• Journal of the Korean Association of Oral and Maxillofacial Surgeons
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• v.34 no.6
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• pp.602-610
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• 2008

Purpose Acrylamide is present in significant quantities in a wide range of commonly consumed human foods. Carcinogenic risk of acrylamide through the consumption of food is a great public concern and in controversy, but it is not properly addressed due to the lack of evidence in humans. While a plenty of data is available on the carcinogenicity in animal models, the studies in humans are limited. Thus, the present study attempted to examine the carcinogenic potentials of acrylamide on the human epithelial cell, which is the target cell origin of the most cancers. Material and method & Result 1. Acrylamide was not cytotoxic up to $100{\mu}M$ as measured by MTT and LDH assays, indicating a relatively low toxicity of this substance in human epithelial cells. 2. The parameters of neoplastic cellular transformation such as cell saturation density, soft-agar colony formation and cell aggregation were analyzed to examine the carcinogenic potential of acrylamide. 3. The neoplastic transformation was further increased with the co-treatment of TPA 4. Antioxidants blocked the generation of Reactive Oxygen Species(ROS) and the GSH depleting agent dramatically increased the ROS production. 5. mRNA levels of fibronectin following acrylamide exposure was increased in a dose-dependent manner, indicating a possible biomarker of acrylamide-induced cellular transformation. Conclusion The present study will provide a valuable basis to compare the interspecies differences in response to carcinogenic potentials of acrylamide. The data on the interspecies differences are essential element in human risk assessment. Thus, our results obtained from the human epithelial cells will contribute to improving the risk assessment of human neoplasm including oral cancer.

• Journal of Soil and Groundwater Environment
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• v.26 no.3
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• pp.37-49
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• 2021

There is domestic Soil Contamination Warning Standard (SCWS) as remediation standard concentration of contaminated soils. No risk should be observed at soil concentration less than SCWS. Therefore, SCWS was evaluated to confirm the risk assessment. Background Concentration of Soil (BGC) and target remediation concentration were also assessed. The results show that Excess Cancer Risk (ECR) of SCWS was the highest in the groundwater intake pathway (Adult: 6.27E-04, Child: 2.81E-04). Total Cancer Risk (TCR) was 7.76E-04 and 4.30E-04 for adult and child, exceeding reference value (10^-6). Hazard Quotient (Non-Carcinogenic Risk, HQ) was the highest in the indoor air inhalation pathway (Adult: 3.64E+03, Child: 8.74E+02). Hazard Index (Total Non-Carcinogenic Risk, HI) exceeded reference value 1. ECR of the BGC was the highest in the groundwater intake pathway (Adult: 1.71E-04, Child: 7.67E-05). TCR was 2.12E-04 for adults and 1.17E-04 for children, exceeding the reference value (10^-6). HQ was the highest in groundwater intake pathway (Adult: 4.10E-01, Child: 1.84E-01). HI was lower than reference value 1 (Adult: 4.78E-01, Child: 2.50E-01). The heavy metal affecting ECR was Arsenic (As). The remediation-concentration of As was 7.14 mg/kg which is higher than BGC (6.83 mg/kg). TCR of As should be less than reference value (10^-6), but it was higher for all of SCWS, BGC and target remediation concentration. Therefore, it is suggested that risk assessment factors should be re-evaluated to fit domestic environmental settings and SCWS should be induced to satisfy the risk assessment.

• Journal of Environmental Impact Assessment
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• v.8 no.2
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• pp.1-8
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• 1999

The research centers on the concentration profile and risk assessment of toxic metals for ambient air in Taejon industrial complex. Airborne concentrations of each toxic metal for risk assessment were obtained from 2-year sampling by high volume air sampler and analysis by ICP-MS and ICP-AES in the complex. The long-term arithmetic mean of human carcinogen, arsenic, hexavalent chromium and nickel subsulfide was 5.53, 2.16 and $3.46ng/m^3$ while the mean of probable human carcinogen, beryllium, cadmium and lead was 0.08, 2.35, $293.29ng/m^3$, respectively. And the long-term arithmetic mean concentration of non-carcinogenic metal, manganese was $55.91ng/m^3$. The point risk estimate for the inhalation of carcinogenic metals was $3.6{\times}10^{-5}$, which was higher than a risk standard of $10^{-5}$. About 75% of the cancer risk was to the inhalation of human carcinogen, arsenic. Thus, it is necessary to properly manage arsenic risk in Taejon industrial complex. The point hazard index by the inhalation of manganese was 1.1. Therefore, an investigation into Taejon industrial complex is needed to obtain more fine long-term concentration data for airborne non-carcinogenic metals including manganese.

• Journal of Korean Society for Atmospheric Environment
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• v.12 no.5
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• pp.555-566
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• 1996

In order to assess the long-term airborne concentrations of 6 metals such as Cr, Cd, Pb, Zn, K, and Na and the associated health resk, a great number of PM-10 samples were collected and analyzed in Kyung Hee University-Suwon Campus for three years from 1991 to 1993. The 3-year average concentration of Pb in respirable particulate matters was 142.6 ng/m$^{3}$ while that of Zn was 1,210.5ng/m$^{3}$. The corresponding hazard index from Pb Zn for the ingalation route was estimated to be 9.5.times.10$^{-2}$ and 3.5.times.10$^{-2}$ , respectively. Therefore, it can be said that there was no adverse chronic health effects by airborne Pb and Zn. However, the 2-year average concentration of Cr(6) was estimated to be 1.3ng/m$^{3}$ shile the 3-year average concentration of Cd was 3.1ng/m$^{3}$. The total cancer risk by these two metals for the inhalation route was estimated to be about 7.2.times.10$^{-6}$ . This order-of-magnitude risk estimate suggests that the ingalation risk in the study area from all carcinogenic metals including As and Ni (subsulfide) might exceed the acceptable risk criteria of 10$^{-5}$ -10$^{-6}$ by U.S.EPA.For a better risk assessment in the future, alveolar deposition of PM-10 in the study area were also discussed and an assessment was done.

• Safety and Health at Work
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• v.2 no.1
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• pp.1-8
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• 2011

The knowledge on the etiology of breast cancer has advanced substantially in recent years, and several etiological factors are now firmly established. However, very few new discoveries have been made in relation to occupational risk factors. The International Agency for Research on Cancer has evaluated over 900 different exposures or agents to-date to determine whether they are carcinogenic to humans. These evaluations are published as a series of Monographs (www.iarc.fr). For breast cancer the following substances have been classified as "carcinogenic to humans" (Group 1): alcoholic beverages, exposure to diethylstilbestrol, estrogen-progestogen contraceptives, estrogen-progestogen hormone replacement therapy and exposure to X-radiation and gamma-radiation (in special populations such as atomic bomb survivors, medical patients, and in-utero exposure). Ethylene oxide is also classified as a Group 1 carcinogen, although the evidence for carcinogenicity in epidemiologic studies, and specifically for the human breast, is limited. The classification "probably carcinogenic to humans" (Group 2A) includes estrogen hormone replacement therapy, tobacco smoking, and shift work involving circadian disruption, including work as a flight attendant. If the association between shift work and breast cancer, the most common female cancer, is confirmed, shift work could become the leading cause of occupational cancer in women.

• Proceedings of the KSEEG Conference
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• 2000.04a
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• pp.59-60
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• 2000

• Journal of Environmental Health Sciences
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• v.33 no.1 s.94
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• pp.1-10
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• 2007

This study accomplished to grasp the present condition of HAPs and to examine efficiently carcinogenic and non-carcinogenic health effects through health risk assessment in new apartments from June, 2004 to May,2005. Moreover, we performed uncertainty analysis by Monte-Carlo analysis to control uncertainty of exposure factors. The major results obtained from this study were as follows. Firstly, cancer risk of formaldehyde for male was $1.67{\times}10^{-5}$ in CTE in point estimation. Cancer risk of formaldehyde was showed $2.94{\times}10^{-3}$ in RME that applied worst case used results of 95 percentile in point estimation. It exceeds $10^{-6}$ of guide line in US EPA. Moreover, cancer risks of formaldehyde for female were $3.98{\times}10^{-5}$ in CTE and $3.93{\times}10^{-3}$ RME. Secondly, every hazard index for non-carcinogenic pollutants was less than 1 of permitted standards in CTE. However, in RME of male, hazard indexes of 1,2-Dichloropropane and Toluene were 1.3 and 2.0, respectively. Hazard indexes of 1,2-Dichloropropane and Totuene for female in RME were 1.7 and 2.6, respectively.

• Journal of the Korean Association of Oral and Maxillofacial Surgeons
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• v.33 no.5
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• pp.437-444
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• 2007

Vinyl acetate has been widely used for the manufacture of polyvinyl alcohol emulsion, which is primary ingredient of adhesive, paints, textile, paperboard coatings, etc. Since these products are plentiful and frequently used around us, workers and consumers are at health risk. International Agency for Research on Cancer(IARC) classified vinyl acetate as group 2B(possibly carcinogenic to humans). Among the organs targeted, the oral cavity is the most vulnerable organ affected by the carcinogenic effects of vinyl acetate. Since the origin of most of oral cancer is derived from the epithelial cells, it is important to understand the carcinogenic potential of vinyl acetate in human epithelial cells. Thus, the present study has attempted to utilize the immortalized human epithelial cell model to assess the carcinogenic potency of this chemical and to understand the underlying mechanisms.

• Safety and Health at Work
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• v.9 no.3
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• pp.290-295
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• 2018

Background: There is little information on the dose-response relationship between exposure to occupational carcinogenic agents and mesothelioma. This study aimed to investigate this association as well as the existence of agents other than asbestos that might cause mesothelioma. Methods: The Swedish component of the Nordic Occupational Cancer (NOCCA) study consists of 6.78 million individuals with detailed information on occupation. Mesothelioma diagnoses recorded in 1961-2009 were identified through linkage to the Swedish Cancer Registry. We determined cumulative exposure, time of first exposure, and maximum exposure intensity by linking data on occupation to the Swedish NOCCA job-exposure matrix, which includes 29 carcinogenic agents and corresponding exposure for 283 occupations. To assess the risk of mesothelioma, we used conditional logistic regression models to estimate hazard ratios and 95% confidence intervals. Results: 2,757 mesothelioma cases were identified in males, including 1,416 who were exposed to asbestos. Univariate analyses showed not only a significant excess risk for maximum exposure intensity, with a hazard ratio of 4.81 at exposure levels 1.25-2.0 fb/ml but also a clear dose-response effect for cumulative exposure with a 30-, 40-, and 50-year latency time. No convincing excess risk was revealed for any of the other carcinogenic agents included in the Swedish NOCCA job-exposure matrix. Conclusion: When considering asbestos exposure, past exposure, even for short periods, might be enough to cause mesothelioma of the pleura later in life.

• Toxicological Research
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• v.34 no.4
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• pp.291-296
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• 2018

Chemical carcinogenesis is a multistep process. Genotoxic carcinogens, which are DNA-reactive, induce DNA adduct formation and genetic alterations in target cells, thereby generating mutated cells (initiation). Subsequently, preneoplastic lesions appear through clonal proliferation of the mutated cells and transform into tumors (promotion and progression). Many factors may influence these processes in a dose-dependent manner. Therefore, quantitative analysis plays an important role in studies on the carcinogenic threshold of genotoxic carcinogens. Herein, we present data on the relationship between key carcinogenic events and their deriving point of departure (PoD). Their PoDs were also compared to those of the carcinogenesis pathway. In an experiment, the liver of rats exposed to 2-amino-3,8-dimethylimidazo-(4,5-f)quinoxaline (MeIQx) was examined to determine the formation of MeIQx-DNA adducts, generation of mutations at LacI transgene, and induction of preneoplastic glutathione S-transferase placental form (GST-P)-positive foci and tumors (benign and malignant). The PoDs of the above key events in the carcinogenicity of MeIQx were increased as the carcinogenesis advanced; however, these PoDs were lower than those of tumor induction. Thus, the order of key events during tumor induction in the liver was as follows: formation of DNA adducts ${\ll}$ Mutations ${\ll}$ GST-positive foci (preneoplasia) ${\ll}$ Tumor (adenoma and carcinoma). We also obtained similar data on the genotoxic and carcinogenic PoDs of other hepatocarcinogens, such as 2-amino-3,8-dimethylimidazo(4,5-f)quinoline. These results contribute to elucidating the existence of a genotoxic and carcinogenic threshold.