| Author: | Yang, Qian |
| Title: | Critical components shaping the health impact of PM2.5 in Hong Kong : insights from chemical speciation, sources, and bioaccessibility |
| Advisors: | Li, Xiangdong (CEE) |
| Degree: | Ph.D. |
| Year: | 2026 |
| Department: | Department of Civil and Environmental Engineering |
| Pages: | xvi, 182 pages : color illustrations |
| Language: | English |
| Abstract: | Air pollution remains a critical global health issue, with fine particulate matter (PM2.5) recognized as a major pollutant due to its ability to penetrate deep into the lung and enter the bloodstream, posing systemic health impacts. In vitro cytotoxicity analysis is widely adopted approaches for quantifying acute cytotoxicity, while health risk assessment is for accessing chronic inhalation-related health impacts induced by PM2.5. Previous health impact assessments of PM2.5 primarily focused on its mass concentration. However, emerging evidence suggests that the health impact of PM2.5 is not always directly correlated with its overall mass, but instead with its specific components, sources, and bioaccessibility. To address these research gaps, this study presents an integrated analysis of PM2.5-related health impacts in Hong Kong, a megacity in south China and one of the world's most traffic-intensive regions. This thesis adopts component-specific and source-resolved perspectives, integrating chemical characterization, source apportionment, bioaccessibility analysis, and assessments of both acute biological toxicity and chronic health risks, to enhance the understanding of PM2.5's health impacts. Not all PM2.5 fractions pose equal risks to human respiratory health. Specific components, despite constituting a small fraction of the total mass, may contribute considerably to inhalation toxicity. Thus, detailed investigations into these highly toxic components are needed. Moreover, the acute and chronic health effects caused by specific emission sources with toxic components are still insufficiently characterized, particularly in densely populated urban environments. Thus, this study firstly detailed the chemical speciation of PM2.5 using the samples collected from roadside, general urban, and coastal background areas in Hong Kong over a year. To evaluate component-specific health impacts, acute cytotoxicity was assessed using intracellular reactive oxygen species (ROS) and cell viability with the BEAS-2B cell line, along with chronic inhalation health risks according to USEPA guidelines. As a result, trace metals were the primary drivers of both acute and chronic toxicity, with EC also contributing significantly, while polycyclic aromatic hydrocarbons (PAHs) had a lesser role. Moreover, to investigate the key sources contributing most to health impacts, the study identified major sources of PM2.5 by Positive matrix factorization (PMF), including secondary aerosols, vehicle emissions, resuspended dust, shipping emissions, sea salt, and a mixed source (i.e., combustion & industrial emissions). Source contributions and regional effects were further analyzed using monthly profiles and back-trajectory airmass clusters via the Hybrid Single-Particle Lagrangian Integrated Trajectory (HYSPLIT) model. To quantify the source-resolved health impacts of PM2.5, we developed a novel source-resolved cytotoxicity model that integrates source profiles with biological toxicity datasets. Our analyses demonstrated two key findings: (1) local on-road traffic emissions dominated the induction of acute ROS (contributing to 84% of acute ROS effects in roadside PM2.5 and 63% in ambient urban PM2.5); (2) in contrast, regional combustion and industrial emissions posed more substantial chronic health risks, especially for aerosols in urban and coastal areas. Building upon our experiments, we observed that even completely insoluble substances could induce cytotoxicity, albeit through mechanisms and toxic effects that may differ from those of bioaccessible substances. This prompted us to consider the impact of bioaccessibility on cytotoxicity. Firstly, an improved extraction method using simulated epithelial lung fluid separated the bioaccessible and lung-fluid-insoluble fractions of PM2.5. The bioaccessibility of key toxic components was then analyzed. Among trace metals, As, Cd, Sb, and V showed high bioaccessibility (50–80%), while Fe, Mn, and Zn exhibited lower bioaccessibility (<20%). Most parent PAHs had bioaccessibility below 10%, indicating that their toxicity primarily stems from insoluble particle phases rather than dissolved forms in lung fluid. A pioneering aspect of this study is the evaluation of in vitro toxicity for both bioaccessible and lung-fluid-insoluble fractions, demonstrating that insoluble components, particularly lung-fluid-insoluble inorganic fractions, significantly induce intracellular ROS. This highlights the need to consider both soluble and insoluble fractions of PM2.5 in further health impact assessments. As a whole, this study enhanced the understanding of PM2.5 health impacts in a densely populated coastal megacity by integrating chemical speciation, toxicological, and bioaccessibility analyses. The findings emphasized the importance of targeted, toxicity-oriented air pollution control strategies and highlighted the need for continued refinement of methodologies and comprehensive risk assessments in future research. |
| Rights: | All rights reserved |
| Access: | open access |
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