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Measurements of size-resolved aerosol concentration and fluxes were made in a forest in the Athabasca Oil Sands Region (AOSR) of Alberta, Canada, in August 2021 with the aim of investigating (a) particle size distributions from different sources, (b) size-resolved particle deposition velocities, and (c) the rate of vertical mixing in the canopy. Particle size distributions were attributed to different sources determined by wind direction. Air mixed with smokestack plumes from oil sands processing facilities had higher number concentrations with peak number at diameters near 70 nm. Aerosols from the direction of open-pit mine faces showed number concentration peaks near 150 nm and volume distribution peaks near 250 nm (with secondary peaks near 600 nm). Size-resolved deposition fluxes were calculated which show good agreement with previous measurements and a recent parameterization. There is a minimum deposition velocity of vd=0.02 cm s−1 for particles of 80 nm diameter; however, there is a large amount of variation in the measurements, and this value is not significantly different from zero in the 68 % confidence interval. Finally, gradient measurements of aerosol particles (with diameters <1 µm) demonstrated nighttime decoupling of air within and above the forest canopy, with median lag times at night of up to 40 min and lag times between 2 and 5 min during the day. Aerosol mass fluxes (diameters <1 µm) determined using flux–gradient methods (with different diffusion parameterizations) underestimate the flux magnitude relative to eddy covariance flux measurements when averaged over the nearly 1-month measurement period. However, there is significant uncertainty in the averages determined using the flux–gradient method.

Measurements of ozone were made using an instrumented tower and a tethersonde located in a forested region surrounded by oil sands production facilities in the Athabasca Oil Sands Region (AOSR). Our observations and modelling show that the concentration of ozone was modified by vertical mixing, photochemical reactions, and surface deposition. Measurements on the tower demonstrated that when winds are from the direction of anthropogenic emissions from oil sand extraction and processing facilities, the ozone mixing ratio in the forest is as much as 10 ppb lower than when winds are from the direction of undisturbed forest. This finding is supported by previous studies which suggest that surplus NOx from oil sands emissions results in ambient ozone titration. Gradients of ozone mixing ratio with height were observed using instruments on a tethered balloon (up to a height of 300 m) as well as a pulley system and 2-point gradients within the canopy. Strong gradients (ozone increasing with height between 0.2 and 0.4 ppb m-1) were measured in the canopy overnight, while daytime gradients were weaker and highly variable. A 1D canopy model was used to simulate the afternoon in-canopy gradient with reduced mixing overnight (suggesting high stability within the canopy), and an ozone deposition velocity of 0.2 cm s-1. Sensitivity simulations using the model suggest the local NO concentration profile and coefficients of vertical diffusivity have a significant influence on the O3 concentrations and profiles in the region.

The emission of SO2 from the Athabasca oil sands region (AOSR) has been shown to impact the surrounding forest area and human exposure. Recent studies using aircraft-based measurements have demonstrated that deposition of SO2 to the forest is at a rate many times higher than model estimates. Here we use the flux/gradient method to estimate SO2 deposition rates at two tower sites in the boreal forest downwind of AOSR SO2 emissions. We use both continuous and passive sampler measurements and compare both techniques. The measurements predict SO2 deposition velocities ranging from 2.1–5.9 cm s-1. There are uncertainties associated with the passive sampler flux/gradient analysis, primarily due to an assumed Schmidt number, a required assumption of independent variables, and potential wind effects. We estimate the total uncertainty as ±2 cm s-1. Accounting for these uncertainties, the measurements are near (or slightly higher than) the previous aircraft-based measurements (1.2–3.2 cm s-1) and significantly higher than model estimates for the same measurement periods (0.1–0.6 cm s-1), suggesting that SO2 has a much shorter lifetime in the atmosphere than is currently predicted by models.

Future urban climates are likely to warm substantively in coming decades as a result of climate change, and greater heat wave severity is anticipated. Moreover, the urban heat island contributes additional heat, especially during evening and night. Infrastructure-based heat reduction strategies can reduce canopy air temperatures during daytime, and to some extent at night. These strategies also have several additional effects beyond air temperature reduction. Here, we apply an early coupling of the WRF mesoscale model with the BEP-Tree urban canopy model to simulate extreme heat events representative of both contemporary and projected future climates for the metropolitan region of Toronto, Canada. Urban and non-urban land cover is derived using the state-of-the-art LCZ Generator methodology. Subsequently, the effectiveness of heat mitigation strategies, including highly reflective surfaces and vegetation, is quantified for the future scenario in the context of the increase in heat wave intensity. Specifically, the neighbourhood- and city-scale climate impacts of street trees across the diurnal cycle are quantified, and the diurnal progression of their local climate effects is discussed with reference to their modifications to multiple physical processes in the canopy. Effects of all heat mitigation strategies on canopy climate, building energy use, and thermal comfort indices are evaluated.

High-performance thermal insulation is a critical need for buildings. This article presents the development and thermal characterization of composite foam insulation boards containing low-cost vacuum insulation cores. The composite foam-vacuum insulation boards were created in a semi-automatic operation in a foam insulation manufacturing plant. The low-cost vacuum insulation is a new technology called modified atmosphere insulation. The production process of modified atmosphere insulation is much simpler than traditional vacuum insulation manufacturing, and it has the potential for significant cost reduction at the same thermal performance. Prototypes of small- and full-scale composite insulation boards were created for testing and evaluation under laboratory and natural weatherization conditions. The laboratory tests showed that the overall thermal resistance of the composite insulation board is at least twice that of current rigid foam insulation used in building envelope. Ongoing test of the composite insulation in a natural exposure test facility indicates that the high thermal performance was retained through handling and installation as well as natural aging over a period of one and a half years.

Immune homeostasis depends upon effective clearance of pathogens while simultaneously preventing autoimmunity and immunopathology in the host. Restimulation-induced cell death (RICD) is one such mechanism where by activated T cells receive subsequent antigenic stimulation, reach a critical signal threshold through the T cell receptor (TCR), and commit to apoptosis. Many details of this process remain unclear, including the role of co-stimulatory and co-inhibitory proteins that influence the TCR signaling cascade. Here we characterize the role of T cell immunoglobulin and mucin domain containing 3 (TIM-3) in RICD regulation. TIM-3 protected newly activated CD8+ effector T cells from premature RICD during clonal expansion. Surprisingly, however, we found that TIM-3 potentiated RICD in late-stage effector T cells. The presence of TIM-3 increased proximal TCR signaling and proapoptotic protein expression in late-stage effector T cells, with no consistent signaling effects noted in newly activated cells with or without TIM-3. To better explain these differences in TIM-3 function as T cells aged, we characterized the temporal pattern of TIM-3 expression in effector T cells. We found that TIM-3 was expressed on the surface of newly activated effector T cells, but remained largely intracellular in late-stage effector cells. Consistent with this, TIM-3 required a ligand to prevent early RICD, whereas ligand manipulation had no effects at later stages. Of the known TIM-3 ligands, carcinoembryonic antigen‐related cell adhesion molecule (CEACAM1) showed the greatest difference in surface expression over time and also protected newly activated cells from premature RICD, with no measurable effects in late-stage effectors. Indeed, CEACAM1 enabled TIM-3 surface expression on T cells, implying a co-dependency for these proteins in protecting expanding T cells from premature RICD. Our findings suggest that co-signaling proteins like TIM-3 and CEACAM1 can alter RICD sensitivity at different stages of the effector T cell response, with important implications for checkpoint blockade therapy.

Vegetation alters urban climates via transpirational cooling; however, unlike shorter vegetation, trees additionally provide shade and shelter. Urban canopy models (UCMs) are coupled with mesoscale models for assessment of neighbourhood-scale climate, but their representation of urban trees is limited. We present BEP-Tree, a multi-layer UCM that integrates trees instead of using the ‘tile’ approach that characterizes most urban mesoscale modelling. BEP-Tree resolves the microclimate underneath trees where outdoor human thermal exposure occurs; these conditions are largely inaccessible to current mesoscale modelling and remote sensing approaches. Moreover, BEP-Tree allows trees to protrude above buildings, enabling assessment of low-rise neighbourhoods. The new model combines existing models, including detailed radiative and hydrodynamic models that assess built-tree interactions, and includes new parameterizations for impacts of tree foliage distribution. BEP-Tree is evaluated against unique datasets from three cities enabling assessment of modelled radiation, energy exchanges and road and air temperatures across the diurnal cycle. Urban trees redirect sensible heat into latent heat and reduce pedestrian-level solar radiation, wind, and temperatures during daytime. Thermal climate and energy exchanges are more sensitive to street tree density than height. Coupled with a mesoscale model, BEP-Tree enables assessment of urban forest-induced neighbourhood-to-city scale climate impacts during fair weather periods.

In healthy individuals, the balance between immune-mediated pathogen clearance and tissue damage is tightly regulated through multiple processes. One such mechanism is restimulation-induced cell death (RICD), a propriocidal apoptotic mechanism that constrains T cell responses. Activated T cells must surpass a high threshold of TCR signal strength to induce pro-apoptotic genes responsible for executing RICD. Because co-receptors such as TIM-3 are thought to modulate TCR signal strength, we hypothesized that TIM-3 can shape the T cell response by tuning RICD sensitivity. We utilized siRNA knockdowns and transfection of wild-type and mutant TIM-3 expression constructs to assay for changes in RICD sensitivity in both immortalized and primary human T cells in vitro. Strikingly, we observed that the effect of altering TIM-3 expression varied temporally during the effector T cell response. Whereas TIM-3 promoted RICD resistance in newly activated T cells, TIM-3 enhanced RICD sensitivity in late-stage effector T cells by boosting TCR-induced FASL and BIM expression in a ligand-independent fashion. Preliminary evidence suggests that this dichotomy may relate to substantial temporal changes in the expression, cellular localization, and glycosylation of TIM-3 in early versus late-stage effector T cells. Overall, these results indicate that TIM-3 influences apoptosis sensitivity differently at distinct phases of the human T cell response, with important implications for the use of checkpoint blockade immunotherapies targeting TIM-3. Our findings may also help to clarify discrepancies in the literature regarding TIM-3 signaling and function in T cells.