What causes chronic bronchitis?

Smoking

Smoking is the most important etiological factor of chronic bronchitis due to the significant spread of tobacco smoking among the population and due to the pronounced aggressive effect on the respiratory system and other organs and systems.

Among males over the age of 10, smoking is up to 35-80% (according to various data), among women 10-20%. Smoking is widespread among young people, especially among adolescents.

According to the Seventh World Congress on Smoking and Health in 1990, smoking caused the death of 3 million people.

More than 1,900 components have been found in tobacco smoke, which have a toxic, mutagenic, carcinogenic effect (nicotine, "tar" consisting of polycyclic aromatic hydrocarbons that have a carcinogenic effect - benzpyrene, cresol, phenol, radioactive substances - polonium, etc. Carbon monoxide; nitrogen oxide, urethane, vinyl chloride, hydrocyanic acid, cadmium, formaldehyde, etc.).

There are the following negative aspects of the effect of smoking on the bronchopulmonary system:

• nicotine interacts with nitrogen oxide, N-nitrosazamines are formed, which contribute to the development of cancer;
• urethane, benzpyrene, vinyl chloride - are carcinogens. Of all these substances, the most studied is the process of biotransformation of benzpyrene - in the respiratory tract it is metabolized by the P450 system to the epoxy compound, which undergoes further changes to form epoxide dihydrodiol and epoxidiol; these substances also have a carcinogenic effect;
• cadmium is a heavy metal that causes severe damage to the cells of the bronchopulmonary system;
• polonium-210 promotes the development of cancer; It is now believed that polonium is adsorbed in tobacco from the atmosphere, its half-life exceeds 138 days;
• the function of the ciliated epithelium of the bronchi, mucociliary transport, i.e. Sharply reduced drainage function of the bronchi; after smoking 15 cigarettes a day, the ciliary epithelium ciliary activity is completely paralyzed; violation of mucociliary clearance contributes to the development of infection in the bronchial tree;
• under the influence of the components of tobacco smoke, the phagocytic function of neutrophils and macrophages decreases;
• the chemical components of tobacco smoke stimulate the proteolytic activity of the bronchial contents in connection with the increase in the neutrophil content in it by 2-3 times in comparison with the norm. Neutrophilic leukocytes produce a large amount of proteolytic enzyme - neutrophil elastase, which contributes to the destruction of elastic lung fibers, which predisposes to the development of emphysema. In addition, high proteolytic activity of bronchial mucus damages the ciliated epithelium of the bronchi;
• under the influence of tobacco smoke, metaplasia of cells of ciliated epithelium and Clara cells (non-ciliary epithelial cells) occurs, they turn into goblet-like mucus. Metaplastic cells can become precursors of cancer cells;
• smoking leads to a decrease in the phagocytic function of neutrophils and alveolar macrophages, and the activity of antimicrobial systems of macrophages also decreases. Alveolar macrophages phagocytose insoluble particles of tobacco smoke (cadmium, polonium, etc.), their cytoplasm acquires a characteristic sand color, the lumps are more intensely colored yellow. Such characteristic morphological changes in alveolar macrophages are considered biological markers of the smoker; a decrease in the cytotoxic activity of alveolar macrophages with respect to tumor cells due to inhibition of the synthesis of interferon and anti-blast cytokine;
• Smoking disrupts the synthesis and function of the surfactant;
• the protective function of the immune system decreases (including the local bronchopulmonary immune system); the quantity and function of killer T-lymphocytes, which normally kill circulating tumor cells and prevent their metastasis, are significantly reduced. As a result of these changes, the probability of developing bronchial carcinoma increases dramatically. Currently, there are data on the occurrence of smoking antibodies to certain components of tobacco smoke and the formation of immune complexes that can cause suppression of the immune response to T- and B-dependent antigens, damage cytotoxic lymphocytes and natural killers;
• It is known that in alveolar macrophages there is an angiotensin-converting enzyme that converts angiotensin I into angiotensin II. Under the influence of smoking, the activity of this enzyme in alveolar macrophages increases, which leads to an increase in the synthesis of angiotensin II, which has a powerful vasoconstrictive effect, and promotes the formation of pulmonary hypertension;
• nicotine promotes the development of allergic reactions. Tobacco smoke is currently considered as an allergen, predisposing to increased synthesis of immunoglobulin E, responsible for the development of atonic reactions. In the serum of smokers, the content of IgE increases, which is associated with sensitization to exoallergens. It was found that the content of histamine in sputum smokers is significantly increased, which correlates with the increase in the number of mast cells in the epithelium. The process of degranulation of mast cells during smoking significantly increases, which leads to the emergence of histamine and other mediators of allergy and inflammation and predisposes to the development of bronchospasm.

At present, it has been reliably established that smoking leads to the development of various bronchopulmonary diseases: chronic bronchitis (including obstructive bronchitis), bronchiolitis obliterans, emphysema, bronchial asthma, lung cancer and lung anomalies in children.

According to epidemiological studies, characteristic signs of chronic bronchitis appear with a smoking experience of 15-20 years, and with a smoking experience of more than 20-25 years there are complications of chronic obstructive bronchitis - pulmonary heart and respiratory failure. Among smokers, chronic bronchitis occurs 2-5 times more often than among non-smokers. Smoking has a huge negative impact on the cardiovascular system. Each cigarette smoked shortens a person's life by 5.5 minutes, the average life expectancy of a smoking person is 15 years shorter than non-smokers.

The negative effect of tobacco smoke is manifested not only with active, but also with passive smoking (ie when in a smoke-filled room and passively inhaling tobacco smoke).

Inhalation of contaminated air

It is established that the incidence of chronic bronchitis among people living in regions with high atmospheric pollution is higher compared to those living in ecologically clean areas. This is due to the fact that inhaling polluted air, a person inhales various pollutants - aggressive substances of a different nature and chemical structure, causing irritation and damage to the bronchopulmonary system. Air pollution usually occurs as a result of entering the atmosphere of waste from modern industrial production, combustion products of various fuels, "exhaust" gases.

The main indicators of air pollution are high concentrations in it of sulfur dioxide and nitrogen (SO2, NO2) and smoke. But, in addition, polluted air can contain hydrocarbon, nitrogen oxides, aldehydes, nitrates and other pollutants. Acute massive air pollution - smog - can lead to severe exacerbation of chronic bronchitis. Smog is formed as a result of rapid air pollution by the products of fuel combustion, in windless weather accumulating under a layer of warm air, which in low places is located above a layer of cold air. Oxides of nitrogen and sulfur in the air combine with water and lead to the formation of sulfuric and nitric acid vapors, the inhalation of which significantly damages the bronchopulmonary system.

Influence of occupational hazards

The professional hazards that cause the development of chronic bronchitis include:

• the impact of various types of dust (cotton, flour, coal, cement, quartz, wood, etc.) - develop the so-called "dust" bronchitis;
• the effect of toxic vapors and gases (ammonia, chlorine, acids, sulfur dioxide, carbon monoxide, phosgene, ozone, vapors and gases formed during gas and electric welding);
• high, or, conversely, low air temperature, drafts and other negative microclimate features in production facilities and shops.

Climatic factors

Development and exacerbation of chronic bronchitis is promoted by a damp and cold climate. Aggravations usually occur in autumn, winter, early spring.

Infection

Most pulmonologists believe that the infectious factor is secondary, joining later, when the conditions for infection of the bronchial tree have already formed under the influence of the aforementioned etiological factors. Thus, the infection contributes to the exacerbation and persistence of chronic bronchitis and is much less likely to be the root cause of its development.

Yu. B. Belousov et al. (1996) give the following data on the etiology of acute and exacerbation of chronic bronchitis (USA, 1989):

• Haemophilus influenzae 50%;
• Streptococcus pneumoniae - 14%;
• Pseudomonas aeruginosa - 14%;
• Moraxella (Neisseria or Branhamella) catarrhalis - 17%;
• Staphylococcus aureus - 2%;
• Other - 3% of cases.

According to Yu Novikov (1995), the main pathogens for exacerbation of chronic bronchitis are:

• Streptococcus pneumoniae - 30.7%;
• Haemophilus influenzae - 21%;
• Streptococcus haemolyticus - 11%;
• Staphylococcus aureus 13.4%;
• Pseudomonas aeruginosa 5%;
• Mycoplasma - 4.9%;
• Uncovered pathogen - 14% of cases

From the data given, it can be seen that the leading role in exacerbation of chronic bronchitis is played by pneumococcus and hemophilic rod. According to 3. V. Bulatova (1980), the causes of exacerbation of chronic bronchitis are:

• monovirus infection - in 15%;
• mixed viral infection - 7%;
• mycoplasma in 35%;
• viruses + mycoplasma - in 13%;
• bacteria - in 30% of cases

Consequently, a major role belongs to a viral or mycoplasma infection. With an exacerbation of purulent bronchitis, an important role is played by microbial associations. After viral bronchitis, the number of colonies of the hemophilic rod increases dramatically in the bronchial secretion of patients.

Infectious agents release a number of toxins that damage the ciliated epithelium of the bronchi. Thus, Haemophilus influenzae produces low molecular weight peptidoglycans that slow the oscillation of the cilia, and lipo-oligo saccharides, contributing to the attrition of the ciliated epithelium. Streptococcus pneumoniae secretes pneumolysin, which slows ciliary fluctuations, causes cell necrosis and creates openings in the cell membrane. Pseudomonas aeruginosa produces piocyanin (L-hydroxyphenazine), which slows ciliary fluctuations and causes cell death with the production of active hydroxyanines, and also produces ramo-lipids that destroy cell membranes and cause cell death.

Postponed acute bronchitis

Untreated acute lingering and recurrent bronchitis can lead to further development of chronic bronchitis, especially in persons predisposed to it and in the presence of contributing factors.

Genetic factors, constitutional predisposition

In the development of chronic bronchitis, an important role is played by hereditary factors and constitutional predisposition. They contribute to the onset of the disease when exposed to the aforementioned etiological factors, as well as under conditions of altered allergic reactivity of the organism. With weighed heredity in chronic bronchitis, the risk of developing this disease in offspring (especially in women) is significantly increased, especially if the mother suffers from chronic bronchitis. There are reports that chronic bronchitis often develops in individuals who have type I haptoglobin, blood group B (III), Rh-factor.

Factors predisposing to the development of chronic bronchitis

To the development of chronic bronchitis predispose:

• chronic tonsillitis, rhinitis, sinusitis, pharyngitis, carious teeth;
• violation of nasal breathing of any nature (for example, the presence of polyposis of the nose, etc.);
• stagnation in the lungs of any genesis;
• alcohol abuse (alcohol taken internally, secreted by the bronchial mucosa and has a damaging effect on it);
• chronic renal failure (the bronchial mucosa secreted by the products of nitrogen metabolism cause its damage).