• Toxicological Research
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• v.6 no.1
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• pp.63-73
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• 1990

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.

• Toxicological Research
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• v.6 no.1
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• pp.61-61
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• 1990

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.

• Journal of the Korea Safety Management & Science
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• v.12 no.3
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• pp.107-119
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• 2010

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.

• Journal of Korean Society for Atmospheric Environment
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• v.8 no.2
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• pp.100-104
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• 1992

The research in this paper centers on a comparative risk assessment for nearby air pollution by carcinogenic metal emission from municipal solid waste incinerators. If a substance is identified as a potential human carcinogen, the carcinogenicity may be related to the chemical form of a substance and the route of exposure. This type of information with regard to carcinogenic uncertainty is incorporated into hazard quantification. In addition to the dioxin emission, the metal emission from municipal solid waste incineration is found to be a major contributor to human cancer risk via the inhalation route. The magnitude of risk by metals is about 5 times greater than that of risk by dioxins. Hexavalent form of chromium and cadmium compounds are major contributors to cancer risk from metal emission. In addition, hexavalent chromium is known to be human carcinogen while 2,3,7,8-TCDD is known to be only probable human carcinogen.

• Toxicological Research
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• v.34 no.4
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• pp.311-324
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• 2018

Arsenic is one of the most toxic environmental toxicants. More than 150 million people worldwide are exposed to arsenic through ground water contamination. It is an exclusive human carcinogen. Although the hallmarks of arsenic toxicity are skin lesions and skin cancers, arsenic can also induce cancers in the lung, liver, kidney, urinary bladder, and other internal organs. Arsenic is a non-mutagenic compound but can induce significant cytogenetic damage as measured by chromosomal aberrations, sister chromatid exchanges, and micronuclei formation in human systems. These genotoxic end points are extensively used to predict genotoxic potentials of different environmental chemicals, drugs, pesticides, and insecticides. These cytogenetic end points are also used for evaluating cancer risk. Here, by critically reviewing and analyzing the existing literature, we conclude that inorganic arsenic is a genotoxic carcinogen.

• Toxicological Research
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• v.18 no.1
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• pp.99-106
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• 2002

The United States Environmental Protection Agency (EPA) characterized the cancer hazard of di(2-ethylhexyl)-phthalate (DEHP) as a B2 group (probable human carcinogen) and proposed "Guide-lines for Carcinogen Risk Assessment". This guidelines proposed alternative methods for analyzing carcinogen dose-response data and for extrapolating the effects of observed at high dose to predict that might occur at lower doses relevant to human exposure. This proposed guidelines state that "If in a particular case, the evidence indicated a threshold, as in the case of carcinogenicity being secondary to another toxicity that has a threshold, the margin of exposure analysis for toxicity is the same as is done for a non-cancer endpoint". DEHP is excellent candidate for reconideration under the new guidelines for carcinogen risk assessment (John Doull et al., 1998). This study is conducted about risk assessment for infant exposure on DEHP in powdered milk wing methodology in EPA's new guideline on carcinogenic risk assessment. Estimated cancer risk of DEHP in powdered milk and cow milk is 2.83$\times$$10^5$ (using cancer potency: 1.4$\times$$10^2$/ (mg/kg/day)) as mean and MOE is 12075 (using selected NOEL 20 mg/kg/day) as mean. mg/kg/day) as mean.

• Environmental Analysis Health and Toxicology
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• v.21 no.2 s.53
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• pp.93-102
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• 2006

Methyl tert-butyl ether (MTBE), an octane booster that is added to the reformulated gasoline, has been a widespread contaminant in aquatic ecosystem. MTBE is a recalcitrant pollutant having low biodegradability. Due to its higher water solubility and low octanol-water partition coefficient, it can be rapidly transported to the surrounding water environment. Also, MTBE is a known animal carcinogen, and is classified as a possible human carcinogen by U. S. Environmental Protection Agency. The adverse effect of MTBE to aquatic biota was widely reported. In Korea, the recent detection of MTBE in groundwater near gasoline filling stations has drawn concern to public health and ecosystem. To address this concern, the effect of MTBE to human health and ecosystem was discussed in this review. Also, ecotoxicity data of MTBE for fish, invertebrates, and algae were extensively compared to estimate the hazard concentration 5($HC_5$) of MTBE as a screening level.

• Environmental Analysis Health and Toxicology
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• v.13 no.1_2
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• pp.27-31
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• 1998

Motor vehicle exhaust is the major cause to the air contamination in Seoul. It includes many toxic chemicals to human health such as aidehyde, PAHs, benzene, xylene, toluene, benzo[a]pyrene, nickel, arsenic and cadmium in gasoline exhaust and formaldehyde, PAHs, 1,3-butadiene, benzene and particulate matter in diesel exhaust. Some chemicals out of them are classified as a human carcinogen. Many large diesel vehicles such as buses and trucks are drivened frequently in Seoul so that the air in Seoul is seriously contaminated by diesel exhaust, especially particulate matter. The amounts of particulate matter from large diesel vehicles may be estimated to be more than 50% of small dust in Seoul. The particles of particulate matter are coated with many toxic chemicals and some of these are considered as a human carcinogen. The cancer risk has to be throughly managed because the population density of Seoul is very high. Government should list hazardous air pollutants in Seoul, assess the exposure of people to toxic pollutants, especially carcinogens and manage human health risk.

• Toxicological Research
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• v.13 no.1_2
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• pp.49-54
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• 1997

PCBs are classified as B2 (Probable human carcinogen) based on the induction of hepatocellular carcinomas in rats and mice from IRIS (Integrated Risk Information System). About 20 years ago, PCBs were phased out for electrical use in Korea, but PCBs were continuously used in the other field. Lately, there has been increasing concern on possible effects of contaminated soil to the other environment and human health. The purpose of this study is to determine PCBs level in soil at some site and to assess the human exposure doses according to exposure routes for people living within sites which expected to be exposed to PCBs. Pollution level of PCBs on the site was monitored using gas liquid chromatography. To assess the transport of PCBs in soil to plant and to air, various transfer factors(diffusion coefficient, bioconcentration factor etc.) were considered in simple calculations. To calculate the residential exposure doses by routes, some equations were considered using assumption value, which define inhalation, ingestion (soil, plant) and derreal uptake pathway. Computated results will be used as risk assessment information for human health evaluation on contaminated soil.

• Korean Journal of Community Nutrition
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• v.2 no.5
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• pp.735-744
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• 1997

The effect of green tea drinking on the hepatocellular chemical cacinogenesis have been studied. Placental glutathione S-transferase(GST-P) positive foci area in a liver tissue, contents of thiobarbituric acid reactive substances(TBARS), total cytochrome P450 and glucose 6-phospphatase(G6P) activity in hepatic microsomes were investigated. Weaning Sprague-Dawley male rats were fed AIN-76A diet with deionized water or green tea infusion, Rats of CTR and CTR+ groups were provided deionized water while GTI and GTI+ groups were provided green tea instead of deionized water for the entire experimental period of 13weeks. Rats of GTP and GTP + groups had deionized water for the first 6 weeks and switched to green tea for the last 7weeks of the experimental period. CTR+, GTI +, and GTP + groups were carcinogen treated groups, Diethylnitrosamine(DEN) was injected as a single dose of 200mg/kg body weight intraperitoneally after 4 weeks of feeding. 2-Acetyla-minofluorene(AAF) was used as a carcinogen proliferater and suppled in the diets of carcinogen treated rats as 0.02% content for the last 6weeks starting from 2weeks after DEN injection. Rats were sacrificed after 13week weeks of feeding. The area and number of GST-P positive foci detected in carcinogen treated rats were decreased by green tea ingestion but when timing and duration of green tea ingestion was delayed after promotion period as in GTP + group, GST-P positive foci were not decreased as much as in GTI+ group. TBARS contents of carcinogen treated rats decreased by 13weeks of green tea ingestion but GTP groups did not show statiscally significant differences. G6P activities tended to decrease by carcinogen treatment but changes were not statiscally significant by green tea ingestion. Total cytochrome P450 contents were increased by carcinogen treatment. Thirteen weeks of green tea ingestion (GTI) also increased to total cytochrome P450 contents while 7weeks of green tea ingestion(GTP) did show any effects. These results suggest that green tea has suppressive effects on hepatocellular chemical carcinogenesis probably through the activities of antioxidant compounds. (Korean J Community utrition 2(5) : 735∼744, 1997)