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To quantify the fine-scale spatial variations and local source impacts of urban ultrafine particle (UFP) concentrations, we conducted 3-6 weeks of continuous measurements of particle number (a proxy for UFP) and other air pollutant (CO, NO 2 , and PM 2.5 ) concentrations at 32 sites in Pittsburgh, Pennsylvania during the winters of 2017 and 2018. Sites were selected to span a range of urban land use attributes, including urban background, near local and arterial roads, traffic intersections, urban street canyon, near-highway, near large industrial source, and restaurant density. The spatial variations in urban particle number concentrations varied by about a factor of three. Particle number concentrations are 2-3 times more spatially heterogeneous than PM 2.5 mass. The observed order of spatial heterogeneity is UFP > NO 2  > CO > PM 2.5 . On average, particle number concentrations near local roads with a cluster of restaurants and near arterial roads are roughly two times higher than the urban background. Particle number concentrations in the urban street canyon, downwind of a major highway, and near large industrial sources are 2-4 times higher than background concentrations. While traffic is known as an important contributor to particle number concentrations, restaurants and industrial emissions also contribute significantly to spatial variations in Pittsburgh. Particle size distribution measurements using a mobile laboratory show that the local spatial variations in particle number concentrations are dictated by concentrations of particles smaller than 50 nm. A large fraction of urban residents (e.g., ~50%) in Pittsburgh live near local sources and are therefore exposed to 50%-300% higher particle number concentrations than urban background location. These locally emitted particles may have greater health effects than background particles., (Copyright © 2018 Elsevier B.V. All rights reserved.)

Positive and negative artifacts of particle-phase organic carbon (p-OC) and the polycyclic aromatic hydrocarbons (PAHs) in gasoline direct injection (GDI) engine exhaust particulate matter (PM) were assessed using an integrated organic gas and particle sampler (IOGAPS). Three configurations (denuder + sorbent impregnated filters (SIFs), upstream Zefluor filter + denuder + SIFs, and standard filter pack + SIFs) were used to collect GDI exhaust samples at cold start and highway cruise operating conditions with no aftertreatment. Approximately 35% of the measured GDI p-OC was attributed to positive artifacts; negative artifacts were not detectable due to low overall SVOC concentrations. GDI engine exhaust PAH concentrations were approximately 10 times higher during cold start than highway cruise. At highway cruise, pyrene and fluoranthene were the dominant PAHs in the undenuded filter pack; downstream of the denuder benzo(a)anthracene was the dominant PAH. From a comparison of our findings to published PAH emission factors we estimate that three-way catalyst conversion efficiencies of PAHs were approximately 80% for 3 of the 15 PAHs measured during highway cruise operation. These conversion efficiencies may be considerably lower during cold start operation when the three-way catalyst has not reached its operating temperature. Our previous work showed that adverse biological responses to GDI engine exhaust exposure may be dominated by the particle phase when measured downstream of a Teflon filter. Understanding the partitioning characteristics of PAHs may help elucidate specific PAHs contributing to this effect., (Copyright © 2018 Elsevier B.V. All rights reserved.)

Gasoline direct injection (GDI) engines are increasingly prevalent in the global vehicle fleet. Particulate matter emissions from GDI engines are elevated compared to conventional gasoline engines. The pulmonary effects of these higher particulate emissions are unclear. This study investigated the pulmonary responses induced by GDI engine exhaust using an ex vivo model. The physiochemical properties of GDI engine exhaust were assessed. Precision cut lung slices were prepared using Balb/c mice to evaluate the pulmonary response induced by one-hour exposure to engine-out exhaust from a laboratory GDI engine operated at conditions equivalent to vehicle highway cruise conditions. Lung slices were exposed at an air-liquid interface using an electrostatic aerosol in vitro exposure system. Particulate and gaseous exhaust was fractionated to contrast mRNA production related to polycyclic aromatic hydrocarbon (PAH) metabolism and oxidative stress. Exposure to GDI engine exhaust upregulated genes involved in PAH metabolism, including Cyp1a1 (2.71, SE=0.22), and Cyp1b1 (3.24, SE=0.12) compared to HEPA filtered air (p<0.05). GDI engine exhaust further increased Cyp1b1 expression compared to filtered GDI engine exhaust (i.e., gas fraction only), suggesting this response was associated with the particulate fraction. Exhaust particulate was dominated by high molecular weight PAHs. Hmox1, an oxidative stress marker, exhibited increased expression after exposure to GDI (1.63, SE=0.03) and filtered GDI (1.55, SE=0.04) engine exhaust compared to HEPA filtered air (p<0.05), likely attributable to a combination of the gas and particulate fractions. Exposure to GDI engine exhaust contributes to upregulation of genes related to the metabolism of PAHs and oxidative stress., (Copyright © 2016 Elsevier B.V. All rights reserved.)