Earticle

In this study, the methods were developed to measure PAHs in the air, metabolites of pyrene and benzo(a)pyrene via human urine, genetic polymorphisms in human buccal cell for evaluation of the health effects about environmental pollution. We have also performed a preliminary molecular epidemiology study on residents in the metropolitan area and workers in workplace for these method applications. The analytical method utilized HPLC(High Performance Liquid chromatography) for metabolites measure of pyrene and benzo(a)pyrene in human urine. Modifying the analytical procedure for the determination of 1-hyroxypyrene(1-OHP), 1 -OH-pyrene-glucuronide(1-OHPG), 7,8-diol- benzo(a)pyrene(Diol) and 7,8,9,10- tetrol-benzo(a)pyrene(Tetrol), we developed HPLC method for the simultaneous determination of 1-OHP, 1-OHPG, diol and tetrol. Metabolites product of pyrene(1-OHP, 1-OHPG) were not significant both in urban and workplace area. The average concentration of 1-OHP and 1-OHPG in participant's urine were 0.037±0.062 and 0.714±1.095 ug/gcreatinine, each. Diol as metabolite product of benzo(a)pyrene was significant between urban and workplace area. The average concentration of diol and tetrol in participant's urine were 0.249±0.528 and 0.750±0.792 ug/gcreatinine, respectively. In the case of CYP1A1, 42.86% of them has homozygous wild type(W) and who has heterozygous variant type(H) was 48.57% and 8.57% of homozygous variant type(M) genetic type. In the case of CYP2E1, 69.44% of them has homozygous wild type(D) type, 25.00% of each has heterozygous variant type (DC) and 5.56% of them has homozygous variant type (CC). Who doesn't have GSTM1 gene was 48.57% and who has GSTM1 gene was 51.43%. Who doesn't have GSTT1 gene was 63.89% in study groups and who has GSTT1 gene was 36.11%. Who has W genetic type, which is homozygous wild type of GSTP1, was 79.41% and H genetic type, which is heterozygous variant type was 20.59%.. Who has C/C genetic type, which is homozygous wild type of NQO1, was 37.14% and C/T genetic type, which is heterozygous variant type was 48.579%. T/T genetic type which is homozygous variant type was 14.29%. Concentration differences of metabolites such as 1-OHP, 1-OHPG, diol and tetrol in urine, which is generated by genetic polymorphism of CYP1A1, CYP2E1 gene of Phase I and GSTM1, GSTT1, GSTP1, NQO1 gene of Phase II, was examined. As a result, GSTM1, GSTP1, CYP1A1, CYP2E1, NQO1 and indicate slight differences depend on the amount of metabolites in urine, it was not statistically significant.

The purpose of this study was to assess the exposure to concentrated ambient fine particulates (i.e. PM2.5 and PM10) and heavy metals in particle and to determine whether lung function in children decreases following exposure to particulate and heavy metals on air pollution. And this study evaluated the usefulness of urinary malondialdehyde (MDA) and 8-hydroxy-deoxyguanosine (8-OHdG) as oxidative stress biomarkers related to the Asian dust event (ADE) and the potential individual effect of genetic polymorphisms of Glutathion S-transferase (GST) M1/T1 enzymes involved in air pollutants metabolisms on lung function was also investigated. The fine particulate and metals exposure assessments are conducted for 42 days duration the spring season. Daily ambient concentrations of PM2.5, PM10 and heavy metals (Fe, Ni, Mn, Pb, and Zn) are collected at elementary school in Deokjeok Island, Korea. The pulmonary functions such as peak expiratory flow rate (PEFR), FEV1, FVC and FEV1/FVC were measured. Forty three children (23 boys and 20 girls, mean age: 9.61 years old) were participated in this study. The levels of PEFR in subjects were measured 3 times a day for study period. Genetic polymorphisms of GSTM1/T1 were assessed by PCR-based methods. Inference on the air pollution and time effects of PEFR data were used by the mixed-model after adjustment of weather information such as temperature, humidity and atmospheric pressure. Daily mean concentrations of PM2.5 and PM10 over the PEFR measurement periods were 20.28±8.35 and 35.29±23.84 ug/m2, respectively. The levels of PM2.5 were significantly correlated with heavy metals (P<0.01). Daily mean PEFR was related with the levels of 24-hour PM2.5, PM10 and their heavy metals. The result shows that the increase of fine particulate concentrations (one day lag) and heavy metals (one day lag) were negatively associated with the PEFR. And PM, metals and GSTM1/T1 genotype were significant predictors for PEFR by mixed model. Levels of urinary 8-OHdG and MDA after the ADE (43.31±61.05 ng/ml) were significantly higher than those the non-ADE (23.01±42.38)(n=42 paired, p=0.02). These results suggest that fine particulate (PM2.5 and PM10), heavy metals and genotypes are statistically significant predictors for pulmonary function such as PEFR. Therefore, the levels of PEFR might be utilized as health effect indicator of fine particle air pollutants exposure. and Our findings also suggest that oxidative markers such as urinary MDA and 8-OHdG levels are increased by the ADE.

In order to develop methods to measure dioxin-like compounds in human serum. In addition to measurement of dioxin-like compounds, we established the method for sampling and storage. The volume of serum for analysis dioxin-like compounds was about 30ml(70ml of whole blood). The serum were stored in refrigerator until analysis. Serum(20-30g) was treated for 4h with 2N KOH/EtOH solution. The solution was extracted with n-hexane and the hexane phase was treated with sulfuric acid. The hexane phase was concentrated and applied to columns packed with multi layer silica gel, AgNO3, alumina and active carbom column. The 6 kinds of purification Method were applied to determine Dioxin-like compounds. The recovery of the dioxin were high in method 1(treated with sulfuric acid and multi-layer silica gel column, alumina column, active carbon column). And method 4(only multi-layer silica gel column) can remove the matrix of blood serum as effectively as a multi-layer silica gel column.

The 70 um polypropylene membrane with 64-80 %porosity could be prepared by using supercritical CO2 instead of organic solvents. The average pore size of the membrane was about 2~5 umwith 10~30 polypropylene wt%. The porosity decreased with an increasing polypropylene concentration and breaking point with 10, 20, and 30 polypropylene wt% was 0.17, 0.24, and 0.46 Kgf/mm2, respectively. A 94% and 99% of initial camphene concentration was extracted in 5 min and 10 min, respectively, and kept constant at 99% over 10 min. The optimum conditions to extract camphene effectively were 45˚C and 150 bar.

본 연구는 광범위한 자료들을 토대로 사실적 기술 방법을 통하여 규명하였으며, 다른 나라에도 적용 자료를 사용하는 토대를 마련하는데 그 목적이 있다. 본 연구는 유럽 사회 내에서 PM10(10um) 수준의 옥외 공기오염 농도를 기준으로 하였다. 모아진 자료들은 거의 모든 나라들의 세계은행 연구 자료들과 지난 10년간 각 지역의 모니터들에 의해 사망률을 조사하였다. EUR A지역은 24.89ug/m3 (세계은행조사)와 35.96ug/m3 (전병적학적조사)으로 나타났다. EUR B지역은 67.01ug/m3 와 53.86ug/m3 이였고, EUR C지역은 55.67ug/m3 와 61ug/m3 으로 조사되었다. 그 결과 EUR A,B,C의 영ㆍ유아 사망자수는 3명, 3387명, 471명으로 나타났다. EUR B지역은 EUR A지역에 비해 2.69배로 옥외 공기오염도가 높은 연고로 사망률이 1.129배가 더 높았다. EUR C지역은 EUR A지역에 비해 2.22배가 높았고, 사망자수는 157배 높았다. 만약 EUR B지역과 C지역에서 40ug/m3 로 옥외 공기오염을 낮추었으면 B지역에서는 연간 1026명의 사망자가 줄었을 것이고, EUR C지역은 281명의 사망자가 줄어들었을 것이다.

This study aimed to identify significant effects of death by the outdoor air pollution between 0-4 years of age infant and babyhood in European countries to adapt the findings of the study into the other countries in a given materials all over the world. Outdoor air pollution was expressed as the mean PM10(10um) concentration for each of the EUR subregions. The exposure data were used to calculate the mortality burden by the World Bank for almost every country and epidemiological studies that measured PM10 concentrations at fix-site monitors in the last 10 years. EUR A regions manifested 24.84 (World Bank investigation),ug/m3 and 35.96(epidemiological investigation) ug/m3 while EUR B showed 67.01ug/m3 and 53.86ug/m3 and EUR C manifested in 55.67,ug/m3 and 61ug/m3. From these results EUR A, B, and C showed each 3 infant of death, 3887 infants death and 471 infants death. EUR B manifested 2.69 times than EUR A, so as to 1.129 times death rate, while EUR C showed 2.22 times air pollution than EUR A so as to 157 times death rate than EUR A. IF PM10 concentrations in EUR B and EUR C decreased to 40,ug/m" it was estimated that in EUR B annually 1026 ARI associated death of children 0-y years of age would have been prevented. The corresponding prevented figures for EUR C should be 281 respectively.