Decades of evidence from laboratory and epidemiological studies demonstrate the adverse health effects of particulate matter (PM). A key driver is PM2.5-induced reactive oxygen species (ROS) formation, which triggers oxidative stress and inflammation via redox-sensitive pathways. This project investigates how the intrinsic chemical reactivity of PM2.5 relates to pro-inflammatory lung responses and chronic disease development. Limited knowledge exists on how PM2.5 oxidative potential (OP) links to inflammatory potency, the balance between exogenous and endogenous ROS, or how acute oxidative insults shape long-term immune memory. We will quantify PM2.5-mediated OP using advanced instrumentation, assess downstream redox and immune responses, and explore epigenetic markers bridging acute and chronic effects in human airway cells.

Objectives:
1. Quantify OP at high time resolution in laboratory and field studies using state-of-the-art instrumentation.
2. Link PM2.5 OP to biological mechanisms by integrating OP data with air–liquid interface (ALI) exposures of human lung models to assess oxidative stress and inflammation.
3. Identify redox-driven epigenetic reprogramming by mapping DNA methylation and histone modifications in cells exposed to PM2.5 of differing OP.
4. Correlate PM2.5 chemistry, OP, and epigenetic biomarkers to predict chronic lung-disease risk and guide health-relevant air-quality metrics.

This TUM–Imperial project will advance mechanistic understanding of PM2.5 toxicity and support more targeted air pollution mitigation strategies.