Pau-Chung ChenProf.

In 1986, Dr. Pau-Chung Chen graduated from Kaohsiung Medical College in Taiwan with a degree in medicine. He then went on to study environmental and occupational medicine at the Institute of Public Health at the National Taiwan University College of Medicine between 1988-1990. In 1991-1995, he earned his MSc and PhD degrees in Epidemiology and Population Health at the London School of Hygiene and Tropical Medicine in the United Kingdom. Currently, Dr. Chen holds the position of Distinguished Professor at the Institute of Environmental and Occupational Health Sciences at the National Taiwan University College of Public Health, as well as being a Distinguished Investigator and Director of the National Institute of Environmental Health Sciences at the National Health Research Institutes. He has dedicated over 30 years to the field of environmental and occupational health sciences and has published over 400 scientific articles. He received the Outstanding Research Award from the Ministry of Science and Technology in 2015 and 2020, an Outstanding Alumni Award from Kaohsiung Medical University in 2018, and has been listed in the world's top 2% scientists since 2020. Dr. Chen served as the chair of the Scientific Committee on Reproductive Hazards in the Workplace (RHICOH) and the International Commission on Occupational Health (ICOH) from 2012-2018. He was also the first chair of the Birth Cohort Consortium of Asia (BiCCA) from 2012-2014. In 2013-2014, he served as an expert witness in the class action of the former workers of Taiwan RCA, and gave oral testimony in court for 7 days, totaling nearly 50 hours. In 2020, he received the National Occupational Safety and Health Award - Personal Contribution Award from the Ministry of Labor. He also served as President of the Taiwan Public Health Association from 2017-2022 and under his tenure, Taiwan became the first in Asia to pass the Public Health Specialists Act in 2020. I was also elected as a Fellow of the Collegium Ramazzini in 2023 and of the International Society of Environmental Epidemiology (ISEEF) in 2024.

20 MARCH

Time	Session

13:10 13:40	Meet the Professor 3 Environmental Hormone Ching Chang LeeTaiwan Moderator Endocrine Disrupting Chemicals Exposure and Human Health Outcomes in Different PopulationsUp to now, public concerns about the impact of EDCs on human health is growing steadily. Phthalates are thyroid, reproductive and developmental toxicants. Maternal hypothyroidism during pregnancy can cause adverse effects in the fetus. Study 1 investigates the association between phthalate exposure and thyroid hormones in pregnant women. After adjusting for age, BMI and gestation, urinary MBP levels showed negative associations with FT4 and T4 (FT4:  = -0.110, P < 0.001; T4:  = -0.112, P = 0.003). Exposure to di-n-butyl phthalate (DBP) may affect thyroid activity in pregnant women. Study 2 evaluates the association between maternal urine excretion, the exposure of fetus to phthalates in amniotic fluid, and the health of newborns. We found a significant positive correlation between creatinine adjusted urinary MBP and amniotic fluid MBP (R2=0.156, P <0.05) in all infants and, only in female infants, a significantly negative correlation between amniotic fluid MBP, AGD (R = −0.31, P <0.06), and the anogenital index adjusted by birth weight (AGI-W) (R = −0.32, P <0.05). Our data clearly show that in utero exposure to phthalates in general has anti-androgenic effects on the fetus. Study 3 investigates the association between exposure to phthalates and female puberty, and assesses the effect of leuprorelin acetate treatment on kisspeptin-54 secretion in girls with CPP. All seven urinary phthalate metabolites in the CPP group were significantly higher than in prepubescent controls. Serum kisspeptin-54 level were higher (P = 0.022) in the CPP group than control group and still significantly higher after adjusting for age (P = 0.03). There was a significant increasing trend (Ptrend = 0.005) between levels of kisspeptin and the stages of puberty. Significantly positive correlation between kisspeptin-54 and urinary MBP (R2 = 0.109, P = 0.024) was found. Study 4 explores the biomarkers of altered testicular function associated with exposure to phthalates: the testosterone and INSL3 secretion of adult men with different fertility states. In multiple regression models controlled for potential confounders, there is an inverse association between urinary levels of MMP), mono-iso-butyl phthalate (MiBP), MEHP, MEHP% and serum TT (P = 0.001, 0.007, 0.042 and 0.012). The inverse associations were also found between urinary levels of MiBP, MBzP, MEHP, MEHP% and serum fT (P = 0.028, 0.017, 0.045 and 0.027). Urinary MBzP and MEHP% were negatively associated with a decrease in serum INSL3 (P = 0.049 and 0.001). We also observed a strong inverse relationship between MEHP% quartiles and serum TT, fT, the TT : LH ratio and INSL3 (Ptrend = 0.003, 0.080, 0.002 and 0.012). Serum INSL3, TT, fT and the TT : LH ratio were lower for men in the highest MEHP% quartile than in the reference group (P = 0.007, 0.002, 0.090 and 0.001). In conclusion, the present study showed that infertile men had poor Leydig cell functionality, higher levels of urinary phthalate metabolites and lower concentrations of androgens or INSL3, or both, which implied that being exposed to phthalates might affect human testicular steroidogenesis by impairing the function of Leydig cells. Study 5 investigated the active mechanisms of how being exposed to phthalates affects the imbalance of androgen and estrogen and the generation of ROS to determine whether both mediated phthalate-induced effects are involved in prostatic enlargement. DEHP metabolite levels, particularly urinary MEHP, were positively associated with androgen, estrogen, hormone ratios, inducible nitric oxide synthetase (iNOS), 8-OHdG, prostate specific antigen (PSA), and prostate volume (PV) (P < 0.05). PV and PSA were positively associated with androgen, estrogen, hormone ratios and oxidative stress markers (P < 0.05). The estimated percentages of exposure to phthalates in prostatic enlargement mediated by androgen, estrogen, and OS markers ranged from 3.5% to 63.1%. Exposure to DEHP promoted the progress of BPH by increasing dihydrotestosterone (DHT), estradiol (E2), the converted enzymes aromatase and 5 reductase, and reactive oxygen species (8-OHdG and iNOS) production. Sex hormones and OS might be important hyperplasia-promoters after a patient has been exposed to phthalates, especially to DEHP. PFAS Exposure and Human Health: From Ubiquity to Urgency Pau-Chung ChenTaiwan Speaker PFAS Exposure and Human Health from Ubiquity to UrgencyPer- and polyfluoroalkyl substances (PFAS), often referred to as “forever chemicals,” are ubiquitous environmental contaminants widely used in industrial and consumer applications. Due to their extreme persistence, bioaccumulation potential, and endocrine-disrupting properties, PFAS have emerged as a major global public health concern. Our research team has conducted a comprehensive and systematic investigation into the human health effects of PFAS across the life course, integrating epidemiological analyses, biomonitoring, and biomarker-based approaches. Our findings demonstrate that PFAS exposure is associated with a broad spectrum of adverse health outcomes. In early life, prenatal and childhood exposure to PFAS has been linked to reduced fetal and childhood growth, disrupted thyroid function, delayed neurodevelopment, increased symptoms of attention deficit/hyperactivity disorder, elevated immunoglobulin E levels, impaired lung function development, and increased risks of childhood asthma. We have also identified associations with altered sex hormone profiles, including reduced testosterone and increased estradiol levels, as well as elevated uric acid concentrations. In adolescents and adults, our collaborative studies further indicate that PFAS exposure interferes with reproductive hormone regulation, accelerates subclinical atherosclerosis—as evidenced by increased carotid intima-media thickness—and elevates the risks of metabolic syndrome, diabetes, and premenopausal breast cancer. Collectively, these findings provide compelling evidence that PFAS exert multi-system effects spanning growth and development, neurobehavior, immune function, cardiometabolic health, and reproductive outcomes, thereby establishing a globally recognized body of evidence on PFAS-related health risks. Beyond scientific discovery, this lecture highlights how epidemiological evidence has informed policy action in Taiwan. In response to mounting health concerns, the use of PFOS was completely phased out beginning in 2017, followed by the progressive replacement of PFOA and related chemicals. PFHxS was subsequently designated as a toxic chemical substance and was effectively banned by the end of 2023, with limited exemptions for research and educational purposes. In 2024, the Executive Yuan approved the national Action Plan for the Management of Per- and Polyfluoroalkyl Substances, marking a critical step toward comprehensive PFAS governance. This lecture underscores the urgent need to translate scientific evidence into preventive action and demonstrates how sustained research can catalyze regulatory change. Addressing PFAS contamination will require coordinated efforts across science, industry, and policy to protect current and future generations from the long-term health consequences of these persistent chemicals. 201DE

Time

Session

13:10

13:40

Meet the Professor 3

Environmental Hormone

Ching Chang LeeTaiwan Moderator Endocrine Disrupting Chemicals Exposure and Human Health Outcomes in Different PopulationsUp to now, public concerns about the impact of EDCs on human health is growing steadily. Phthalates are thyroid, reproductive and developmental toxicants. Maternal hypothyroidism during pregnancy can cause adverse effects in the fetus. Study 1 investigates the association between phthalate exposure and thyroid hormones in pregnant women. After adjusting for age, BMI and gestation, urinary MBP levels showed negative associations with FT4 and T4 (FT4:  = -0.110, P < 0.001; T4:  = -0.112, P = 0.003). Exposure to di-n-butyl phthalate (DBP) may affect thyroid activity in pregnant women. Study 2 evaluates the association between maternal urine excretion, the exposure of fetus to phthalates in amniotic fluid, and the health of newborns. We found a significant positive correlation between creatinine adjusted urinary MBP and amniotic fluid MBP (R2=0.156, P <0.05) in all infants and, only in female infants, a significantly negative correlation between amniotic fluid MBP, AGD (R = −0.31, P <0.06), and the anogenital index adjusted by birth weight (AGI-W) (R = −0.32, P <0.05). Our data clearly show that in utero exposure to phthalates in general has anti-androgenic effects on the fetus. Study 3 investigates the association between exposure to phthalates and female puberty, and assesses the effect of leuprorelin acetate treatment on kisspeptin-54 secretion in girls with CPP. All seven urinary phthalate metabolites in the CPP group were significantly higher than in prepubescent controls. Serum kisspeptin-54 level were higher (P = 0.022) in the CPP group than control group and still significantly higher after adjusting for age (P = 0.03). There was a significant increasing trend (Ptrend = 0.005) between levels of kisspeptin and the stages of puberty. Significantly positive correlation between kisspeptin-54 and urinary MBP (R2 = 0.109, P = 0.024) was found. Study 4 explores the biomarkers of altered testicular function associated with exposure to phthalates: the testosterone and INSL3 secretion of adult men with different fertility states. In multiple regression models controlled for potential confounders, there is an inverse association between urinary levels of MMP), mono-iso-butyl phthalate (MiBP), MEHP, MEHP% and serum TT (P = 0.001, 0.007, 0.042 and 0.012). The inverse associations were also found between urinary levels of MiBP, MBzP, MEHP, MEHP% and serum fT (P = 0.028, 0.017, 0.045 and 0.027). Urinary MBzP and MEHP% were negatively associated with a decrease in serum INSL3 (P = 0.049 and 0.001). We also observed a strong inverse relationship between MEHP% quartiles and serum TT, fT, the TT : LH ratio and INSL3 (Ptrend = 0.003, 0.080, 0.002 and 0.012). Serum INSL3, TT, fT and the TT : LH ratio were lower for men in the highest MEHP% quartile than in the reference group (P = 0.007, 0.002, 0.090 and 0.001). In conclusion, the present study showed that infertile men had poor Leydig cell functionality, higher levels of urinary phthalate metabolites and lower concentrations of androgens or INSL3, or both, which implied that being exposed to phthalates might affect human testicular steroidogenesis by impairing the function of Leydig cells. Study 5 investigated the active mechanisms of how being exposed to phthalates affects the imbalance of androgen and estrogen and the generation of ROS to determine whether both mediated phthalate-induced effects are involved in prostatic enlargement. DEHP metabolite levels, particularly urinary MEHP, were positively associated with androgen, estrogen, hormone ratios, inducible nitric oxide synthetase (iNOS), 8-OHdG, prostate specific antigen (PSA), and prostate volume (PV) (P < 0.05). PV and PSA were positively associated with androgen, estrogen, hormone ratios and oxidative stress markers (P < 0.05). The estimated percentages of exposure to phthalates in prostatic enlargement mediated by androgen, estrogen, and OS markers ranged from 3.5% to 63.1%. Exposure to DEHP promoted the progress of BPH by increasing dihydrotestosterone (DHT), estradiol (E2), the converted enzymes aromatase and 5 reductase, and reactive oxygen species (8-OHdG and iNOS) production. Sex hormones and OS might be important hyperplasia-promoters after a patient has been exposed to phthalates, especially to DEHP.

PFAS Exposure and Human Health: From Ubiquity to Urgency

Pau-Chung ChenTaiwan Speaker PFAS Exposure and Human Health from Ubiquity to UrgencyPer- and polyfluoroalkyl substances (PFAS), often referred to as “forever chemicals,” are ubiquitous environmental contaminants widely used in industrial and consumer applications. Due to their extreme persistence, bioaccumulation potential, and endocrine-disrupting properties, PFAS have emerged as a major global public health concern. Our research team has conducted a comprehensive and systematic investigation into the human health effects of PFAS across the life course, integrating epidemiological analyses, biomonitoring, and biomarker-based approaches. Our findings demonstrate that PFAS exposure is associated with a broad spectrum of adverse health outcomes. In early life, prenatal and childhood exposure to PFAS has been linked to reduced fetal and childhood growth, disrupted thyroid function, delayed neurodevelopment, increased symptoms of attention deficit/hyperactivity disorder, elevated immunoglobulin E levels, impaired lung function development, and increased risks of childhood asthma. We have also identified associations with altered sex hormone profiles, including reduced testosterone and increased estradiol levels, as well as elevated uric acid concentrations. In adolescents and adults, our collaborative studies further indicate that PFAS exposure interferes with reproductive hormone regulation, accelerates subclinical atherosclerosis—as evidenced by increased carotid intima-media thickness—and elevates the risks of metabolic syndrome, diabetes, and premenopausal breast cancer. Collectively, these findings provide compelling evidence that PFAS exert multi-system effects spanning growth and development, neurobehavior, immune function, cardiometabolic health, and reproductive outcomes, thereby establishing a globally recognized body of evidence on PFAS-related health risks. Beyond scientific discovery, this lecture highlights how epidemiological evidence has informed policy action in Taiwan. In response to mounting health concerns, the use of PFOS was completely phased out beginning in 2017, followed by the progressive replacement of PFOA and related chemicals. PFHxS was subsequently designated as a toxic chemical substance and was effectively banned by the end of 2023, with limited exemptions for research and educational purposes. In 2024, the Executive Yuan approved the national Action Plan for the Management of Per- and Polyfluoroalkyl Substances, marking a critical step toward comprehensive PFAS governance. This lecture underscores the urgent need to translate scientific evidence into preventive action and demonstrates how sustained research can catalyze regulatory change. Addressing PFAS contamination will require coordinated efforts across science, industry, and policy to protect current and future generations from the long-term health consequences of these persistent chemicals.

201DE

Pau-Chung ChenProf. Taiwan

20 MARCH