Micol Introna. Photo: Stella Papadopoulou

Participate in the PhD Defence online on Zoom: https://stockholmuniversity.zoom.us/j/63760546931

Abstract
Transport-related particles originate from both combustion and non-combustion sources. At street level, vehicles emit significant amounts of particulate matter into the atmosphere. Similarly, subway systems represent polluted microenvironments where particle emissions primarily result from friction between brakes, rails, and wheels. When inhaled, these airborne particles can pose serious health risks and contribute to the onset of various diseases. Particles smaller than 2.5 µm in diameter (PM2.5) are of particular concern because they can reach deep areas of the respiratory system, accumulate in the alveoli, and be potentially toxic. However, based on their sources, PM2.5 can differ in composition and therefore have different toxicological effects. In vitro toxicological assessments are typically conducted under submerged conditions, where particles collected on filters are resuspended in liquid and administered to cell cultures. While this method has limitations in simulating real-world exposure, air–liquid interface (ALI) systems offer a more physiologically relevant approach by allowing direct aerosol exposure to cultured cells. However, most of ALI studies have been conducted in laboratories where aerosols were lab-generated or re-aerosolized after filter collection. 

This thesis aimed to bridge the gap between laboratory-based toxicological assessments and real-world exposure scenarios by conducting in situ experiments focused on transport-related PM2.5. A novel mobile ALI exposure system was developed, allowing direct exposure of human respiratory cells to ambient PM2.5 in urban environments. In situ toxicological exposures were performed using human alveolar epithelial cells alone or in co-culture with immune cells. In parallel, submerged exposures were conducted using two cell models (human alveolar epithelial cells and immune cells). These cells were exposed to suspensions with increasing particle doses to investigate dose–response relationships. Filter-collected PM2.5 samples were also analyzed chemically to identify potentially toxic compounds.

Cytotoxic and pro-inflammatory effects of freshly emitted PM2.5 were assessed in three settings: (i) in a road tunnel, (ii) in a subway station in Stockholm, and (iii) in a tribology laboratory to compare the emissions from different brake materials. During 2-hour ALI exposures, the average deposited PM2.5 dose was 1.4 ± 0.8 μg/cm² in the road tunnel, 0.12 ± 0.07 µg/cm² in the subway, and 4.03 ± 2.48 µg/cm² in the tribology lab. Submerged experiments demonstrated inflammatory responses, particularly in immune cells, following PM2.5 exposure from the road tunnel and subway. In contrast, ALI experiments showed no significant effects, likely due to lower deposited doses. Chemical analysis of the PM2.5 from the subway revealed high levels of polycyclic aromatic hydrocarbons (PAHs), typically released from combustion processes. The tribology campaign indicated that non-asbestos organic brake materials reduced cell viability in ALI exposures, while other materials showed no significant toxicological effects under any tested condition. This thesis demonstrated the feasibility and value of field-based toxicological research. Future studies should focus on increasing the dose delivery in the ALI system, extending exposure durations, and expanding the range of transport-related environments investigated to better understand the health risks of urban air pollution.