Risk factors for COPD include both individual susceptibility factors and environmental factors, which interact with each other. Individual factors Certain genetic factors can increase the risk of developing COPD. A known genetic factor is α1-antitrypsin deficiency. Severe α1-antitrypsin deficiency is associated with emphysema formation in nonsmokers. Emphysema caused by α1-antitrypsin deficiency has not been officially reported so far in China. Bronchial asthma and airway hyperresponsiveness are risk factors for COPD, and airway hyperresponsiveness may be related to certain genetic and environmental factors of the organism. Environmental factors 1, smoking: smoking is an important factor in the development of COPD. Smokers have a higher rate of abnormal lung function, a faster annual rate of decline in FEV1, and more smokers die from COPD than non-smokers. Passive smoking may also contribute to respiratory symptoms and the development of COPD. Smoking in pregnant women may affect the growth of fetal lungs and development in the womb, and have an effect on fetal immune system function. 2, occupational dust and chemical substances: when occupational dust and chemical substances (fumes, allergens, industrial exhaust and indoor air pollution, etc.) are too concentrated or exposed for too long, can lead to the occurrence of COPD unrelated to smoking. Exposure to certain specific substances, irritants, organic dusts and allergens can increase airway reactivity. 3, air pollution: chemical gases such as chlorine, nitrogen oxide, sulfur dioxide, etc., have an irritating and cytotoxic effect on the bronchial mucosa. When airborne soot or sulfur dioxide increases significantly, acute COPD attacks increase significantly. Other dusts such as silica, coal dust, cotton dust and cane dust also stimulate the bronchial mucosa, which impairs the airway clearance function and creates conditions for bacterial invasion. The large amount of fumes from cooking and soot from biofuels are associated with the onset of COPD, and indoor air pollution from biofuels may have a synergistic effect with smoking. 4, Infection: Respiratory infections are another important factor in the onset and exacerbation of COPD. Viruses also play a role in the onset and progression of COPD. Severe lower respiratory tract infections in childhood are associated with reduced lung function and the onset of respiratory symptoms in adulthood. 5. Socioeconomic status: The onset of COPD is associated with the socioeconomic status of the patient. This may be intrinsically linked to differences in the degree of indoor and outdoor air pollution, nutritional status or other and socioeconomic status. Pathogenesis The pathogenesis is not fully understood. It is generally accepted that COPD is characterized by chronic inflammation of the airways, lung parenchyma and pulmonary vasculature, with an increase in alveolar macrophages, T-lymphocytes (especially CD8+) and neutrophils in different parts of the lung, and in some patients, eosinophilia. Activated inflammatory cells release a variety of mediators, including leukotriene-B4 (LTB4), interleukin-8 (1L-8), tumor necrosis factor-α (TNF-α), and others. These mediators can disrupt the structure of the lung and/or promote a neutrophil inflammatory response. In addition to inflammation, protease and anti-protease imbalances in the lung, oxidative and antioxidant imbalances, and autonomic nervous system dysfunction (e.g., abnormal distribution of cholinergic neuroreceptors) also play an important role in COPD pathogenesis. Inhalation of noxious particles or gases can lead to lung inflammation; smoking induces inflammation and directly damages the lungs; and various risk factors for COPD can produce similar inflammatory processes that lead to the development of COPD.