Journal of Korean Society of Occupational and Environmental Hygiene
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v.21
no.4
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pp.227-235
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2011
The objective of this study was to analyze 157 processes of 145 industries that exceeded Korean Occupational Exposure Limits (KOEL) for carcinogen during the 11 year period from 1999 to 2009. The data included number of industry and workers exposed, type of carcinogen and their exceeded ratio, type and size of industry in each year. These data were collected by 46 regional employment & labor offices in Korea using work environment monitoring reports. The result showed that, in each year, about 10 industries exceed their carcinogen exposure limit. The most common carcinogen exceeding KOEL were found to be formaldehyde, benzene, ethylene oxide and chromium VI. The carcinogen with the highest level of over-exposure were in the order of formaldehyde, benzene, ethylene oxide and asbestos. Fabricated metal product manufacturing industry were found to be most vulnerable against carcinogen with 11.1% of them exceeding carcinogen KOEL followed by electronic components manufacturing industry (8.3%), chemical products manufacturing industry (6.3%), and electrical equipments manufacturing industry (4.9%). The industry employing less than 50 workers had the highest percentage of exceeding carcinogen KOEL with 52.8%. The result also showed that strengthening KOEL for benzene and asbestos helped reduce the level of carcinogen over-exposure. Based on these results, strengthening the KOEL or new regulation turned out to help reduce the carcinogen over-exposure level. Benzene, ethylene oxide and chromium VI were the most frequently over-exposed carcinogen with the highest level. Therefore, these chemicals need to be regulated with a highest priority to improve the workplace environment. The results also show that the small-sized industries employing less than 50 workers was the most vulnerable against carcinogen exposures. Therefore, more government support are needed for these small-sized industries to help them to improve their workplace environment.
The aim of this study was to compare the carcinogen classification systems of developed countries or global organizations with domestic system under Industrial Safety and Health Act (ISHA). We selected the representative institutions which had carcinogen classification system such as International Agency for Research on Cancer (IARC), National Toxicological Program (NTP), Environmental Protection Agency (US-EPA), American Conference of Governmental Industrial Hygienists (ACGIH), and European Union (EU). We collected the carcinogen lists issued by 5 institutions, and merged by CAS number of each chemical with Microsoft Access 7.0. We found that confirmed human carcinogens, probable human carcinogens and possible human carcinogens were 34, 179, and 252, respectively. All of the institutions classified chemicals as 2 (NTP), 3 (EU) or 5 (IARC, ACGIH, US-EPA) categories based on the weight of scientific evidences for carcinogenicity and periodically updated the carcinogen list by regular procedure. However, a total of 90 chemicals could be classified as carcinogen under ISHA in Korea. There was no procedure or system which periodically update the carcinogen lists. In addition, the status of carcinogen classification according to regulation was confused. In conclusion, these findings suggest that the carcinogen classification and management system should be amended by consideration of systems of advanced institutions and the domestic regulation system.
Human exposure to environmental carcinogens can be detected by a number of methods including immunoassay, $^{32}P-postlabeling$ assay, and fluorescence technique. These assays have been applied to measure biological markers of carcinogen-adducts formed with macromolecules such as DNA, RNA and protein. In an attempt to investigate causal relationships between carcinogen exposure and tumor formation, specific carcinogen-adducts have been quantitated from human tissues and body fluids of cancer patients, occupational workers heavily exposed to certain carcinogens, smokers and controls. Carcinogens studied for biological human monitoring include benzo(a)pyrene, aflatoxin B1, UV light, ethylene oxide, 8-methoxypsoralen, 4-aminobiphenyl, vinyl choride, N-nitrosamine, cisplatin and other chemotherapeutic agents. Relevance of human monitoring for cancer research, progress in this field, methods to detect carcinogen-adducts are reviewed here. It is hoped that these approaches will be used for the risk assessment of carcinogen exposure, cancer etiology study and cancer prevention in humans.
Human exposure to environmental carcinogens can be detected by a number of methods including immunoassay, $^{32}P$-postlabeling assay, and fluorescence technique. These assays have been applied to measure biological markers of carcinogen-adducts formed with macromolecules such as DNA, RNA and protein. In an attempt to investigate causal relation ships between carcinogen exposure and tumor formation, specific carcinogen-adducts have been quantitated from human tissues and body fluids of cancer patients, occupational workers heavily exposed to certain carcinogens, smokers and controls. Carcinogens studied for biological human monitoring include benzo(a)pyrene, aflatoxin B1, UV light, ethylene oxide, 8-methoxypsoralen, 4-aminobiphenyl, vinyl chloride, N-nitrosamine, cisplatin and other chemotherapeutic agents. Relevance of human monitoring for cancer research, progress in this field, methods to detect carcinogen-adducts are reviewed here. It is hoped that these approaches will be used for the risk assessment of carcinogen exposure, cancer etiology study and cancer prevention in humans.
The influences of dietary supplement of citron tea on the hepatocellular chemical carcinogenesis have been studied by examining placental glutathione S-transferase(GST-P) positive foci area in a liver tissue, contents of total cytochrome P450, thiobarbituric acid reactive substances(TBARS) and glucose 6-phosphatase(G6Pase) in hepatic microsome and glutathione S-transferase(GST) activity. Weaning Sprague-Dawley male rats were fed AIN76 diet with or without citron tea supplement. Rats of CTR and CTR+ groups were fed diet without citron tea supplement while CDI and CDI+ groups were fed diet with citron tea supplement for the entire experimental period(13 weeks). Rats of CDP and CDP+ groups were fed diet without citron tea supplement for the first 7 weeks and swiched to citron tea containing diet for the last 6 weeks of experimental period. CTR+, CDI+ and CDP+ groups were carcinogen treated group. Diethylnitrosamine(DEN) was used as a carcinogen initiator and injected to the rats of carcinogen treated groups as a single dose of 200 mg/kg body weight intraperitoneally after 4 weeks of feeding. 2-Acethylaminofiuorene(AAF) was used as a carcinogen promoter and supplied in the diets of carcinogen treated rats as 0.02% content for the last 6 weeks starting from 2 weeks after DEN injection. Rats were sacrificed after 13 weeks of feeding. Liver/body weight ratio and GST activities were increased by carcinogen treatment. However, they were not changed by citron tea supplement. Total cytochrome P450 contents were not changed by carcinogen treatment or citron tea supplement. TBARS contents of carcinogen treated rats showed tendency to decrease by citron tea supplement. G6Pase activity decreased by carcinogen treatment and citron tea supplement. The area of GST-P positive foci detected in carcinogen treated rats were decreased by citron tea supplement and not affected by the timing and the duration of citron tea supplement. These results suggest that citron tea has suppressive effects on hepatocellular chemical carcinogenesis probably through antioxidant compounds by decreasing TBARS contents.
This study was done to investigate the effects of different dietary oils on hepatic mitochondrial lipid compositon, adenine nucleotide translocase(AdNT) and ATPase activities in carcinogen treated rats. Sixty male Sprague-Dawley rats, weighing 50∼60g, were fed three different types of dietary oil, beef tallow(BT), corn oil(CO) and sardine oil(SO) at 15% by weight for 14 weeks. Three weeks after feeding rats were intraperitoneally injected with a single dose of diethylnitrosamine(200mg/Kg BW). After five weeks rate fed 0.02% acetylaminofluorene contating diet for 6 weeks, and after seven weeks 0.05% phenobarbital containing diet for 7 weeks. At 14th week, rats were sacrificed and hepatic mitochondrial lipid composition, AdNT and ATPase activities were determined. Percent liver weight per body weight was significantly by carcinogen treatment. Analysis of mitochondrial lipid composition showed that body cholesterol and phospholipid contents were not affected by dietary oils but significantly increased by carcinogen treatment. Individual phospholipid composition as well as phosphatidyl ethanolamine/phosphatidyl choline ratio were altered by either dietary oils or carcinogen treatment. Fatty acid composition was changed by dietary oils but not much by carcinogen treatment. AdNT activity was affected by dietary oils in only carcinogen treated groups. ATPase activity was affected by dietary oils in only carcinogen nontreated groups. These data indicate that both dietary oils and caricinogen treatment can change mitochondrial lipid composition and thereby change AdNT and ATPase activities. Particularly effects of carcinogen treatment on cholesterol/phopholipid ratio, phospholipid compositon and ATPase activity were different among dietary oil groups. Therefore it is suggested that different dietary oils can somewhat modulate the changes of mitochnodrial lipid composition and membrane bound enzyme activites during hepatocarcinogenesis.
The purpose of this study was to determine the effects of taurine supplementation on the hepatic lipid peroxidation, activiteis of defense enzymes and membrane stability during rat hepatocarcinogenesis. Hepatocarcinogenesis was induced by Solt & Farber modification. Lipid peroxide contents of carcinogen treated group which was not supplemented with taurine were lower than those of control group. This might be that peroxide is decreased because of the activation of detoxifing enzyme. Glutathione S-transferase(GST) activites of carcinogen treated groups were significantly (p<0.05) increased compared to those of control groups. The GST activities of group supplemented with taurine before treatment of carcinogen and during the all period of experiment were only less increased. In carcinogen treated groups, glutathione peroxidase(GPx) activites of groups supplemented with taurine were higher than those of non supplemented group. By carcinogen treatemtn, glucose 6-phosphatase(G6Pase) activites, index of membrane stability were decreased, but in carcinogen treated groups supplemented with taurine, they were less decreased. These results suggest that taurine supplementation seems to inhibit lipid peroxidation, to change the activities of defense enzymes and to prevent to membrane disintegration during chemically induced hepatocarcinogenesis.
Background: Occupational cancer is a global health issue. The Korean CARcinogen EXposure (K-CAREX), a database of CARcinogen EXposure, was developed for the Korean labor force to estimate the number of workers exposed to carcinogens by industry. The present study aimed to estimate the intensity of exposure to carcinogens by industry, in order to supply complementary information about CARcinogen EXposure intensity to the K-CAREX. Methods: We used nationwide workplace monitoring data from 2014 to 2016 and selected target carcinogens based on the K-CAREX list. We computed the 95th percentile levels of measurements for each industry by carcinogens. Based on the 95th percentile level relative to the occupational exposure limit, we classified the CARcinogen EXposure intensity into five exposure ratings (1-5) for each industry. Results: The exposure ratings were estimated for 21 carcinogenic agents in each of the 228 minor industry groups. For example, 3,058 samples were measured for benzene in the manufacturing industry of basic chemicals. This industry was assigned a benzene exposure rating of 3. Conclusions: We evaluated the CARcinogen EXposure ratings across industries in Korean workers. The results will provide information on the exposure intensity to carcinogens for integration into the K-CAREX. Furthermore, it will aid in prioritizing control efforts and identifying industries of concern.
Cancer has been the leading cause of death in Korea for the last 30 years. Cancer patients' 5-year survival rate between 2005 and 2009 was 62.0%, representing a highly advanced standard of care, as much as developed countries in the EU and the US. The Korean government formulated its first 10-year plan for cancer control in 1996 and has been carrying out a second 10-year plan for cancer control since 2006. But despite the Korean government's efforts, the cancer burden in Korea continues to increase. Many separate laws have gone into effect concerning the management of carcinogen exposure. However, there are no integrated regulatory laws or management systems against carcinogen exposure in Korea. Dead zones remain where carcinogen exposure cannot be controlled properly in Korea. In this paper, we suggest the need to establish a national carcinogen list based on international harmonization as a prerequisite for a paradigm shift in cancer control policy from treatment to primary prevention.
Kim, Hyoung-Chun;Chun, Wan-Jhoo;Lee, Hyun-Woo;Kwon, Myung-Sang;Song, Kye-Yong;Jhoo, Wang-Kee
YAKHAK HOEJI
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v.36
no.2
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pp.180-187
/
1992
This study investigated the hypothesis that carcinogen-induced elevation of oxyradical during the hepatocarcinogenesis in rat. The hepatic preneoplastic lesions in the Spraque-Dawley rats were induced by the carcinogen treatment such as diethylnitrosamine(DEN) and acetylaminofluorene(AAF) in combination with partial hepatectomy(PH). The liver sample was taken at 2, 6, 10 and 16 months after carcinogen treatments followed by PH. Carcinogen treatments initially increased the indices of oxidative damage(activities of xanthine oxidase and production rates of superoxide anion, microsomal hydrogen peroxide, hydroxyl radical) in the liver compared to PH groups. However, cytosolic hydrogen peroxide did not change significantly throughout the full time period. Of hydrogen peroxide scavenger, the catalase was remained lower than PH groups, whereas the peroxidase was increased after carcinogen treatments. Morphologically, the immunohistochemical analysis with glutathione-S-transferase of a placenta form(GSTP) antibody was used to detect the induction of preneoplastic nodules. During the hepatocarcinogenesis, both production rate of hydroxyl radical and activity of glutathione-S-transferase(GST) markedly increased with the appearance of the preneoplastic nodule. These results indicated that the hydroxyl radical of reactive oxygen species seemed to have a major influence on the hepatocarcinogenesis and the effect of time after removal of the carcinogen also appeared to be highly critical in the hepatocarcinogenesis.
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