個人簡歷

Education/Training:

• PhD. Division of Pathophysiology and Repair, School of Biosciences, Cardiff University, UK
• MSc. Occupational Medicine and Industrial Hygiene, School of Public Health, National Taiwan University, Taiwan
• BSc. Occupational Safety and Health, School of Public Health, China Medical University, Taiwan

Professional and Research Experience:

• 2024-present: Vice Director, TMU Research Center of Thoracic Medicine, Taipei Medical University, Taipei, Taiwan
• 2023-present: Visiting Professor, National Heart & Lung Institute, Imperial College London, UK

Awards and Honors:

• 2023: Elected Full Member, Sigma Xi, The Scientific Research Honor Society
• 2022, 2023, 2024: Taipei Medical University Research Excellent Award
• 2021: World's Top 2% Scientists 2021, Stanford University (Elsevier)
• 2022: Taipei Medical University Top Research Article Award

Selected Publications:

• Chen, X-Y.#, Kao, C.#, Peng, S-W., Chang, J-H.*, Lee, Y-L.*, Laiman, V., Chung, K.F., Bhavsar, P.K., Heriyanto, D.S., Chuang, K-J., Chuang, H-C.* (2023) Role of DCLK1/Hippo Pathway in Type II Alveolar Epithelial Cells Differentiation in Acute Respiratory Distress Syndrome. Molecular Medicine 29, p159.
• Tran, H.M., Lin, Y-C., Tsai, F-J., Lee, K-Y., Chang, J-H., Chung, C-L., Chung, K.F., Chuang, K-J., Chuang, H-C.* (2023) Short-term mediating effects of PM2.5 on climate-associated COPD severity. Science of the Total Environment 903, p166523.
• Chen, T-C.#, Lo, Y-C.#, Li, S-J., Lin, Y-C., Chang, C-W., Lian, Y-W., Laiman, V., Hsiao, T-C., Chuang, H-C.*, Chen, Y-Y.* (2023) Assessing traffic-related air pollution-induced fiber-specific white matter degradation associated with motor performance declines in aged rats. Ecotoxicology and Environmental Safety 263, p115373.

Abstract

Chinese Title:

空氣汙染與肺部疾病：從流行病學到毒理學的跨領域研究

English Title:

Air Pollution and Respiratory Disease: From Epidemiology to Toxicology

Abstract

Chronic obstructive pulmonary disease (COPD) is a significant global public health concern, currently the fourth-leading cause of death worldwide, and projected to become the third-leading cause by 2020. While smoking is a well-known risk factor for COPD, a notable proportion of COPD patients are non-smokers, suggesting other contributing factors. Epidemiological evidence indicates that acute exacerbations (AEs) of COPD are associated with typical urban levels of particulate matter (PM). PM exposure has been shown to reduce lung function, contributing to the development and progression of COPD. In one cohort study, a unit increase in PM2.5 (particulate matter less than 2.5 um in aerodynamic diameter) concentration was associated with a 2.3% rise in COPD AEs. Furthermore, participants exposed to PM2.5 levels above 15.4 μg/m³ exhibited a 54% higher risk of COPD AEs compared to those in a reference group.

Recent U.S. cohort studies have correlated chronic air pollution exposure with emphysema progression, using CT imaging and lung function measurements. Findings show that prolonged exposure to ambient pollutants, particularly PM2.5 and NOx, is associated with increased emphysema, a hallmark of COPD. Cellular senescence, a state where cells permanently cease to divide, has been implicated in aging and age-related diseases like COPD. Alveolar type II epithelial cells (AECII), which produce surfactant and regenerate type I alveolar cells (AECI) after injury, act as alveolar progenitor cells essential for maintaining alveolar integrity.

Increased apoptosis of alveolar epithelial cells contributes to the development of emphysematous changes in COPD by disrupting the natural regenerative process, in which cells lost to apoptosis are typically replaced through cell proliferation. Research indicates that emphysema is associated with abnormal alveolar cell turnover, marked by both heightened proliferation and apoptosis, which progressively destroys alveolar structures and reduces lung surface area—a defining characteristic of emphysema. In COPD patients, accelerated senescence of alveolar cells is commonly observed, contributing to abnormal cell turnover and substantial cell loss in emphysematous lungs. Understanding the phenotypes of COPD in response to air pollution exposure is therefore crucial to addressing these pathological changes.