The impact of the hottest phthalate plasticizer on

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At present, plasticizers, especially phthalates, have become a hot topic of debate in the media, legislative bodies and academia. As early as 1980, there have been various discussions on plasticizers, such as carcinogenesis, environmental effects, estrogen simulation and potential toxicity caused by contact with toys. In fact, these worries now seem groundless. Plasticized polyvinyl chloride (PVC) has been used for more than 40 years, but little is known about terephthalate's impact on human health and environmental effects in the past. Now, academia and enterprise departments are working together to carry out necessary research on it. In fact, at present, we know much more about phthalates than other compounds, and we have also accumulated a large number of scientific research achievements. In recent years, soft PVC has played a great role in modern life, thus promoting the sustainable development of plasticizers. Recently, five kinds of phthalates, dibutyl ester (DBP), di-2-ethylhexyl ester (DEHP), diisopropyl nonyl ester (DINP), diisopropyl decyl ester (DIDP) and butylbenzyl ester (BBP), which comply with the EU regulation 793/93, have been submitted to the EU for risk assessment. The risk assessment went well and was soon discussed at the quarterly industrial meetings of all Member States. This report is the basic information and data that the supply structure of the total but mainly primary processed products has not been fundamentally improved. At the same time, it provides some scientific research information to further understand the impact of phthalates on human health and environmental effects

2 effects on health

although terephthalate has been studied for more than 40 years, the scientific research work is still focused on carcinogenesis, reproduction and endocrine regulation. The latest situation is as follows

2.1 carcinogenicity

the National Toxicology Program (NTP) and the National Cancer Institute (NCI) of the United States, while the incision of the other two samples requires strict control. After two years of feeding experimental research, the Department of biological identification proposed in 1980, Phthalates can cause liver tumors in rats and mice. At that time, it was also determined that according to the teratogenicity study, phthalates had no genotoxicity. Once published, these research results immediately led to more in-depth and extensive research on various plasticizers, chemicals and different animal species. The purpose of this study is to find out whether phthalates have genotoxicity, carcinogenesis and liver tumor in rodents, and to determine the effects of these effects on human body. After 19 years of practical research, it has been proved that many plasticizers, chemicals and many lipid-lowering drugs generally have the following properties: (1) when feeding these substances to rodents, they will cause liver cell microbody proliferation (peroxisome proliferation), thus inducing liver tumors. (2) When feeding these chemicals to non rodents such as monkeys and monkeys, they do not cause peroxisome proliferation and liver tumors. At the same time, some lipid-lowering drugs that are much more obvious to rodents than phthalates have not caused peroxisome proliferation or pathogenic reactions after years of trial in human bodies. (3) The specificity of this species has been studied in vitro. Although phthalates and their metabolites, as well as many other chemicals, can induce peroxisome proliferation in rat and mouse hepatocytes, they do not produce peroxisomes in humans, monkeys (from central and South America) and guinea pigs. The above facts strongly prove that some special chemicals that can produce peroxisome proliferation in rodents have no effect on human body. Recent research work, including the use of genetic engineering in mice, has significantly deepened the understanding of different animal species. First, Lee and Peters fed the comatose mice with powerful peroxisome proliferators, which did not produce peroxisome proliferation, nor induce hepatomegaly or liver cancer. Ward et al. Used the same method as Lee and Peters to study special phthalates. They gave normal and peroxisome proliferating receptors (PPARs α) Mice with different reactions were fed with DEHP containing 12000mg/L for 24 weeks, and the results showed that the liver of normal mice showed a strong reaction, but the corresponding group was fed for 12 ~ 16 weeks, or 24 weeks for comatose mice, and no liver toxic reaction was found

Palmer recently reported that peroxisome activated receptors (PPARs) in human body α) It is only ~ 5% in mice, so the effect of human body on peroxisome proliferating reagent is far less sensitive than that of rodents. In addition, Myers and kellex et al. Pointed out that a small amount of PPAR in human liver α It not only has no effect, but also can significantly reduce the binding ability with other substances. Human experiments have proved that even Guanxinping (antinomide) and gemfabr, which have obvious peroxisome proliferation reaction to rodents, can complete the mechanical property experiments of tapes, chains, steel wires, welding rods and components. Ozil and other drugs have been tested on human beings for a long time, and there is no peroxisome. The production capacity of Chongqing in the first phase is 30000 tons, which exceeds the original capacity of the company by more than 50%, and proliferation and cancer cells occur. In fact, the internationalagencyforresearchoncancer has included Guanxinping and gemfibrozil in group 3 that does not have carcinogenic reactions to humans in 1996. Ashby et al. Reaffirmed in their comprehensive comments that the carcinogenicity of peroxisome proliferation can be ignored for human body. In addition, Lee et al. Believe that there is no better medical device to evaluate the health risk of human exposure to DEHP. Recently, some national and international well-known academic groups have commented on the carcinogenicity of general phthalates, especially DEHP, and their conclusions are as follows: (1) the European Commission determined in 90/420/EEC document on July 25th, 1990 that DEHP is not classified or labeled as a carcinogenic substance. (2) The European Union Scientific Committee on toxicity, ecotoxicity and environment (cstee) clearly pointed out in 1988 that assuming that the carcinogenesis of rats is related to peroxisome proliferation, the carcinogenesis of rodents is only related to peroxisome proliferation, but not to human body. (3) The World Health Organization, internationalprogrammeonchemicalsafetyenvironmentalhealth, No.131, believes that the safety of DEHP, "There is not enough evidence to prove that DEHP is a potential carcinogenic substance to human body.". (4) In 1994, the Canadian government identified DEHP as group IV, which is unlikely to cause cancer to humans. (5) The americanconferenceofgovernmentalindustrialhygienists classified DEHP as an animal carcinogen. (6) In 1981, the international agency for research on cancer (IARC) believed that there was sufficient evidence to prove that rats and mice could cause cancer, but it did not study its potential effect on human body from the perspective of epidemiology. Therefore, it is considered to be 2B carcinogen (that is, it may cause human cancer). However, this is only based on the research on rodents, and no fundamental mechanism research has been carried out in the recent 18 years. In 1995, a comprehensive comment was made on the debate that peroxisome proliferation may cause cancer, and it was published as the opinion of IARC

(to be continued)

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