NH3 is a precursor of PM2.5 which deteriorates urban air quality, affects human health and impacts the global radiation budget. Since vehicles are important sources of NH3 in urban areas, we have satisfactorily studied the possibility of measuring NH3 emissions from gasoline and SCR-equipped diesel light duty vehicles during real driving on-road operation using a portable FTIR. The performance of the portable FTIR resulted to be comparable to that of a laboratory-based FTIR during a series of experiments performed in the Vehicle Emission Laboratory (VELA) using the World-harmonized Light-duty Test Cycle (WLTC). Higher on-road NH3 emission factors were obtained for the gasoline vehicle than for the diesel. High NOx emissions were measured from the diesel vehicle, indicating a low efficiency of the DeNOx system, SCR. On-road NH3 emission factors were ~2 times lower than during the laboratory tests at 23 C for both vehiclesNH3 emissions were not observed for the diesel vehicle during cold start operation. However, NH3 cold start emissions from the gasoline vehicle were up to 2 orders of magnitude higher than during the entire road trips, ranging from 45 to 134 mg km-1. Cold start emissions are of paramount importance as they commonly take place in urban areas. Hence, future urban reductions in PM2.5 might need to take into consideration the introduction of NH3 emissions limits for passenger cars.JRC.C.4-Sustainable Transpor

The transport sector is one of the main sources air pollutants. Different exhaust after-treatment systems have been implemented over the years to control the emissions of criteria pollutants. However, while reducing the emissions of the target compounds these systems can lead to the emissions of other pollutants and/or greenhouse gases such as NH₃ or N₂O. Following the implementation of the Real Driving Emissions (RDE) test procedure in the EU, vehicles have been equipped with more complex after-treatment configurations. The impact that these technologies may have on the emissions of non-regulated pollutants during real-world driving have not been evaluated until now. In the current study we present the on-road emissions of a series of non-regulated pollutants, including NH₃, N₂O, CH₄ and HCHO, measured with a portable FTIR from a series of Euro 6d, Euro 6c and Euro 6d-TEMP, gasoline diesel and compressed natural gas (CNG) vehicles during real-world testing. The obtained results show that it is possible to measure N₂O, NH₃, CH₄ and HCHO during on-road operation. The results also highlight the importance of the measurement of the emissions of these pollutants during real-world driving, as the emissions of NH₃ (a particulate matter precursor) and those of N₂O and CH₄ (green-house gases) can be high from some vehicle technologies. NH₃ emissions were up to 49 mg/km for gasoline passenger cars, up to 69 mg/km for the CNG light-commercial vehicle and up to 17 mg/km a diesel passenger car equipped with a selective catalytic reduction system (SCR). On the other hand, N₂O and CH₄ emissions accounted for up to 9.8 g CO₂ eqv/km for a diesel passenger car equipped with a combination of diesel oxidation catalysts (DOC), lean NO_x traps (LNT), SCR and possibly an ammonia slip catalyst ASC.

The biological effects induced by complete engine emissions in a 3D model of the human airway (MucilAir^TM) and in human bronchial epithelial cells (BEAS-2B) grown at the air–liquid interface were compared. The cells were exposed for one or five days to emissions generated by a Euro 5 direct injection spark ignition engine. The general condition of the cells was assessed by the measurement of transepithelial electrical resistance and mucin production. The cytotoxic effects were evaluated by adenylate kinase (AK) and lactate dehydrogenase (LDH) activity. Phosphorylation of histone H2AX was used to detect double-stranded DNA breaks. The expression of the selected 370 relevant genes was analyzed using next-generation sequencing. The exposure had minimal effects on integrity and AK leakage in both cell models. LDH activity and mucin production in BEAS-2B cells significantly increased after longer exposures; DNA breaks were also detected. The exposure affected CYP1A1 and HSPA5 expression in MucilAir^TM. There were no effects of this kind observed in BEAS-2B cells; in this system gene expression was rather affected by the time of treatment. The type of cell model was the most important factor modulating gene expression. In summary, the biological effects of complete emissions exposure were weak. In the specific conditions used in this study, the effects observed in BEAS-2B cells were induced by the exposure protocol rather than by emissions and thus this cell line seems to be less suitable for analyses of longer treatment than the 3D model.