Harmful substances in cigarettes smoking is a well-known fact …… different cigarettes when lit release different chemicals, but the main number of tar and carbon monoxide and other chemicals. Cigarettes ignited to produce substances harmful to humans are broadly divided into six categories: (1) aldehydes, nitrides, olefins, these substances have an irritating effect on the respiratory tract; (2) nicotine, can stimulate sympathetic nerves, causing damage to the intima; (3) amines, cyanide and heavy metals, these are toxic substances; (4) benzpyrene, arsenic, cadmium, methylhydrazine, amino phenols, other radioactive substances. These substances have carcinogenic effects; (5) phenolic compounds and formaldehyde, these substances have accelerated cancer; (6) carbon monoxide can reduce the ability of red blood cells to transport oxygen to the whole body. First, the carcinogenic effect of smoking has been recognized as carcinogenic. Epidemiological surveys show that smoking is an important causative factor for lung cancer, especially squamous epithelial cell carcinoma and small cell undifferentiated carcinoma. The risk of lung cancer in smokers is 13 times higher than that in nonsmokers, and 45 times higher than that in 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. Smokers who are also exposed to chemical carcinogens (such as asbestos, nickel, uranium, and arsenic) have a higher risk of developing lung cancer. The polycyclic aromatic hydrocarbons in tobacco smoke need to be metabolized by polycyclic aromatic hydrocarbon hydroxylase before they are cytotoxic and mutagenic, 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 significant increase in the incidence of cancer in its offspring. Second, the cardiovascular and cerebrovascular effects of many studies that 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% 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, and the incidence of myocardial infarction is 2-6 times higher in the former than in the latter. The incidence of coronary heart disease was 9 to 12 times higher in those with hypertension, high cholesterol and smoking. Smoking is responsible for 30% to 40% of cardiovascular deaths, and the increase in mortality is proportional to the amount of smoking. Nicotine and carbon monoxide in cigarette smoke are recognized as the main harmful factors causing coronary atherosclerosis, but their exact mechanism is not yet fully understood. Most scholars believe that lipid changes, platelet function and blood rheology abnormalities play an important role. High-density lipoprotein cholesterol (HDL-C) stimulates the production of prostacyclin (PGI2), the most potent vasodilator and inhibitor of platelet aggregation, in vascular endothelial cells. 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 can increase plasma fibrinogen levels, leading to dysfunction of the coagulation system; smoking can also affect the metabolism of arachidonic acid, resulting in a decrease in PGI2 production and a relative increase in thromboxane A2, leading to vasoconstriction and increased platelet aggregation. All of these may promote the occurrence and development of coronary heart disease. Because of myocardial hypoxia, which increases myocardial stress and decreases the threshold for ventricular fibrillation, smokers with coronary artery disease are more likely to develop arrhythmias and have an increased risk of sudden death. It is 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. Experimental studies have found that 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 enlarged, 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 non-smokers. The mechanism may be due to the activation of the lower respiratory mononuclear macrophage system as a result of the stimulation of smoke particles and noxious gases. MN moves 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 destruction of alveolar wall septa and interstitial fibrosis. It has been reported that nearly 13 million people in the United States suffered from COPD in 1986 and more than 90,000 died in 1991, with smoking being its main cause. Chronic bronchitis is two to four times higher in smokers than in nonsmokers, and is proportional to the amount and years of smoking, and 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 non-smokers, and can inhibit the pancreatic secretion of sodium bicarbonate, resulting in increased acid load on the duodenum, inducing ulcers. Tobacco nicotine can reduce the tone of the pyloric sphincter, making it easy for bile to reflux, thus weakening the defense factors of the gastric and duodenal mucosa, prompting chronic inflammation and ulcers, and delaying the healing of existing ulcers. In addition, smoking can reduce the tension 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. Smoking in pregnant women can cause 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. These hazards are due to carbon monoxide and other harmful substances in smoke entering the fetal bloodstream, forming carboxyhemoglobin and causing hypoxia; at the same time, nicotine constricts blood vessels, reducing the fetal blood supply and nutrient supply, thus affecting the normal growth and development of the fetus. Ninety percent of lung cancers, 75 percent of COPD and 25 percent of coronary heart disease in women are related to smoking. The rate of death from breast cancer is 25% higher in women who smoke than in non-smoking women. Nicotine has been shown to lower sex hormone production and kill sperm, reducing sperm count, morphological abnormalities and viability, resulting in a reduced 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 and unconsciously inhale smoke dust particles and various toxic substances. The concentration of harmful substances inhaled by passive smokers is not lower than that of smokers, and the cold smoke exhaled by smokers contains one times more tar than the hot smoke inhaled by smokers, two times more benzopyrene, and four times more carbon monoxide. 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. A large number of epidemiological surveys have shown that the lung cancer rate of wives whose husbands 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 5,000 pregnant women and found that when the husband smokes more than 10 cigarettes a day, the prenatal mortality rate of their fetus increases by 65%; the more they smoke, the higher the mortality rate. More children in smoking families suffer from respiratory diseases than in non-smoking families.