• Proceedings of the Korea Environmental Mutagen Society Conference
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• 2004.05a
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• pp.79-79
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• 2004

• Biomedical Science Letters
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• v.11 no.2
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• pp.143-152
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• 2005

To investigate the exposure effect of polycyclic aromatic hydrocarbons (PAHs), we analyzed the relationship between urinary 8-hydroxydeoxyguanosine (8-OHdG) concentration and PAHs exposure. The study population contained 44 workers in steel-pipe coating and paint manufacture industries. We measured airborne total PAHs as an external dose, urinary 1-hydroxypyrene (1-OHP) as an internal dose of PAHs exposure, and urinary 8-OHdG as an effective dose of oxidative DNA damage. There was significant correlation between the urinary concentration of l-OHP and the environmental concentration of PAHs, pyrene, urinary cotinine, AST, and GGT. The mean of urinary 8-OHdG was $17.07\pm1.706{\mu}g/g$ creatinine in workers exposed to airborne PAHs. There was significant correlation between the urinary concentration of 8-0HdG and the airborne concentration of PAHs. From the results of stepwise multiple regression analysis about 8-OHdG, significant independents was total PAHs. In this study, there were significant correlation between the urinary concentration of 8-OHdG and the airborne concentration of PAHs. The urinary 1-OHP was effective index as a biomarker of airborne PAHs in workplace. But it was influenced by non-occupational PAHs source, smoking and biomarkers of liver function test.

• Journal of Preventive Medicine and Public Health
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• v.41 no.1
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• pp.61-67
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• 2008

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 $0.02\;{\mu}mol/mol$ creatinine, $0.47\;{\mu}mol/mol$ creatinine, 0.14 g/g creatinine and $0.95\;{\mu}mol/g$ creatinine, respectively. Those values for the elderly were $0.07{\mu}mol/mol$ creatinine, $1.87{\mu}mol/mol$ creatinine, 0.11 g/g creatinine and $1.18\;{\mu}mol/g$ 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. Conclusions : 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.

• Environmental Analysis Health and Toxicology
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• v.21 no.4 s.55
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• pp.375-380
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• 2006

Endocrine disrupting chemicals (EDC) have been emphasized due to their threats in human health. Waste incinerator emission has been emphasized as a source of EDC including polychlorinateddibenzofurans(PCDD/F) and other carcinogenic polycyclic aromatic hydrocarbons (PAHs). Urinary 1-hydroxypyrene (1-OHP) has been used as an exposure biomarker for the PAHs. On the other hand, etheno-DNA adducts, e.g. 1, $N^6-ethenodeoxyadenosine({\varepsilon}dA)$, has been developed as an useful effective or response biomarker for carcinogenesis. Thus, I investigated association between urinary 1-OHP and ${\varepsilon}dA$ levels due to distance from an incinerator which was built more 10 years ago in the middle of a farm in P city. I designated the EDC-high and low exposed group due to distance from the incinerator, i.e. within 2.5km and $5.0{\sim}7.5km$ from the incinerator, respectively. The study subjects were age and sex-matched males and females (mean age, $61.3{\pm}9.6$ yrs; total 40 persons, male, 10; female, 10 for the each group). Urinary 1-OHP and ${\varepsilon}dA$ were analyzed with HPLC-FD and IP-HPLC-FD, respectively. As results, the distance from the incinerator was not associated with urinary 1-OHP nor ${\varepsilon}dA$ levels (p=0.43 and 0.82, respectively). On the other hand, urinary ${\varepsilon}dA$ levels were significantly higher in the hyperlipidemia group (N=10) than normal group (N=30). In conclusion, urinary 1-OHP nor ${\varepsilon}dA$ levels can not be suggested as an incinerator-related exposure nor effective biomarker. However, not only distance from the incinerator bot also systemic approaches including wind and soil contamination are required to assume exposure levels of incinerator-related EDC.

• Journal of Environmental Health Sciences
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• v.37 no.6
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• pp.474-481
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• 2011

This study investigated urinary metabolites of polycyclic aromatic hydrocarbons (PAHs) in the urine of smokers and non-smokers by liquid chromatography triple quordrupole tandem mass spectroscopy (LC/MS/MS). Compounds analyzed for urinary biomarkers of PAHs were five mono-hydroxylated PAHs metabolites; 1-naphthol, 2-naphthol, 1-hydroxypyrene(1-OHP), 3-phenanthrol, 2-fluorenol. Urine samples were pretreated by enzymatic hydrolysis and solid phase extraction method. Smokers were composed of 17 men and five women; non-smokers 17 men and 16 women. Smoking increased urinary concentrations of five PAHs metabolites significantly higher than those of nonsmokers. Statistically significant correlations among the five PAHs metabolites were shown. The results suggest that LC/MS/MS technology should be useful in the environmental health discipline.

• Journal of Preventive Medicine and Public Health
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• v.38 no.3
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• pp.345-350
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• 2005

Objectives : 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.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.6
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• pp.2699-2705
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• 2014

This study was to undertaken to investigate the impacts of AhR, CYP1A1, GSTM1 genetic polymorphisms on the R273G mutation in exon 8 of the tumor suppressor p53 gene (TP53) among polycyclic aromatic hydrocarbons (PAHs) exposed to coke-oven workers. One hundred thirteen workers exposed to PAH and 82 control workers were recruited. We genotyped for polymorphisms in the AhR, CYP1A1, GSTM1, and TP53 R273G mutation in blood by PCR methods, and determined the levels of 1-hydroxypyrene as PAH exposure marker in urine using the high pressure liquid chromatography assay. We found that the distribution of alcohol users and the urinary excretion of 1-OHP in the exposed workers were significantly higher than that of the control workers (p=0.004, p<0.001, respectively). Significant differences were observed in the p53 genotype distributions of smoking subjects (p=0.01, 95%CI: 1.23-6.01) and PAH exposure (p=0.008, 95%CI: 1.24-4.48), respectively. Further, significant differences were observed in the p53 exon 8 mutations for the genetic polymorphisms of Lys/Arg for AhR (p=0.02, 95%CI: 0.70-15.86), Val/Val for CYP1A1 (p=0.04, 95%CI: 0.98-19.09) and null for GSTM1 (p=0.02, 95%CI: 1.19-6.26), respectively. Our findings indicated that polymorphisms of PAH metabolic genes, such as AhR, CYP1A1, GSTM1 polymorphisms may interact with p53 genetic variants and may contribute to PAH related cancers.

• Journal of Preventive Medicine and Public Health
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• v.39 no.2
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• pp.130-134
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• 2006

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 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.