Harmful substances in cigarettes: (1) aldehydes, nitrides, olefins, these substances have an irritating effect on the respiratory tract. (2) Nicotine, which can stimulate sympathetic nerves and cause endothelial damage. (3) amines, cyanide and heavy metals, which are toxic substances. (4) benzpyrene, arsenic, cadmium, methylhydrazine, aminophenol, other radioactive substances. All of these substances have carcinogenic effects. (5) Phenolic compounds and formaldehyde, etc. These substances have the effect of accelerating carcinogenesis. (6) carbon monoxide, can reduce the ability of red blood cells to transport oxygen to the whole body. I. Carcinogenic effects: Smoking is one of the important causative factors of lung cancer, especially squamous epithelial cell carcinoma and small cell undifferentiated carcinoma. The risk of lung cancer for smokers is 13 times higher than that for nonsmokers, and 45 times higher than that for nonsmokers if they smoke more than 35 cigarettes per day. The mortality rate of lung cancer among smokers is 10-13 times higher than that of nonsmokers. About 85% of lung cancer deaths are caused by smoking. The polycyclic aromatic hydrocarbons in tobacco smoke need to be metabolized by polycyclic aromatic hydrocarbon hydroxylase to have cytotoxic and mutagenic effects, and the concentration of this hydroxylase is higher in smokers than in nonsmokers. Smoking decreases the activity of natural killer cells, thereby reducing the body’s ability to monitor, kill, and remove tumor cell growth, which further explains why smoking is a high risk factor for the development of many cancers. The incidence of laryngeal cancer is more than ten times higher in smokers than in nonsmokers. There is a 3-fold increase in the incidence of bladder cancer, which may be related to the beta-naphthylamine in smoke. In addition, smoking is associated with the occurrence of lip, tongue, oral cavity, esophagus, stomach, colon, pancreatic, kidney, and cervical cancers. Clinical studies and animal experiments have shown that the carcinogenic substances in smoke can also affect the fetus through the placenta, resulting in a significantly higher incidence of cancer in its offspring. Second, the cardiovascular and cerebrovascular effects: smoking is a major risk factor for many cardiovascular and cerebrovascular diseases, the incidence of coronary heart disease, hypertension, cerebrovascular disease and peripheral vascular disease in smokers are significantly higher. Statistics show that 75 percent of patients with coronary heart disease and hypertension have a history of smoking. The incidence of coronary heart disease is 3.5 times higher in smokers than in nonsmokers, the death rate of coronary heart disease is 6 times higher in the former than in the latter, the incidence of myocardial infarction is 2-6 times higher in the former than in the latter, and pathological autopsy also reveals that coronary atherosclerotic lesions are more extensive and severe in the former than in the latter. Thirty to 40% of deaths from cardiovascular disease are caused by smoking, and the increase in mortality is directly proportional to the amount of smoking. Nicotine and carbon monoxide in cigarette smoke are recognized as the main harmful factors causing coronary atherosclerosis. Smoking can damage vascular endothelial cells and cause lower serum HDL-C, higher cholesterol, and lower PGI2 levels, thus causing peripheral vascular and coronary artery constriction, wall thickening, luminal narrowing, and slowed blood flow, resulting in myocardial hypoxia. Nicotine can also promote platelet aggregation. Carbon monoxide in cigarette smoke combines with hemoglobin to form carboxyhemoglobin, which affects the oxygen-carrying capacity of red blood cells and causes tissue hypoxia, thus inducing coronary artery spasm. As a result of tissue hypoxia, compensatory erythrocytosis is caused, which increases blood viscosity. In addition, smoking increases plasma fibrinogen levels, leading to dysfunction of the coagulation system; smoking also affects the metabolism of arachidonic acid, resulting in decreased PGI2 production and a relative increase in thromboxane A2, leading to vasoconstriction and increased platelet aggregation. It has been reported that the risk of stroke in smokers is 2 to 3.5 times higher than in nonsmokers; if smoking and hypertension coexist, the risk of stroke increases nearly 20 times. In addition, smokers are susceptible to occlusive arteriosclerosis and occlusive thromboarteritis. Smoking can cause chronic obstructive pulmonary disease (COPD for short), which eventually leads to pulmonary heart disease. Third, the impact on the respiratory tract: smoking is one of the main causes of chronic bronchitis, emphysema and chronic airway obstruction. Long-term smoking can damage and shorten the cilia of the bronchial mucosa and affect the clearance function of the cilia. In addition, the submucosal glands become hyperplastic and hypertrophic, with increased mucus secretion and altered composition, which can easily obstruct the fine bronchi. In dog experiments, exposure to large amounts of smoke and dust can cause emphysematous changes. A study at the Institute of Respiratory Diseases, China Medical University, found that lower respiratory macrophages (AM), neutrophils (PMN) and elastase were significantly increased in smokers compared to nonsmokers. The mechanism may be due to the stimulation of smoke particles and noxious gases, the lower respiratory mononuclear macrophage system is activated, and the activated AM can release elastase in addition to PMN chemotactic factors, causing In addition to releasing elastase, the activated AM also releases PMN chemotactic factors that allow PMN to move from capillaries to the lungs. Activated AM also releases macrophage growth factor, which attracts fibroblasts; and PMN releases large amounts of toxic oxygen radicals and protein hydrolases including elastase and collagenase, which act on elastin, polymyxin, basement membrane and collagen fibers of the lung, leading to disruption of alveolar wall septa and interstitial fibrosis. Chronic bronchitis is two to four times higher in smokers than in nonsmokers and is proportional to the amount and years of smoking. Patients often have chronic cough, sputum, and dyspnea with activity. Pulmonary function tests show airway obstruction, reduced pulmonary compliance, ventilation and diffusion function and decreased arterial partial pressure of oxygen. COPD predisposes to spontaneous pneumothorax. Smokers often suffer from chronic pharyngitis and vocal fold inflammation. Fourth, the impact on the digestive tract: smoking can cause an increase in gastric acid secretion, generally 91.5% more than nonsmokers, and can inhibit the pancreatic secretion of sodium bicarbonate, resulting in an increase in the duodenal acid load, inducing ulcers. Tobacco nicotine can make the pyloric sphincter muscle tone is reduced, so that bile is easy to reflux, thus weakening the gastric and duodenal mucosa defense factors, prompting chronic inflammation and ulcers, and delay the healing of the original ulcer. In addition, smoking can reduce the tone of the lower esophageal sphincter, which can easily cause reflux esophagitis. Fifth, other: smoking is more harmful to women than men, smoking women can cause menstrual disorders, conception difficulties, ectopic pregnancy, low estrogen, osteoporosis and early menopause. Pregnant women who smoke are prone to spontaneous abortion, fetal growth retardation, and low birth weight. Other conditions such as preterm labor, stillbirth, early placental abruption, and placenta praevia may be associated with smoking. Smoking during pregnancy can increase fetal mortality before and after birth and the incidence of congenital heart disease. The rate of death from breast cancer is 25% higher in women who smoke than in non-smoking women. Nicotine has been shown to reduce sex hormone production and kill sperm, resulting in a decrease in sperm count, abnormal morphology, and decreased viability, which reduces the chance of conception. Smoking can also cause damage to testicular function, male hypogonadism and sexual dysfunction, leading to male infertility. Smoking can cause tobacco amblyopia, and smoking in the elderly can cause macular degeneration, which may be due to atherosclerosis and an increased rate of platelet aggregation, contributing to local hypoxia. Recently, a study in the United States found that smoking in strong noise can cause permanent hearing loss, and even deafness. Sixth, passive smoking: refers to people who live and work around smokers, unconsciously inhaling smoke dust particles and various toxic substances. The concentration of harmful substances inhaled by passive smokers is not lower than that of smokers, smokers exhale cold smoke, smoke tar content than smokers inhale hot smoke in 1 times more, benzo(a)pyrene 2 times more, carbon monoxide 4 times more. Studies have found that women who regularly smoke passively in the workplace have a higher incidence of coronary heart disease than those who do not or rarely smoke passively in the workplace. According to an international sample survey, 50% of the patients with cancer caused by smoking are passive smokers. Numerous epidemiological surveys have shown that the prevalence of lung cancer in wives of husbands who smoke is 1.6 to 3.4 times higher than that of husbands who do not smoke. Passive smoking in pregnant women can affect the normal growth and development of the fetus. Some scholars have analyzed more than 5000 pregnant women and found that when the husband smokes more than 10 cigarettes a day, the prenatal mortality rate of his fetus increases by 65%; the more he smokes, the higher the mortality rate. More children in smoking families suffer from respiratory diseases than in non-smoking families.