title: Secondary effects of catalytic diesel particulate filters: reduced aryl hydrocarbon receptor-mediated activity of the exhaust.
abstract: 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.
authors.affiliation: Laboratory for Analytical Chemistry, Swiss Federal Laboratories for Materials Testing and Research, Uberlandstrasse 129, CH-8600 Dübendorf, Switzerland.
authors.forename: Daniela
authors.initials: D
authors.lastname: Wenger
authors.forename: Andreas C
authors.initials: AC
authors.lastname: Gerecke
authors.forename: Norbert V
authors.initials: NV
authors.lastname: Heeb
authors.forename: Markus
authors.initials: M
authors.lastname: Zennegg
authors.forename: Martin
authors.initials: M
authors.lastname: Kohler
authors.forename: Hanspeter
authors.initials: H
authors.lastname: Naegeli
authors.forename: Renato
authors.initials: R
authors.lastname: Zenobi
mesh_terms: D000393:Air Pollutants / Q000032:analysis*; D000397:Air Pollution / Q000517:prevention & control*; D000818:Animals; D001572:Benzofurans / Q000032:analysis; D002384:Catalysis; D045744:Cell Line, Tumor; D003300:Copper / Q000737:chemistry; D003510:Cyclohexanes / Q000737:chemistry; D000072338:Dibenzofurans, Polychlorinated; D005374:Filtration / Q000379:methods; D005742:Gasoline; D017930:Genes, Reporter / Q000235:genetics; D007501:Iron / Q000737:chemistry; D008156:Luciferases / Q000235:genetics; D000072317:Polychlorinated Dibenzodioxins / Q000031:analogs & derivatives / Q000032:analysis; D011084:Polycyclic Aromatic Hydrocarbons / Q000032:analysis; D051381:Rats; D018336:Receptors, Aryl Hydrocarbon / Q000819:agonists* / Q000235:genetics; D001335:Vehicle Emissions / Q000032:analysis*
chemical_list: D000393:Air Pollutants; D001572:Benzofurans; D003510:Cyclohexanes; D000072338:Dibenzofurans, Polychlorinated; D005742:Gasoline; D000072317:Polychlorinated Dibenzodioxins; D011084:Polycyclic Aromatic Hydrocarbons; D018336:Receptors, Aryl Hydrocarbon; D001335:Vehicle Emissions; D003300:Copper; D007501:Iron; D008156:Luciferases; C518164:1,6-dichlorohexane