Impact of low- and high-oxidation diesel particulate filters on genotoxic exhaust constituents.

Diesel exhaust contains several genotoxic compounds that may or may not penetrate diesel particulate filters (DPFs). Furthermore, the DPF-supported combustion of soot and adsorbed compounds may lead to the formation of additional pollutants. Herein, we compare the impact of 14 different DPFs on emissions of known genotoxic compounds. During a four year period, these DPFs were tested on a heavy duty diesel engine, operated in the ISO 8178/4 C1 cycle. Integral samples, including gas-phase and particle-bound matter were taken. All DPFs were efficient wall-flow filters with solid particulate number filtration efficiencies eta > 98%. On the basis of their CO, NO, and NO(2) emission characteristics, two different filter families were distinguished. DPFs with high oxidation potential (hox, n = 8) converted CO and NO besides hydrocarbons, whereas low oxidation potential DPFs (lox, n = 6) did not support CO and NO oxidation but still converted hydrocarbons. Lox-DPFs reduced NO(2) from 1.0 +/- 0.3 (engine-out) to 0.42 +/- 0.11 g/kWh (eta = 0.59), whereas hox-DPFs induced a NO(2) formation up to 3.3 +/- 0.7 g/kWh (eta = -2.16). Emissions of genotoxic PAHs decreased for both filter families. Conversion efficiencies varied for individual PAHs and were lower for lox- (eta = 0.31-0.87) than for hox-DPFs (eta = 0.75-0.98). Certain nitro-PAHs were formed indicating that nitration is an important step along PAH oxidation. For example, 1-nitronaphthalene emissions increased from 11 to 17 to 21 microg/L without, with lox-, and hox-DPFs respectively, whereas 2-nitronaphthalene emissions decreased from 25 to 19 to 4.7 microg/L. In contrast to our expectations, the nitration potential of lox-DPFs was higher than the one of hox-DPFs, despite the intense NO(2) formation of the latter. The filters converted most genotoxic PAHs and nitro-PAHs and most soot particles, acting as carriers for these compounds. Hox-DPF exhaust remains oxidizing and therefore is expected to support atmospheric oxidation reactions, whereas lox-DPF exhaust is reducing and consuming oxidants such as ozone, when mixed with ambient air.

In vitro estrogenicity of ambient particulate matter: contribution of hydroxylated polycyclic aromatic hydrocarbons.

Atmospheric particulate matter (PM1) was collected at an urban and a rural site in Switzerland during a hibernal high air pollution episode and was investigated for estrogenicity using an estrogen-sensitive reporter gene assay (ER-CALUX). All samples that were tested induced estrogen receptor-mediated gene expression in T47D human breast adenocarcinoma cells. Observed estrogenic activities corresponded to 17beta-estradiol (E2) CALUX equivalent concentrations ranging from 2 to 23 ng E2-CEQ per gram of PM1 (particulate matter of < or = 1 microm aerodynamic diameter) and from 0.07 to 1.25 pg E2-CEQ per m(3) of sampled air. There was a strong correlation between the PM1 estrogenicity of the urban and rural sites (r = 0.92). Five hydroxylated polycyclic aromatic hydrocarbons (hydroxy-PAHs), which show structural similarities to E2, were assessed for their estrogenic activity. The following order of estrogenic potency was found: 2-hydroxychrysene > 2-hydroxyphenanthrene > 1-hydroxypyrene > 2-hydroxynaphthalene > 1-hydroxynaphthalene. Three of these hydroxy-PAHs, namely 2-hydroxyphenanthrene, 2-hydroxynaphthalene and 1-hydroxynaphthalene, were detected in all PM1 extracts. However, they contributed only 0.01-0.2% to the overall estrogenic activity. Hence, mainly other estrogenic compounds not yet identified by chemical analysis must be responsible for the observed activity. The temporal trend of PM1 estrogenicity at the urban and rural site, respectively, was compared with the time course of several air pollutants (NO2, NO, SO2, O3, CO) and meteorological parameters (temperature, humidity, air pressure, solar irradiation, wind velocity). However, specific emission sources and formation processes of atmospheric xenoestrogens could not be elucidated. This study showed that ambient particulate matter contains compounds that are able to interact with estrogen receptors in vitro and potentially also interfere with estrogen-regulated pathways in vivo.

Secondary effects of catalytic diesel particulate filters: conversion of PAHs versus formation of nitro-PAHs.

Diesel particulate filters (DPFs) are a promising technology to detoxify diesel exhaust. However, the secondary combustion of diesel soot and associated compounds may also induce the formation of new pollutants. Diesel soot is rated as carcinogenic to humans and also acts as a carrier for a variety of genotoxic compounds such as certain polycyclic aromatic hydrocarbons (PAHs) or nitrated PAHs (nitro-PAHs). Furthermore, diesel exhaust contains considerable amounts of nitric oxide (NO), which can be converted to more powerful nitrating species like nitrogen dioxide (NO2), nitric acid (HNO3), and others. This mix of compounds may support nitration reactions in DPFs. Herein we report effects of two cordierite-based, monolithic, wall-flow DPFs on emissions of genotoxic PAHs and nitro-PAHs and compare these findings with those of a reporter gene bioassay sensitive to aryl hydrocarbons (AHs). Soot combustion was either catalyzed with an iron- or a copper/iron-based fuel additive (fuel-borne catalysts). A heavy duty diesel engine, operated according to the 8-stage ISO 8178/4 C1 cycle, was used as test platform. Emissions of all investigated 4- to 6-ring PAHs were reduced by about 40-90%, including those rated as carcinogenic. Emissions of 1- and 2-nitronaphthalene increased by about 20-100%. Among the 3-ring nitro-PAHs, emissions of 3-nitrophenanthrene decreased by about 30%, whereas 9-nitrophenanthrene and 9-nitroanthracene were found only after DPFs. In case of 4-ring nitro-PAHs, emissions of 3-nitrofluoranthene, 1-nitropyrene, and 4-nitropyrene decreased by about 40-60% with DPFs. Total AH-receptor (AHR) agonist concentrations of diesel exhaust were lowered by 80-90%, when using the iron- and copper-based DPFs. The tested PAHs accounted for < 1% of the total AHR-mediated response, indicating that considerable amounts of other aryl hydrocarbons must be present in filtered and unfiltered exhaust. We conclude that both DPFs detoxified diesel exhaust with respect to total aryl hydrocarbons, including the investigated carcinogenic PAHs, but we also noticed a secondary formation of selected nitro-PAHs. Nitration reactions were found to be stereoselective with a preferential substitution of hydrogen atoms at peri-positions. The stereoisomers obtained are related to combustion chemistry, but differ from those formed upon atmospheric nitration of PAHs.

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.

Catalytic diesel particulate filters reduce the in vitro estrogenic activity of diesel exhaust.

An in vitro reporter gene assay based on human breast cancer T47D cells (ER-CALUX) was applied to examine the ability of diesel exhaust to induce or inhibit estrogen receptor (ER)-mediated gene expression. Exhaust from a heavy-duty diesel engine was either treated by iron- or copper/iron-catalyzed diesel particulate filters (DPFs) or studied as unfiltered exhaust. Collected samples included particle-bound and semivolatile constituents of diesel exhaust. Our findings show that all of the samples contained compounds that were able to induce ER-mediated gene expression as well as compounds that suppressed the activity of the endogenous hormone 17beta-estradiol (E2). Estrogenic activity prevailed over antiestrogenic activity. We found an overall ER-mediated activity of 1.63 +/- 0.31 ng E2 CALUX equivalents (E2-CEQs) per m(3) of unfiltered exhaust. In filtered exhaust, we measured 0.74 +/- 0.07 (iron-catalyzed DPF) and 0.55 +/- 0.09 ng E2-CEQ m(-3) (copper/iron-catalyzed DPF), corresponding to reductions in estrogenic activity of 55 and 66%, respectively. Our study demonstrates that both catalytic DPFs lowered the ER-mediated endocrine-disrupting potential of diesel exhaust.

Secondary effects of catalytic diesel particulate filters: copper-induced formation of PCDD/Fs.

Potential risks of a secondary formation of polychlorinated dibenzodioxins/furans (PCDD/Fs) were assessed for two cordierite-based, wall-through diesel particulate filters (DPFs) for which soot combustion was either catalyzed with an iron- or a copper-based fuel additive. A heavy duty diesel engine was used as test platform, applying the eight-stage ISO 8178/4 C1 cycle. DPF applications neither affected the engine performance, nor did they increase NO, NO2, CO, and CO2 emissions. The latter is a metric for fuel consumption. THC emissions decreased by about 40% when deploying DPFs. PCDD/F emissions, with a focus on tetra- to octachlorinated congeners, were compared under standard and worst case conditions (enhanced chlorine uptake). The iron-catalyzed DPF neither increased PCDD/F emissions, nor did it change the congener pattern, even when traces of chlorine became available. In case of copper, PCDD/F emissions increased by up to 3 orders of magnitude from 22 to 200 to 12 700 pg I-TEQ/L with fuels of < 2, 14, and 110 microg/g chlorine, respectively. Mainly lower chlorinated DD/Fs were formed. Based on these substantial effects on PCDD/F emissions, the copper-catalyzed DPF system was not approved for workplace applications, whereas the iron system fulfilled all the specifications of the Swiss procedures for DPF approval (VERT).