Asthma is a chronic airway disease characterized by an excessive inflammatory response to both specific and chemical stimuli (1). Some agents that induce this response are known, while others are not. As a result of repeated exposures with these agents, the disease gradually worsens and secondary changes in bronchial normal responses occur.
As a result of smoking, toxic agents containing many harmful substances that directly affect the airways are encountered, while regional inflammation in the lungs is also triggered. Persistent and persistent airway inflammation occurs in both chronic obstructive pulmonary disease (chronic bronchitis + emphysema) and smoking-related lung diseases such as asthma (2).
Smoking can trigger an acute (sudden) attack in asthmatic patients; In addition, there is a very close relationship between asthma severity and exposure to cigarettes (3-5). This information is also supported by animal models (6,7). Our recent information shows that active smoking is an important risk factor for the onset of asthma in adults (8).
Smoking-related airway inflammation
Smoking causes persistent airway inflammation. Smoking contains a large amount of toxic and carcinogenic substances, therefore it causes damage to bronchial cells in the short and medium term (9). Biological and molecular mechanisms cause damage by acting in different ways but together (10). In addition to abnormal changes in bronchial cells, abnormalities in the programmed cell death (apoptosis) system occur as a result of dysfunctions in some cells (macrophages and other inflammatory cells) involved in molecular repair mechanisms. As a result of all these, deterioration in apoptosis and marophage phagocytosis, unexpected death (necrosis) in cells, and finally, irreversible bronchial narrowing occur (11-13). In addition, it has been observed that smokers without asthma have airway inflammation when compared to non-smokers (14-17).
Inflammatory cells in the airway in smokers with asthma
Inflammation in the form of neutrophils in the airway wall (mostly CD8+ T cells and macrophages) and neutrophils in the bronchial fluids (sputum) in smokers It has been observed that there is an increase in cells (14,18). In lung biopsy sections, an increase in eosinophils, which is the most important cell in allergy, was found in smokers compared to non-smokers (19). Although there are not enough publications on smokers with asthma, it has been shown that exposure to cigarette smoke increases bronchial hyperexcitability in experimental animal asthma models, and eosinophil and allergic-type Th-2 cytokine response increases in these samples following allergen stimulation (20,21).
Cytokines and other mediators in smokers with asthma
In the sputum of smokers with asthma, there is an increase in the cytokine called IL-8, which is used to call neutrophil-type inflammatory cells to the lungs, as a result of which inflammatory cells are collected in the lung and these changes are caused by smoking. is related to the amount; we see that the patient’s pulmonary function tests (such as FEV1) are impaired (22). Likewise, it has been shown that the levels of tissue-destroying proteins (eosinophilic cationic protein = ECP) of sputum allergy cells increase in smokers with asthma (22). IL-18 cytokine is an important cytokine responsible for the development of the Th-1 type, which operates anti-allergic mechanisms. Therefore, this cytokine also suppresses the development of Th-2, which operates the allergic mechanisms. A significant decrease was found in IL-18 levels in both asthmatic and non-asthmatic smokers compared to non-smokers. This effect was found to be particularly prominent in asthmatics (23). With all these findings, it can be said that smoking turns the immune response (immune response) towards the allergic type, Th-2, in asthmatic patients.
It was observed that nitric oxide (NO) levels, which are known to expand the bronchi, also decreased in smokers with asthma who did not receive cortisone (steroid) treatment, compared to non-smokers with asthma (24). Cigarette smoking probably lowers the NO level by suppressing (inhibiting) the enzyme that produces NO. In addition, oxidative stress has been observed to increase in smokers with asthma (25,26). It is also known that neurogenic inflammation contributes to the event in smokers with asthma (27).
Airway remodeling in smokers with asthma
Abnormal remodeling and remodeling of tissues in asthmatic patients is a fact. Remodeling was found to be much more severe in smokers with asthma (28).
IgE and smoking
In the general population, there is a positive correlation between smoking and specific IgE levels, which are allergy antibodies against house dust mites (29).
Passive smoking
With passive smoking, an increase in the incidence of asthma is observed, especially in children, along with an increase in the incidence of cough, wheezing, bronchitis, bronchiolitis, pneumonia, and deterioration in lung function tests. While the prevalence and severity of asthma are increased by passive smoking, attacks are also seen more frequently. For this reason, an increase is observed in the frequency of admission to the emergency department (30,31). These risks are particularly associated with family smoking at an early age.
According to a recent study conducted in Germany, the relationship between passive smoking and allergic sensitization in adults was evaluated. Although not statistically significant, a positive correlation was found between passive smoking and the incidence of allergic sensitization and allergic rhinitis (32).
In conclusion, it is certain that there is a non-negligible relationship between smoking, allergic sensitization and asthma. For this reason, we should direct our patients to quit smoking and recommend that they be protected from passive smoking.
Resources
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20. Seymour BW, Schelegle ES, Pinkerton KE, et al. Secondhand smoke increases bronchial hyperreactivity and eosinophilia in a murine model of allergic aspergillosis. Clin Dev Immunol 2003; 10: 35–42.
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23. McKay A, Komai-Koma M, MacLeod K, et al. Interleukin-18 levels in induced sputum are reduced in asthmatic and normal smokers. Clin Exp Allergy 2004; 34: 904–10.
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27. Kwong K, Wu ZX, Kashon M, et al. Chronic smoking enhances tachykinin synthesis and airway responsiveness in guinea pigs. Am J Respir Cell Mol Biol 2001; 25: 299–305.
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29. Jarvis D, Chinn S, Lucynska C, Burney P. The association of smoking with sensitization to common environmental allergens: results from the European Community Health Survey. J Allergy Clin Immunol 1999; 104: 934–40.
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32. Topp R, Thefeld W, Wichmann HE, Heinrich J. The effect of environmental tobacco smoke exposure on allergic sensitization and allergic rhinitis in adults. Indoor Air 2005 Aug;15(4):222-7.
Wishing you healthy days…
Prof. Dr. Cengiz KIRMAZ
