Rough breath sounds are abnormal breath sounds caused by mild edema or inflammatory infiltration of the bronchial mucosa resulting in an unsmooth or narrowed wall, resulting in poor airflow entry. It is seen in the early stages of bronchial and pulmonary inflammation. Etiology: Under normal conditions, the respiratory tract has a well-developed defense function, which can play the role of filtration, warming and humidification of the inhaled air; the ciliary movement of the airway mucosal surface and the cough reflex, through which foreign bodies and pathogenic microorganisms can be removed from the airway. Secretory IgA is also present in the lower respiratory tract, which has an anti-pathogenic microbial effect. Therefore, the lower respiratory tract is generally maintained in a purified state. The whole body or local defense and immune function of the respiratory tract is reduced, especially in elderly people, who are highly susceptible to chronic bronchitis and recurrent attacks that do not heal. 1, smoking is the main factor in the development of the disease, cigarettes contain tar, nicotine and cyanuric acid and other chemicals, can damage the airway epithelial cells, so that the cilia movement and macrophage phagocytosis is reduced, resulting in a decrease in airway purification function. They can also stimulate submucosal receptors and make the parasympathetic nerve hyperfunction, causing bronchial smooth muscle contraction, resulting in increased airway resistance, as well as increased glandular secretion, cupped cell hyperplasia, bronchial mucosa congestion and edema, mucus accumulation, which can easily induce infection. In addition, cigarette smoke increases the production of toxic oxygen radicals, induces the release of proteases from neutrophils, inhibits the anti-protease system, destroys pulmonary elastic fibers, and induces the development of emphysema. Studies have shown that the prevalence of chronic bronchitis in smokers is 2 to 8 times higher than in nonsmokers, and the longer the smoking age, the greater the amount of smoke, the higher the prevalence. 2, atmospheric pollution harmful gases such as sulfur dioxide, nitrogen dioxide, chlorine and ozone on the airway mucous membrane epithelium have stimulating and cytotoxic effects. It is reported that when airborne soot or sulfur dioxide exceeds 1000 μg/m3, acute attacks of chronic bronchitis increase significantly. Other dust such as silica, coal dust, cane dust, cotton dust, etc. can also stimulate damage to the bronchial mucosa, so that the lung clearance function suffers damage, creating conditions for bacterial infection. 3, infection factors infection is one of the important factors in the occurrence and development of chronic bronchitis. The main reason for the acute onset of this disease is viral, mycoplasma and bacterial infections. Viral infections are common with influenza virus, rhinovirus, adenovirus and respiratory syncytial virus. Bacterial infections include Streptococcus pneumoniae, Haemophilus influenzae, Cattamora and Staphylococcus. Bacterial infections occur every time secondary to viral or mycoplasma infections on the basis of damaged airway mucosa. 4, allergic factors wheezing chronic bronchitis patients, more allergic history, a variety of allergens to stimulate the positive rate of skin testing is also high, the number of eosinophils in the sputum and histamine content and blood IgE has a tendency to increase, some patients in the serum rheumatoid factor positive and T lymphocyte subpopulation distribution abnormal, so it is believed that atopy and immune factors are related to the occurrence of the disease. However, it is also believed that atopy should be a factor in the development of asthma, and such patients should actually belong to the category of asthma or chronic bronchitis combined with asthma. 5, other chronic bronchitis acute attacks in the winter more, so the weather factors should be considered as one of the important factors in the development of the disease. The cold air can stimulate the glands to secrete more mucus and weaken the cilia movement, weakening the airway defense function. It can also cause bronchial smooth muscle spasm by reflex, mucosal vasoconstriction, and local blood circulation disorder, which is conducive to secondary infection. Most patients with this disease have autonomic dysfunction, and some patients have hyperparasympathetic function and increased airway reactivity compared to normal subjects. In addition, hypoadrenocorticism, impaired cellular immune function, reduced lysozyme activity, low nutrition, and vitamin A and C deficiency in the elderly can increase airway mucosal vascular permeability and diminish epithelial repair function. There is no conclusive evidence as to whether genetic factors are related to the development of chronic bronchitis. 6, the elderly gonads and adrenal cortex function decline, laryngeal reflexes weaken, respiratory defense function degeneration, monocyte – phagocyte system function decline, also can make the development of chronic bronchitis increased. 7, nutrition also has a certain impact on bronchitis, vitamin C deficiency, the body’s resistance to infection is reduced, vascular permeability increased; vitamin A deficiency, can make the bronchial mucosa of the columnar epithelial cells and mucosa repair function is weakened, lysozyme activity is reduced, prone to chronic bronchitis. The genetic factors are related to the development of chronic bronchitis, which has not been confirmed so far. α1-antitrypsin severe deficiency can cause emphysema, but no symptoms of airway lesions, suggesting that it is not directly related to chronic bronchitis.