In vitro assessment of aryl hydrocarbon, estrogen, and androgen receptor-mediated activities of secondary organic aerosols formed from the oxidation of polycyclic aromatic hydrocarbons and furans.

Biomass burning constitutes a significant source of fine particulate matter (PM) in the atmosphere, particularly during winter due to residential wood heating. This source also emits substantial quantities of volatile and semi-volatile organic compounds, leading through (photo-)chemical and physical processes, to the formation of secondary organic aerosols (SOAs), accounting for a significant fraction of PM. The current understanding of the biological effects of SOA resulting from the oxidation of major gaseous precursors emitted by biomass burning (e.g., polycyclic aromatic hydrocarbons (PAHs), phenols, furans) is still limited. Mechanism-based in vitro cellular bioassays targeting toxicologically relevant modes of action have proven valuable in assessing and quantifying the overall biological activity of complex mixtures like SOA, thereby revealing the presence of toxicologically relevant compounds. The main objective of this study was to investigate, using a battery of in vitro mechanism-based cellular bioassays, the aryl hydrocarbon (AhR), estrogen (ER), and androgen receptor (AR)-mediated activities of laboratory-generated SOA resulting from the oxidation of four PAHs and three furans. SOA was produced using an oxidation flow reactor (OFR) under either daytime (OH radicals) or nighttime (NO radicals) conditions. Furan-derived SOA did not exhibit any biological activity with the targeted endpoints. PAH-derived SOA, formed from AhR weakly or inactive PAHs, showed significant AhR-mediated activities. Notably, SOA resulting from naphthalene and acenaphthylene + acenaphthene demonstrated the highest AhR activation potency, with greater activities observed for SOA formed through NO radical oxidation. No endocrine-disrupting activity was observed for the PAH-derived SOA, similar to the individual parent PAHs (with the exception of fluorene and phenanthrene PAHs which were weekly anti-androgenic). These findings underscore the substantial contribution of PAH-derived SOA to the AhR-mediated activities of PM.