The World Health Organization has proven with science and facts that smoking is a major killer that increasingly threatens human health. China is the world’s largest tobacco country, and the latest survey in 2010 showed that there are still nearly 300 million smokers in China. Recently, studies have found that smoking is also a serious risk to male reproductive health. Smokers’ sperm density decreases by 13-17% compared to non-smokers, and sperm density decreases even more significantly in people with heavy smoking index. Smoking decreases sperm motility and viability, especially the linear movement of sperm. There is a dose-response relationship between changes in sperm density and sperm motility and smoking. Smoking causes an increase in sperm malformation and an increase in the proportion of head-defective and ovoid sperm, as well as an increase in microdroplets in the sperm cytoplasm and an increase in the proportion of immature sperm. The frequency of chromosomal damage in Golgi- and Cap-phase sperm cells was 1.15% in smokers and 0.82% in nonsmokers who were infertile. Nicotine is able to induce double-stranded DNA breaks in mirrors and is a potential oxidizing factor for sperm plasma membrane and DNA integrity. Smoking increases the fragility of sperm DNA, increases the sensitivity of sperm to acidic mutagens, and increases DNA breakage. Smoking increases ploidy chromosomal sperm, which increases the risk of aneuploidy syndrome. Acrosome protease activity is reduced in smokers compared to nonsmokers, and acrosome response is significantly diminished. Markable alterations in the number and arrangement of genetic filament microtubules and genetic filament aberrations occurred in smokers compared to nonsmokers. The percentage of convoluted sperm correlated with heavy smoking, and convolution of the tail filaments within the plasma membrane was seen electron microscopically. Cigarettes contain a large number of toxic substances such as nicotine, cotinine, benzo[a]pyrene, and cadmium. Nicotine can affect the morphology and sperm density of spermatozoa. Seminal fluid levels of cotidine and 3-hydroxycotidine were negatively correlated with sperm motility, and cotidine levels were negatively correlated with sperm linear motility. There was a significant correlation between seminal plasma cotinine concentration (positively correlated with smoking) and percentage of abnormally morphologic spermatozoa. The testis is one of the major target organs for cadmium, causing hemorrhagic necrosis of some testicular tissues by damaging the blood-testis barrier, acting on the chromosomes of mesenchymal cells and damaging the spermatogenic epithelium. benzo[a]pyrene is present in cigarette smoke and reduces sperm motility by increasing sperm hyperactivation and premature acrosome reaction. Studies have found that exposure of nonsmokers’ sperm to smokers’ seminal plasma diminishes sperm motility, acrosome response, and MDA levels. Nicotine alters the hypothalamic-pituitary axis, stimulating the release of growth hormone, cortisol, pressor hormone, and prolactin, which in turn inhibits the release of luteinizing hormone and prolactin. Studies have reported an increase in 17β estradiol and a decrease in luteinizing hormone, follicle stimulating hormone and prolactin in smokers. Ramlau reported a dose-response relationship between serum T, LH and LH/ free-T and smoking. However, there are also controversial reports of no significant changes in FSH, LH, and T in smokers compared to nonsmokers. In rats exposed to cigarette smoke, testicular mesenchymal and germ cells were reduced and supporting cells were damaged. Testicular ultrastructure showed a series of changes: increased subbasal collagen fibers, thickening of the lamina propria, and separation of peritubular cells. Mitochondria were morphologically diverse with increased irregular cristae and high electron density matrix, accumulation of lipid droplets, and multinuclear formation in the cells. N-Aminose, total phosphate, zinc and acid phosphatase secreted by the seminal vesicles were decreased in smokers, indicating that smoking has a damaging effect on the seminal vesicles and prostate. Vitamin E is the most essential antioxidant in semen, and the level of vitamin E in human seminal plasma is 0-10 mg/dl, which is 9 times higher than the level in blood. Serum vitamin E levels decreased by 20-40% in heavy smokers, and semen quality could be improved with vitamin E supplementation therapy. Serum levels of zinc, copper and SOD were decreased in moderate and heavy smokers compared to nonsmokers, and were negatively correlated with the total amount and duration of smoking. Cigarette smokers had a 48% increase in leukocytes in semen, a 107% decrease in ROS levels, and a 10-point decrease in ROS-TAC scores. Components of cigarette smoke can induce oxidative damage to sperm DNA through the blood-testis barrier, leading to changes in semen quality. Vitamin E’s in semen correlated with sperm density, sperm motility, and percentage of normal sperm morphology. The process of smoking produces various toxic oxygen reactive substances, such as superoxide anions and oxygen radicals, which not only have a damaging effect on blood vessels, affect testicular blood flow, cause testicular spermatogenic dysfunction and increase malformed spermatozoa, but also cause oxidative stress, which can cause mitochondrial and DNA damage. Varant reported that smoking significantly increased the risk of erectile dysfunction, with a cumulative composite smoking index (pack-years) adjusted OR=1.68, with an OR=2.30 for those with a smoking index ≥20. Edoardo concluded from a survey of 16724 patients that after adjusting for confounding factors such as age, marital status, education, alcohol consumption, physical activity, and pathological Rahman reported that those who smoked since 1994 and developed vascular disease in 1994-1999 had a higher OR for ED in 1999-2004 than nonsmokers. The risk of ED was three times higher in smokers (IDR 3.1), and it is believed that smoking causes erectile dysfunction by causing vascular lesions. Specifically, prolonged smoking has damaging effects on the vascular endothelium, peripheral nerves, and ultrastructure of tissues, mediating the effects of chronic smoking on erectile function. More specifically, smoking increases the production of reactive groups (ROS), decreases the biological activity of NO, leads to impaired relaxation of endothelial smooth muscle in the penis, and affects penile erection. Although some studies have presented controversial conclusions regarding the effects of smoking on semen parameters, sex hormones, etc., the idea that smoking acts on various parts of the male reproductive system, leading to decreased male fertility, has been accepted by most scholars. This is especially true for those whose semen quality is on the borderline of normal. In addition, cigarettes can damage sperm DNA and mutate it, and they contain a large number of mutagens, so out of a sense of responsibility for the health of the next generation, we are determined to quit smoking and achieve the goal of human reproductive health.