What causes chronic bronchitis?

The disease is associated with long-term irritation of the bronchi by various harmful factors (smoking, inhalation of air polluted with dust, smoke, carbon monoxide, sulfur dioxide, nitrogen oxides and other chemical compounds) and recurrent respiratory infection (respiratory viruses, Pfeiffer's bacillus, pneumococci), less often occurs with cystic fibrosis, alpha1-antitrypsin deficiency. Predisposing factors are chronic inflammatory and suppurative processes in the lungs, upper respiratory tract, decreased resistance of the body, hereditary predisposition to respiratory diseases.

Smoking

Smoking is the most important etiological factor of chronic bronchitis due to the significant prevalence 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 10 years of age, 35-80% smoke (according to various sources), among women 10-20%. Smoking is widespread among young people, especially among teenagers.

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

More than 1900 components have been found in tobacco smoke that have a toxic, mutagenic, and carcinogenic effect (nicotine; "tar" consisting of polycyclic aromatic hydrocarbons that have a carcinogenic effect - benzopyrene, cresol, phenol; radioactive substances - polonium, etc.; carbon monoxide; nitrogen oxide; urethane; vinyl chloride; hydrocyanic acid; cadmium; formaldehyde, etc.).

The following negative aspects of the impact of smoking on the bronchopulmonary system are highlighted:

• Nicotine interacts with nitric oxide, forming N-nitrosodimines, which contribute to the development of cancer;
• urethane, benzpyrenes, vinyl chloride - are carcinogens. Of all the substances listed, the process of benzpyrene biotransformation has been studied the most - in the respiratory tract it is metabolized by the P450 system to an epoxide compound, which undergoes further changes with the formation of epoxide dihydrodiol and epoxide diol; these substances also have a carcinogenic effect;
• Cadmium is a heavy metal that causes significant damage to the cells of the bronchopulmonary system;
• polonium-210 promotes cancer development; it is currently believed that polonium is adsorbed into tobacco from the atmosphere, its half-life exceeds 138 days;
• the function of the ciliated epithelium of the bronchi and mucociliary transport are impaired, i.e. the drainage function of the bronchi is sharply reduced; after smoking 15 cigarettes a day, the motor activity of the cilia of the ciliated epithelium is completely paralyzed; impaired mucociliary clearance contributes to the development of infection in the bronchial tree;
• under the influence of tobacco smoke components, the phagocytic function of neutrophils and macrophages decreases;
• chemical components of tobacco smoke stimulate the proteolytic activity of bronchial contents due to an increase in the content of neutrophils in it by 2-3 times compared to the norm. Neutrophilic leukocytes produce a large amount of the proteolytic enzyme - neutrophil elastase, which promotes the destruction of elastic fibers of the lungs, which predisposes to the development of pulmonary emphysema. In addition, high proteolytic activity of bronchial mucus damages the ciliated epithelium of the bronchi;
• under the influence of tobacco smoke, metaplasia of ciliated epithelial cells and Clara cells (non-ciliary epithelial cells) occurs, they are transformed into goblet-shaped mucus-forming cells. 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 the antimicrobial systems of macrophages also decreases. Alveolar macrophages phagocytize insoluble particles of tobacco smoke (cadmium, polonium, etc.), their cytoplasm acquires a characteristic sandy color, the lumps are more intensely colored yellow. Such characteristic morphological changes in alveolar macrophages are considered biological markers of a smoker; a decrease in the cytotoxic activity of alveolar macrophages in relation to tumor cells has been noted due to the suppression of the synthesis of interferon and antineoplastic cytokine;
• Smoking disrupts the synthesis and function of surfactant;
• the protective function of the immune system (including the local bronchopulmonary immune system) is reduced; the number and function of T-lymphocyte killers, which normally kill circulating tumor cells and prevent their metastasis, are significantly reduced. As a result of these changes, the likelihood of developing bronchial carcinoma increases sharply. Currently, there is data on the occurrence of antibodies to some components of tobacco smoke in smokers 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 alveolar macrophages contain angiotensin-converting enzyme, which 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 vasoconstrictor effect, and contributes to the formation of pulmonary hypertension;
• Nicotine contributes to the development of allergic reactions. Tobacco smoke is currently considered an allergen that predisposes to increased synthesis of immunoglobulin E, responsible for the development of atonic reactions. The content of IgE in the blood serum of smokers increases, which is associated with sensitization to exoallergens. It has been established that the content of histamine in the sputum of smokers is significantly increased, which correlates with an increase in the number of mast cells in the epithelium. The process of degranulation of mast cells during smoking is significantly enhanced, which leads to the release of histamine and other mediators of allergy and inflammation and predisposes to the development of bronchospasm.

It has now been reliably established that smoking leads to the development of various bronchopulmonary diseases: chronic bronchitis (including obstructive), obliterating bronchiolitis, pulmonary emphysema, bronchial asthma, lung cancer and lung abnormalities in children.

According to epidemiological studies, characteristic signs of chronic bronchitis appear after 15-20 years of smoking, and after 20-25 years of smoking, complications of chronic obstructive bronchitis appear - pulmonary heart disease 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 smoker is 15 years shorter than that of non-smokers.

The negative impact of tobacco smoke manifests itself not only in active, but also in passive smoking (i.e. when in a smoky room and passively inhale tobacco smoke).

Inhalation of polluted air

It has been established that the incidence of chronic bronchitis among people living in regions with high air pollution is higher than among people living in ecologically clean areas. This is due to the fact that when inhaling polluted air, a person inhales various pollutants - aggressive substances of various natures and chemical structures that cause irritation and damage to the bronchopulmonary system. Air pollution usually occurs as a result of the release into the atmosphere of waste from modern industrial production, combustion products of various types of fuel, and "exhaust" gases.

The main indicators of air pollution are considered to be high concentrations of sulfur and nitrogen dioxides (SO2, NO2) and smoke. But, in addition, polluted air may contain hydrocarbons, 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 fuel combustion products, which in windless weather accumulate under a layer of warm air, which in low places is located above a layer of cold air. Nitrogen and sulfur oxides contained 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.

The impact of occupational hazards

Occupational hazards that cause the development of chronic bronchitis include:

• exposure to various types of dust (cotton, flour, coal, cement, quartz, wood, etc.) - so-called "dust" bronchitis develops;
• the influence 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 features of the microclimate in production facilities and workshops.

Climatic factors

The development and exacerbation of chronic bronchitis is facilitated by damp and cold climate. Exacerbations usually occur in autumn, winter, early spring.

Infection

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

Yu. B. Belousov et al. (1996) provide 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%;
• Others - 3% of cases.

According to Yu. Novikov (1995), the main pathogens in exacerbations of chronic bronchitis are:

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

From the data presented it is evident that the leading role in the exacerbation of chronic bronchitis is played by pneumococcus and Haemophilus influenzae. According to Z. V. Bulatova (1980), the causes of exacerbation of chronic bronchitis are:

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

Consequently, a major role belongs to viral or mycoplasma infection. In case of exacerbation of purulent bronchitis, microbial associations play a significant role. After viral bronchitis, the number of colonies of Haemophilus influenzae in the bronchial secretion of patients increases sharply.

Infectious agents secrete a number of toxins that damage the ciliated epithelium of the bronchi. Thus, Haemophilus influenzae produces low-molecular peptide glycans that slow down the oscillations of the cilia, and lipooligosaccharides that promote the exfoliation of the ciliated epithelium. Streptococcus pneumoniae secretes pneumolysin, which slows down ciliary oscillations, causes cell necrosis, and creates holes in the cell membrane. Pseudomonas aeruginosa produces pyocyanin (L-hydroxyphenazine), which slows down ciliary oscillations and causes cell death with the production of active hydroxyanines, and also produces rhamnolipids that destroy cell membranes and cause cell death.

Acute bronchitis

Untreated acute, protracted and recurrent bronchitis can cause the development of chronic bronchitis in the future, especially in people predisposed to it and in the presence of contributing factors.

Genetic factors, constitutional predisposition

Hereditary factors and constitutional predisposition play a major role in the development of chronic bronchitis. They contribute to the development of the disease under the influence of the above-mentioned etiological factors, as well as under conditions of altered allergic reactivity of the body. With a burdened heredity for chronic bronchitis, the risk of developing this disease in offspring (especially in women) increases significantly, especially if the mother suffers from chronic bronchitis. There are reports that chronic bronchitis more often develops in people with type I haptoglobin, blood group B (III), Rh-phagocytosis.

Factors predisposing to the development of chronic bronchitis

The following factors predispose to the development of chronic bronchitis:

• chronic tonsillitis, rhinitis, sinusitis, pharyngitis, dental caries;
• disruption of nasal breathing of any nature (for example, the presence of nasal polyposis, etc.);
• congestion in the lungs of any origin;
• alcohol abuse (alcohol taken orally is secreted by the bronchial mucosa and has a damaging effect on it);
• chronic renal failure (products of nitrogen metabolism secreted by the bronchial mucosa cause its damage).