Unveiling the Importance of Organic Hydroxy Acids-Related Autoxidation Pathway in Isoprene Secondary Organic Aerosol Formation: Insights from Aerosol Tracer Composition in the Pearl River Delta.

Isoprene-derived secondary organic aerosol (iSOA) forms through complex, nitrogen oxide (NOx) dependent oxidation pathways. Low-NOx conditions favor the IEPOX pathway, yielding 2-methyltetrols (MTLs), whereas high-NOx environments promote the HMML pathway, producing 2-methylglyceric acid (2MGA). Additionally, isoprene-derived highly oxygenated molecules (iHOMs), formed via autoxidation mechanisms involving rapid H-shift reactions of peroxy radicals and analogous H-shifts of alkoxy radicals under atmospherically relevant conditions, may also contribute to iSOA formation. However, their ambient abundance and atmospheric significance remain poorly constrained. Through year-long, regional measurements of PM2.5 across nine sites in the Pearl River Delta (PRD), we quantified six iHOM species. The measured iHOMs had an annual mean concentration of 2.69 ± 3.52 ng m-3, with higher concentrations in summer and autumn, and were dominated by methyltartaric acids (MTA, 71%). The relative proportions of particle-phase iSOA tracers for the HOM (MTA), HMML (2MGA), and IEPOX (MTLs) pathways were 10%, 11%, and 79%, respectively. Box model simulations showed that their corresponding gas-phase intermediates, the peroxide isomer set (PIS), HMML, and IEPOX, accounted for 25%, 22%, and 53%, respectively. Together, the ambient observations and model results indicate that the IEPOX pathway makes the largest contribution to iSOA formation in the polluted PRD, whereas the MTA-related HOM pathway and HMML pathway make smaller but non-negligible contributions, particularly in winter. Moreover, pathway partitioning is associated with the isomeric distribution of isoprene hydroxy peroxy radicals (ISOPO2): the HOM pathway originates from limited δ-ISOPO2 (6.5 ± 3.0%), whereas IEPOX and HMML pathways arise from β-ISOPO2 (93.5 ± 3.0%), with HMML formation further modulated by competition between the MPAN + OH reaction and the temperature-dependent MPAN decomposition.