• 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.

• Journal of Food Hygiene and Safety
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• v.9 no.3
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• pp.133-139
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• 1994

The pyrolytic formation of benzo[a]pyrene during the cooking procedure was analysed in beef, pork, pacific saury, rice, and soybean by HPLC. In raw foods, benzo[a]pyrene (B[a]P) was not detected or negligible, but it was increasingly formed when foods were boiled (0.010~0.037 ppb) and more dramatically during broiling (0.302~0.851 ppb) in a time dependent manner. Human daily intake of B[a]P in Koreans and cancer risk assessment were estimated based on food consumption per capita and carcinogenic potency of B[a]P. When cooked foods were consumed for entire life time, cancer risk was estimated to bo 1.77$\times$10-6>1.65$\times$10-7>1.32$\times$10-8 by the order of broiled, boiled, and raw foods consumption. These data suggest that broiled foods produce more benzo[a]pyrene than water boiled foods. Thus cooking procedure is an important factor for the formation of carcinogens and needs to bo modified to reduce cancer risk for man.

• Journal of Food Hygiene and Safety
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• v.15 no.3
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• pp.267-270
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• 2000

This study was designed to predict the risk of a hazard chemical, vinyl chloride, by applying dose-response assessment that are one of the major process in practicing risk assessment. After extrapolating from the high dose exposure of vinyl chloride based upon animal carcinogenic data to the low dose exposed to human using several mathematical models, we calculated the cancer potency factors as well as virtually safe dose and the resulted values were compared. This process will provide the new insight to assess the risk of a chemical accurately imposed to human in the future.

• Journal of Korean Society for Atmospheric Environment
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• v.12 no.5
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• pp.567-576
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• 1996

Air pollution has been recognized for many years as a factor which heightens the risk of cancer. Extractable polycyclic organic matters in air particulates have been recognized as to have carcinogenic effects. This study examined the health risks posed by organic substances of air particulates in Seoul based on methodelogies that have been developed for conducting risk posed by organic substances of sir particulates in Seoul based on methodologies that have been developed for conducting risk assessment of complex -chemical-mixture. The data used in this study was obtained from air samples collected in a heavy traffic area of Seoul (Shinchon) from 1986 to 1994. The mean concentration of total supended pariculates was 158.0.mu.g/m/msup 3/, 5% of which is consisted of organic matter. The excess cancer risk from benzo(a)pyrene (BaP) was estimated to be 3.48.times.10$^{-6}$ by applying BaP unit risk estimates to the mean concentration. 8.74ng/m BaP equivalents of potency method was 1.0.times.10$^{-3}$ . The calculated risk from EOM were comparably higher than that from benzo(a)pyrene and exceeded the acceptable risk level.

• Asian Pacific Journal of Cancer Prevention
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• v.13 no.6
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• pp.2429-2435
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• 2012

Methyl isocyanate may have a role in cancer etiology, although the link is unclear. There is evidence in the literature that it can induce cancer in animals but the carcinogenic potency is weak. Pheochromocytoma of adrenal medulla and acinar cell tumors of pancreas have been observed in methyl isocyanate exposed animals. Conversely, emerging data from population-based epidemiological studies are contradictory since there is no evidence of such cancers in methyl isocyanate exposed humans. Recently, we reported a high prevalence of breast and lung cancers in such a population in Bhopal. In vitro findings appearing in the latest scientific literature suggest that genomic instability is caused by methyl isocyanate analogs in lung, colon, kidney, ovary epithelial cells, and that hepatocytes may undergo oncogenic transformation, have obvious implications. The conflicting information prompted us to present this update over the last three decades on methyl isocyanate-induced cancers after an extensive literature search using PubMed. While the pertinent literature remains limited, with a scarcity of strong laboratory analyses and field-epidemiological investigations, our succinct review of animal and human epidemiological data including in vitro evidences, should hopefully provide more insight to researchers, toxicologists, and public health professionals concerned with validation of the carcinogenicity of methyl isocyanate in humans.

• Proceedings of the Korea Society of Environmental Toocicology Conference
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• 2003.05a
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• pp.194-194
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• 2003

The International Agency for Research on Cancer (IARC, 1989) has classified whole diesel exhaust as probably carcinogenic to humans. Diesel exhaust particulate matter (DPM) adsorbs different chemical substances including PAHs and nitroarenes. DPM is emphasized because it is a major component of diesel exhaust, it is suspected of contributing to a health hazard. Diesel exhaust is a complex mixture of carbon particles and associated organics and inorganics, and it is not known what fraction or combination of fractions cause the health effects [cancer effects, noncancer effects (respiratory tract irritation/inflammation and changes in lung function)] that have been observed with exposure to diesel exhaust. In order to identify which chemical classes are responsible for the majority of the observed biological activities, we performed a particular biological/chemical analysis. Respirable particulate matter (PM2.5: <2.5mm) was collected from diesel engine exhaust using a high-volume sampler equipped with a cascade impactor. Particulate oganic matter was extracted by the dichloromethane/sonication method and the crude extract was fractionated according to EPA recommended procedure into seven fractions by acid-base partitioning and silica gel column chromatography. We examined genotoxic potentials of diesel exhaust particulate matter using novel genotoxicity tests, which are rapid, simple and sensitive methods for assessing DNA-damage at the DNA and chromosomal level (comet assay, in vitro MN test and Ames test). Higher genotoxic potency was observed in non polar fractions and several PAHs were detected by GC-MS, such as 1,2,5,6 dibenzanthracene, chrysene, 1,2-benzanthracene, phenanthrene and fluoranthene.

• Journal of Korean Society of Occupational and Environmental Hygiene
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• v.3 no.1
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• pp.14-21
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• 1993

N-Heterocyclic aromatics (NHA) are widely occurring environmental pollutants formed during the pyrolysis of nitrogen-containing organic chemicals. NAH are found in significant amounts in tobacco condensates, synthetic fuels, polluted river sediment, and effluents from the heating of coal. Following topical application 7H-dibenzo[c, g]carbazole (DBC) induces cancer in liver as well as skin, indicating that dermal exposure can lead to systemic effect. DBC and dibenz[a,j]acridine (DBA) are examples of NHA. The potency of many carcinogenic compounds is related, at least in part, to the efficiency of their biological activation. We undertook studies to determine which initial metabolites lead to the formation of high levels of carcinogen-DNA adducts in vivo. DBC and DBA's, DBA, trans-DBA-1,2-dihydrodiol (DBA-1,2-DHD), trans-DBA-3,4-dihydrodiol (DBA-3,4-DHD), and trans-DBA-5,6-dihydrodiol (DBA-5,6-DHD), were applied to the skin of mice. There were six adducts that were related to DBC application. These addusts were seen in the target organ, liver at high levels, but at very low levels in non-target organs, skin, lung and kidney. In skin, DBA produced two distinct adducts. The same two adducts were seen when DBA-3,4-DHD was applied. In addition the total adduct level elicited by DBA-3,4-DHD higher than that of parent compound. Two adducts were seen when DBA-5,6-DHD was applied, but these were very different from adducts seen with DBA. These results suggested that activation of DBA to DNA-binding compounds in skin includes initial formation of DBA-3,4-DHD.

• Toxicological Research
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• v.21 no.4
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• pp.339-345
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• 2005

Aflatoxins are produced by Aspergillus flavus, parasiticus that grows in improperly stored cereals. Aflatoxin $B_1\;(AFB_1)$ is a potent hepatocarcinogen in a variety of experimental animals including human beings. In spite of a high attention to the hepatocarcinogenecity of aflatoxins, the relative toxicity of other types $(AFB_2,\;AFG_1\;and\;AFG_2)$ of the toxins is not fully clarified. Sprague-Dawley male rats were orally administered with $AFB_1,\;AFB_2,\;AFG_1\;and\;AFG_2$ at the dose of 250, 1250, and $2500\;{\mu}g/kg$ body weight. Animals were then killed at 12, 24 or 48 hrs following aflatoxin adminstration. Subsequently the relative weight of liver was measured and histopathological examination on the liver was performed. Level of 8-OxodG and expression of ras gene in the liver was determined. The relative liver weights at high doses of $AFB_1\;and\;AFG_1$ was significantly low. The treatment of $AFB_1$ at the high dose of $2500\;{\mu}g/kg$ showed vacuolar degeneration and centrilobular hepatic necrosis with inflammatory cells. The pathological changes by $AFB_2\;AFG_1,\;and\;AFG_2$ were not clearly found. The formation of 8-OxodG by $AFB_1$ increased in a dose-dependent manner up to 24 hrs after a single treatment of $AFB_1$ thereafter decreased to the level of the control. The treatments of $AFB_2\;AFG_1,\;and\;AFG_2$ showed an inconsistent pattern in the formation of 8-OxodG in the liver of rats with increasing time. The expression of ras oncogene in the liver by $AFB_1$ at the dose of $1250\;{\mu}g/kg$ was increased twice compared to the control. The treatments of $AFB_2\;AFG_1,\;and\;AFG_2$ at all doses decreased the expression of ras in the liver. These results in the present study indicate that $AFB_1$ among aflatoxins with low comparable levels is the most toxic as determined by early biomarkers such as 8-OxodG formation and ras expression. However, the levels of 8-OxodG and ras as biomarkers were not useful to predict the relative hepatocarcinogenicity of aflatoxins to $AFB_1$ in the present model. Further studies are required to look for other biomarkers to predict carcinogenic potency of aflatoxins.