnosis on the polyneuritic type. Characteristic burning pain, paresthesia, less weakness in the extremities, possible small muscle hypertrophy, hyperkeratosis, hair loss, white transverse striae on the nails (Mees strips). Possible development of toxic hepatitis.

Treatment see Professional Polyneuropathies. As a specific agent apply unitiol (according to the conventional scheme), sulphide baths. At an intoxication of a mild degree - treatment in out-patient conditions, at an intoxication of average gravity - in the conditions of a hospital. With employment, contact with toxic substances is excluded.

Mercury intoxication is possible during mercury mining, production of measuring instruments, pesticides. The ingestion of metallic mercury is not dangerous.

Mercury is a thiol poison blocking the sulfhydryl groups of tissue proteins; This mechanism underlies polymorphic disorders in the CNS. Mercury has a pronounced tropism to the deep sections of the brain.

Clinically for acute intoxication, mercury vapor is characterized by headache, fever, diarrhea, vomiting, after a few days, hemorrhagic syndrome and ulcerative stomatitis develop. The initial stage of chronic intoxication with mercury vapor proceeds according to the type of vegetovascular dystonia, neurasthenia (irritable weakness, headache, intermittent sleep, drowsiness during the day). Characteristic of small, irregular finger tremor, tachycardia, excessive sweating, "play" of the vasomotors, shine of the eyes. Increases the function of the thyroid gland, adrenal cortex; Dysfunction of the ovaries. Significant intoxication proceeds according to the type of asthenovegetative syndrome. There is a growing headache, asthenia, disturbing persistent insomnia, painful dreams. Characteristic symptom of "mercury eretism" - shyness, self-doubt, with excitement - hyperemia of the face, palpitation, sweating. Typical vascular instability, cardialgia. It is possible to develop a syndrome of hypothalamic dysfunction with vegetovascular paroxysms. As the disease progresses, the syndrome of encephalopathy is formed, and psychopathological disorders increase. Changes in the internal organs are of a disregulatory nature (cardioneurosis, dyskinesia). Often observed subfebrile.

Treatment. To remove mercury from the body, use unitiol (according to the conventional scheme), iv infusion of sodium thiosulphate (20 ml of 30% solution, per course 15-20 infusions), succimer or D-penicillamine, hydrogen sulphide baths. In the initial stage-outpatient or sanatorium treatment, a temporary transfer (for a period of 2 months) to work outside contact with mercury. At the expressed displays - hospital treatment, transfer to other work.

The carbon disulfide intoxication occurs in the production of viscose fibers (silk, cord, staple), cellophane, in the chemical industry (solvent), in agriculture (insecticides). Carbon disulfide causes enzyme-mediator action; Binds to amino acids, forms dithiocarbamic acids, blocks copper-containing enzymes, disrupts the exchange of vitamins B6, PP, serotonin, tryptamine. Has a pronounced tropism to the deep sections of the brain; Violates vegetovascular and neuroendocrine regulation.

Clinic of acute intoxication with mild form resembles intoxication, is reversible. Heavy forms are accompanied by coma, a lethal outcome is possible. After leaving the coma, encephalopolyneuritis is formed.

Chronic intoxication is distinguished by a combination of vegeto-vascular, neuroendocrine and psychopathological disorders with vegetosensory polyneuropathy. In the initial stage, vegetative-vascular dystonia, cerebral asthenia, and light vegetosensory polyneuropathy are revealed. As the disease grows, the stage of organic disorders - encephalopathy - is characterized by a variety of cerebral syndromes; Obligate are hypothalamic syndromes. Characteristic tactile, elementary and hypnagogic hallucinations, senestopathies, violation of the body scheme, mnestiko-intellectual disorders, depression. In the stage of organic disorders, persistent arterial hypertension, hyperlipidemia is often observed. In severe cases of intoxication, it is possible to develop encephalomyelonepineuritis or parkinsonism.

Treatment is carried out in a hospital. The drugs improving the metabolism and blood supply of the brain and peripheral nervous system are shown. Effectively, the appointment of vitamin B6, zntsefabola. With the growth of functional disorders, even at the initial stage, translation into work is necessary, excluding contact with carbon disulfide; At the expressed forms working capacity is steadily lowered.

Intoxication with tevetraethyl lead (TPP) is possible in the manufacture of TPP, the manufacture of mixtures, in the motor transport industry. TPP directly affects all parts of the brain, it has tropism for the hypothalamic departments and reticular formation of the trunk; Leads to a disruption of the metabolism of the brain.

In acute poisoning there is a latent period from 6-8 hours to 2 days. For symptoms and treatment, see Tetraethyl lead in the chapter "Acute poisoning". Clinic of chronic intoxication of TPP and ethyl liquid resembles a clinic of worn out acute intoxication: against a background of persistent headache and insomnia, psychopathological disorders are revealed; Vegetative triad: arterial hypotension, bradycardia, hypothermia; Sensation of "hair in the mouth"; Formed encephalopathy, personality psychopathy.

Clinic of chronic intoxication with leaded gasoline is characterized by vegetative vascular dystonia (cerebral angiodystonia), neurotic disorders (increased excitability, restless sleep, intimidating dreams). With the deepening of intoxication, vegetosensory polyneuropathy, microfocal cerebral symptomatology are revealed. There may be attacks of narcolepsy or muscle weakness. Treatment is non-specific, aimed at mitigating asthenic and psycho-vegetative disorders, improving the metabolism of the brain. Morphine compounds, chloral hydrate, bromide preparations are contraindicated. Treatment of severe psychopathological disorders is carried out in a psychiatric hospital.

Reverse development of the process is possible only with light intoxication, in most cases, it is recommended to transfer to another job; In patients with encephalopathy there may be a complete loss of ability to work.

Intoxication with gasolines. The nature of the action is narcotic, irritating. Pathways-respiratory organs, skin; Is excreted through the lungs, with urine. Acute intoxication is accompanied by headache, irritation of the mucous membranes, flushing of the face, dizziness, a sense of intoxication, euphoria. In severe cases - psychomotor agitation, delirium, loss of consciousness (see also Petrol in the chapter "Acute poisoning"). Chronic intoxications are characterized by asthenovegetative syndrome, neurotic disorders.

Treatment - according to conventional schemes. Diseases of blood caused by the effects of poisons. Depending on the nature of the lesion, four groups of occupational blood diseases are identified.

The first group is characterized by oppression of hemopoiesis and, more rarely, myeloproliferative process. At the heart of the disease - intoxication with benzene and its homologues, chlorine derivatives of benzene, hexamethylenediamine, chlororganic pesticides, etc.; Ionizing radiation. It affects hemopoiesis at the level of polypotent stem cells, which leads to a decrease in their content in the bone marrow and spleen, as well as a violation of the ability of these cells to differentiate. Chronic intoxication with benzene as the most typical representative of the poisons of this group occurs clinically with predominant suppression of hemopoiesis and damage to the nervous system, as well as changes in other organs and systems. An easy degree of intoxication is characterized by moderate leukopenia, thrombocytopenia, reticulocytosis; Possible nasal bleeding, bleeding gums, bruises on the skin. Neurasthenic or asthenovegetative syndrome develops. As the severity of intoxication increases, the severity of hemorrhagic diathesis increases, a tendency to hypotension, a violation of the functional capacity of the liver, myocardial dystrophy, the appearance of symptoms of polyneuropathy, toxic encephalopathy. In the blood - increased leukopenia, thrombocytopenia, anemia (deep pancytopenia); Reticulocytosis is replaced by reticulocytopenia; Increased ESR. In sternal points, compensatory activation of hematopoiesis with mild degree and hypoplasia is severe.

Treatment is carried out in a hospital. With mild degree - vitamins C, P, group B. With hemorrhagic syndrome - vikasol, aminocaproic acid, calcium chloride. Deep pancytopenia requires repeated hemotransfusions in combination with corticosteroid hormones, gemostimulators, anabolic hormones (nerobol). Treatment of other syndromes is symptomatic.

The prognosis is favorable when contact with toxic substances is stopped and adequate therapy is carried out. Rational employment is recommended. With a decrease in working capacity, a referral to VTEK.

The second group is characterized by the development of hypochromic hypersideremic sideroblastic anemia. At the heart of the disease is intoxication with lead and its inorganic compounds.

Lead - thiol poison, blocking sulfhydryl, as well as carboxyl and amine groups of enzymes that provide the process of biosynthesis of porphyrins and heme. As a result of disruption of heme biosynthesis, protoporphyrin and iron accumulate in erythrocytes, in non-hemoglobin iron in serum, and a large amount of deltaaminolevulinic acid (ALA) and coproporphyrin (CP) is released in the urine. Lead also has a damaging effect directly on red blood cells, reducing the duration of their life.

The clinical picture of lead intoxication is composed of several syndromes, the leading of which is the damage of blood and porphyrin metabolism. The initial form is characterized only by laboratory changes in the form of an increase in the number of reticulocytes, basophilic-granular erythrocytes in the blood and ALA and CP in the urine. With a mild form, along with an increase in these shifts, there are signs of asthenovegetative syndrome and peripheral polyneuropathy. For the expressed form, not only the further increase in blood changes and disturbances of porphyrin metabolism, but also the development of anemia, intestinal colic, marked neurologic syndromes (asthenovegetative, polyneuropathy, encephalopathy), signs of toxic hepatitis are characteristic.

With lead colic there is a sharp cramping pain in the abdomen, persistent constipation, arterial hypertension, mild leukocytosis, an increase in body temperature, and the release of urine of dark red color due to hypercoppororphyrinuria. Colic is always accompanied by a marked anemic syndrome.

Diagnosis of intoxication is based on the data of profanamnesis, the results of clinical and laboratory studies. Lead intoxication must be differentiated from blood diseases (hypochromic iron deficiency, hemolytic anemia, thalassemia), porphyria, acute abdomen, lesions of the nervous system and liver of unprofessional etiology.

Treatment is carried out in a hospital. The main method of excretory and pathogenetic therapy is the use of complexones: tetacin-calcium, pentacin, D-penicillamine (according to the generally accepted scheme). Colic is stopped by administering 20 ml of a 10% solution in / in tetacin calcium (up to 2 times on the first day of treatment). In the presence of polyneuropathy and other syndromes, treatment is sympathetic. Recommended foods high in protein, calcium, iron, sulfur; Vegetables, fruits, juices (pectins) are introduced into the diet. Sanatorium-and-spa treatment is shown (Pyatigorsk, Sernovodsk, Matsesta).

The prognosis for the initial and mild form is favorable. In severe form, contact with lead and other toxic substances must be avoided. With a decline in working capacity - the direction of the WTEC.

The third group of occupational diseases of the blood is hemolytic anemia. At the heart of the disease - intoxication with arsenic hydrogen, phenylhydrazine, methyhemoglobin-forming agents (oxidizers, amino and nitro derivatives of benzene).

Pathogenesis: pathological oxidation (oxidative hemolysis), leading to accumulation of peroxide compounds. This leads to functional and structural changes in hemoglobin, irreversible shifts in lipids of erythrocyte membranes, and inhibition of sulfhydryl group activity.

Clinically, with mild intoxication, weakness, headache, nausea, chills, hysteria of the sclera are observed. With the expressed form of the latent period (2-8 hours), there is a period of progressive homolysis, accompanied by growing weakness, headache, pain in the epigastric region and the right upper quadrant, lower back, nausea, vomiting, fever. In the blood - a decrease in hemoglobin, erythrocytopenia, reticulocytosis (up to 200-300 0/00), leukocytosis with a shift to the left. In the urine - hemoglobinuria, protenuria. Urine becomes dark red, sometimes black. Temperature tepe 38-39 gr. C. On the 2nd-3rd day jaundice appears, bilirubinemia increases. On the 3-5th day, the liver and kidneys are involved in the process. With timely treatment, the recovery period lasts from 4 to 6-8 weeks. When poisoning with arsenic hydrogen, symptoms of general toxic effects (myocardiopathy, arterial hypotension, polyneuropathy, etc.) are also observed.

Treatment. The victim is removed from the gassed room and ensures complete peace. Apply antidotes: mekaptid (1 ml of 40% solution in / m, with severe forms up to 2 ml, repeated administration after 6-8 h), antarsin (1 ml of 5% solution w / m). Along with these preparations, unitiol (5 ml of a 5% solution w / m) is administered. For the purpose of detoxification and elimination of symptoms of hepatic and renal failure, forced diuresis, alkalization of plasma, vitamin therapy are used. It shows early hemodialysis. Antibacterial agents and symptomatic therapy are recommended.

The prognosis for mild forms is favorable, with severe-possible residual effects (functional deficiency of the liver, kidneys, anemia) leading to a prolonged decline in ability to work. Prevention: ensuring the clean air environment. Alarm system about the presence in the air of the working zone of arsenic hydrogen.

The fourth group is characterized by the formation of pathological blood pigments - carboxyhemoglobin (HbCO) and mettemoglobin (MtHb). At the heart of the disease - intoxication with carbon monoxide (CO) and methemoglobin-forming agents (amino and nitro compounds of benzene, bertholets salt, etc.).

Pathogenesis: the combination of CO with iron of hemoglobin, the oxidation of hemoglobin by methemoglobin-forming agents of hemoglobin into trivalent leads to the formation of pathological pigments - HbCO and MtHb. As a consequence, hemic hypoxia develops. CO also binds to divalent iron of a number of tissue biochemical systems (myoglobin, cytochrome, etc.), causing the development of histotoxic hypoxia. Hypoxic syndrome leads to the defeat of the central nervous system in the first place.

Symptoms and treatment. Acute intoxication with carbon monoxide - see Carbon monoxide in the chapter "Acute poisoning". In addition to the typical form of CO-intoxication, atypical forms are distinguished: apoplexy (fulminant), fainting and euphoric, characterized by CNS damage and acute vascular insufficiency. Diagnosis of acute intoxication of CO is based on the establishment of the fact of increased concentration of CO in the air of the work zone, clinical data, an increase in the content of HbCD in the blood.

Forecast in the absence of residual phenomena is favorable. In the presence of persistent long-term consequences, the direction to WTEC.

Prevention: systematic monitoring of CO concentration in indoor air. The clinical picture of acute intestinal infections and methemoglobin-forming agents. At a mild degree, cyanosis of mucous membranes, auricles, general weakness, headache, dizziness are observed. Consciousness is preserved. In the blood, the MtHb level does not exceed 20%. With an average degree, the cyanosis of the mucous membranes and skin increases. There is a headache, dizziness, plaited speech, disorientation, uncertainty of gait. Short-term loss of consciousness. Lability of the pulse, shortness of breath, increased tendon reflexes, sluggish response of pupils to light. In the blood, the MtHb level rises to 30-50%, the Heinz-Ehrlich body (erythrocytes with pathological inclusions) is determined. The duration of this period is 5-7 days. Severe degree is manifested by sharp cyanosis of the skin and mucous membranes, severe headache, dizziness, nausea, vomiting. There are prostration, alternating with a sharp excitement, clinical-tonic convulsions, involuntary defecation and urination, tachycardia, hepatomegaly. In the blood, the MtHb level is more than 50%, the number of Heinz-Ehrlich bodies reaches 50 ° / dd and more.

On the 5th-7th day, secondary hemolytic anemia develops, accompanied by reticulocytosis, macrocytosis and normoblastosis. Hemoglobinuria can lead to kidney syndrome. Relapses of intoxication caused by the release of poison from the depot (liver, adipose tissue) and the re-formation of MtHb are noted. This is facilitated by drinking alcohol, a hot shower. Duration of intoxication - 12-14 days. With medium and severe forms, there may be signs of toxic damage to the liver.

Chronic intoxication with methaemoglobin agents is characterized, in addition to regenerative anemia, by liver, nervous system (asthenovegetative syndrome, vegetovascular dystonia), eye (cataract), urinary tract (from cystitis to bladder cancer). The development of these syndromes depends on the chemical structure of the poison.

Diagnosis of intoxication is based on the data of sanitary-hygienic characteristics, clinical and laboratory studies (MtHb, Heinz-Ehrlich body). Treatment. Oxygenotherapy. With hypocapnia, short-term inhalation of the carbogen; Iv injection of 1% methylene blue solution (1-2 ml / kg in 5% glucose solution), chromosomal, 50-100 ml of 30% sodium thiosulfate solution, 30-50 ml of 40% glucose solution with ascorbic acid; In / m 600 μg of vitamin B12. In very severe forms - blood substitution (at least 4 liters). According to the indications - forced diuresis; Symptomatic therapy. Treatment of chronic intoxication is symptomatic.

Forecast in the absence of residual phenomena is favorable. In the presence of persistent consequences - the direction of the WTEC.

Diseases caused by exposure to hepatotropic substances. Among the chemicals, a group of hepatotropic poisons is isolated, intoxication which leads to liver damage. These include chlorinated hydrocarbons (carbon tetrachloride, dichloroethane, tetrachloroethane, etc.), benzene and its derivatives (aniline, trinitrotoluene, styrene, etc.), some pesticides (mercury, chlorine and organophosphorus compounds). Hepatic syndrome is observed under the influence of a number of metals and metalloids (lead, arsenic, fluorine, etc.), monomers used to produce polymeric materials (nitrile acrylic acid, dimethylformamide, etc.).

Intoxications of the listed compounds occur in their production or use as solvents, the starting products for the production of aromatic compounds, organic dyes in various industries, in agriculture.

Pathogenesis. The chemical directly acts on the hepatic cell, its endoplasmic reticulum and the membranes of the endoplasmic reticulum of the hapatocytes, which is accompanied by a violation of membrane permeability with the release of enzymes into the blood and a decrease in protein synthesis. Allergic mechanism of development of toxic hepatitis also has significance.

Clinical picture. In its course, toxic hepatitis can be acute and chronic. Acute liver damage develops on the 2nd-5th day after intoxication and is characterized by an increase in the liver, its painful palpation, and increased jaundice. The degree of expression of these changes depends on the severity of intoxication. A significant increase in the activity of enzymes to serum: alanine and aspartate aminotransferase, lactate dehydrogenase, fructose monophosphate aldolase; Hyperbilirubinemia with predominance of the fraction of bilirubinglucuronide, as well as urobilinuria and bile pigments in the urine. In severe cases hypoproteinemia with hypo-albuminemia, a reduced amount of beta-lipoproteins and phospholipids in the blood. One of the signs of hepatic insufficiency is hemorrhagic syndrome - from microhematuria to massive bleeding.

In the development and course of acute occupational hepatitis, in contrast, primarily from viral hepatitis A (Botkin's disease), a number of features are noted that have differential diagnostic significance. Thus, for acute toxic hepatitis is characterized by the absence of splenomegaly, leukopenia, less severity of dyspeptic disorders. In addition, acute professional hepatitis occurs against the background of other clinical manifestations, characteristic of this or that intoxication. Timely treatment usually leads to a fairly rapid recovery (in 2-4 weeks) with restoration of liver function. The clinical picture of chronic toxic hepatitis is very scarce. Patients complain of a decrease in appetite, bitterness in the mouth, dull pain in the right upper quadrant, worsening after acute and fatty foods, unstable stools. The will in the right hypochondrium can have a paroxysmal character with irradiation in the right scapula and arm. There is icterity of the sclera, less frequent icterus of the skin, moderate enlargement of the liver, soreness in her palpation, positive symptoms of gallbladder irritation. Dyskinesia of the gallbladder is observed; Moderate hyperbilirubinemia due to an increase in the fraction of free bilirubin in mild forms of hepatitis, and at expressed ones - due to bilirubinglucuronide or both of its fractions; A moderate increase in the activity of enzymes in the blood, including fructose monophosphate aldolase. The protein spectrum of blood serum is changed due to moderate hypoalbuminemia and hypergammaglobulinemia. The course of chronic toxic hepatitis is usually benign, and after elimination of the harmful factor, complete recovery is possible, but in some cases development of cirrhosis of the liver is noted.

Diagnosis of occupational toxic hepatitis is carried out taking into account other symptoms and syndromes characteristic of this or that intoxication. Treatment is carried out in a hospital. When the poison is ingested, gastric lavage (10-15 l of water) followed by 150 ml of vaseline oil or 30-60 g of salt laxative. The first day after poisoning shows a combination of methods of forced diuresis with the use of diuretics (urea, mannitol, furosemide). In the presence of symptoms of intoxication - hemodialysis or blood substitution. Lipotropic drugs - intravenously drip 30 ml of 20% choline chloride solution together with 600 ml of 5% glucose solution, B vitamins, vitamin E intramuscularly 1 ml 4-6 times a day, trasilol, countercala, cocarboxylate, tutamic acid, antioiotics. Symptomatic therapy. With chronic toxic liver damage of mild degree-therapeutic nutrition, vitamin therapy, cholagogue, duodenal sounding. Infusion of IV glucose, lipotrol drugs (choline chloride, methionine, lipid). Treatment in an outpatient setting. In severe forms or exacerbation of chronic hepatitis apply sirep, progepar, hepalon. Treatment in hospital. Sanatorium treatment: Borjomi, Jermuk, Essentuki, Zheleznovodsk, Pyatigorsk, Morshin, Truskavets.

The prognosis is favorable. The ability to work is determined by the severity of intoxication, residual phenomena, age, the profession of the patient and working conditions.

Diseases caused by the effects of kidney poisons. This group of diseases consists of toxic kidney nephropathies, kidney damage caused by chemicals, heavy metals and their compounds (mercury, lead, cadmium, lithium, bismuth, etc.), organic solvents (carbon tetrachloride, dichloroethane, ethylene glycol), hemolytic poisons (arsenious hydrogen , Phenylhydrazine, methemoglobin-forming agents).

Pathogenesis: direct toxic effect on the kidney tissue and disorder of renal blood flow on the background of a violation of the general circulation. Immunological (toxic-allergic) mechanism of kidney damage is also possible.

Clinical picture. Renal damage is one of the nonspecific syndromes of acute and chronic intoxication. However, with a number of acute intoxications, toxic nephropathy can play a dominant role in the clinical picture, and with chronic cadmium poisoning, kidney damage takes a leading place in the intoxication clinic. Toxic kidney damage is manifested by acute renal failure (ARF), chronic tubulointerstitial nephropathy, acute and chronic glomerulonephritis. In hemoglobinuria nephrosis - one of the forms of arterial hypertension caused by intoxication with hemolytic poisons - hemoglobinuria, proteinuria, oliguria, which is transferred in severe cases to anuria, are observed.

For nephronecrosis ("excretory" necrosis), caused by compounds of heavy metals, characterized by pronounced opiguria, mild proteinuria, microhematuria, rapidly growing uremia. OPN is also observed in cases of intoxication with glycols, chlorinated hydrocarbons.

Chronic tubopointerstitsialnaya nephropathy develops with chronic intoxications with salts of heavy metals and, first of all, cadmium. Cadmium nephropathy is manifested by proteinuria with the release of low-molecular proteins (beta (two) -microglobubins). The development of slowly progressing anemia is possible. An increase in the amount of beta (two) micro-globulins in urine is an early sign of cadmium intoxication.

Treatment. The main principle of treating OPP is the fight against shock and hemodynamic disorders, removal of the nephrotoxic agent from the body (see Acute Renal Failure). Toxic nephropathy with chronic occupational intoxications does not require special medical measures.

The prognosis depends on the form of the toxic arsenic. In some cases, the transition of OPN to CRF is possible.

One form of occupational lesions of the urinary tract is benign swelling of the bladder (papilloma) followed by transformation into cancer (aromatic amine compounds - benzidine, alpha and beta-naphthylamine).