21 research outputs found
Regional Air Quality Management Aspects of Climate Change: Impact of Climate Mitigation Options on Regional Air Emissions
We
investigate the projected impact of six climate mitigation scenarios
on U.S. emissions of carbon dioxide (CO<sub>2</sub>), sulfur dioxide
(SO<sub>2</sub>), and nitrogen oxides (NO<sub>X</sub>) associated
with energy use in major sectors of the U.S. economy (commercial,
residential, industrial, electricity generation, and transportation).
We use the EPA U.S. 9-region national database with the MARKet Allocation
energy system model to project emissions changes over the 2005 to
2050 time frame. The modeled scenarios are two carbon tax, two low
carbon transportation, and two biomass fuel choice scenarios. In the
lower carbon tax and both biomass fuel choice scenarios, SO<sub>2</sub> and NO<sub>X</sub> achieve reductions largely through pre-existing
rules and policies, with only relatively modest additional changes
occurring from the climate mitigation measures. The higher carbon
tax scenario projects greater declines in CO<sub>2</sub> and SO<sub>2</sub> relative to the 2050 reference case, but electricity sector
NO<sub>X</sub> increases. This is a result of reduced investments
in power plant NO<sub>X</sub> controls in earlier years in anticipation
of accelerated coal power plant retirements, energy penalties associated
with carbon capture systems, and shifting of NO<sub>X</sub> emissions
in later years from power plants subject to a regional NO<sub>X</sub> cap to those in regions not subject to the cap
Environmental Particulate (PM2.5) Augments Stiffness-Induced Alveolar Epithelial Cell Mechanoactivation of Transforming Growth Factor Beta
<div><p>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.</p></div
Average Source Apportionment for South Dekalb PM2.5 Collection.
<p>Average Source Apportionment for South Dekalb PM2.5 Collection.</p
Average Comparison of AQS and ASACA Particle Composition for Species of Interest.
<p>Average Comparison of AQS and ASACA Particle Composition for Species of Interest.</p
Exposure of RLE-6TN cells to increased stiffness and PM2.5 increases intracellular ROS.
<p>RLE-6TN cells were cultured on PA gels of increasing substrate stiffness with either no PM2.5 (A) or 10µg/cm<sup>2</sup> PM2.5 (B) and intracellular ROS levels were measured by the DCFH<sub>2</sub>-DA oxidation assay. Three independent triplicate experiments were performed and statistical significance is shown between substrates (A) and in comparison to the matched no PM2.5 controls (B). ** (p<0.01) and *** (p<0.001).</p
RLE-6TN cells are viable up to a concentration of 10µg/cm<sup>2</sup>.
<p>(A) Schematic illustrating process of PM2.5 collection for cell culture experiments. (B) RLE-6TN cells were cultured with increasing concentrations of isolated PM2.5 for 24 hours and analyzed using the trypan blue assay. Approximately 100% of cells were viable through a concentration of 10µg/cm<sup>2</sup>. Treatment with concentrations above 10µg/cm<sup>2</sup> resulted in significant cell death. Significance shown for * (p<0.01)</p
Stiffness-mediated activation of TGFβ is increased by addition of PM2.5.
<p>RLE-6TN cells were cultured for 5 days on substrates of increasing stiffness with or without the addition of each concentration of PM2.5 and levels of TGFβ activation were determined using the MLEC bioluminescence co-culture assay. Statistical significance is shown for each concentration of PM2.5 within its same substrate stiffness (* p<0.001).</p
Exposure to PM2.5 results in elongated cell phenotype and increased cell cortical stiffness.
<p>RLE-6TN cells were cultured on Fn-PA gels or Fn- or Ln-coated glass for 5 days with the addition of 10µg/cm<sup>2</sup>, 1µg/cm<sup>2</sup>, or 0.1µg/cm<sup>2</sup> concentrations of PM2.5, and changes in the actin cytoskeleton were analyzed by phalloidin staining of actin filaments and quantified as mean fluorescent staining of actin per cell (A-R). Single cell cortical stiffness of RLE-6TN cells cultured on 8 kPa gels were measured by AFM and significance shown for each group compared to the No PM2.5 control (S). Cell circularity was calculated from acquired images. Values closer to 1 indicate a more rounded, epithelial like cell (T). Experiments were performed in triplicate, representative images are presented and significance shown for * (p<0.05), ** (p<0.01) and *** (p<0.001).</p
Improving the Accuracy of Daily PM<sub>2.5</sub> Distributions Derived from the Fusion of Ground-Level Measurements with Aerosol Optical Depth Observations, a Case Study in North China
The
accuracy in estimated fine particulate matter concentrations
(PM<sub>2.5</sub>), obtained by fusing of station-based measurements
and satellite-based aerosol optical depth (AOD), is often reduced
without accounting for the spatial and temporal variations in PM<sub>2.5</sub> and missing AOD observations. In this study, a city-specific
linear regression model was first developed to fill in missing AOD
data. A novel interpolation-based variable, PM<sub>2.5</sub> spatial
interpolator (PMSI<sub>2.5</sub>), was also introduced to account
for the spatial dependence in PM<sub>2.5</sub> across grid cells.
A Bayesian hierarchical model was then developed to estimate spatiotemporal
relationships between AOD and PM<sub>2.5</sub>. These methods were
evaluated through a city-specific 10-fold cross-validation procedure
in a case study in North China in 2014. The cross validation <i>R</i><sup>2</sup> was 0.61 when PMSI<sub>2.5</sub> was included
and 0.48 when PMSI<sub>2.5</sub> was excluded. The gap-filled AOD
values also effectively improved predicted PM<sub>2.5</sub> concentrations
with an <i>R</i><sup>2</sup> = 0.78. Daily ground-level
PM<sub>2.5</sub> concentration fields at a 12 km resolution were predicted
with complete spatial and temporal coverage. This study also indicates
that model prediction performance should be assessed by accounting
for monitor clustering due to the potential misinterpretation of model
accuracy in spatial prediction when validation monitors are randomly
selected
Stiffness mediated ROS production is TGFβ dependent.
<p>RLE-6TN cells were cultured on PA gels of increasing stiffness with or without the addition of 10 µg/cm<sup>2</sup> and exposure to a TGFβ blocking antibody for 5 days. Levels of intracellular ROS were measured by the DCFH<sub>2</sub>-DA oxidation and assay. Three independent triplicate experiments were performed and statistical significance is shown between the PM2.5 groups with or without the TGFβ antibody. *** (p<0.001)</p