Causes of bronchial asthma

The main predisposing factors for the development of bronchial asthma factors are currently considered:

• heredity;
• atopy;
• hyperreactivity of the bronchi.

G. B. Fedoseev attributed to predisposing factors also biological defects of healthy people.

[1]

Heredity and bronchial asthma

Hereditary predisposition to bronchial asthma is revealed in 46.3% of patients, if one parent has bronchial asthma, the probability of developing a bronchial asthma in a child is 20-30%, and if both parents are sick, it reaches 75%. In general, it is considered that the risk of developing bronchial asthma in a child whose parents have signs of atopy is 2-3 times higher than that of a child from parents who do not have it.

At present, a polygenic type of inheritance of predisposition to bronchial asthma is assumed.

Genetic markers of predisposition to bronchial asthma are certain HLA antigens (the main histocompatibility complex located on the short arm of the 6 chromosome, the genes controlling the 2 and 4 components of the complement, the B-factor of theperdin, and the genes that control the immune response-Ir- genes).

As established by EN Barabanova (1993) and MA Petrova (1995), antigens B13, B21, B35 and DR5 are much more common in patients with bronchial asthma compared to healthy people. There are reports of frequent occurrence in patients with bronchial asthma also of antigens A2, B7, B8, B12, B27, DR2. The presence of these antigens significantly increases the risk of developing bronchial asthma. In contrast, antigens A28, B14, BW41, DR1 are "protective" against the development of bronchial asthma.

Currently, two asthmatic genes have been found in mice that cause bronchial hypersensitivity (hyperreactivity).

In humans, the main genes of predisposition to bronchial asthma are contained in chromosomes 5 and 11, with a cluster of IL4 genes playing a special role. It is believed that the genetic basis of bronchial asthma is represented by a combination of genetic predisposition to the development of atopy and hyperreactivity of the bronchi. Each of these genetic predisposition factors significantly increases the likelihood of bronchial asthma.

Atopy

Atopy is the body's ability to produce an increased amount of IgE (reactin) in response to the effects of environmental allergens. At the same time, the level of IgE is raised in the blood of patients, positive skin tests with allergens are noted, and in the anamnesis there are indications of various manifestations of allergy.

Atopy is extremely often present in patients with bronchial asthma and their next of kin. The ability to synthesize IgE is under genetic control and is inherited.

[2], [3], [4], [5], [6], [7], [8]

Hyperreactivity of the bronchi

Hyperreactivity of the bronchi is an increased reaction of the bronchi to an irritant effect, while the development of bronchospasm is possible. This same effect in most healthy individuals does not cause a bronchospastic reaction. It is established that the ability to hyperreactivity of the bronchi is also inherited.

In 1996, F. Kummer reported that individuals predisposed to the development of bronchial asthma, identified changes in 4, 5, 6, 11 chromosomes, responsible for bronchial hyperreactivity in contact with exoallergenic (mainly proteinaceous nature).

Biological defects in practically healthy individuals

This predisposing factor is also of great importance, because under the influence of various causes (exacerbation of chronic respiratory diseases, contact with allergens, neuropsychic stress, chemical irritants, adverse weather conditions, etc.), a clinical manifestation of these defects occurs and bronchial asthma develops.

According to GB Fedoseev, biological defects can be the following:

• defects at the level of the whole organism (defects in the functioning of the immune, nervous, endocrine systems);
• defects at the organ level (hyperreactivity of the bronchi to biologically active substances, pollutants, allergens, violation of the local bronchopulmonary protection system);
• defects at the cellular level (mast cell instability, excessively high release of biologically active substances in their degranulation, dysfunction of eosinophils, macrophages and other cells);
• defects at the subcellular level (defects of membrane-receptor complexes, in particular, reduced activity of beta2-adrenoreceptors, disturbances of the oxidant-antioxidant system, etc.).

[9], [10], [11], [12], [13],

Causal factors of bronchial asthma

Under the influence of causative factors, in fact, predisposing factors, including biological defects, actually occur, and bronchial asthma develops.

[14], [15],

Allergens

Allergens are the main etiological factor of bronchial asthma.

[16], [17]

Household allergens

The main representative of household allergens is house dust. It contains various substances: the remains of various tissues, particles of the epidermis of man and animals, allergens of insects, pollen of plants, fungi (most often antigens of mold fungi - rhizopus, mucor, alternative, penicillium, etc.), bacteria, library dust and other components.

However, allergenic properties of house dust are caused, first of all, by ticks. More than 50 species of mites were found in house dust. The most important are Dermatophagoides pteronissinus, Dermatophagoides farinae, Dermatophagoides microceras and Euroglyphis mainei. Typically, Dermatophagoides pteronissinus (54-65%), Dermatophagoides farinae (36-45%) dominate in the dwelling houses, barnacles of the family Acaridae (27%) and Euroglyphis mainei (14%) are less common.

In 1 g of household dust can contain several thousand ticks. Places of their habitation are bedding (pillows, mattresses, blankets), carpets, upholstered furniture, feather beds. The most optimal conditions for the life of mites are air temperature 25-27 ° C, humidity 70-80%.

Ticks D. Pteronissinus eat scales of the epidermis, their life span is 2.5-3 months, the female lays 20-40 eggs, the period of their development is about 6 days.

Ticks are ubiquitous, except for areas with arctic climate and high-altitude areas. At an altitude of 1,000 m above sea level, only single mites are found, and at an altitude of more than 1600 m they are absent. The mites die at temperatures above 60 ° C and at temperatures below 1b-18 ° C.

Allergenic activity is possessed by the feces of mites - a particle about 10-20 μm in size. These particles enter the respiratory tract along with the inhaled air. In D.pteronissinus allergens of 7 groups, D.farinae - 3, D.microceras - 1 have been identified. Methods of enzyme immunoassay have been developed for the determination of mite allergens in house dust.

Home dust and ticks contained in it cause the development of not only allergic bronchial asthma, but allergic rhinitis, urticaria, atopic dermatitis, and Quincke edema.

Bronchial asthma, caused by sensitization to house dust, has the following characteristics:

• often there are night attacks of suffocation, since at night there is a close contact of the patient with bedding and the allergens of domestic dust contained in them;
• year-round patient is disturbed by attacks of bronchial asthma, if he permanently resides in his apartment, as the contact with home dust continues constantly, but attacks disappear or decrease when the patient is outside the home environment (business trip, hospital, etc.);
• bronchial asthma often worsens in the cold season (during this period the apartment tries to increase the air temperature and it becomes optimal for mites, in addition, at this time, the saturation of residential premises with dust);
• bronchial asthma exacerbated when cleaning the apartment, shaking carpets, etc .;

Epidermal allergens

Epidermal allergens include particles of the epidermis, dandruff, animal wool (dogs, cats, cows, horses, pigs, rabbits, laboratory animals), birds, as well as allergens of the epidermis and human hair. In addition, allergens are also contained in saliva, urine, feces of animals and birds.

The most frequent source of allergens are cats. Every fourth patient with bronchial asthma does not tolerate contact with the cat. The main allergens of cats are found in wool, saliva and urine.

In patients with epidermal allergies, it is possible to develop severe allergic reactions even to the first administration of tetanus, rabies, antidiphtheria, antibotulinemic sera, immunoglobulins and other protein preparations. This is due to the presence of antigenic similarity of epidermal allergens (primarily, horse dander) and blood plasma proteins.

[18], [19], [20], [21], [22], [23]

Injectable allergens

Insect allergens are allergens of insects (bees, bumblebees, wasps, mosquitoes, midges, cockroaches, etc.). Allergens of insects get into the blood of a person through the blood (with bites), by inhalation or by contact. Especially great is the role of cockroaches, allergens are contained in their saliva, faeces, tissues. The poison of insects contains biogenic amines (histamine, serotonin, acetylcholine, etc.), proteins (apamin, melittan), enzymes (phospholipase A2, hyaluronidase, proteases, etc.). Allergens are proteins and enzymes. The remaining substances contribute to the development of toxic, inflammatory and bronchospastic effect. Melittin, along with an allergenic effect, can also cause degranulation of mast cells and histamine release.

The strongest allergens are also daphnia - a component of the feed of aquarium fish.

Insect professional asthma is possible (on silk-processing production due to sensitization to butterfly's papillo-damp dust, in beekeeping).

Pollen allergens

Pollen of many plants has allergic properties and causes allergies - pollinosis (allergic rhinitis, conjunctivitis, bronchial asthma). Antigenic properties are due to the proteins contained in it. Pollinosis can be caused by 200 species of plants, pollen has sizes up to 30 microns and deeply penetrates the respiratory tract, causing bronchial asthma. Pollen of trees contains 6 antigens, herbs - up to 10 antigens. The most common are the following types of pollen, which causes bronchial asthma:

• pollen of grasses (timothy, hedgehog, foxgrass, ryegrass, fescue, bluegrass, grass, nettle, plantain, sorrel, ragweed, wormwood);
• pollen of flowers (buttercup, dandelion, daisy, poppy, tulip, etc.);
• pollen bushes (dog rose, lilac, elder, hazelnut, etc.);
• pollen of trees (birch, oak, ash, poplar, willow, chestnut, pine, alder, etc.).

The most common pollen bronchial asthma occurs in the following terms: from mid-April to the end of May (flowering trees); June-July (flowering of meadow grasses); August-September (pollen of weeds appears in the air). Exacerbations of the disease occur, as a rule, during the stay outside the city, in the forest, in the meadows, in the country, in the hike, in the village. Especially bad patients suffer from windy weather, since at that time there is an abundance of pollen in the air. As a rule, pollen bronchial asthma is combined with other manifestations of pollinosis - allergic rhinitis and conjunctivitis, less often - hives, dermatitis, edema Quincke.

It is extremely important for a practical doctor to know about the possibility of cross-sectional food allergy and intolerance of certain medicinal plants in patients with pollen bronchial asthma.

Fungal Allergens

Allergy to fungi is detected in 70-75% of patients with bronchial asthma. The most allergenic are fungi of the genera Penicillium, Aspergillus, Mucor.Alternaria, Candida. Mushrooms and their spores are part of house dust, present in the air, on the soil, on the skin, in the intestines. Spores mold molds inhaled in the upper and lower respiratory tract. Among antigens of fungi, the most allergenic are the cell wall lipoproteins, both spore and mycelium.

It has been established that fungi and their antigens cause the development of I, II or IV types of hypersensitivity by Gell and Coombs. Bronchial asthma caused by fungi is often accompanied by intolerance to foods containing mushrooms (beer, kvass, dry wines, lactic acid products, antibiotics), fungal skin lesions. The condition of patients worsens in wet weather, while staying in a damp room (especially with the growth of mold on the walls). Many patients have a seasonal pattern of exacerbations of fungal bronchial asthma. For example, bronchial asthma caused by Alternaria, Candida mushrooms is more often exacerbated during the warm season and less often in winter. This is due to the fact that the concentration of spores of these fungi increases in the warm months of the year. With bronchial asthma caused by fungi of the genera Penicillium, Aspergillium, there is no seasonal course of the disease, as the amount of spores of these fungi in the air remains high throughout the year.

Fungi can also cause occupational bronchial asthma due to their use in industry and agriculture (production of antibiotics, enzymes, vitamins, hormones, beer, bread, lactic acid products, yeast, protein-vitamin concentrate).

Food allergens

Food allergy is the cause of asthma in 1-4% of adults. The most allergenic products are: milk (its main antigens are casein / beta-lactoglobulin, alpha-lactoglobulin), chicken eggs (the main antigens are ovalbumin, ovomucoid, ovo-transferrin), wheat flour (contains 40 antigens), rye flour 20 antigens), fish, meat.

Cross-allergy to medicines

A drug	Preparations to which there is a cross-provoking allergy (they can not be used for allergy to allergies to drugs, named in the first column)
Euphyllin, diaphylline	Derivatives of ethylenediamine (suprastin, ethambutol)
Acetylsalicylic acid (citramone, aspen, ascofen, sedalgin, etc.)	Non-steroidal anti-inflammatory drugs and preparations containing them (baralgin, maxigan, spasmalgon, trigan, spazgan, teofedrine, pentalgin, etc.).
Novocaine	Local anesthetics (anesthesin, lidocaine, dicaine, trimecaine), sulfonamides, sulfanylurea derivatives for the treatment of diabetes mellitus, diuretics (dichlorothiazide, cyclomethiazide, furosemide, bufenox, clopamid, indapamide)
Iodine	Radiopaque substances, inorganic iodides (potassium iodide, Lugol's solution), thyroxine, triiodothyronine
Penicillin and its derivatives	Cephalosporins

Some products can cause the development of bronchial asthma due to the high content of biogenic amines and their liberators (citrus fruits, strawberries, strawberries, tomatoes, chocolate, cheese, pineapples, sausages, beer). Food intolerance is often caused by special food additives and dyes, which are contained in fruit juices, drinks, sausages, sausages, sweets and other products, confectionery, canned food.

[24], [25], [26], [27], [28], [29], [30]

Medicinal allergens

Drugs may cause an exacerbation and worsening of the course of bronchial asthma in 10% of patients (Hunt, 1992). Medications can also be a direct cause of asthma. The mechanisms of development of drug bronchial asthma are different, which is due to the peculiarities of the action of the drugs themselves. The following mechanisms are known for the development of bronchial asthma under the influence of medications.

Medicinal allergy

A number of drugs cause the development of bronchial asthma by the mechanism of immediate hypersensitivity with the formation of IgE and IgG4. These drugs include antibiotics of the penicillin group, tetracycline, cephalosporins, nitrofuran derivatives, serums, immunoglobulins, etc. Both the drugs themselves, as well as their compounds with blood proteins and metabolic products of medicines act as allergens.

It should be remembered about the possibility of cross-allergy to medicines

Pseudoallergia

With pseudoallergia, bronchospastic syndrome is caused not by allergies, but by one of the following mechanisms:

• a violation of the metabolism of arachidonic acid (non-steroidal anti-inflammatory drugs);
• liberation of histamine from mast cells by a non-immune route (muscle relaxants, opium preparations, polyglucin, hemodez, radiopaque substances);
• activation of complement, its fraction of C3a, C5a cause release of histamine from mast cells (radiogenic contrast substances);
• by the release of serotonin (derivatives of rauwolfia, cristepin, triresid, adelphane, raunatin, reserpine).

Bronchospastic effect as a manifestation of the basic pharmacological activity of the drug

The following groups of medicinal products have this effect:

• beta2-adrenoblockers (blockade of beta2-adrenergic receptors causes the development of bronchospasm);
• holinomimetiki - proserin, pilocarpine, galantamine (they activate the acetylcholine receptors of the bronchi, which leads to their spasmodic);
• ACE inhibitors (bronhosuzhivayuschy effect due to increased blood levels of bradykinin).

Professional allergens

According to Bardana (1992), Brooks (1993), in 2-15% of patients, the cause of asthma is production factors. At present, about 200 substances are known to cause the development of occupational (industrial) bronchial asthma. Professional bronchial asthma can be allergic, non-allergic and mixed. Allergic bronchial asthma occurs due to the sensitization of patients to production allergens, with the development of type I allergic reaction with the formation of IgE and IgG4.

Non-allergic occupational bronchial asthma is caused by substances that are not allergens and thus do not cause an allergic (immunological) reaction.

Non-allergic occupational bronchial asthma includes the following types of diseases:

• asthma workers in the cotton processing industry due to the inhalation of cotton dust and flax. Plant dust contributes to the degranulation of mast cells of lung tissue and the release of histamine from them, under the influence of which histamine receptors are excited and bronchospasm sets in;

Allergens that cause professional bronchial asthma

Allergens	Type of professional activity
Wood dust (oak, maple, birch, mahogany)	Furniture manufacture
Flowers	Flower Greenhouses
Wheat flour (in the form of inhalation)	Bakery, milling industry
Green coffee beans (coffee dust)	Coffee production
Tea	Production, packaging of tea
Tobacco	Tobacco production
Epidermal allergens of animals	Livestock, work in vivariums, zoos, veterinarians
Allergens of birds (chickens, ducks, geese)	Work on poultry farms
Dust of castor oil beans	Manufacture of castor oil
Papillious dust (scales of bodies and wings of butterflies)	The silk-processing industry (coconut, grenade, weaving)
Grain mite	Work on grains
Medicines (antibiotics, enzymes, immunoglobulins, vaccines, serums)	Pharmaceutical industry, work with drugs in medical institutions
Salts of platinum	Metalworking and chemical industry, photography
Nickel salts	Casting of steel, galvanic
Chromium salts	Cement, steel production
Sac subtilis enzymes	Manufacture of detergents
Trypsin, pancreatin, papain, bromelin	Pharmaceutical industry
Diisocyanates	Production of polyurethane, glue, automotive paints
Anhydrides (phthalic, trimellitin, maleic)	Production and use of epoxy glue, paints
Dimethylethanolamine	Manufacture of aerosol paints
Ethylenediamine	Refrigeration plants
Glutaraldehyde, paraphenylenediamine, acrylates	Production of glue, artificial fibers
Persulfates	Photocopy service

Note: salts of platinum, cobalt, nickel, chromium are usually haptens, which, when combined with proteins, form highly active allergens (antigens)

• The asthma of meat packers develops as a result of the separation of chemical substances from the packaging polyvinylchloride film during technological processes associated with hot wire. The origin of these substances and the mechanism of development of this type of bronchial asthma is still unknown;
• asthma workers employed in industries associated with the use of formaldehyde (chemical industry, plastics, rubber, morgues, forensic laboratories). The development of bronchial asthma is due to the direct irrigation effect of formaldehyde on bronchial muscles;
• asthma, which occurs during the first day after inhalation of various irrigants in a high concentration (gases, smoke, smog). As isocyanates in this situation, isocyanates, sulfur compounds, chlorine, phosgene, tear gases, welding vapors, acetic acid, etc.,

Mixed professional bronchial asthma develops with the involvement of allergic and non-allergic mechanisms. This group includes the following types of bronchial asthma:

• bronchial asthma caused by isocyanates. These compounds are used in the manufacture of glue, paints, artificial fibers, polymeric materials, they evaporate easily and enter the respiratory tract of workers. In the origin of this type of bronchial asthma is important as an allergic mechanism - the production of specific antibodies IgE and IgG4 to cisocyanates, and non-allergic mechanisms (blockade of beta 2-adrenergic receptors of the bronchi, the irritative effect);
• bronchial asthma in cabinetmakers - occurs in carpenters in the manufacture of furniture from red cedar. In its dust contains plikatikova acid, with its inhalation specific IgE antibodies are formed, the activation of complement occurs. In addition, plicatic acid blocks the beta2-adrenergic receptors of the bronchi. A mixed mechanism of development of bronchial asthma also occurs when working with wood from other breeds.

Combined effects of allergens and pollutants

Pollutants significantly increase the effect of allergens. "Pollutant + allergen" complexes can act as superantigens and cause bronchial hyperreactivity even in persons not predisposed to bronchial asthma.

[31], [32], [33], [34], [35]

Endogenous etiological factors

Endogenous factors are not allergens and cause the development of nonallergic bronchial asthma.

The endogenous factors include the following:

• a metabolic disorder of arachidonic acid under the influence of aspirin (acetylsalicylic acid). In persons suffering from such a metabolic defect under the influence of aspirin from arachidonic acid, the synthesis of leukotrienes is enhanced, which leads to the development of bronchospasm;
• hyperreactivity of the bronchi in relation to physical exertion (asthma of physical effort develops); neuropsychic factors - can be the reason for a rather rare neuro-psychic variant of bronchial asthma. It should also be taken into account that psycho-emotional stressful situations can very often cause an exacerbation of any variant of bronchial asthma. Stressful situations cause the development of neuro-reflex reactions leading to bronchospasm and a fit of suffocation;
• dyshormonal disorders - play a leading role in the development of special variants of bronchial asthma associated with ovarian dysfunction and insufficiency of the glucocorticoid function of the adrenal glands.

[36], [37], [38], [39], [40], [41]

Factors contributing to the occurrence of bronchial asthma

These factors significantly increase the risk of developing bronchial asthma when exposed to causative factors.

[42], [43], [44], [45],

Respiratory infections

Respiratory infections are one of the most important factors contributing to the development of bronchial asthma in adults and children. GB Fedoseev (1992) identifies the infectious-dependent form of bronchial asthma. Infectious dependence is understood as a condition in which the occurrence and / or course of bronchial asthma depends on the effects of various infectious antigens (viruses, bacteria, fungi). Especially important is the role of acute viral respiratory infections. The most common occurrence and progression of bronchial asthma is associated with influenza viruses, respiratory syncytial virus, rhinovirus, parainfluenza virus. Respiratory viruses damage the ciliated epithelium of the bronchial mucosa, increase its permeability for various types of allergens, toxic substances. Along with this, under the influence of respiratory viral infection, the sensitivity of the irritant receptors of the submucosal layer of the bronchi increases sharply. Thus, under the influence of viral infection, the hyperreactivity of the bronchi increases dramatically. In addition, a viral infection is involved in the formation of allergic inflammation of the bronchi, the possibility of induction of the synthesis of virus-specific IgE is established. A certain role in the development of bronchial asthma is also played by bacterial infection and fungi.

Air pollutants

"Pollutants are various chemical substances that, when stored in the atmosphere in high concentrations, can cause deterioration in human health" (AV Emel'yanov, 1996). It is established that the pollutants undoubtedly contribute to the onset of bronchial asthma, they realize the phenotypic hereditary predisposition to it. Bronchial asthma is an ecologically dependent disease, especially in children. As indicated in the national Russian program "Bronchial asthma in children, strategy, treatment and prevention" (1997), bronchial asthma in children is a sensitive marker of air pollution. The most widespread pollutants are carbon monoxide, sulfur dioxide and nitrogen dioxide, metals, ozone, dust, products of incomplete combustion of gasoline (oil hydrocarbons, formaldehyde, etc.).

Especially dangerous and aggressive for the respiratory tract is smog: industrial and photochemical. Industrial smog is the result of incomplete combustion of liquid and solid fuels, it dominates in industrial regions. The main components of industrial (industrial) smog are sulfur dioxide in complex with solid particles, some of them can be allergens. The photochemical smog is formed in places of congestion of motor transport under the influence of sunlight - photochemical reactions are activated in the exhaust gases. The main components of photochemical smog - nitrogen dioxide, ozone.

The source of pollutants are industrial enterprises, factories, factories (emissions of incomplete combustion of liquid and solid fuels, sulfur dioxide and other substances into the atmosphere), vehicle exhaust gases, chemicals used in agriculture (pesticides, herbicides). In addition, pollutants are present in human dwellings, their sources are household chemicals, heating appliances, perfume products, stoves, fireplaces, synthetic coatings and upholstery materials, various types of glue, paints. In the air of living rooms there are oxides of nitrogen, carbon monoxide, sulfur dioxide, formaldehyde, isocyanates, tobacco smoke. Pollutants have a variety of effects on the respiratory tract:

• cause significant irritation of theirritic receptors (sulfur dioxide, acids, various solids, dust), which leads to the development of bronchospasm;
• damage the ciliated epithelium and increase the permeability of the epithelial layer of the bronchi, which creates favorable conditions for the action of immunocompetent cells of the bronchopulmonary system and exoallergens (ozone, nitrogen dioxide and other pollutants);
• stimulate the production of inflammatory mediators and allergies, as they contribute to the degranulation of mast cells and basophils.

Thus, the pollutants of atmospheric air and living rooms contribute to the development of bronchial inflammation, dramatically increase the hyperreactivity of the bronchi and thereby contribute to both the development of bronchial asthma and its aggravation.

[46], [47], [48], [49]

Smoking and passive smoking

According to modern concepts, smoking is one of the main factors affecting the occurrence and course of bronchial asthma. Tobacco smoke contains a large number of substances that have a toxic, irritant effect (including on the irritative receptors), a carcinogenic effect. In addition, tobacco smoke dramatically reduces the function of the local bronchopulmonary defense system, primarily the ciliary epithelium of the bronchial mucosa (details of the effect of tobacco smoke on the respiratory tract). Ultimately, inflammation of the mucous membrane, sensitization and hyperreactivity of the bronchi develops under the influence of tobacco smoke components, which contributes to the development of bronchial asthma. The same negative impact has also passive smoking - staying in a smoked room and inhaling tobacco smoke. "Passive smokers" absorb the same amount of nicotine and other toxic substances of tobacco smoke from the smoke-free air of the premises, as the active smoker. Passive smokers are also more likely to have food and pollen sensitization compared to people living in premises where no one smokes.

Factors contributing to exacerbation of bronchial asthma (triggers)

Triggers are the factors that cause exacerbation of bronchial asthma. Under the influence of triggers, the inflammatory process in the bronchi is stimulated or bronchial spasm is provoked.

The most frequent triggers are allergens, respiratory infections, air pollution, eating foods that are allergic to the patient, physical activity, meteorological factors, medicines. One of the most important factors that cause exacerbation of bronchial asthma is physical activity. Hyperventilation, which occurs during physical exertion, causes cooling and dryness of the bronchial mucosa, which provokes bronchospasm. There is a special form of bronchial asthma caused by physical activity.

Exacerbation of bronchial asthma can also cause unfavorable weather conditions. Patients with bronchial asthma are extremely meteosensitive. Exacerbation of bronchial asthma is most often promoted by the following meteorological factors:

• low temperature and high humidity of atmospheric air - these factors are particularly unfavorable for patients with bronchial asthma who have fungal sensitization, as in these meteorological conditions the concentration of fungal spores in the air increases; in addition, these conditions contribute to the formation of industrial smog;
• significant drop or increase in atmospheric pressure;
• air pollutants;
• sunny windy weather - adversely affects the full-bodily bronchial asthma (the wind carries pollen of plants, ultraviolet irradiation increases the antigenic properties of pollen);
• changing the earth's magnetic field;
• storm.

To the factors aggravating the course of bronchial asthma, it is necessary to include also some medicines: beta-adrenoblockers (block beta2-adrenoreceptors of bronchi), non-steroidal anti-inflammatory drugs (enhance leukotriene synthesis), drugs rauwolfia (increase the activity of acetylcholine receptors of the bronchi), etc.

[50], [51], [52],