Emissions from a flex fuel GDI vehicle operating on ethanol fuels show marked contrasts in chemical, physical and toxicological characteristics as a function of ethanol content.

ABSTRACT

This study assessed the gaseous and particulate emissions, as well as the toxicological properties of particulate matter (PM) from a flex fuel vehicle equipped with a wall-guided gasoline direct injection engine over triplicates cold-start and hot-start LA92 cycles. The vehicle was operated on a Tier 3 E10 fuel, an E10 fuel with higher levels of aromatics than the Tier 3 E10, an E30, and an E78 blend. Total hydrocarbon (THC), non-methane hydrocarbon (NMHC), carbon monoxide (CO), particulate emissions, and gaseous toxics (of benzene, toluene, ethylbenzene, xylenes (BTEX), and 1,3-butadiene) reduced for E30 and E78 blends compared to both E10 fuels. Formaldehyde and acetaldehyde emissions substantially increased with the higher ethanol blends. The high aromatic E10 fuel increased the emissions of THC, NMHC, particulates, and BTEX compared to the Tier 3 E10 fuel and the higher ethanol blends, as well as showed higher concentrations of accumulation mode particles. The GDI PM did not exhibit any measurable mutagenicity at the PM concentrations tested. Cytotoxicity varied only within a small range and concentrations of PM, eliciting a cytotoxic response similar to those by ambient aerosol. The outcomes of our two measures of PM oxidative potential (macrophage ROS and DTT) were significantly correlated, with the E78 blend exhibiting the least oxidative potential and the E30 the greatest. Gene expression analysis at both the mRNA and protein level indicates that there is the potential for GDI PM emissions to contribute to inflammation and etiology of disease such as asthma, and in contrast to the ROS and DTT outcomes, the E78 fuel PM exhibited the greatest potential to elicit pro-inflammatory cytokine (TNFα) production. Overall, the trends in toxicity emission rates (activity/mi) across the ethanol blends was driven primarily by PM mass emission rate contrasts and only secondarily by the differences in intrinsic toxicity of the PM.