Although the etiology and pathogenesis have not been clearly defined, it is usually believed to be related to the following factors: 1. Smoking: a large number of studies have shown that smoking is the primary cause of the progressive increase in lung cancer mortality. Benzo(a)pyrene, nicotine, nitrosamine and a small amount of radioactive element polonium in cigarette smoke have carcinogenic effect, especially easy to cause squamous epithelial cell carcinoma and undifferentiated small cell carcinoma. Compared with non-smokers, the risk of lung cancer in smokers is 4-10 times higher on average, and in heavy smokers it can be 10-25 times higher. There is a clear quantity-one-effect relationship between the amount of cigarettes smoked and lung cancer. The younger the age of smoking initiation, the longer the duration of smoking, and the greater the amount of cigarettes smoked, 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 a day is equivalent to a radiation dose of 1.2mGy. Passive or environmental smoking is also a cause of lung cancer. The risk of lung cancer among nonsmoking wives whose husbands smoke is twice that of wives in families where neither spouse smokes, and the risk increases with the amount of smoking done by the husband. It is encouraging to note that the risk of lung cancer decreases each year after quitting smoking, and can be halved after 1-5 years of cessation. Research results in the United States show that the risk of lung cancer decreases progressively during the period of 2-15 years after smoking cessation, and the incidence rate thereafter is equivalent to that of lifelong non-smokers. 2. Occupational carcinogenic factors: Occupational factors confirmed to cause lung cancer include asbestos, arsenic, chromium, nickel, beryllium, coal tar, mustard gas, trichloromethyl ether, chloromethyl ether, the heating products of tobacco as well as radon and radon daughters gas produced by decaying radioactive substances such as uranium, radium, etc., ionizing and microwave radiation, etc. These factors can make the risk of lung cancer occur. These factors can increase the risk of lung cancer by 3-30 times. Among them, asbestos is a recognized carcinogen, and the incidence of lung cancer, pleural and peritoneal mesothelioma in exposed persons is significantly higher, with a latent period of up to 2O years or more. Asbestos-exposed smokers have a lung cancer mortality rate eight times that of non-exposed smokers. In addition, there is a close relationship between uranium exposure and lung cancer, especially small cell lung cancer, and smoking can significantly aggravate this risk. Air pollution: air pollution includes indoor small environment and outdoor 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 of substances for lung cancer risk factors, especially for female adenocarcinoma of the greater impact. Oil smoke released from heating during cooking is also a carcinogenic factor that cannot be ignored. In the atmosphere of heavy industrial cities, there are carcinogenic substances such as 3,4-benzopyrene, arsenous oxide, radioactive substances, nickel, chromium compounds and non-combustible aliphatic hydrocarbons. The amount of benzo(a)pyrene contained in the air inhaled daily by residents of large, heavily polluted cities can exceed the content of 20 paper cigarettes and increase the carcinogenic effect of paper cigarettes. Every increase of 1ug/m2 of benzo(a)pyrene content in the atmosphere can increase the mortality rate of lung cancer by 1%-15%. 4. Ionizing radiation: large doses of ionizing radiation can cause lung cancer, and the effects produced by different rays are different, such as the atomic bomb in Hiroshima, Japan, which released neutrons and a-rays, and Nagasaki, which had only a-rays, and the risk of the former suffering from lung cancer is higher than that of the latter. The United States reported in 1978 that the source of ionizing radiation in the general population was about 49.6% from nature, 44.6% from medical irradiation, and 36.7% from X-ray diagnosis. 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 level of β-carotene in serum also have high risk of lung cancer. Epidemiological investigation data also show that more consumption of green, yellow and orange vegetables and fruits containing β-carotene and foods containing vitamin A can reduce the risk of lung cancer, and this protective effect is especially obvious for people who are smoking or former smokers. 6.Other predisposing factors: American Cancer Society lists tuberculosis as one of the factors of lung cancer. The risk of lung cancer in people with tuberculosis is 10 times higher than that of the normal population. Its main histologic type is adenocarcinoma. In addition, viral infection, fungal toxins (Aspergillus flavus), etc., may also play a role in the occurrence of lung cancer. 7. Heredity and genetic changes: after long-term exploration and research, it is now gradually recognized that lung cancer may be a disease that develops from external causes through internal causes. The above mentioned external factors can induce malignant transformation of cells and irreversible genetic changes, including activation of proto-oncogenes, inactivation of oncogenes, activation of auto-feedback secretion loop and inhibition of apoptosis, which lead to uncontrolled cell growth. These genetic alterations arise in a multistep, randomized fashion over a long period of time. The mechanisms by which many genes become oncogenic are unclear, but these alterations ultimately involve the loss of control of key physiological functions of the cell, including proliferation, apoptosis, differentiation, signaling and motility. Oncogenes closely associated with lung cancer include 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 include mismatch repair genes such as hMSH2 and hPMS1, and telomerase expression.