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Yong Dae Kim 3 Articles
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.
DOI: https://doi.org/10.3961/jpmph.2008.41.1.61
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  • 45 Download
  • 6 Crossref
AbstractAbstract PDF
OBJECTIVES
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.
Summary

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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
    Yun-Hee Choi, Lita Kim, Da-An Huh, Kyong Whan Moon, Min-Sung Kang, Yong-Jin Lee
    Marine Pollution Bulletin.2024; 199: 116041.     CrossRef
  • Sex-Specific Effects of Combined Heavy Metal Exposure on Blood Pressure: A Bayesian Kernel Machine Regression Analysis
    In-Gwon Kim, Seonmi Hong, Sojeong Yim, Jang-Hun Jeong, Kyunghi Choi, Ju-Hee Lee, Young-Seoub Hong, Sang-Yong Eom, Heon Kim, Yong-Dae Kim
    Atmosphere.2024; 15(10): 1157.     CrossRef
  • Urinary oxidative stress biomarkers among local residents measured 6 years after the Hebei Spirit oil spill
    Jung-Ah Kim, Su Ryeon Noh, Hae-Kwan Cheong, Mina Ha, Sang-Yong Eom, Heon Kim, Myung-Sook Park, Yeonhee Chu, Seung-Hwa Lee, Kyungho Choi
    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
    Doo-Nam Oh, Kyung-Choon Lim, Seungmi Park
    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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  • 85 Download
AbstractAbstract PDF
OBJECTIVES
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.
Summary
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.
  • 2,721 View
  • 80 Download
AbstractAbstract PDF
OBJECTIVE
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.
Summary

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