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Abstract:We built an emission inventory (EI) for the megacity of Bogotá, Colombia for 2012, which for the first time augments traditional industrial and mobile sources by including commercial sources, biogenic sources, and resuspended dust. We characterized the methodologies for estimating each source annually, and allocated the sources to hourly and 1 km 2 spatial resolution for use as inputs for air quality modeling purposes. A resuspended particulate matter (RPM) emission estimate was developed using the first measurements of road dust loadings and silt content for the city. Results show that mobile sources dominate emissions of CO 2 (80%), CO (99%), VOC (68%), NO x (95%), and SO 2 (85%). However, the newly estimated RPM comprises 90% of total PM 10 emissions, which are at least onefold larger than the PM 10 emissions from combustion processes. The 2012 EI was implemented in a chemical transport model (CTM) in order to understand the pollutants' fate and transport. Model evaluation was conducted against observations from the city's air quality monitoring network in two different periods. Modeling results for O 3 concentrations showed a good agreement, with mean fractional bias (MFB) of +11%, and a mean fractional error (MFE) of +35% with observations, but simulated PM 10 concentrations were strongly biased high (MFB +57%, MFE +68%), which was likely due to RPM emissions being overestimated. NO x , CO, and SO 2 were also biased high by the model, which was probably due to emissions not reflecting current fleet conditions. Future work aims to revise emission factors for mobile sources, which are the main sources of pollutants to the atmosphere.

Railyards have the potential to influence localfine particulate matter (aerodynamic diameter < or = 2.5 microm; PM2.5) concentrations through emissions from diesel locomotives and supporting activities. This is of concern in urban regions where railyards are in proximity to residential areas. Northwest of Atlanta, Georgia, Inman and Tilford railyards are located beside residential neighborhoods, industries, and schools. The PM2.5 concentrations near the railyards is the highest measured amongst the state-run monitoring sites (Georgia Environmental Protection Division, 2012; http://www.georgiaair.org/amp/report.php). The authors estimated fuel-based black carbon (BC) and PM2.5 emission factors for these railyards in order to help determine the impact of railyard activities on PM2.5 concentrations, and for assessing the potential benefits of replacing current locomotive engines with cleaner technologies. High-time-resolution measurements of BC, PM2.5, CO2, and wind speed and direction were made at two locations, north and south of the railyards. Emissions factors (i.e., the mass of BC or PM2.5 per gallon of fuel burned) were estimated by using the downwind/upwind difference in concentrations, wavelet analysis, and an event-based approach. By the authors' estimates, diesel-electric engines used in the railyards have average emission factors of 2.8 +/- 0.2 g of BC and 6.0 +/- 0.5 g of PM2.5 per gallon of diesel fuel burned. A broader mix of railyard supporting activities appear to lead to average emission factors of 0.7 +/- 0.03 g of BC and 1.5 +/- 0.1 g of PM2.5 per gallon of diesel fuel burned. Railyard emissions appear to lead to average enhancements of approximately 1.7 +/- 0.1 microg/m3 of PM2.5 and approximately 0.8 +/- 0.01 microg/m3 of BC in neighboring areas on an annual average basis. Uncertainty not quantified in these results could arise mainly from variability in downwind/upwind differences, differences in emissions of the diverse zones within the railyards, and the influence of on-road mobile source emissions.

Dysfunctional pulmonary homeostasis and repair, including diseases such as pulmonary fibrosis (PF), chronic obstructive pulmonary disease (COPD), and tumorigenesis have been increasing over the past decade, a fact that heavily implicates environmental influences. Several investigations have suggested that in response to increased transforming growth factor - beta (TGFβ) signaling, the alveolar type II (ATII) epithelial cell undergoes phenotypic changes that may contribute to the complex pathobiology of PF. We have previously demonstrated that increased tissue stiffness associated with PF is a potent extracellular matrix (ECM) signal for epithelial cell activation of TGFβ. The work reported here explores the relationship between tissue stiffness and exposure to environmental stimuli in the activation of TGFβ. We hypothesized that exposure of ATII cells to fine particulate matter (PM2.5) will result in enhanced cell contractility, TGFβ activation, and subsequent changes to ATII cell phenotype. ATII cells were cultured on increasingly stiff substrates with or without addition of PM2.5. Exposure to PM2.5 resulted in increased activation of TGFβ, increased cell contractility, and elongation of ATII cells. Most notably, on 8 kPa substrates, a stiffness greater than normal but less than established fibrotic lung, addition of PM2.5 resulted in increased cortical cell stiffness, enhanced actin staining and cell elongation; a result not seen in the absence of PM2.5. Our work suggests that PM2.5 exposure additionally enhances the existing interaction between ECM stiffness and TGFβ that has been previously reported. Furthermore, we show that this additional enhancement is likely a consequence of intracellular reactive oxygen species (ROS) leading to increased TGFβ signaling events. These results highlight the importance of both the micromechanical and biochemical environment in lung disease initiation and suggest that individuals in early stages of lung remodeling during fibrosis may be more susceptible than healthy individuals when exposed to environmental injury adjuvants.

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