From primary to secondary aerosol: chemical transformation and toxicity of gasoline vehicle exhaust under contrasting driving conditions

Secondary organic aerosol (SOA) formation from gasoline vehicle exhaust represents a significant contributor to urban air pollution, yet the integrated effects of driving dynamics, atmospheric ageing, and gas-particle interactions on aerosol toxicity remain poorly characterised. This study investigated primary and secondary particle emissions from a plug-in hybrid Euro 6 gasoline vehicle equipped with a gasoline particulate filter (GPF), tested under two chassis dynamometer driving cycles of contrasting aggressiveness: a mild Real Driving Emissions cycle (mRDE) and a highly dynamic Combined cycle, each under cold and hot engine operation. Diluted exhaust was photochemically aged in a Tampere Secondary Aerosol Reactor (TSAR) and characterised physically, chemically, and toxicologically. Chemical analysis included offline quantification of particle-bound polycyclic aromatic hydrocarbons (PAHs), nitro-PAHs (NPAHs), oxy-PAHs (OPAHs), and water-soluble elements, alongside real-time aerosol mass spectrometry (SP-AMS). Toxicological assessment used a mobile Air-Liquid Interface (ALI) system to expose human lung epithelial (A549) cells to fresh and aged whole exhaust and gas-phase-only streams. Atmospheric ageing consistently shifted aerosol composition from a mixed primary aerosol to an organic-dominated secondary aerosol (organic fraction increasing from ∼60% to ∼87%), enhanced ultrafine particle formation, and increased the deposited particle dose. Whole exhaust exposures produced stronger cytotoxic and inflammatory responses than gas-phase-only exposures across all conditions. For the tested vehicle and experimental conditions, driving dynamics exerted the strongest influence on biological response, while atmospheric ageing amplified the particle-associated biological response. Cold-start operation had a more moderate effect, primarily manifested through changes in gaseous emissions rather than particle toxicity.