Although the etiology and pathogenesis are not yet clear, the following factors are commonly believed to be involved: Smoking: Numerous studies have shown that smoking is the primary cause of progressive increase in lung cancer mortality. Benzo(a)pyrene, nicotine, nitrosamines, and small amounts of radioactive elements such as polonium in cigarette smoke are carcinogenic, and are particularly likely to cause squamous epithelial cell carcinoma and undifferentiated small cell carcinoma. Compared with nonsmokers, the risk of lung cancer is on average 4-10 times higher in smokers, and up to 10-25 times higher in heavy smokers. There is a clear quantitative-effect relationship between the amount of smoking and lung cancer, with the younger the age at which smoking begins, the longer the duration of smoking, and the greater the amount of smoking, the higher the incidence of lung cancer. The cancer risk of one cigarette is equivalent to 0,01-0,04mGy of radiation, and smoking 30 paper cigarettes per day is equivalent to 1,2mGy of radiation dose. Passive smoking or environmental smoking is also a cause of lung cancer. The risk of lung cancer among non-smoking wives whose husbands smoke is twice as high as that of wives in households where both spouses do not smoke, and the risk increases with the amount of smoking by the husband. Encouragingly, the risk of lung cancer decreases each year after quitting smoking, and is reduced by half after 1-5 years of quitting. Studies in the United States have shown that the risk of lung cancer decreases progressively between 2 and 15 years after quitting, after which the incidence is equivalent to that of a lifetime nonsmoker. Occupational carcinogenic factors: Occupational factors that have been identified to cause human lung cancer include asbestos, arsenic, chromium, nickel, beryllium, coal tar, mustard gas, trichloromethyl ether, chloromethyl ether, heating products of tobacco, and radon and radon gas produced during the decay of radioactive substances such as uranium and radium, ionizing radiation and microwave radiation. These factors can increase the risk of lung cancer by 3 to 30 times. Among them, asbestos is a recognized carcinogen, and the incidence of lung cancer, pleural and peritoneal mesothelioma is significantly higher in those exposed, with a latency period of 2O years or more. Smokers exposed to asbestos have eight times the lung cancer mortality rate of non-exposed smokers. In addition, there is a strong relationship between uranium exposure and lung carcinogenesis, particularly small cell lung cancer, and smoking can significantly increase this risk. Air pollution: Air pollution includes indoor small environment and outdoor large environment pollution, indoor passive smoking, fuel combustion and cooking process may produce carcinogens. Some data show that indoor use of coal, exposure to soot or its incomplete combustion products are risk factors for lung cancer, especially for female adenocarcinoma. Oil fumes released by heating during cooking are also a carcinogenic factor that cannot be ignored. In the atmosphere of heavy industrial cities, there are carcinogens such as 3,4-benzopyrene, arsenic oxide, radioactive substances, nickel, chromium compounds, and non-combustible aliphatic hydrocarbons. The amount of benzopyrene contained in the air inhaled daily by residents of heavily polluted large cities can exceed the content of 20 paper cigarettes and increase the carcinogenic effect of paper cigarettes. For every 1ug/m2 increase in atmospheric benzo(a)pyrene content, the mortality rate of lung cancer can increase by 1%-15%. Ionizing radiation: Large doses of ionizing radiation can cause lung cancer, and different rays produce different effects, such as neutrons and a-rays released by the atomic bomb in Hiroshima, Japan, and only a-rays in Nagasaki, the former has a higher risk of lung cancer than the latter. The United States in 1978 reported that the source of ionizing radiation in the general population is about 49,6% from nature, 44,6% for medical exposure, and ionizing radiation from X-ray diagnosis can account for 36,7%. Diet and nutrition: Some studies have shown that less consumption of vegetables and fruits containing β-carotene increases the risk of lung cancer. People with low serum beta carotene levels also have a higher risk of lung cancer. Epidemiological data also suggest that higher consumption of green, yellow, and orange vegetables and fruits containing beta carotene and foods containing vitamin A may reduce the risk of lung cancer, and this protective effect is particularly pronounced in current or former smokers. Other predisposing factors: The American Cancer Society lists tuberculosis as a factor in the development of lung cancer. People with tuberculosis have 10 times the risk of developing lung cancer compared to the normal population. Its main histological type is adenocarcinoma. In addition, viral infections, fungal toxins (aflatoxins), etc., may also play a role in the development of lung cancer. Genetic and genetic alterations: After a long period of exploration and research, it is now gradually recognized that lung cancer may be a disease in which exogenous causes develop through endogenous causes. The aforementioned exogenous factors can induce malignant transformation of cells and irreversible genetic alterations, including activation of proto-oncogenes, inactivation of oncogenes, activation of the self-feedback secretion loop and inhibition of apoptosis, leading to uncontrolled cell growth. These genetic alterations arise in a multistep, stochastic manner over a long period of time. The mechanisms by which many genes become oncogenic are unclear, but these alterations ultimately involve the deregulation of key cellular physiological functions, including proliferation, apoptosis, differentiation, signaling and motility. The main oncogenes that are closely associated with lung cancer are the ras and myc gene families, c-erbB-2, Bcl-2, c-fos, and c-jun genes. Related oncogenes include p53, Rb, CDKN2, FHIT gene, etc. Molecular alterations associated with lung cancer development and progression also include abnormalities in mismatch repair genes such as hMSH2 and hPMS1, and telomerase expression. Note: Please refer to the clinic for specific medications and be guided by your doctor in an interview.