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Heon Kim 16 Articles
Association Between MicroRNA196a2 rs11614913 Genotypes and the Risk of Non-Small Cell Lung Cancer in Korean Population
Young-Seoub Hong, Ho-Jin Kang, Jong-Young Kwak, Byung Lae Park, Chang-Hun You, Yu-Mi Kim, Heon Kim
J Prev Med Public Health. 2011;44(3):125-130.   Published online May 17, 2010
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AbstractAbstract PDF

The microRNA (miRNA) miR-196a2 may play an important role in lung cancer development and survival by altering binding activity of target mRNA. In this study, we evaluated their associations with the susceptibility of non-small cell lung cancers (NSCLC) by case-control study in a Korean population.


We performed genotyping analyses for miR-196a2 rs11614913 T/C at miRNA regions in a case-control study using blood samples of 406 NSCLC patient and 428 cancer-free control groups.


The total C allele frequencies for miR-196a2 were 48.8% for the patients and 45.6% for the controls; and the genotype frequencies of TT, TC, and CC were 23.7%, 55.2%, and 21.1% for the patients and 31.1%, 46.35%, and 22.4% for the controls (p<0.05). Participants who possesses TC/CC genotypes showed high risk for NSCLC compared to those possessed TT genotypes (OR, 1.42; 95% CI, 1.03 to 1.96). The association was persisted in 60 and older age group, male, smokers, those without family history for cancer. However, no significant association of CC genotypes in recessive genetic model was observed.


In conclusion, this case-control study provides evidence that miR-196a2 rs11614913 C/T polymorphisms are associated with a significantly increased risk of NSCLC in a dominant model, indicating that common genetic polymorphisms in miR-196a2 rs11614913 are associated with NSCLC. The association of miR196a2 rs11614913 polymorphisms and NSCLC risk require confirmation through additional larger studies.



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  • Effect of miR-196a2 rs11614913 Polymorphism on Cancer Susceptibility: Evidence From an Updated Meta-Analysis
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  • Authors’ reply to Jayaraj et al. ‘s Letter to the Editor re: MIR196A2 rs11614913 contributes to susceptibility to colorectal cancer in Iranian population: A multi-center case-control study and meta-analysis
    Monir Sadat Haerian, Batoul Sadat Haerian, Saadat Molanaei, Farid Kosari, Shahram Sabeti, Farahnaz Bidari-zerehpoosh, Ebrahim Abdolali
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    Koki Katayama, Shimon Nakashima, Hiroo Ishida, Yutaro Kubota, Masataka Nakano, Tatsuki Fukami, Yasutsuna Sasaki, Ken-ichi Fujita, Miki Nakajima
    Non-coding RNA Research.2021; 6(3): 123.     CrossRef
  • The Molecular Analysis of rs11614913 Polymorphism from miRNA196a Gene and Its Relationship with TNF-α Gene Expression in Cervical Cancer
    Ahmad Hamta, Fatemeh Hajihassani
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  • Association of mir-196a-2 rs11614913 and mir-149 rs2292832 Polymorphisms With Risk of Cancer: An Updated Meta-Analysis
    Jalal Choupani, Ziba Nariman-Saleh-Fam, Zahra Saadatian, Elaheh Ouladsahebmadarek, Andrea Masotti, Milad Bastami
    Frontiers in Genetics.2019;[Epub]     CrossRef
  • Impacts of single nucleotide polymorphisms in three microRNAs (miR-146a, miR-196a2 and miR-499) on the susceptibility to cervical cancer among Indian women
    Nisha Thakur, Pallavi Singhal, Ravi Mehrotra, Mausumi Bharadwaj
    Bioscience Reports.2019;[Epub]     CrossRef
  • Micro-RNA 196a2 expression and miR-196a2 (rs11614913) polymorphism in T1DM: a pilot study
    Alshaymaa A. Ibrahim, Abeer Ramadan, Aliaa Ahmed Wahby, Mirhane Hassan, Hend M. Soliman, Tamer A. Abdel Hamid
    Journal of Pediatric Endocrinology and Metabolism.2019; 32(10): 1171.     CrossRef
  • MIR196A2 rs11614913 C > T polymorphism correlates with an increased risk of hepatopulmonary syndrome in liver cirrhosis: a case–control study in China
    Hai‐Yong Chen, Yao‐Min Chen, Jian Wu, Fu‐Chun Yang, Zhen Lv, Xiao‐Feng Xu, Shu‐Sen Zheng, Sang‐Sang Liao, Yi‐Hui Luo
    Hepatology Research.2017; 47(8): 793.     CrossRef
  • Association of miR-196a2 rs11614913 and miR-499 rs3746444 polymorphisms with cancer risk: a meta-analysis
    Wanjun Yan, Xiaoyan Gao, Shuqun Zhang
    Oncotarget.2017; 8(69): 114344.     CrossRef
  • MiR-196a2 and lung cancer in Chinese non-smoking females: a genetic association study and expression analysis
    Zhihua Yin, Zhigang Cui, Yangwu Ren, Lingzi Xia, Hang Li, Baosen Zhou
    Oncotarget.2017; 8(41): 70890.     CrossRef
  • Somatic Mutation of the SNP rs11614913 and Its Association with Increased MIR 196A2 Expression in Breast Cancer
    Huanhuan Zhao, Jingman Xu, Dan Zhao, Meijuan Geng, Haize Ge, Li Fu, Zhengmao Zhu
    DNA and Cell Biology.2016; 35(2): 81.     CrossRef
  • MicroRNA-196a2 Biomarker and Targetome Network Analysis in Solid Tumors
    Eman A. Toraih, Manal S. Fawzy, Eman A. Mohammed, Mohammad H. Hussein, Mohamad M. EL-Labban
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    Genetic Testing and Molecular Biomarkers.2016; 20(10): 579.     CrossRef
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    Muhammad Abu-Elmagd, Mourad Assidi, Hans-Juergen Schulten, Ashraf Dallol, Peter Natesan Pushparaj, Farid Ahmed, Stephen W Scherer, Mohammed Al-Qahtani
    BMC Medical Genomics.2015;[Epub]     CrossRef
  • Functional Genetic Variants in Pre-miR-146a and 196a2 Genes are Associated with Risk of Lung Cancer in North Indians
    Kushaldeep Kaur Sodhi, Charu Bahl, Navneet Singh, Digamber Behera, Siddharth Sharma
    Future Oncology.2015; 11(15): 2159.     CrossRef
  • Quantitative assessment of the association between miR-196a2 rs11614913 polymorphism and cancer risk: evidence based on 45,816 subjects
    Zhengjun Kang, Yuhui Li, Xiaokai He, Tao Jiu, Jinxing Wei, Fengyan Tian, Chaohui Gu
    Tumor Biology.2014; 35(7): 6271.     CrossRef
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  • Effects of common polymorphisms rs2910164 in miR-146a and rs11614913 in miR-196a2 on susceptibility to colorectal cancer: a systematic review meta-analysis
    D. Wan, W. Gu, G. Xu, C. Shen, D. Ding, S. Shen, S. Wang, X. Gong, S. He, Q. Zhi
    Clinical and Translational Oncology.2014; 16(9): 792.     CrossRef
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    Asian Pacific Journal of Cancer Prevention.2014; 15(5): 2101.     CrossRef
  • Effects of Common Polymorphism rs11614913 in Hsa-miR-196a2 on Lung Cancer Risk
    Zhengrong Yuan, Xu Zeng, Dan Yang, Weilu Wang, Zhihua Liu, Giuseppe Viglietto
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    Zhiwei Chen, Ling Xu, Xiangyun Ye, Shengping Shen, Ziming Li, Xiaomin Niu, Shun Lu, Ramon Andrade de Mello
    PLoS ONE.2013; 8(4): e61008.     CrossRef
  • Association between microRNA Polymorphisms and Cancer Risk Based on the Findings of 66 Case-Control Studies
    Xiao Pin Ma, Ting Zhang, Bo Peng, Long Yu, De Ke Jiang, Georgina L. Hold
    PLoS ONE.2013; 8(11): e79584.     CrossRef
  • Different Effects of Three Polymorphisms in MicroRNAs on Cancer Risk in Asian Population: Evidence from Published Literatures
    Yeqiong Xu, Ling Gu, Yuqin Pan, Rui Li, Tianyi Gao, Guoqi Song, Zhenlin Nie, Liping Chen, Shukui Wang, Bangshun He, Sadashiva Karnik
    PLoS ONE.2013; 8(6): e65123.     CrossRef
  • Opportunities and Challenges for Selected Emerging Technologies in Cancer Epidemiology: Mitochondrial, Epigenomic, Metabolomic, and Telomerase Profiling
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  • The association of miR-146a rs2910164 and miR-196a2 rs11614913 polymorphisms with cancer risk: a meta-analysis of 32 studies
    Jianbo Wang, Qingwei Wang, Hong Liu, Na Shao, Bingxu Tan, Guangyu Zhang, Kai Wang, Yibin Jia, Wei Ma, Nana Wang, Yufeng Cheng
    Mutagenesis.2012; 27(6): 779.     CrossRef
  • Mechanistic Roles of Noncoding RNAs in Lung Cancer Biology and Their Clinical Implications
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    Genetics Research International.2012; 2012: 1.     CrossRef
  • A Genetic Variant in miR-196a2 Increased Digestive System Cancer Risks: A Meta-Analysis of 15 Case-Control Studies
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  • Comprehensive Review of Genetic Association Studies and Meta-Analyses on miRNA Polymorphisms and Cancer Risk
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    PLoS ONE.2012; 7(11): e50966.     CrossRef
  • miR-196a2 polymorphisms and susceptibility to cancer: A meta-analysis involving 24,697 subjects
    Experimental and Therapeutic Medicine.2012; 3(2): 324.     CrossRef
  • miR-196a2 C allele is a low-penetrant risk factor for cancer development
    Li-Xin Qiu, You Wang, Zu-Guang Xia, Bo Xi, Chen Mao, Jia-Lei Wang, Bi-Yun Wang, Fang-Fang Lv, Xiang-Hua Wu, Ling-Qing Hu
    Cytokine.2011; 56(3): 589.     CrossRef
Effects of the Exposure to Polycyclic Aromatic Hydrocarbons or Toluene on Thiobarbituric Acid Reactive Substance Level in Elementary School Children and the Elderly in a Rural Area.
Dae Seon Kim, Chul Ho Lee, Sang Yong Eom, Tackshin Kang, Yong Dae Kim, Heon Kim
J Prev Med Public Health. 2008;41(1):61-67.
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AbstractAbstract PDF
Polycyclic aromatic hydrocarbons (PAH) and toluene have been reported to induce reactive oxygen species and oxidative stress. This study was performed to investigate the effects of low level exposure to PAHs or toluene on the lipid peroxidation level in elementary school children and the elderly in a rural area. METHODS: Forty seven elementary school children and 40 elderly people who were living in a rural area and not occupationally exposed to PAH or toluene were the subjects of this study. Information about active or passive smoking and diet was obtained using a self-administered questionnaire. The urinary 1-hydroxypyrene (1-OHP), 2-naphthol, hippuric acid and thiobarbituric acid reactive substance (TBARS) concentrations were measured, and these values were corrected with the urinary creatinine concentration. RESULTS: In school children, the geometric means of the urinary 1-OHP, 2-naphthol, hippuric acid and TBARS levels were 0.02 ymol/mol creatinine, 0.47 micron mol/mol creatinine, 0.14 g/g creatinine and 0.95 micron mol/g creatinine, respectively. Those values for the elderly were 0.07 micron mol/mol creatinine, 1.87 micron mol/mol creatinine, 0.11 g/g creatinine and 1.18 micron mol/g creatinine, respectively. The mean levels of urinary 1-OHP, 2-naphthol and TBARS were significantly higher in the elderly subjects than in the children. The urinary TBARS level was not correlated with the urinary 1-OHP, 2-naphthol and hippuric acid, but they were correlated with the age of the subjects. CONCLSIONS: These results suggest that low level inhalation exposure to PAH or toluene does not markedly increase lipid peroxidation, and age is a significant determinant of lipid peroxidation.


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  • Association between oil spill clean-up work and thyroid cancer: Nine years of follow-up after the Hebei Spirit oil spill accident
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    Marine Pollution Bulletin.2024; 199: 116041.     CrossRef
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    Science of The Total Environment.2017; 580: 946.     CrossRef
  • Concentration of volatile organic compounds(VOCs) in ambient air and level of residents in industrial area
    Kyungsook Woo, Heejin Park, Tackshin Kang, Geunbae Kim, Junmin Jeon, Bongki Jang, Jongwha Lee, Busoon Son
    Journal of Korean Society of Occupational and Environmental Hygiene.2015; 25(1): 104.     CrossRef
  • Health Effects of Exposure to Oil-contaminated Water Using Biological Markers: Focusing on G Village near the Area of Daecheon Beach
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    Journal of Korean Biological Nursing Science.2013; 15(2): 74.     CrossRef
  • Urinary metabolites before and after cleanup and subjective symptoms in volunteer participants in cleanup of the Hebei Spirit oil spill
    Mina Ha, Hojang Kwon, Hae-Kwan Cheong, Sinye Lim, Seung Jin Yoo, Eun-Jung Kim, Seok Gun Park, Jeongae Lee, Bong Chul Chung
    Science of The Total Environment.2012; 429: 167.     CrossRef
Effects of Oxidative DNA Damage and Genetic Polymorphism of the Glutathion Peroxidase 1 (GPX1) and 8-Oxoguanine Glycosylase 1 (hOGG1) on Lung Cancer.
Chul Ho Lee, Kye Young Lee, Kang Hyeon Choe, Yun Chul Hong, Sung Il Noh, Sang Yong Eom, Young Jun Ko, Yan Wei Zhang, Dong Hyuk Yim, Jong Won Kang, Heon Kim, Yong Dae Kim
J Prev Med Public Health. 2006;39(2):130-134.
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AbstractAbstract PDF
Oxidative DNA damage is a known risk factor of lung cancer. The glutathione peroxidase (GPX) antioxidant enzyme that reduces hydrogen peroxide and lipid peroxides plays a significant role in protecting cells from the oxidative stress induced by reactive oxygen species. The aim of this case-control study was to investigate effects of oxidative stress and genetic polymorphisms of the GPX1 genes and the interaction between them in the carcinogenesis of lung cancer. METHODS: Two hundreds patients with lung cancer and 200 age- and sex-matched controls were enrolled in this study. Every subject was asked to complete a questionnaire concerning their smoking habits and their environmental exposure to PAHs. The genotypes of the GPX1 and 8-oxoguanine glycosylase 1 (hOGG1) genes were examined and the concentrations of urinary 1-hydroxypyrene (1-OHP), 2-naphthol and 8-hydroxydeoxyguanosine (8-OH-dG) were measured. RESULTS: Cigarette smoking was a significant risk factor for lung cancer. The levels of urinary 8-OH-dG were higher in the patients (p<0.001), whereas the urinary 1-OHP and 2-naphthol levels were higher in the controls. The GPX1 codon 198 polymorphism was associated with an increased risk of lung cancer. Individuals carrying the Pro/Leu or Leu/Leu genotype of GPX1 were at a higher risk for lung cancer (adjusted OR=2.29). In addition, these individuals were shown to have high urinary 8-OH-dG concentrations compared to the individuals with the GPX1 Pro/Pro genotype. On the other hand, the polymorphism of the hOGG1 gene did not affect the lung cancer risk and the oxidative DNA damage. CONCLUSIONS: These results lead to a conclusion that individuals with the GPX1 Pro/Leu or Leu/Leu genotype would be more susceptible to the lung cancer induced by oxidative stress than those individuals with the Pro/Pro genotype.
Effects of Oxidative DNA Damage Induced by Polycyclic Aromatic Hydrocarbons and Genetic Polymorphism of the Paraoxonase-1 (PON1) Gene on Lung Cancer.
Chul Ho Lee, Kye Young Lee, Kang Hyeon Choe, Yun Chul Hong, Yong Dae Kim, Jong Won Kang, Heon Kim
J Prev Med Public Health. 2005;38(3):345-350.
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AbstractAbstract PDF
Polycyclic aromatic hydrocarbons (PAHs), which are risk factors for lung cancer, have been reported to induce oxidative DNA damage. The paraoxonase (PON) plays a significant role in the detoxification of a variety of organophosphorous compounds, with paraoxonase-1 (PON1) being one of the endogenous free-radical scavenging systems in the human body. The aim of this case-control study was to investigate the effects of PAH exposure, oxidative stress and the Q192R polymorphism of PON1 genes, and their interactions in the carcinogenesis of lung cancer. METHODS: One hundred and seventy seven lung cancer patients and 177 age- and sex-matched controls were enrolled in this study. Each subject was asked to complete a questionnaire concerning their smoking habits and environmental exposure to PAHs. The Q192R genotypes of the PON1 gene was examined, and the concentrations of urinary 1-hydroxypyrene (1-OHP), 2-naphthol and 8- hydroxydeoxyguanosine (8-OH-dG) measured. RESULTS: Cigarette smoking was found to be a significant risk factor for lung cancer. The urinary 8-OH-dG level was higher in the patients, whereas the urinary 1-OHP and 2- naphthol levels were higher in the controls. There was a significant correlation between the urinary levels of 8-OHdG and 1-OHP in both the cases and controls. The PON1 polymorphism was associated with an increased risk of lung cancer. Individuals carrying the Q/Q genotype of the PON1 gene were found to be at higher risk of developing lung cancer. There was a significant correlation between the urinary levels of 8-OH-dG and 1-OHP in those with the PON1 Q/Q genotype. CONCLUSIONS: These results lead to the conclusion that PAHs would induce oxidative DNA damage, especially in individuals with the PON1 Q/Q genotype. Therefore, people with the PON1 Q/Q genotype would be more susceptible to lung cancer than those with the R/R or Q/R genotypes of the PON1 gene.
The Exposure Status and Biomarkers of Bisphenol A in Shipyard Workers.
Sang Baek Koh, Cheong Sik Kim, Jun Ho Park, Bong Suk Cha, Jong Ku Park, Heon Kim, Soung Hoon Chang
Korean J Prev Med. 2003;36(2):93-100.
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AbstractAbstract PDF
Because shipyard workers are involved with various manufacturing process, they are exposed to many kinds of hazardous materials. Welders especially, are exposed to bisphenol-A (BPA) during the welding and flame cutting of coated steel. This study was conducted to assess the exposure status of the endocrine disruptor based on the job-exposure matrix. The effects of the genetic polymorphism of xenobiotic enzyme metabolisms involved in the metabolism of BPA on the levels of urinary metabolite were investigated. METHODS: The study population was recruited from a shipyard company in the K province. A total of 84 shipbuilding workers 47 and 37 in the exposed and control groups, respectively, were recruited for this study. The questionnaire variables included, age, sex, use of personal protective equipment, smoking, drinking and work duration. The urinary metabolite was collected in the afternoon and correction made for the urinary creatinine concentration. The of the CYP1A1, CYP2E1 and UGT1A6 genotypes were investigated using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) methods with the DNA extracted from venous blood. RESULTS: The urinary BPA level in the welders group was significantly higher than in the control group (p< 0.05). The urinary BPA concentration with the wild type UGT1A6 was higher than the other UGT1A6 genotypes, but with no statistical significant. From themultiple regression analysis of the urinary BPA, the regression coefficient for job grade was statistically significant (p< 0.05). CONCLUSIONS: The grade of exposure to BPA affected the urinary BPA concentration was statistically significant. However, the genetic polymorphisms of xenobiotics enzyme metabolism were not statistically significant. Further investigation of the genetic polymorphisms with a larger sample size is needed.
Urinary 1-Hydroxypyrene and 2-Naphthol as a Biological Exposure Markers of Total Suspended Particulate in the General Population .
Jong Won Kang, Soo Hun Cho, Heon Kim, Daehee Kang, Chul Ho Lee
Korean J Prev Med. 2000;33(3):306-312.
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AbstractAbstract PDF
Polycyclic aromatic hydrocarbons (PAH) are well known environmental pollutants. The measurement of PAH in ambient air is not commonly used, because it is quite difficult to perform and is unreliable. Using biomarkers of PAH can be an alternative approach to this problem. The PAH in ambient air is absorbed in particulate matter. Total suspended particulate(TSP) or particulate matter of less than 10 micrometer in diameter (PM10) can be easily measured. Therefore, TSP or PM10 can be used as a surrogate measurements of ambient air PAH. CONCLUSIONS: We investigated whether the urinary concentration of two biomarkers of PAH, 1-hydroxypyrene (1-OHP) and 2-naphthol, could reflect the total suspended particulate in the general population. METHODS: In order to exclude the effects of occupational exposure and smoking, first grade middle school students were included in this study. Four middle schools within a one kilometer boundary of ambient air monitoring stations were selected. Total suspended particulate was regarded as the marker of airborne PAH. Diet and smoking data were collected by self administered questionnaires, and spot urine samples were collected. Urinary 1-OHP and 2-naphthol were analyzed by high performance liquid chromatography. RESULTS: The correlation between urinary 1-OHP, 2-naphthol and passive smoking was not statistically significant. The correlation between urinary 1-OHP and TSP indices was not statistically significant. The correlations between urinary 2-naphthol and TSP of two lag days, one lag day, and zero lag days were statistically significant. The statistical significance of two lag days was the strongest (p=0.001), one lag day was the next (p=0.0275), and zero lag days was the weakest (p=0.0349). CONCLUSION: Our results imply that the urinary concentration of 2-naphthol can be applied as a PAH exposure marker for the general population with low PAH exposure.
A Case-Control Study on Effects of Genetic Polymorphisms of GSTM1, GSTT1, CYP1A1 and CYP2E1 on Risk of Lung Cancer.
Hong Mei Nan, Heon Kim, Jong Won Kang, Jang Whan Bae, Kang Hyeon Choe, Ki Hyeong Lee, Seung Taik Kim, Choong Hee Won, Yong Min Kim
Korean J Prev Med. 1999;32(2):123-129.
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AbstractAbstract PDF
This study was performed to investigate effects of genetic polymorphisms of glutathione S-transferase M1 (GSTM1), glutathione S-transferase M1 (GSTT1), cytochrome P450 1A1 (CYP1A1) and cytochrome P450 2E1 (CYP2E1) on lung cancer development. METHODS: Ninety-eight lung cancer patients and 98 age-sex matched non-cancer patients hospitalized in Chungbuk National University Hospital from March 1997 to August 1998, were the subjects of this case-control study. Direct interview was done and genotypes of GSTM1, GSTT1, CYP1A1 and CYP2E1 were investigated using multiplex PCR or PCR-RFLP methods with DNA extracted from venous blood. Effects of the polymorphisms of GSTM1, GSTT1, CYP1A1 and CYP2E1, lifestyle factors including smoking, and their interactions on lung cancer were statistically analyzed. RESULTS: GSTM1 was deleted in 67.01% of the cases and 58.16% of the controls, and the odds ratio(95% CI) was 1.46(0.82-2.62). GSTT1 deletion was 58.76% for the lung cancer patients and 50.00% for the controls OR:1.43(0.81-2.51). The frequencies of Ile/Ile, Ile/Val and Val/Val of the CYP1A1 polymorphisms were 59.18%, 35.71%, and 5.10% for the cases, and 52.04%, 45.92%, 2.04% for the controls, respectively. Risk of lung cancer was not associated with polymorphism of CYP1A1 (x2trend=0.253, p-value>0.05). The respective frequency of c1/c1, c1/c2, c2/c2 genotypes for CYP2E1 were 50.00%, 42.86%, 7.14% for the lung cancer patients, and 66.33%, 30.61%, 3.06% for the controls (x2trend=5.783, p<0.05). c2 allele was a significant risk factor for lung cancer. We also observed a significant association of cigarette smoking history with lung cancer risk. The odds ratio(95% CI) of cigarette smoking was 3.03(1.58-5.81). In multiple logistic analysis including genotypes of GSTM1, GSTT1, CYP1A1 and CYP2E1, and smoking habit, only smoking habit came out to be a significant risk factor for lung cancer. CONCLUSION: Genetic polymorphisms of GSTM1, GSTT1, CYP1A1 and CYP2E1 are not so strongly associated with lung cancer as lifestyle factors including cigarette smoking.
Effects of Exposure to Hexavalent Chromium on the Level of 8-Hydroxydeoxyguanosine and the Activities of Superoxide Dismutase and 8-Hydroxyguanine Endonuclease in Rat Lung .
Heon Kim, Hun Sik Kim, Rosa Kim, Hyeon Yeong Kim, Jae Hwang Jeong
Korean J Prev Med. 1999;32(1):101-107.
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AbstractAbstract PDF
To determine the effects of exposure to hexavalent chromium, 93 male Sprague-Dawley rats were exposed to hexavalent chromium solution. METHODS: Rats were divided into 4 groups and exposed to 0.1 ml of 0 mM, 0.4 mM, 2.0 mM, and 10.0 mM potassium chromate in the first experiment, and to 0.1 ml of 0 mM, 20 mM, 40 mM, and 80 mM in the second for consecutive 3 days by tracheal instillation. Three and 10 rats were the controls for the first and the second experiments, respectively. Lung tissues were then removed to measure the 8-hydroxydeoxyguanosine (8-OH-dG) level using the HPLC-ECD method, superoxide dismutase (SOD) activity using the cytochrome C method, and 8-hydroxyguanine endonuclease activity using the oligonucleotide nicking assay. RESULTS: The results showed no significant linear relationship between chromium exposure level and 8-OH-dG level or 8-hydroxyguanine endonuclease activity. In the first experiment, 8-OH-dG level and 8-hydroxyguanine endonuclease activity increased in 0.4 mM group, and then decreased in 2.0 mM and 10.0 mM groups. The correlation coefficients between 8-OH-dG level and 8-hydroxyguanine endonuclease activity was statistically significant (P<0.01), and total SOD activity was elevated by chromium exposure in a dose-dependent manner (P<0.05). In contrast, there was no significant dose-response pattern or correlation in the second experiment. CONCLUSIONS: Based on the fact that there was no linear relationship between chromium dose and 8-OH-dG level or activity of the repair enzyme, it seems unlikely that 8-OH-dG formation is the major mechanism of chromium carcinogenesis.
A case-control study on the effects of the genetic polymorphisms of N-acetyltransferase 2 and glutathione S-transferase mu and theta on the risk of bladder cancer.
Heon Kim, Wun Jae Kim, Hyung Lae Lee, Moo Song Lee, Cheol Hwan Kim, Ro Sa Kim, Hong Mei Nam
Korean J Prev Med. 1998;31(2):275-284.
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AbstractAbstract PDF
Activities of enzymes involved in the metabolism of various carcinogenic xenobiotics is one of the most important host factors for cancer occurrence. N-acetyltransferase (NAT) and glutathione S-transferases (GST) are enzymes which reduce the toxicity of activated carcinogenic metabolites. Slow N-acetylation and lack of GST mu (GSTM1) were reported as risk factors of bladder cancer. GST theta (GSTT1), which is another type of GST, was reported to be deleted at higher proportion among Koreans. Since cause of bladder cancer is not fully explained by single risk factor, many kinds of enzymes would be involved in the metabolism of carcinogens excreted in urine. This study was performed to investigate whether the polymorphisms of NAT2, GSTM1 and GSTT1 are risk factors of bladder cancer and to evaluate the effects of their interaction on bladder cancer development. Sixty-seven bladder cancer and 67 age- and sex-matched non-cancer patients hospitalized in Chungbuk National University Hospital from March to December 1996, are the subjects of this case-control study. Questionnaire interview was done and the genotypes of NAT2, GSTM1 and GSTT1 were identified using PCR methods with DNA extracted from venous blood. The effects of the polymorphism of NAT2 and GSTM1 and their interaction on bladder cancer were statistically tested after controlling the other risk factors. The frequencies of slow, intermediate, and rapid acetylators were 3.0%, 38.8%, and 58.2% for the cases, and 7.6%, 40.9%, and 51.5% for the controls, respectively. The risk of bladder cancer was not associated with the increase of NAT2 activity(x(2) trend=l.18, P-value>0.05). GSTM1 was deleted in 68.7% of the cases and 49.3% of the controls (x(2)=5.21, P-value<0.05), and the odds ratio (95% CI) was 2.23 (l.12 - 4.56). GSTT1 deletion, the rate of which were 26.9% for the bladder cancer patients and 43.3% for the controls, was a significant protective factor against bladder cancer. Smoking history, turned out to be insignificant as a risk factor of bladder cancer (OR=l.85, 95% CI: 0.85 - 4.03), and occupation could not be tested because of the extremely small number of occupational history related to the increase of bladder cancer. In multiple logistic analysis controlling the effects of other risk factors, GSTM1 deletion was the only significant risk factor for bladder cancer (OR: 2.56, 95% CI: l.22-5.36, P-value<0.05), but slow acetylation and GSTT1 deletion were not. These results suggest that GSTM1 deletion may, be a significant risk factor of bladder cancer. Since there have been much debates on causal relationship between slow acetylation and GSTT1 deletion, and bladder cancer, further studies are needed.
A Case-control Study for Assessment of Risk Factors of Breast Cancer by the p53 Mutation .
Heon Kim, Se Hyun Ahn, Moo Song Lee
Korean J Prev Med. 1998;31(1):15-26.
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p53 is the most frequently mutated gene in female breast cancer tissues and the prognosis of breast cancer could be changed by mutation of the gene. This study was performed to examine risk factors for breast cancer subtypes classified by p53 mutation and to investigate the roles of p53 gene mutation in carcinogenesis of breast cancer. The study subjects were 81 breast cancer patients and 121 controls who were matched to cases 1:1 or 1:2 by age, residence, education level and menopausal status. All the subjects were interviewed by a well-trained nurse with standardized questionnaire on reproductive factors, and were asked to fill the self-administrative food frequency and 24 hour recall questionnaires. p53 gene mutation in the cancer tissue was screened using polymerase chain reaction (PCR)-single strand conformational polymorphism (SSCP) method. Mutation type was identified by direct sequencing of the exon of which mobility shift was observed in SSCP analysis. Mutations were detected in p53 gene of 25 breast cancer tissues. By direct sequencing, base substitutions were found in 20 cancer tissues (10 transition and 10 transversion), and frame shift mutations in 5 (4 insertions and 1 deletion). For the whole cases and controls, risk of breast cancer incidence decreased when the parity increased, and increased when intake amount of total calory, fat, or protein increased. Fat and protein were statistically significant risk factors for breast cancer with p53 mutation. For breast cancer without p53 mutation, protein intake was the only significant dietary factor. These results suggests that causes of p53 positive breast cancer would be different from those of p53 negative cancer, and that dietary factors or related hormonal factors induce mutation of p53, which may be the first step of breast cancer development or a promoter following some unidentified genetic mutations.
The effects of chromium exposure on sister chromatid exchange and concentration of 8-hydroxydeoxyguanosine.
Sang Hwan Han, Soo Hun Cho, Heon Kim, Soo Min Park, Mina Ha, Young Soo Joo, Ho Jang Kwon, Yong Dae Kwon, Myung Hee Kwon
Korean J Prev Med. 1995;28(2):511-525.
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To elucidate some DNA adducts as a biological marker for workers of chromate pigment, the effects of chromium exposure on the formation of 8-hydroxydeoxyguanosine(8-OH-dG) and sister chromatid exchanges(SCEs) frequency in 38 workers of a pigment plant in Bucheon which utilized lead chromates, were examined. The chromium contents of venous blood and urine were measured as working environmental exposure level. The concentrations of 8-OH-dG in DNA isolated from lymphocytes were determined with high performance liquid chromatography and electrochemical detector and denoted as a molar ratio of 8-OH-dG to deoxyguanosine(dG). The SCEs frequency were analyzed in DNA isolated from lymphocytes. A significant correlation was found between creatinine adjusted urine chromium concentration and the molar ratio of 8-OH-dG to dG(r=0.47, p<0.01). After adjusting the current smoking habit, the correlation coefficient was increased(r=0.62, p<0.05). However, there was no significant correlation between the SCE frequency and chromium exposure. This significant results between molar ratio of 8-OH-dG to dG and chromium exposure are in good agreement with in vitro studies that support the importance of DNA adduct formation for the carcinogenic effect of chromium.
A Case-Control Study of Primary Liver Cancer and Liver Disease History.
Dong Hyun Kim, Byung Joo Park, Keun Young Yoo, Yoon Ok Ahn, Hyo Suk Lee, Chung Yong Kim, Sang Il Lee, Moo Song Lee, Hyung Sik Ahn, Heon Kim, Tae Soo Park
Korean J Prev Med. 1994;27(2):217-225.
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The relationship between past liver disease history and the risk of primary liver cancer was analyzed in a hospital-based case-control study conducted in Seoul on 165 patients with histologically or serologically confirmed hepatocellular carcinoma and individually age-and sex-matched 165 controls in hospital for ophthalmologic, ontologic, or nasopharyngeal problems. Significant association were observed for liver diseases occurring 5 or more years before liver cancer diagnosis[OR, 4.9;97% confidence interval(CI), 1.6~14.0) and family history of liver disease(OR, 9.0;95% CI, 2.1~38.8). These associations were mot appreciably modified by allowance for major identified potential confounding factors, From these results, it is possible to speculate that liver cell injuries caused by Considering the significant effect of family history of liver diseases on PLCA risk after adjusting past liver disease history, there might be genetic susceptibility in the carcinogenic mechanism of liver cancer. Further investigations are needed to clarify the effect of family history of liver disease on PLCA risk.
Effects of Hyperoxia on 8-Hydroxydeoxyguanosine Formation in Carbon Monoxide Exposed Rats.
Heon Kim, Soo Hun Cho, Myung Hee Chung
Korean J Prev Med. 1994;27(1):84-106.
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Hyperbaric oxygen(HBO) therapy for carbon monoxide(CO) poisoning eventually inducing the hypoxia-reoxygenation condition, may produce oxygen free radicals, which forms 8-hydroxydeoxyguanosine(8-OH-dG) by attacking C-8 position of deoxy-guanosine (dG) in DNA. Effects of oxygen partial pressure or duration of HBO therapy with or without CO poisoning on the tissue 8-OH-dG formation were investigated. Male Sprague-Dawley rats were grouped and exposed to air(control group), 4000ppm of CO for 10 to 30 minutes(CO only group), air for 30 minutes after 30 minute exposure to 4000ppm of CO(CO-air exposure group), HBO after 30 minute exposure to 4000ppm of CO(CO-HBO group), or HBO therapy for 10-120 minutes (HBO only group). The 8-OH-dG concentrations in the brain and the lung tissues were measured with high performance liquid chromatography and electrochemical detector (ECD). Average concentrations of the 8-OH-dG of each group were statistically compared. In the brain tissues, 8-OH-dG concentrations of the CO only group, the CO-air exposure group, and the CO-HBO group did not significantly differ from those of the control group. Similar insignificance was also found between the CO-HBO group and the HBO only groups. No appreciable dose-response relationship was observed between the 8-OH-dG concentration and the oxygen partial pressure or the duration of HBO. However, the 8-OH-dG concentrations of the 30 minute CO only group were higher than those of the CO-air exposure group (p-value<0.05). In the lung tissues, there were no significant differences between the 8-OH-dG concentrations of the control group and those of the CO only group, the CO-air exposure group, and the CO-HBO group. However, mean 8-OH-dG concentration of the CO-air exposure group was significantly higher than that of the CO only group under the same CO exposure condition(p-value<0.05). With the duration of CO exposure, the 8-OH-dG concentrations of the lung tissues decreased significantly (p-value<0.05). The concentrations of 8-OH-dG in the lung tissues proportionally increased with the duration of HBO, but no such relation was observed with the oxygen partial pressure. These results suggest that the brain may be more resistant to oxygen free radicals as compared with the lungs, and that oxygen toxicity following HBO may be affected by factors other than oxygen free radicals.
Effects Of Glue Sniffing On Weight Increase Or Central Nervous System Of Young Rat.
Heon Kim, Sun Min Kim, Soo Hun Cho
Korean J Prev Med. 1993;26(2):222-230.
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Industrial glues, known as 'Bonds' in Korea, contain many kinds of organic solvents, and glue sniffing of youths became one of the social problems in Korea. Mixed exposures to solvents by glue sniffing may induce chronic toxicities different from those by exposures to solvents of single component. To test effects of the glue sniffing on weight gain or central nervous system, two groups of 20 male Sprague-Dawley rats were exposed to air(control group) or vapors of the glues to narcotic status(exposed group), and weight check, tail flick test, hot plate test, rotarod treadmill test were done on the 14th, 24th, 36th, 45th, 53rd, 86th, 102nd, 117th, 134th and 151st days after the first exposure. On the 188th day, their brains were excised and examined by a pathologist. Weight gain, controlled against time change, showed significant difference between the groups, but response times in tail flick test, hot plate tests, and rotarod treadmill test didn't. In pathological examination with blind method, no macroscopic or microscopic difference were found between the two groups. These results suggests that organic lesion in central nervous system may not ensue glue sniffing, but, before firm conclusion, more studies in various exposure conditions should be followed.
Carboxyhemoglobin Dissociation Pattern by Age in the Rat.
Sun Min Kim, Heon Kim, Soo Hum Cho
Korean J Prev Med. 1991;24(4):507-515.
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One, two, six and ten week old Sprague-Dawley rats were exposed to carbon monoxide at 3,700 ppm for 30 minutes, and carboxyhemoglobin was measured immediateley, 5, 30, 60, 90, 120 minutes after the exposure. In each time after the exposure, the means of the carboxyhemoglobin levels were "compared among the week age groups. The regression analysis was done using the natural logarithm. of the carboxyhemoglobin concentration as a dependent variable and the time after the exposure. as an independent vaiable. From the regression equation, the half lives of the carboxyhemoglobin were calculated. The one week old rats showed significantly higher carboxyhemoglobin level than other week age rats in the entire time after the exposure. The corrected carboxyhemoglobin concentration calculated by subtracting the normal carboxyhemoglobin level from the me cured carboxyhemoglobin at each age group, showed no uniform differences.
The Effect Of Gunshot Or Cannonade Training During Military Service On Hearing Threshold Levels.
Heon Kim, Soo Hun Cho, Hyun Sul Lim
Korean J Prev Med. 1991;24(1):86-92.
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To test if exposure history to rifle fire or cannonade training during military duty can induce hearing loss, history of personal military service and history of gunshot exposure were asked to 228 male college students with self-administrative questionnaire. Otoscopic examination and Rinne's test were performed if any abnormal finding was detected by pure-tone audiometry. Average hearing threshold levels of 500 Hz, 1,000 Hz, 2,000 Hz, 4,000 Hz and threshold levels at 4,000 Hz were calculated for 112 students who were remained after exclusion of cases with history of ear disease, of ototoxic drug administration, and of neuropsychiatric disease, and mean of those were compared between group of students who have completed military duty (completed group) and group of those who have not (not-completed group), and between group exposed(exposed group) and group unexposed to gunshot sound(unexposed group). Mean of average hearing threshold level and mean of threshold levels at 4,000 Hz of completed group and those of exposed group were higher than those of not-completed group and unexposed group, respectively. Proportion of cases that average threshold level was greater than 40 dB of threshold levels at 4,000 Hz was greater than 50 dB were higher also in completed group and exposed group than in duty not-completed group and unexposed group, respectively. Multiple linear regression analysis including age, duration of military service, degree of gunshot sound exposure as independent variables and average hearing threshold level as dependant variable, was performed in order to estimate the effect of age on hearing, and any considerable effect of age on hearing could not be found. In conclusion, hearing impairment can be induced by rifle fire or cannonade training.

JPMPH : Journal of Preventive Medicine and Public Health