Secondary effects of catalytic diesel particulate filters: reduced aryl hydrocarbon receptor-mediated activity of the exhaust.

Diesel exhaust contains numerous toxic substances that show different modes of action such as triggering aryl hydrocarbon receptor (AhR)-mediated pathways. We investigated AhR-mediated activity of exhaust generated by a heavy-duty diesel engine operated with or without iron- or copper/iron-catalyzed diesel particulate filters (DPFs). AhR agonists were quantified using the DR-CALUX reporter gene assay (exposure of cells for 24 h). We found 54-60 ng 2,3,7,8-tetrachlorodibenzo-p-dioxin CALUX equivalents (TCDD-CEQs) per m3 of exhaust in unfiltered samples and 6-16 ng TCDD-CEQ m3 in DPF-treated samples. DPF applications decreased TCDD-CEQ concentrations by almost 90%. Concentrations of known AhR agonists were determined with GC/HRMS and converted to TCDD-CEQ concentrations using compound-specific relative potency values. The analyzed nine polycyclic aromatic hydrocarbons (PAHs) and the 172,3,7,8-chlorinated dibenzodioxins/furans (23,7,8-PCDD/Fs) contributed only marginally (0.6-1.6%) to the total agonist concentration. However, both DPFs also decreased concentrations of individual PAHs by 7(0-80%. Variation of the assay exposure time (8, 24, 48,72, and 96 h) revealed that AhR-mediated activity decreased over time and reached a plateau after 72 h, which was most likely due to biotransformation of AhR agonists by the exposed H4IIE cells. At the plateau, we measured 1-2 ng TCDD-CEQ m(-3) in both an unfiltered and a filtered exhaust sample. Our findings show that DPFs are a promising technology to detoxify diesel exhaust regarding compounds with AhR-mediated activity.