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Abstract. 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.

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.

Abstract. 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. Background air from undeveloped forested areas air showed a peak number concentration for diameters near 70 nm while air mixed with upgrader smokestack plumes had higher number concentrations with peak number between diameters of 70 and 80 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 PM1 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. PM1 fluxes 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.