Biomedical subjects

Yun-Chul Hong

Publications and source records attributed to Yun-Chul Hong.

12 recordsLinked to original sources

PubMed2025

Stratifying Lung Adenocarcinoma Risk with Multi-ancestry Polygenic Risk Scores in East Asian Never-Smokers.

BACKGROUND: Lung adenocarcinoma (LUAD) in never-smokers is a major public health burden, especially among East Asian women. Polygenic risk scores (PRSs) are promising for risk stratification but are primarily developed in European-ancestry populations. We aimed to develop and validate single- and multi-ancestry PRSs for East Asian never-smokers to improve LUAD risk prediction. METHODS: PRSs were developed using genome-wide association study summary statistics from East Asian (8,002 cases; 20,782 controls) and European (2,058 cases; 5,575 controls) populations. Single-ancestry models included PRS-25, PRS-CT, and LDpred2; multi-ancestry models included LDpred2+PRS-EUR128, PRS-CSx, and CT-SLEB. Performance was evaluated in independent East Asian data from the Female Lung Cancer Consortium (FLCCA) and externally validated in the Nanjing Lung Cancer Cohort (NJLCC). We assessed predictive accuracy via AUC, with 10-year and (age 30-80) absolute risks estimates. RESULTS: The best multi-ancestry PRS, using East Asian and European data via CT-SLEB (clumping and thresholding, super learning, empirical Bayes), outperformed the best East Asian-only PRS (LDpred2; AUC=0.629, 95% CI:0.618,0.641), achieving an AUC of 0.640 (95% CI:0.629,0.653) and odds ratio of 1.71 (95% CI:1.61,1.82) per SD increase. NJLCC Validation confirmed robust performance (AUC =0.649, 95% CI: 0.623, 0.676). The top 20% PRS group had a 3.92-fold higher LUAD risk than the bottom 20%. Further, the top 5% PRS group reached a 6.69% lifetime absolute risk. Notably, this group reached the average population 10-year LUAD risk at age 50 (0.42%) by age 41, nine years earlier. CONCLUSIONS: Multi-ancestry PRS approaches enhance LUAD risk stratification in East Asian never-smokers, with consistent external validation, suggesting future clinical utility.

East Asian never smokers↗

PubMed2003

Multiple biomarkers study in painters in a shipyard in Korea.

Shipbuilding workers are exposed to a variety of genotoxic compounds including polycyclic aromatic hydrocarbons (PAHs). A limited number of studies have been conducted to evaluate biomarkers related to PAH exposure in painters in the shipyard industry. We examined this in 208 workers recruited from a shipyard located in South Korea. Employees were grouped into three exposure groups: (1) 111 painters using coal tar paints, (2) 70 painters using general paints, and (3) 27 on-site controls using no paints. Levels of urinary 1-hydroxypyrene glucuronide (1-OHPG), as internal dose of PAH exposure, were measured by synchronous fluorescence spectroscopy. Glutathione S-transferase (GST) M1 and T1 genotypes were assessed by a multiplex polymerase chain reaction (PCR)-based method, aromatic-DNA adducts in peripheral white blood cells were measured by 32P-postlabeling, and glycophorin A (GPA) variant frequencies in red blood cells were assessed by flow cytometry. Information on demographic characteristics, smoking habits, diet, job title and use of personal protective equipment (e.g. respiratory and dermal) were collected by self-administered questionnaire. Average urinary 1-OHPG levels in coal tar paint (2.24 micromol/mol creatinine) and general paint (1.38 micromol/mol creatinine) users were significantly higher than in on-site controls (0.62 micromol/mol creatinine) (P<0.001). Paint use, irrespective of the type of paints, and smoking (yes/no) were positively associated with urinary 1-OHPG levels, whereas green tea consumption (yes/no) was negatively associated with the 1-OHPG levels. No significant effect in the 1-OHPG levels were observed for the GSTM1 and GSTT1 genotypes. Aromatic-DNA adduct levels tended to be higher in coal tar paint users (P = 0.06) and painters (P = 0.07) compared to on-site controls. No differences in adduct levels were observed, between the two groups of painters, and the combined group showed greater adduct levels than on-site controls (P = 0.05). GPA mutation frequencies measured in 55 individuals with MN heterozygote genotypes were not significantly different among the three exposure groups, and no correlation was observed between urinary 1-OHPG levels and aromatic-DNA adducts or GPA mutation frequency. These results suggest that painters in the shipyard were exposed to significant amounts of PAHs and possibly to other genotoxic aromatic compounds, and that urinary 1-OHPG may be a potential biomarker of PAH exposure in this population.

Adult↗

PubMed2003

The lag-effect pattern in the relationship of particulate air pollution to daily mortality in Seoul, Korea.

To assess differences in the lag-effect pattern in the relationship between particulate matter less than 10 microm in aerodynamic diameter (PM(10)) and cause-specific mortality in Seoul, Korea, from January 1995 to December 1999, we performed a time-series analysis. We used a generalized additive Poisson regression model to control for time trends, temperature, humidity, air pressure, and the day of the week. The PM(10) effect was estimated on the basis of the time-series models using the 24-h means and the quadratic distributed-lag models using a cumulative 6-day effect. One interquartile range increase in the 6-day cumulative mean of PM(10) (43.12 microg/m(3)) was associated with an increase in non-accidental deaths [3.7%, 95% confidence interval (CI): 2.1, 5.4], respiratory disease (13.9%, 95% CI: 6.8, 21.5), cardiovascular disease (4.4%, 95% CI: -1.0, 9.0), and cerebrovascular disease (6.3%, 95% CI: 2.3, 10.5). We found the following patterns in the disease-specific lag-effect window: respiratory mortality was more affected by air pollution level on the day of death, whereas cardiovascular deaths were more affected by the previous day's air pollution level. Cerebrovascular deaths were simultaneously associated with the air pollution levels of the same day and the previous day. The patterns in the lag effect from the distributed-lag models were similar to those of a series of time-series models with 24-h means. These results contribute to our understanding of how exposure to air pollution causes adverse health effects.

Adolescent↗

PubMed2003

Ischemic stroke associated with decrease in temperature.

BACKGROUND: Some studies suggest low temperatures can affect mortality, especially deaths associated with circulatory and respiratory conditions. METHODS: We investigated the association between ischemic stroke onset and decrease in temperature in 545 patients over a 3-year period (January 1998 to December 2000) in Incheon, Korea. We used a case-crossover study design to assess changes in the risk of ischemic stroke during a brief hazard period after exposure to decrease in temperature. For each subject, the case period was matched to 2 control periods exactly 1 week before and after onset of the ischemic stroke. RESULTS: Decreased ambient temperature was associated with risk of acute ischemic stroke. The strongest effect was seen on day after exposure to cold weather. The odds ratio (OR) for an interquartile range decrease in temperature was 2.9 (95% confidence interval [CI] = 1.5-5.3). The risk period was 24-48 hours after cold exposure. Risk estimates associated with decreased temperature were greater in the winter than in the summer. Women, persons greater than 65 years of age, nonobese persons, and those with previous hypertension or hypercholesterolemia were more susceptible to cold-induced ischemic stroke. CONCLUSIONS: These results suggest that stroke occurrence rises with decreasing temperature, and that even a moderate decrease in temperature can increase the risk of ischemic stroke. Susceptible people should take steps to protect themselves from cold, especially in the winter.

Age Factors↗

PubMed2003

Effects of the GSTM1 and GSTT1 polymorphisms on the relationship between maternal exposure to environmental tobacco smoke and neonatal birth weight.

The purpose of the investigation was to determine whether genetic polymorphisms in enzymes that metabolize exogenous chemicals modulate the effects of environmental tobacco smoke (ETS) exposure on birth weight. A survey was conducted from 2000 to 2001 among 266 pregnant women who were hospitalized for delivery and on their singleton live births. We determined maternal GSTM1 and GSTT1 polymorphisms by polymerase chain reaction and measured the urinary cotinine of pregnant women at delivery by radioimmunoassay. Birth weight was found to decrease significantly with increasing concentrations of maternal urinary cotinine (P < 0.05). The interactive effect of exposure to ETS and the presence of the GSTT1 polymorphism was found to be significant by multivariate analysis (P < 0.01), whereas the interactive effect of exposure to ETS and the presence of GSTM1 polymorphism did not reach statistical significance (P = 0.21). A combination of the GSTM1-null and the GSTT1 null-genotypes was found to exacerbate the effect of maternal exposure to ETS on birth weight more than the presence of either genotype alone. Our data indicate that maternal exposure to ETS negatively affects neonatal birth weight, and the adverse effect of maternal exposure to ETS on neonatal birth weight could be modified by the maternal metabolic genotypes, GSTM1 and GSTT1.

Adult↗

PubMed2003

Infant susceptibility of mortality to air pollution in Seoul, South Korea.

OBJECTIVE: Susceptibility of target populations to air pollution is an important issue, because air pollution policies and standards should be based on the susceptibilities of those at particular risk. To evaluate which age group is more susceptible to the adverse health effects of air pollution, we compared the effects of air pollution on mortality among postneonates, those aged 2 to 64 years, and those over 65 years of age. DESIGN: Daily counts of total and respiratory death along with daily levels of meteorological variables and air pollutants were analyzed using generalized additive Poisson regression. The relative risks (RR) of mortality for interquartile changes of the levels of particulate matter <10 micro m (PM(10)) were calculated on the same day. RESULTS: For postneonates, the RR of total mortality for an interquartile change (42.9 micro g/m(3)) in PM(10) (RR: 1.142; 95% confidence interval [CI]: 1.096-1.190) was greatest among age groups. Next were the elderly over 65 years of age (RR: 1.023; 95% CI: 1.022-1.024). Regarding respiratory mortality, RR for an interquartile change of PM(10) in postneonates (RR: 2.018; 95% CI: 1.784-2.283) was also greater than those in the other groups. CONCLUSIONS: These results agree with the hypothesis that infants are most susceptible to PM(10) in terms of mortality, particularly respiratory mortality.

Adolescent↗

PubMed2002

Genetic susceptibility of term pregnant women to oxidative damage.

Genetic polymorphisms involved in the activation and detoxification of exogenous chemicals and in the production and scavenging of reactive oxygen species may modulate the levels of oxidative injury biomarker. We investigated 81 pregnant women in Inchon, Korea. In addition to a questionnaire survey, urinary concentrations of 8-hydroxydeoxyguanosine (8-OH-dG) and malondialdehyde (MDA) were measured as oxidative injury biomarkers. Cytochrome P-450(CYP)1A1, CYP2E1, glutathione S-transferase (GST)M1 and GSTT1 polymorphisms and myeloperoxidase (MPO) and manganese superoxide dismutase (MnSOD) polymorphisms were evaluated to determine the effect of genetic modification on urinary 8-OH-dG and MDA. The concentrations of urinary 8-OH-dG were significantly elevated in the presence of the MnSOD variant genotype (P=0.04) and in the case of GSTM1 null status (P=0.02) by multivariate regression. The concentrations of urinary MDA were not affected significantly by the genetic polymorphisms. This result shows that oxidative stress injury is modified by some heritable polymorphisms, including GSTM1 and MnSOD.

8-Hydroxy-2'-Deoxyguanosine↗

PubMed2002

Association of air pollution with school absenteeism due to illness.

OBJECTIVE: To assess the association of air pollution and school absenteeism among elementary students. DESIGN: Time-series analysis of air pollution and school absenteeism data with controlling for long-term trends, seasonality, day of the week, and holiday as well as meteorologic variables. SETTING: School absenteeism data for the period from March 2, 1996, to December 22, 1999, were collected from student attendance reports of one elementary school in Seoul, Korea. MAIN OUTCOME MEASURES: The number of daily illness-related absences was analyzed against the daily levels of air pollution by generalized additive Poisson regression. The relative risks of absenteeism for air pollution exposure of interquartile ranges (the range from the lowest 25% of the value to the lowest 75% of the value) on absenteeism were calculated on the same day. RESULTS: Exposure to air pollutants such as particulate matter of 10 micro m or less in aerodynamic diameter (PM(10)), sulfur dioxide, and ozone, was associated with illness-related absenteeism. The estimated relative risks were 1.06 (95% confidence interval, 1.04-1.09) per 42.1- micro g/m( 3) increase in PM(10), 1.09 (95% confidence interval, 1.07-1.12) per 5.68-part per billion increase in sulfur dioxide, and 1.08 (95% confidence interval, 1.06-1.11) per 15.94-part per billion increase in ozone. There was no significant relationship between nitrogen dioxide level and illness-related absenteeism. CONCLUSION: Air pollution is associated with illness-related absences among elementary students.

Absenteeism↗

PubMed2002

Air pollution and asthma among children in Seoul, Korea.

BACKGROUND: As information about the health risks associated with air pollution has become available, attention has focused increasingly on susceptible persons such as children and persons with preexisting respiratory diseases, such as asthma. METHODS: We investigated the association between outdoor air pollution and asthma attacks among children under 15 years of age in Seoul, Korea. We estimated the relative risks of hospitalization associated with an interquartile range (IQR) increase in pollutant concentrations and used time series analysis of the counts by means of the generalized additive Poisson model. RESULTS: The estimated relative risk of hospitalization for asthma was 1.07 (95% confidence interval [CI] = 1.04-1.11) for particulate matters less than or equal to 10 microm in aerodynamic diameter (IQR = 40.4 microg/m3); 1.11 (95% CI = 1.06-1.17) for sulfur dioxide (IQR = 4.4 ppb); 1.15 (95% CI = 1.10-1.20) for nitrogen dioxide (IQR = 14.6 ppb); 1.12 (95% CI = 1.07-1.16) for ozone (IQR = 21.7 ppb); and 1.16 (95% CI = 1.10-1.22) for carbon monoxide (IQR = 1.0 ppm). CONCLUSIONS: These findings support the hypothesis that air pollution at levels below the current standards of Korea is harmful to sensitive subjects such as asthmatic children.

Adolescent↗

PubMed2002

Air pollution: a new risk factor in ischemic stroke mortality.

BACKGROUND AND PURPOSE: Air pollution is known to be associated with cardiovascular disease, but little is known about the occurrence of stroke in relation to air pollution. We investigated the association between acute stroke mortality and air pollution over a 7-year period (January 1991 through December 1997) in Seoul, Korea. METHODS: A generalized additive model was used to regress daily stroke death counts for each air pollutant, controlling for time trends, day of the week, and meteorological influences such as temperature, relative humidity, and atmospheric pressure. Ischemic and hemorrhagic stroke deaths were examined separately. RESULTS: The effects of air pollutants on ischemic stroke mortality were statistically significant, whereas this was not the case for hemorrhagic stroke mortality. We observed estimated relative risks of 1.03 (95% CI, 1.00 to 1.06) and 1.04 (95% CI, 1.01 to 1.08) for ischemic stroke mortality for each interquartile range increase in total suspended particulates and sulfur dioxide concentrations on the same day. We also found significantly increased relative risks of 1.04 (95% CI, 1.01 to 1.07) for nitrogen dioxide with a 1-day lag, of 1.06 (95% CI, 1.02 to 1.09) for carbon monoxide with a 1-day lag, and of 1.06 (95% CI, 1.02 to 1.10) for ozone with a 3-day lag for each interquartile range increase. CONCLUSIONS: These findings indicate that air pollutants are significantly associated with ischemic stroke mortality, which suggests an acute pathogenetic process in the cerebrovascular system induced by air pollution.

Air Pollution↗

PubMed2002

Effects of air pollutants on acute stroke mortality.

The relationship between stroke and air pollution has not been adequately studied. We conducted a time-series study to examine the evidence of an association between air pollutants and stroke over 4 years (January 1995-December 1998) in Seoul, Korea. We used a generalized additive model to regress daily stroke death counts for each pollutant, controlling for seasonal and long-term trends and meteorologic influences, such as temperature, relative humidity, and barometric pressure. We observed an estimated increase of 1.5% [95% confidence interval (CI), 1.3-1.8%] and 2.9% (95% CI, 0.3-5.5%) in stroke mortality for each interquartile range increase in particulate matter < 10 microm aerodynamic diameter (PM(10)) and ozone concentrations in the same day. Stroke mortality also increased 3.1% (95% CI, 1.1-5.1%) for nitrogen dioxide, 2.9% (95% CI, 0.8-5.0%) for sulfur dioxide, and 4.1% (95% CI, 1.1-7.2%) for carbon monoxide in a 2-day lag for each interquartile range increase in single-pollutant models. When we examined the associations among PM(10) levels stratified by the level of gaseous pollutants and vice versa, we found that these pollutants are interactive with respect to their effects on the risk of stroke mortality. We also observed that the effects of PM(10) on stroke mortality differ significantly in subgroups by age and sex. We conclude that PM(10) and gaseous pollutants are significant risk factors for acute stroke death and that the elderly and women are more susceptible to the effect of particulate pollutants.

Adolescent↗

PubMed2002

Benzo[a]pyrene-induced DNA-protein crosslinks in cultured human lymphocytes and the role of the GSTM1 and GSTT1 genotypes.

We investigated the influence of glutathione S-transferase M1 (GSTM1) and glutathione S-transferase T1 (GSTT1) polymorphisms upon DNA-protein crosslinks (DPC) induced by benzo[a]pyrene (B[a]P) in cultured human lymphocytes. Lymphocyte samples were collected from 30 healthy nonsmoking hospital administrative workers. DPC was detected with KCl-SDS assay and the distributions of GSTM1 and GSTT1 were determined by polymerase chain reaction. B[a]P was found to induce a significant dose-responsive increase in cytotoxicity and DPC regardless of the genotypes (p<0.05). We did not find statistically significant genetic modification effect of GSTM1 and GSTT1 polymorphisms in the cytotoxicity and DPC formation (p>0.05). In terms of the genes examined, the level of cytotoxicity and DPC formation were found to be highest in the GSTM1-null and GSTT1-null cells. In conclusion, B[a]P induced a significant increase in the cytotoxicity and the level of DPC formation in cultured human lymphocytes. Our findings suggest that DPC could be used as a biomarker of B[a]P exposure.

Adult↗