Chronic obstructive pulmonary disease (COPD) is a group of common preventable and treatable diseases characterized by persistent airflow limitation, and there are many factors involved in the pathogenesis of COPD that are not well understood and have yet to be studied. In recent years, it is believed that COPD-related pathogenic factors include both individual susceptibility factors and environmental factors. The most important environmental factors are smoking and exposure to occupational dust. In addition, chemical substances, infections, socioeconomic status, etc. have an impact. 1, air pollution harmful gases in the atmosphere such as sulfur dioxide, nitrogen dioxide, chlorine, etc. can damage the airway mucosa epithelium, so that the cilia clearance function decreases, mucus secretion increases, increasing the conditions for bacterial infection. 2, oxidative stress There are many studies that show an increase in oxidative stress in COPD patients. The main oxidants are superoxide anion (O2-), hydroxyl radical (OH), hypochlorous acid (HClO), H2O2 and nitric oxide (NO). Oxides can directly act and destroy many biochemical macromolecules such as proteins, lipids and nucleic acids, leading to cellular dysfunction or cell death, and can also destroy the extracellular matrix; cause protease-anti-protease imbalance; promote inflammatory responses, such as activation of transcription factor NF-κB, involved in the transcription of a variety of inflammatory factors, such as IL-8, TNF-а, NO-inducible synthase and epoxide inducible enzymes. 3, smoking As an important pathogenic factor, the prevalence of chronic bronchitis is 2-8 times higher in smokers than in nonsmokers, and the longer the smoking age, the greater the amount of smoking, the higher the prevalence of COPD. Tobacco contains tar, nicotine and hydrocyanic acid and other chemicals, as described in the first section of this chapter, cigarettes can damage airway epithelial cells and cilia movement, prompting the bronchial mucus glands and cup cells to proliferate and hypertrophy, mucus secretion increases, so that the airway purification capacity is reduced. It also increases oxygen radical production, induces neutrophils to release proteases, destroys lung elastic fibers, and induces emphysema formation. 4, occupational dust and chemical substances Exposure to occupational dust and chemical substances, such as smoke, allergens, industrial exhaust and indoor air pollution, may produce COPD similar to smoking when the concentration is too high or too long. 5, inflammatory mechanisms Chronic inflammation of the airways, lung parenchyma and pulmonary vasculature is a characteristic change in COPD, and inflammatory cells such as neutrophils, macrophages and T lymphocytes are involved in the COPD pathogenesis. Activation and aggregation of neutrophils is an important part of the inflammatory process in COPD, causing a chronic mucus hypersecretion state and destruction of lung parenchyma through the release of neutrophil elastase, neutrophil tissue proteinase G, neutrophil proteinase 3 and matrix metalloproteinases. 6, Infectious factors Similar to chronic bronchitis, infection is also an important factor in the development of COPD. 7, protease-anti-protease imbalance Protein hydrolase has a damaging and destructive effect on tissues; anti-protease has an inhibitory function on elastase and other proteases, of which a1-antitrypsin (a1-AT) is the most active one. Increased protease or insufficient anti-protease can lead to the destruction of tissue structure and emphysema. Inhalation of harmful gases and substances can lead to increased production or activity of protease, while decreased production or accelerated inactivation of anti-protease; at the same time, oxidative stress, smoking and other risk factors can also reduce the activity of anti-protease. Congenital a1-antitrypsin deficiency is mostly seen in individuals of Northern European origin and has not been officially reported in China. 8, other such as autonomic dysfunction, malnutrition, temperature changes, etc. may be involved in the occurrence and development of COPD.