The npj Clean Air RCT-style controlled exposure trial (double-blind, n=15 healthy UK volunteers) demonstrates that 60-minute exposures to diesel exhaust, woodsmoke, cooking emissions, and limonene SOA—normalized to identical PM levels—produce divergent short-term respiratory and cognitive signatures after four hours. Respiratory impairment ranked highest for limonene SOA, followed by woodsmoke, while diesel and woodsmoke paradoxically boosted psychomotor speed, potentially via NOX-mediated vasodilation. This challenges the prevailing regulatory focus on bulk PM2.5 mass, as the original MedicalXpress coverage underplays how the study’s small, healthy sample limits extrapolation to elderly or comorbid populations where cumulative lung-brain axis inflammation may accelerate neurodegeneration. A 2017 Lancet observational cohort (n>2 million) linked long-term NO2 and PM exposure to 1.3-fold higher dementia incidence, yet lacked mechanistic granularity now supplied here; likewise, a 2022 Environmental Health Perspectives meta-analysis flagged source heterogeneity but relied on ambient monitoring rather than controlled mixtures. The trial’s internal validity is strong due to within-subject design, yet absence of inflammatory biomarker data or diverse demographics represents a clear gap. These acute shifts imply repeated daily micro-exposures in urban indoor settings could compound into elevated dementia trajectories, demanding policy that differentiates combustion versus secondary organic aerosols rather than uniform PM thresholds.