Causes of bronchial asthma

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

• heredity;
• atopy;
• bronchial hyperreactivity.

G. B. Fedoseyev also includes biological defects in healthy people among the predisposing factors.

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Heredity and bronchial asthma

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

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

Genetic markers of predisposition to bronchial asthma are considered to be certain HLA antigens (the major histocompatibility complex, located on the short arm of chromosome 6; here are also located the genes that control the 2nd and 4th components of complement, the B-factor properdin, as well as the genes that control the immune response - Ir genes).

As established by E. N. Barabanova (1993) and M. A. Petrova (1995), antigens B13, B21, B35 and DR5 are much more common in patients with bronchial asthma than in healthy people. There are reports of the frequent occurrence of antigens A2, B7, B8, B12, B27, DR2 in patients with bronchial asthma. The presence of these antigens significantly increases the risk of developing bronchial asthma. On the contrary, antigens A28, B14, BW41, DR1 are “protective” with respect to the development of bronchial asthma.

Two asthmatic genes have now been identified in mice that cause bronchial hypersensitivity (hyperreactivity).

In humans, the main genes predisposing to bronchial asthma are contained in chromosomes 5 and 11, with the IL4 gene cluster 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 bronchial hyperreactivity. Each of these genetic predisposition factors significantly increases the likelihood of developing bronchial asthma.

Atopy

Atopy is the body's ability to produce increased amounts of IgE (reagins) in response to environmental allergens. In this case, the blood of patients has increased levels of IgE, positive skin tests with allergens are noted, and the anamnesis contains indications of various manifestations of allergies.

Atopy is extremely common in patients with bronchial asthma and their close relatives. The ability to synthesize IgE is under genetic control and is inherited.

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Bronchial hyperreactivity

Bronchial hyperreactivity is an increased reaction of the bronchi to an irritant, which may lead to bronchospasm. This same effect does not cause a bronchospastic reaction in most healthy individuals. It has been established that the ability to hyperreactivity of the bronchi is also inherited.

In 1996, F. Kummer reported that in individuals predisposed to developing bronchial asthma, changes were found on chromosomes 4, 5, 6, and 11, which are responsible for bronchial hyperreactivity upon contact with an exoallergen (mainly of a protein nature).

Biological defects in apparently healthy individuals

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

According to G. B. 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 (bronchial hyperreactivity to biologically active substances, pollutants, allergens; disruption of the local bronchopulmonary defense system);
• defects at the cellular level (instability of mast cells, excessively high release of biologically active substances during 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-adrenergic receptors, disorders of the oxidant-antioxidant system, etc.).

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Causal factors of bronchial asthma

Under the influence of causal factors, the predisposing factors, including biological defects, are actually realized, and bronchial asthma develops.

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Allergens

Allergens are the main etiological factor of bronchial asthma.

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Household allergens

The main representative of household allergens is house dust. It contains various substances: remains of various tissues, particles of human and animal epidermis, insect allergens, plant pollen, fungi (most often these are mold fungi antigens - rhizopus, mucor, alternaria, penicillium, etc.), bacteria, library dust and other components.

However, the allergenic properties of house dust are primarily due to mites. More than 50 species of mites have been found in house dust. The most important are Dermatophagoides pteronissinus, Dermatophagoides farinae, Dermatophagoides microceras and Euroglyphis mainei. Dermatophagoides pteronissinus (54-65%) and Dermatophagoides farinae (36-45%) usually predominate in residential premises; less common are barn mites of the Acaridae family (27%) and Euroglyphis mainei (14%).

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

D. pteronissinus ticks feed on epidermal scales, their lifespan is 2.5-3 months, the female lays 20-40 eggs, their development period is about 6 days.

Ticks are widespread everywhere, except for areas with an arctic climate and high mountain areas. At an altitude of 1,000 m above sea level, only single ticks are found, and at an altitude of more than 1,600 m, they are absent. Ticks die at temperatures above 60°C and at temperatures below 16-18°C.

Allergenic activity is possessed by mite excrements - a particle of about 10-20 microns in size. These particles enter the respiratory tract along with inhaled air. Allergens of 7 groups have been identified in D.pteronissinus, D.farinae - 3, D.microceras - 1. Currently, enzyme immunoassay methods have been developed to determine mite allergens in house dust.

House dust and the mites it contains cause the development of not only allergic bronchial asthma, but also allergic rhinitis, urticaria, atopic dermatitis, and Quincke's edema.

Bronchial asthma caused by sensitization to house dust has characteristic features:

• Night attacks of suffocation are often observed, since at night the patient has close contact with bedding and the house dust allergens contained in it;
• the patient is bothered by attacks of bronchial asthma all year round if he permanently lives in his apartment, since there is constant contact with house dust, but the attacks disappear or decrease when the patient is outside the home environment (business trip, hospital, etc.);
• bronchial asthma often worsens during the cold season (it is during this period that they try to increase the air temperature in the apartment and it becomes optimal for ticks; in addition, at this time the saturation of living spaces with dust increases);
• bronchial asthma is aggravated by cleaning the apartment, shaking carpets, etc.;

Epidermal allergens

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

The most common source of allergens are cats. Every fourth patient with bronchial asthma cannot stand contact with a cat. The main cat allergens are found in fur, saliva and urine.

Patients with epidermal allergy may develop severe allergic reactions even to the first administration of anti-tetanus, anti-rabies, anti-diphtheria, anti-botulinum serums, immunoglobulins and other protein preparations. This is explained by the presence of antigenic similarity between epidermal allergens (primarily horse dandruff) and blood plasma proteins.

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Insect allergens

Insect allergens are insect allergens (bees, bumblebees, wasps, mosquitoes, midges, cockroaches, etc.). Insect allergens enter the human bloodstream through blood (through bites), inhalation, or contact. Cockroaches play a particularly important role; allergens are contained in their saliva, feces, and tissues. Insect venom contains biogenic amines (histamine, serotonin, acetylcholine, etc.), proteins (apamin, melitgan), enzymes (phospholipase A2, hyaluronidase, proteases, etc.). Allergens are proteins and enzymes. Other substances contribute to the development of toxic, inflammatory, and bronchoconstrictive effects. Melittin, along with its allergenic effect, can also cause degranulation of mast cells and histamine release.

Daphnia, a component of aquarium fish food, are also strong allergens.

Insect-induced occupational asthma is possible (in silk processing production due to sensitization to papillary dust of butterflies, in beekeeping).

Pollen allergens

The pollen of many plants has allergenic properties and causes allergies - hay fever (allergic rhinitis, conjunctivitis, bronchial asthma). Antigenic properties are due to the proteins it contains. Hay fever can be caused by 200 plant species, pollen is up to 30 microns in size and penetrates deep into the respiratory tract, causing bronchial asthma. Tree pollen contains 6 antigens, grass pollen - up to 10 antigens. The most common types of pollen causing bronchial asthma are:

• grass pollen (timothy, orchard grass, foxtail, ryegrass, fescue, bluegrass, wheatgrass, nettle, plantain, sorrel, ragweed, wormwood);
• flower pollen (buttercup, dandelion, daisy, poppy, tulip, etc.);
• pollen of shrubs (rose hips, lilac, elderberry, hazelnut, etc.);
• tree pollen (birch, oak, ash, poplar, willow, chestnut, pine, alder, etc.).

Pollen bronchial asthma most often occurs during the following periods: from mid-April to the end of May (trees bloom); June-July (meadow grasses bloom); August-September (weed pollen appears in the air). Exacerbations of the disease usually occur during a stay outside the city, in the forest, in the meadows, at the dacha, on a hiking trip, in the village. Patients tolerate windy weather especially poorly, since at this time there is an extremely large amount of pollen in the air. As a rule, pollen bronchial asthma is combined with other manifestations of hay fever - allergic rhinitis and conjunctivitis, less often - urticaria, dermatitis, Quincke's edema.

It is extremely important for a practicing physician to know about the possibility of cross-food allergies and intolerance to 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 fungi are of the genera Penicillium, Aspergillus, Mucor.Alternaria, Candida. Fungi and their spores are part of house dust, are present in the air, on the soil, on the skin, in the intestines. Spores of mold fungi enter the upper and lower respiratory tract by inhalation. Among fungal antigens, the most allergenic are lipoproteins of the cell wall of both spores and mycelium.

It has been established that fungi and their antigens cause the development of I, II or IV types of hypersensitivity according to Gell and Coombs. Bronchial asthma caused by fungi is often accompanied by intolerance to products containing fungi (beer, kvass, dry wines, fermented milk products, antibiotics), fungal skin lesions. The condition of patients worsens in humid weather, when staying in a damp room (especially with mold growth on the walls). Many patients have a seasonal nature of exacerbations of fungal bronchial asthma. For example, bronchial asthma caused by Alternaria, Candida fungi often worsens in the warm season and less often in winter. This is explained by the fact that the concentration of spores of these fungi increases in the warm months of the year. In bronchial asthma caused by fungi of the Penicillium, Aspergillium genera, there is no seasonality of the course of the disease, since the number of spores of these fungi in the air remains high throughout the year.

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

Food allergens

Food allergy is the cause of bronchial 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 (it contains 20 antigens), fish, meat.

Cross-allergy to drugs

Preparation	Drugs that cause cross-allergy (they cannot be used in case of allergy to the drugs listed in the first column)
Eufillin, diaphyllin	Ethylenediamine derivatives (suprastin, ethambutol)
Acetylsalicylic acid (citramon, asphen, askofen, sedalgin, etc.)	Non-steroidal anti-inflammatory drugs and drugs containing them (baralgin, maxigan, spazmalgon, trigan, spazgan, theofedrine, pentalgin, etc.).
Novocaine	Local anesthetics (anesthesin, lidocaine, dicaine, trimecaine), sulfonamides, sulfonylurea derivatives for the treatment of diabetes mellitus, diuretics (dichlorothiazide, cyclomethiazide, furosemide, bufenox, clopamide, indapamide)
Iodine	Radiocontrast agents, 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 their high content of biogenic amines and their liberators (citrus fruits, strawberries, wild strawberries, tomatoes, chocolate, cheese, pineapples, sausages, beer). Food intolerance is often caused by special food additives and dyes contained in fruit juices, drinks, sausages, hot dogs, sweets and other products, confectionery, canned goods.

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Drug allergens

Medicines can be the cause of exacerbation and worsening of bronchial asthma in 10% of patients (Hunt, 1992). Medicines can also be the direct cause of bronchial asthma. The mechanisms of drug-induced bronchial asthma development are different, which is due to the specific action of the medicines themselves. The following mechanisms of bronchial asthma development under the influence of medicines are known.

Drug 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 and their compounds with blood proteins and the products of drug metabolism act as allergens.

It is important to remember the possibility of cross-allergy to medications.

Pseudoallergy

In pseudoallergy, the bronchospastic syndrome is caused not by an allergy, but by one of the following mechanisms:

• arachidonic acid metabolism disorder (non-steroidal anti-inflammatory drugs);
• release of histamine from mast cells by non-immune means (muscle relaxants, opium preparations, polyglucin, hemodez, radiocontrast agents);
• activation of complement, its fractions C3a, C5a cause the release of histamine from mast cells (X-ray contrast agents);
• serotonin liberation (rauvolfia derivatives, cristepin, trireside, adelfan, raunatin, reserpine).

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

The following groups of drugs have this effect:

• beta2-adrenergic blockers (blockade of beta2-adrenergic receptors causes the development of bronchospasm);
• cholinomimetics - proserin, pilocarpine, galantamine (they activate acetylcholine receptors of the bronchi, which leads to their spasm);
• ACE inhibitors (the bronchoconstrictive effect is due to an increase in the level of bradykinin in the blood).

Professional allergens

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

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

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

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

Allergens that cause occupational asthma

Allergens	Type of professional activity
Wood dust (oak, maple, birch, mahogany)	Furniture production
Flowers	Flower greenhouses
Wheat flour (in the form of inhalations)	Bakery and flour milling industry
Green coffee beans (coffee dust)	Coffee production
Tea	Production, packaging of tea
Tobacco	Tobacco production
Animal epidermal allergens	Animal husbandry, work in vivariums, zoos, veterinarians
Bird allergens (chickens, ducks, geese)	Work on poultry farms
Castor Oil Bean Dust	Castor oil production
Papillon dust (scales from the bodies and wings of butterflies)	Silk processing industry (cocoon winding, grenage workshops, weaving production)
Grain mite	Work in grain warehouses
Medicines (antibiotics, enzymes, immunoglobulins, vaccines, serums)	Pharmaceutical industry, work with drugs in medical institutions
Platinum salts	Metalworking and chemical industry, photography
Nickel salts	Steel casting, galvanizing
Chromium salts	Production of cement, steel
Sac subtilis enzymes	Production of detergents
Trypsin, pancreatin, papain, bromelain	Pharmaceutical industry
Diisocyanates	Production of polyurethane, glue, car paints
Anhydrides (phthalic, trimellitic, maleic)	Production and use of epoxy glue, paints
Dimethylethanolamine	Aerosol paint production
Ethylenediamine	Refrigeration units
Glutaraldehyde, paraphenylenediamine, acrylates	Production of glue, artificial fibers
Persulfates	Photocopying

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

• meat packers' asthma - develops as a result of chemicals being released from PVC packaging film during technological processes involving hot wire. The origin of these substances and the mechanism of development of this type of bronchial asthma are still unknown;
• asthma of workers employed in industries involving the use of formaldehyde (chemical industry, plastics and rubber production, morgues, forensic laboratories). The development of bronchial asthma is caused by the direct irrigative effect of formaldehyde on the bronchial muscles;
• asthma that occurs within the first 24 hours after inhalation of various irritants in high concentrations (gases, smoke, smog). Irritants in this situation include isocyanates, sulfur compounds, chlorine, phosgene, tear gases, welding fumes, acetic acid, etc.

Mixed occupational bronchial asthma develops with the participation 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 production of glue, paints, artificial fibers, polymeric materials, they easily evaporate and enter the respiratory tract of workers. In the origin of this type of bronchial asthma, both an allergic mechanism - the production of specific antibodies IgE and IgG4 to isocyanates, and non-allergic mechanisms (blockade of beta 2-adrenoreceptors of the bronchi, irritant effect) are important;
• bronchial asthma in cabinetmakers - occurs in carpenters when making furniture from red cedar. Its dust contains plicatic acid, when inhaled, specific IgE antibodies are formed, and complement is activated. In addition, plicatic acid blocks beta2-adrenoreceptors of the bronchi. A mixed mechanism of bronchial asthma development also occurs when working with other types of wood.

Combined effects of allergens and pollutants

Pollutants significantly enhance the action of allergens. Complexes of "pollutant + allergen" can act as superantigens and cause bronchial hyperreactivity even in people not predisposed to bronchial asthma.

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Endogenous etiological factors

Endogenous factors are not allergens and cause the development of non-allergic bronchial asthma.

Endogenous factors include the following:

• a disorder of arachidonic acid metabolism under the influence of aspirin (acetylsalicylic acid). In individuals suffering from such a metabolic defect, under the influence of aspirin, the synthesis of leukotrienes from arachidonic acid increases, which leads to the development of bronchospasm;
• hyperreactivity of the bronchi in relation to physical exertion (development of asthma of physical exertion); neuropsychic factors - can be the cause of a rather rare neuropsychic variant of bronchial asthma. It should also be taken into account that psycho-emotional stressful situations can very often be the cause of exacerbation of any variant of bronchial asthma. Stressful situations cause the development of neuroreflex reactions leading to bronchospasm and an attack 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.

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Factors contributing to the development of bronchial asthma

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

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Respiratory infections

Respiratory infections are one of the most important factors contributing to the development of bronchial asthma in adults and children. G. B. Fedoseyev (1992) identifies an infection-dependent form of bronchial asthma. Infection 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). The role of acute viral respiratory infections is especially important. Most often, the occurrence and progression of bronchial asthma is associated with influenza viruses, respiratory syncytial virus, rhinovirus, and parainfluenza virus. Respiratory viruses damage the ciliated epithelium of the bronchial mucosa, increasing its permeability to various types of allergens and toxic substances. Along with this, under the influence of a respiratory viral infection, the sensitivity of irritant receptors of the bronchial submucosal layer sharply increases. Thus, under the influence of viral infection, bronchial hyperreactivity increases sharply. In addition, viral infection participates in the formation of allergic inflammation of the bronchi, the possibility of inducing the synthesis of virus-specific IgE has been established. Bacterial infection and fungi also play a certain role in the development of bronchial asthma.

Air pollutants

"Pollutants are various chemical substances that, when accumulated in the atmosphere in high concentrations, can cause deterioration of human health" (A. V. Yemelyanov, 1996). It has been established that pollutants undoubtedly contribute to the development of bronchial asthma, realizing the phenotypic hereditary predisposition to it. Bronchial asthma is an environmentally dependent disease, this is especially relevant in childhood. 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 and nitrogen dioxides, metals, ozone, dust, products of incomplete combustion of gasoline (petroleum hydrocarbons, formaldehyde, etc.).

Smog is especially dangerous and aggressive for the respiratory tract: 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 smog are sulfur dioxide in combination with solid particles, some of which can be allergens. Photochemical smog is formed in places where vehicles accumulate under the influence of sunlight - photochemical reactions are activated in the exhaust gases. The main components of photochemical smog are nitrogen dioxide and ozone.

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

• cause significant irritation of irritant receptors (sulfur dioxide, acids, various solid particles, 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 influence of immunocompetent cells of the bronchopulmonary system and exoallergens (ozone, nitrogen dioxide and other pollutants);
• stimulate the production of inflammatory and allergy mediators, as they promote the degranulation of mast cells and basophils.

Thus, pollutants of atmospheric air and living spaces contribute to the development of bronchial inflammation, sharply increase bronchial hyperreactivity and thereby contribute to both the development of bronchial asthma and its exacerbation.

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Smoking and passive smoking

According to modern concepts, smoking is one of the main factors influencing the occurrence and course of bronchial asthma. Tobacco smoke contains a large number of substances that have a toxic, irritating effect (including on irritant receptors), and a carcinogenic effect. In addition, tobacco smoke sharply reduces the function of the local bronchopulmonary defense system, primarily the ciliated epithelium of the bronchial mucosa (more about the effect of tobacco smoke on the respiratory tract). Ultimately, under the influence of tobacco smoke components, inflammation of the mucous membrane, sensitization and hyperreactivity of the bronchi develop, which contributes to the development of bronchial asthma. Passive smoking - staying in a smoky room and inhaling tobacco smoke - has the same negative effect. "Passive smokers" absorb as much nicotine and other toxic substances in tobacco smoke from the smoky air of rooms as an active smoker. Passive smokers also have significantly higher rates of food and pollen sensitization compared to people living in non-smoking environments.

Factors that contribute to the exacerbation of bronchial asthma (triggers)

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

An exacerbation of bronchial asthma can also be caused by unfavorable meteorological conditions. Patients with bronchial asthma are extremely sensitive to the weather. The following meteorological factors most often contribute to an exacerbation of bronchial asthma:

• low temperature and high humidity of the atmospheric air - these factors have a particularly adverse effect on patients with bronchial asthma who have fungal sensitization, since in these weather conditions the concentration of fungal spores in the air increases; in addition, these conditions contribute to the formation of industrial smog;
• a significant drop or increase in atmospheric pressure;
• air pollution by pollutants;
• sunny windy weather - has an adverse effect on pollinosis bronchial asthma (wind carries plant pollen, ultraviolet radiation increases the antigenic properties of pollen);
• change in the earth's magnetic field;
• storm.

Factors that aggravate the course of bronchial asthma also include certain medications - these are beta-blockers (block beta2-adrenergic receptors of the bronchi), non-steroidal anti-inflammatory drugs (increase the synthesis of leukotrienes), rauwolfia preparations (increase the activity of acetylcholine receptors of the bronchi), etc.

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