People have realized that smoking can cause cancer. Epidemiological investigation shows that smoking is one of the important pathogenic factors of lung cancer, especially squamous cell carcinoma and small cell undifferentiated carcinoma. The risk of lung cancer of smokers is 13 times that of non-smokers. If you smoke more than 35 cigarettes a day, your risk is 45 times that of non-smokers. The mortality rate of lung cancer in smokers is 10 ~ 13 times higher than that in non-smokers. About 85% of lung cancer deaths are caused by smoking. If smokers are exposed to chemical carcinogens (such as asbestos, nickel, uranium and arsenic, etc. ), the risk of lung cancer will be higher. PAHs in tobacco smoke are cytotoxic and mutagenic only after being metabolized by PAH hydroxylase, and the concentration of this hydroxylase in smokers is higher than that in non-smokers. Smoking will reduce the activity of natural killer cells, thus weakening the body's function of monitoring, killing and clearing tumor cells, which further explains that smoking is a high risk factor for many cancers. The incidence of laryngeal cancer in smokers is ten times higher than that in non-smokers. The incidence of bladder cancer increased by 3 times, which may be related to β -naphthylamine in smoke. In addition, smoking is also related to the occurrence of lip cancer, tongue cancer, oral cancer, esophageal cancer, gastric cancer, colon cancer, pancreatic cancer, renal cancer and cervical cancer. Clinical research and animal experiments show that carcinogens in smoke can also affect the fetus through the placenta, leading to a significant increase in the incidence of cancer in its offspring.

Second, the impact on cardiovascular and cerebrovascular diseases.

Many studies believe that smoking is the main risk factor of many cardiovascular and cerebrovascular diseases, and the incidence of coronary heart disease, hypertension, cerebrovascular disease and peripheral vascular disease of smokers has increased significantly. Statistics show that 75% of patients with coronary heart disease and hypertension have a history of smoking. The incidence of coronary heart disease in smokers is 3.5 times higher than that in non-smokers, the mortality of coronary heart disease is 6 times higher than that in non-smokers, and the incidence of myocardial infarction is 2-6 times higher than that in non-smokers. Hypertension, high cholesterol and the incidence of coronary heart disease in smokers increased by 9 ~ 12 times. 30% ~ 40% of cardiovascular deaths are caused by smoking, and the increase of mortality is directly proportional to the amount of smoking. Nicotine and carbon monoxide in smoking are considered to be the main harmful factors causing coronary atherosclerosis, but the exact mechanism is not fully understood. Most scholars believe that blood lipid changes, platelet function and abnormal hemorheology play an important role. High density lipoprotein cholesterol (HDL-C) can stimulate vascular endothelial cells to produce prostacyclin (PGI2), which is the most effective substance to dilate blood vessels and inhibit platelet aggregation. Smoking can damage vascular endothelial cells, and cause the decrease of serum HDL-C, the increase of cholesterol and the decrease of PGI2-2 level, thus causing contraction of peripheral blood vessels and coronary arteries, wall thickening, lumen stenosis and slow blood flow, resulting in myocardial hypoxia. Nicotine can also promote platelet aggregation. Carbon monoxide in 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. Due to tissue hypoxia, compensatory erythrocytosis and blood viscosity increase. In addition, smoking can increase the level of plasma fibrinogen, leading to dysfunction of coagulation system; Smoking can also affect the metabolism of arachidonic acid, reduce PGI2 _ 2 production and increase thromboxane A _ 2 relatively, thus causing vasoconstriction and increasing platelet aggregation. All these may promote the occurrence and development of coronary heart disease. Due to myocardial hypoxia, myocardial stress increases and ventricular fibrillation threshold decreases, so patients with coronary heart disease who smoke are more prone to arrhythmia and the risk of sudden death increases.

It is reported that the risk of stroke of smokers is 2 ~ 3.5 times that of non-smokers. If smoking and hypertension coexist, the risk of stroke will increase nearly 20 times. In addition, smokers are prone to arteriosclerosis obliterans and thromboangiitis obliterans. Smoking will lead to chronic obstructive pulmonary disease, and eventually lead 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 research shows that long-term smoking can damage and shorten the cilia of bronchial mucosa and affect the cilia removal function. In addition, submucosal gland hyperplasia, hypertrophy, increased mucus secretion, composition has also changed, easy to block bronchioles. In dog experiments, exposure to a large amount of smoke can cause changes in emphysema. A study by the Institute of Respiratory Diseases of China Medical University found that the number of macrophages (AM), neutrophils (PMN) and elastase in the lower respiratory tract of smokers was significantly higher than that of non-smokers. The mechanism may be due to the stimulation of smoke particles and harmful gases, which activated the mononuclear phagocyte system in the lower respiratory tract. Activated AM not only releases elastase, but also releases PMN chemokines, which makes PMN transfer from capillaries to lungs. Activated AM also releases macrophage growth factor to attract fibroblasts. However, PMN releases a large number of toxic oxygen free radicals and proteolytic enzymes, including elastase and collagenase, which act on elastin, mucin, basement membrane and collagen fibers of the lung, thus leading to the destruction of alveolar septa and interstitial fibrosis. It is reported that there were nearly130 thousand COPD patients in the United States during 1986, and more than 90 thousand people died in 199 1 year. Smoking is the main reason. The probability of smokers suffering from chronic bronchitis is 2 ~ 4 times higher than that of non-smokers, and it is directly proportional to the amount of smoking and the number of years of smoking. Patients often have chronic cough, expectoration and dyspnea during activities. Pulmonary function examination showed airway obstruction, decreased lung compliance, ventilation function and diffusion function, and decreased arterial oxygen partial pressure. Even young asymptomatic smokers have slight pulmonary dysfunction. Chronic obstructive pulmonary disease is prone to spontaneous pneumothorax. Smokers often suffer from chronic pharyngitis and vocal cord inflammation.

Fourth, the impact on the digestive tract.

Smoking can increase gastric acid secretion, which is generally 965438 0.5% higher than that of non-smokers, and can inhibit the secretion of sodium bicarbonate by pancreas, thus increasing duodenal acid load and inducing ulcer. Nicotine in tobacco can reduce the tension of pyloric sphincter, make bile easy to reflux, thus weaken the defense factors of gastric and duodenal mucosa, promote chronic inflammation and ulcer, and delay the healing of original ulcer. In addition, smoking can reduce the tension of lower esophageal sphincter and easily cause reflux esophagitis.

Verb (short for verb) others

Smoking is more harmful to women than to men. Smoking can lead to menstrual disorder, difficulty in conception, ectopic pregnancy, low estrogen, osteoporosis and early menopause. Smoking in pregnant women is easy to cause spontaneous abortion, fetal growth retardation and low birth weight. Others such as premature delivery, stillbirth, early placental abruption and placenta previa may be related to smoking. Smoking during pregnancy will increase the mortality before and after birth and the incidence of congenital heart disease. The above hazards are due to the fact that harmful substances such as carbon monoxide in smoke enter the fetal blood to form carboxyhemoglobin, which leads to hypoxia; At the same time, nicotine constricts blood vessels and reduces the blood supply and nutrition supply of the fetus, thus affecting the normal growth and development of the fetus. 90% of lung cancer, 75% of chronic obstructive pulmonary disease and 25% of coronary heart disease in women are related to smoking. The mortality rate of breast cancer in smoking women is 25% higher than that in non-smoking women. Studies have proved that nicotine can reduce the secretion of sex hormones, kill sperm, reduce the number of sperm, abnormal morphology, reduce vitality, and thus reduce the chance of pregnancy. Smoking can also cause testicular function damage, male sexual dysfunction and sexual dysfunction, leading to male infertility. Smoking can cause tobacco amblyopia, and smoking in the elderly can cause macular degeneration, which may be caused by local hypoxia caused by arteriosclerosis and increased platelet aggregation rate. Recently, an American study found that smoking in strong noise can lead to permanent hearing loss and even deafness.

Sixth, passive smoking.

It means that people who live and work around smokers 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. In the cold smoke exhaled by smokers, the content of smoke tar is 1 times higher than that in the hot smoke inhaled by smokers, 2 times higher than that of benzopyrene and 4 times higher than that of carbon monoxide. It is found that the incidence of coronary heart disease in women who often smoke passively in the workplace is higher than that in women who don't smoke passively in the workplace or rarely smoke passively in the workplace. According to an international sampling survey, 50% of cancer patients caused by smoking are passive smokers. A large number of epidemiological surveys show that the prevalence rate of lung cancer of husbands who smoke is 1.6 ~ 3.4 times that of non-smoking husbands. Passive smoking in pregnant women will 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, his prenatal mortality rate increases by 65%; The more you smoke, the higher the death rate. Children from smoking families are more likely to suffer from respiratory diseases than children from non-smoking families.

Seven, quit smoking

To sum up, it can be seen that smoking is harmful to human health. After quitting smoking, its toxic effects will gradually decrease, and most diseases can be reversed to varying degrees, which will help reduce the incidence and mortality of COPD, coronary heart disease and cancer. This shows the importance of quitting smoking. Health education should strengthen the publicity and education of smoking is harmful to health, prohibit smoking in public places, restrict the advertisements of tobacco companies, and print the sign "Smoking is harmful to health" on cigarette cases. There are many ways to quit smoking, such as acupuncture, candy and tea, but the most important way is psychological victory. When smokers really realize the harm of smoking, they will make up their minds to quit smoking as soon as possible.