Carcinogens in the environment come from a wide range of sources, some from nature and some from artificial synthesis. Natural carcinogens can come from plants (such as thapsigargin, safrole), bacteria (such as Escherichia coli can synthesize ethanethionine, intestinal flora can synthesize nitrosamines under certain conditions), molds (such as aflatoxin, fusarium) and so on. But many more are from synthetic (such as polycyclic aromatic hydrocarbons, amine compounds, anti-cancer drugs, etc.), industrial products (such as certain chemical materials, dyes, pesticides, drugs, etc.) or daily life environment (such as cigarette smoke, food cooking thermal cracking products contain a variety of carcinogenic substances). There are many ways for chemical carcinogens in the environment to enter the human body, mainly through the digestive tract, respiratory tract and skin contact. Many indirect carcinogens can become final carcinogens through oxidation, reduction, hydrolysis and other chemical reactions with the participation of cytochrome P-450 mixed function oxidase, various reductases or hydrolytic enzymes. The final carcinogen is mostly an electrophilic molecule, which can interact with nucleophilic groups in DNA, RNA, proteins and other biological macromolecules, causing DNA damage or forming DNA adducts, chromosomal aberrations, cell mutations and carcinogenesis. The methylation level of cellular DNA plays a regulatory role in gene expression, and chemical carcinogens can cause a decrease in the methylation level of cytosine in cells, which may activate certain oncogenes and cause cellular malignancy. On the other hand, some carcinogens are inactivated or excreted after the binding reaction of glucuronosyltransferase, glutathione transferase, sulfotransferase and acetate transferase. The presence and activity of various enzymes in the body are regulated by the genetic phenotype of the body, so the process of in vivo activation of chemical carcinogens causing tumorigenesis is influenced by environmental factors as well as controlled by the genetic background of the body. The genetic phenotypes of individuals in the human population vary greatly, thus determining the sensitivity of different individuals to chemical carcinogens. Since the metabolic activation of carcinogens varies greatly, some chemicals are carcinogenic to one animal but not to humans or another animal. Even if they are carcinogens, the difference in their carcinogenic ability is very large. For example, with 1 / 1 billion concentration of aflatoxin B1 has been easy to successfully induce liver cancer in rats, while safrole feed is required for a few percent of the concentration to induce success, the difference between the two hundreds of thousands of times. The difference in the strength of chemical carcinogens is so great that it is of great practical importance to estimate their realistic hazards. For example, it is clear that saccharin is a very weak bladder carcinogen, it is estimated that the United States about 50 million people apply saccharin, it is estimated that each year may cause about 50 cases of bladder cancer patients; but if the ban on saccharin, people will turn to a large number of applications of sugar, the total number of deaths caused by worsening diabetes, cardiovascular disease, obesity, etc. more than 50 cases of bladder cancer serious many times, so the United States did not strictly prohibit saccharin. The United States does not strictly prohibit saccharin. Ultraviolet light (Uv) has a relationship with the occurrence of skin tumors. Sunlight is the main source of human exposure to ultraviolet light, which accounts for about 5% of the energy of surface sunlight. The wavelength of ultraviolet light is 100-400mm, and it is divided into A, B and C, namely UVA (315-400mm), UVB (280-315mm) and UVC (100-280mm). In the ultraviolet light of the surface daylight, UVA accounts for about 95% UVB accounts for 5%, UVC is completely absorbed by the atmosphere can not reach the ground. UVB irradiation can cause cellular DNA breakage and DNA-protein cross-linking and chromosomal aberrations. UVB can also inhibit the immune function of the skin and make mutated cells easily escape from the body’s immune surveillance, which are conducive to the occurrence of squamous and basal cell carcinoma of the skin, and may also have an effect on causing melanoma. According to statistics, the incidence of head and neck skin squamous carcinoma and basal cell carcinoma is often higher among outdoor workers than indoor workers. In recent years, due to environmental degradation, the ozone in the atmosphere has decreased and the earth’s ozone hole has emerged, the intensity of ultraviolet radiation at the surface will increase dramatically, and the potential risk of inducing human skin cancer will increase greatly. It is estimated that the reduction of atmospheric ozone by 1%, skin cancer will increase by 2% to 6%, and the United States will increase by 10,000 to 20,000 skin cancer patients each year. These problems have attracted the great attention of scientists in various countries.