Yun-Chul Hong

Background: Per- and polyfluoroalkyl substances (PFAS) are persistent synthetic chemicals detected in populations, including children, through exposure from food, drinking water, and consumer products. Although growing evidence links PFAS exposure to altered pediatric lipid profiles, few longitudinal studies have determined whether developmental timing during early childhood is more strongly associated with lipid alterations than exposure magnitude. Methods: Serum PFAS concentrations and lipid levels, including total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), and triglycerides (TG), were measured in 212 children from the Environment and Development of Children cohort at ages 2, 4, 6, and 8 years. Generalized additive mixed models (GAMMs) characterized longitudinal dose–response relationships, tested whether associations varied by exposure age, and whether baseline concentrations at age 2 years were associated with lipid trajectories from ages 2 to 8 years. Age-specific linear regression models (lagged and concurrent) and quantile-based g-computation (q-gcomp) were used to estimate age-specific associations and joint effects of the PFAS mixture on lipid levels at age 8 years. Results: In age-pooled GAMMs at ages 2, 4, 6, and 8 years, exposure-response relationships varied in both shape and direction across PFAS compounds for all lipid outcomes, including linear, non-linear and inverse patterns. Baseline PFAS concentrations at age 2 years were not associated with the rate of age-related change in any lipid outcome from ages 2 to 8 years. By contrast, in age-specific regression models evaluating lipid levels at age 8 years, higher HDL-C was associated with PFAS exposure at ages 6 and 8 years, and most associations remained significant after false discovery rate correction. In q-gcomp analyses, the PFAS mixture was positively associated with HDL-C at age 8 years for exposures measured at ages 6 and 8 years. Conclusion: In age-specific analysis, childhood PFAS exposure was associated with higher HDL-C concentrations, and the strength of this association varied by exposure age rather than corresponding directly to exposure magnitude. These findings suggest that developmental timing should be considered when evaluating the effects of childhood PFAS exposure on blood lipids, and require confirmation in larger longitudinal cohort studies.

Objective This study aims to assess the effectiveness of air pollution reduction policies across ASEAN member states, with a particular focus on identifying implementation gaps. It further seeks to examine how development finance contributes to enabling or constraining these policy efforts, especially in the context of rapid urbanization, industrialization, and recurrent transboundary haze in the region. Methods We employed a mixed-methods design. Quantitatively, we analyzed population-weighted annual PM₂.₅ concentrations from 2010 to 2021 using data from the State of Global Air 2020.Qualitatively, we conducted a systematic review of peer-reviewed and grey literature using AIassisted screening and analyzed official development assistance (ODA) data from major multilateral and bilateral donors. Findings PM₂.₅ levels have generally declined in ASEAN since 2010, although concentrations remain high in Myanmar, Cambodia, and Thailand. Countries with strong regulatory frameworks and financial support showed greater reductions. Periods of increased ODA investment (e.g., 2011, 2013, 2017) coincided with notable PM₂.₅ declines, although these patterns reflect temporal associations rather than causal effects. However, national air quality standards remain poorly aligned with WHO guidelines, and air monitoring systems vary significantly. Transboundary haze and limited political commitment continue to hinder regional enforcement and cooperation. Conclusion Policy effectiveness in ASEAN appears to be associated with national commitment and financial accessibility, rather than determined by any single policy or funding mechanism. Strengthened regional governance, alignment of air quality and climate agendas, and targeted development finance are essential to achieving WHO air quality standards. ASEAN-specific policy mechanisms and sustained international cooperation will be critical to closing the implementation gap and improving health outcomes.

Background: Ischemic heart disease (IHD) continues to rank among the leading global causes of mortality, consistently linked to long-term exposure to fine particulate matter (PM _2.5 ). Despite a declining trend in the annual average PM _2.5 concentration in Seoul, they still fail to meet the air quality standards set by the Korean Ministry of Environment (15 µg/m ³ ). We aim to estimate the IHD mortality attributable to PM _2.5 and the health benefits derived from reducing PM _2.5 concentration in Seoul, South Korea, between 2016 and 2020. Methods: We utilized machine-learning-based PM _2.5 data, Global Exposure Mortality Model, mortality data, and population data to estimate the burden of IHD mortality attributed to PM _2.5 and the benefits in IHD mortality associated with reductions in PM _2.5 concentration in Seoul between 2016 and 2020. We also estimated the health benefits by considering the reference concentration in three reduction scenarios. Results: During the study period, the average PM _2.5 concentration was 23.5 µg/m ³ , with 10,971 IHD deaths among individuals aged ≥ 25 years. We estimated 2,861 excess IHD deaths (aged ≥ 25 years) attributable to PM _2.5 exposure between 2016 and 2020. Under the PM _2.5 reduction scenario, achieving a PM _2.5 concentration of 15 µg/m ³ corresponds to an avoidable mortality rate of approximately 8%. Conclusions: Our study assessed the burden of IHD mortality attributable to ambient PM _2.5 and the potential health benefits associated with its reduction in Seoul between 2016 and 2020. The findings suggest that continued efforts to reduce PM _2.5 concentrations could significantly mitigate IHD mortality, particularly in the context of an aging population.

Background: Lung adenocarcinoma 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 lung adenocarcinoma risk prediction. Methods: PRSs were developed using genome-wide association study summary statistics from East Asian (8002 cases; 20 782 controls) and European (2058 cases; 5575 controls) populations. Single-ancestry models included a PRS with 25 single nucleotide variants (PRS-25), PRS clumping and thresholding (CT), and LDpred2; multi-ancestry models included LDpred2 plus European PRS-128, PRS-CSx, and clumping and thresholding, super learning, empirical Bayes (CT-SLEB). Performance was evaluated in independent East Asian data from the Female Lung Cancer Consortium and externally validated in the Nanjing Lung Cancer Cohort. We assessed predictive accuracy via area under the curve operating procedure (AUC), with 10-year and (ages 30-80 years) absolute risks estimates. Results: The best multi-ancestry PRS, using East Asian and European data via CT-SLEB, outperformed the best East Asian-only (LDpred2; AUC = 0.629, 95% confidence interval [CI] = 0.618 to 0.641), achieving an AUC of 0.640 (95% CI = 0.629 to 0.653) and odds ratio of 1.71 (95% CI = 1.61 to 1.82) per standard deviation increase. Nanjing Lung Cancer Cohort validation confirmed robust performance (AUC = 0.649, 95% CI = 0.623 to 0.676). The top 20% PRS group had a 3.92-fold higher lung adenocarcinoma 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 lung adenocarcinoma risk at age 50 years (0.42%) by age 41 years, 9 years earlier. Conclusions: Multi-ancestry PRS approaches enhance lung adenocarcinoma risk stratification in East Asian never-smokers, with consistent external validation, suggesting future clinical utility.

Objective: The influence of climate change on infectious disease dynamics is a subject of interest, but it demands robust scientific evidence. This study explores the short-term and long-term relationships between meteorological factors and the incidence of scrub typhus (ST) in South Korea. Methods: From 2001 to 2018, data on meteorological conditions and weekly ST cases were sourced from national databases. A generalized additive model was used to visualize the relationship, while a generalized linear model was applied to measure the association’s strength. Mean annual temperature change was used as a proxy for climate change in long-term analysis. Despite the small sample size, generalized and mixed-effect models were employed to minimize geographical effects. Results: The number of ST cases was linearly related to the mean temperature 13 weeks prior, above a threshold temperature of 13.3–18.5°C. A 0.1°C increase in mean temperature was associated with a 25% increase in ST cases (OR 1.25, 95% CI: 1.21, 1.29). In line with the short-term trend, the annual incidence of ST increased by 33% (OR 1.33, 95% CI: 1.26, 1.41) for every 0.1°C increase in annual mean temperature compared to the previous 30 years. Conclusions: Higher mean temperatures during summer were associated with the increased ST cases in the following autumn. Annual mean temperature increases compared to 30 years ago were also associated with higher annual incidence of ST. These findings suggest that global warming has influenced the incidence of ST.