Mechanistic air pollution modeling is essential in air quality management, yet the extensive expertise and computational resources required to run most models prevent their use in many situations ...where their results would be useful. Here, we present InMAP (Intervention Model for Air Pollution), which offers an alternative to comprehensive air quality models for estimating the air pollution health impacts of emission reductions and other potential interventions. InMAP estimates annual-average changes in primary and secondary fine particle (PM2.5) concentrations-the air pollution outcome generally causing the largest monetized health damages-attributable to annual changes in precursor emissions. InMAP leverages pre-processed physical and chemical information from the output of a state-of-the-science chemical transport model and a variable spatial resolution computational grid to perform simulations that are several orders of magnitude less computationally intensive than comprehensive model simulations. In comparisons run here, InMAP recreates comprehensive model predictions of changes in total PM2.5 concentrations with population-weighted mean fractional bias (MFB) of -17% and population-weighted R2 = 0.90. Although InMAP is not specifically designed to reproduce total observed concentrations, it is able to do so within published air quality model performance criteria for total PM2.5. Potential uses of InMAP include studying exposure, health, and environmental justice impacts of potential shifts in emissions for annual-average PM2.5. InMAP can be trained to run for any spatial and temporal domain given the availability of appropriate simulation output from a comprehensive model. The InMAP model source code and input data are freely available online under an open-source license.
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DOBA, IZUM, KILJ, NUK, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK
Significance Our assessment of the life cycle air quality impacts on human health of 10 alternatives to conventional gasoline vehicles finds that electric vehicles (EVs) powered by electricity from ...natural gas or wind, water, or solar power are best for improving air quality, whereas vehicles powered by corn ethanol and EVs powered by coal are the worst. This work advances the current debate over the environmental impacts of conventional versus alternative transportation options by combining detailed spatially and temporally explicit emissions inventories with state-of-the-science air quality impact analysis using advanced chemical transport modeling. Our results reinforce previous findings that air quality-related health damages from transportation are generally comparable to or larger than climate change-related damages.
Commonly considered strategies for reducing the environmental impact of light-duty transportation include using alternative fuels and improving vehicle fuel economy. We evaluate the air quality-related human health impacts of 10 such options, including the use of liquid biofuels, diesel, and compressed natural gas (CNG) in internal combustion engines; the use of electricity from a range of conventional and renewable sources to power electric vehicles (EVs); and the use of hybrid EV technology. Our approach combines spatially, temporally, and chemically detailed life cycle emission inventories; comprehensive, fine-scale state-of-the-science chemical transport modeling; and exposure, concentration–response, and economic health impact modeling for ozone (O ₃) and fine particulate matter (PM ₂.₅). We find that powering vehicles with corn ethanol or with coal-based or “grid average” electricity increases monetized environmental health impacts by 80% or more relative to using conventional gasoline. Conversely, EVs powered by low-emitting electricity from natural gas, wind, water, or solar power reduce environmental health impacts by 50% or more. Consideration of potential climate change impacts alongside the human health outcomes described here further reinforces the environmental preferability of EVs powered by low-emitting electricity relative to gasoline vehicles.
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Fine particulate matter (PM2.5) air pollution exposure is the largest environmental health risk factor in the United States. Here, we link PM2.5 exposure to the human activities responsible for PM2.5 ...pollution. We use these results to explore “pollution inequity”: the difference between the environmental health damage caused by a racial–ethnic group and the damage that group experiences. We show that, in the United States, PM2.5 exposure is disproportionately caused by consumption of goods and services mainly by the non-Hispanic white majority, but disproportionately inhaled by black and Hispanic minorities. On average, non-Hispanic whites experience a “pollution advantage”: They experience ∼17% less air pollution exposure than is caused by their consumption. Blacks and Hispanics on average bear a “pollution burden” of 56% and 63% excess exposure, respectively, relative to the exposure caused by their consumption. The total disparity is caused as much by how much people consume as by how much pollution they breathe. Differences in the types of goods and services consumed by each group are less important. PM2.5 exposures declined ∼50% during 2002–2015 for all three racial–ethnic groups, but pollution inequity has remained high.
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The identification of lymphocyte subsets with non-overlapping effector functions has been pivotal to the development of targeted therapies in immune-mediated inflammatory diseases (IMIDs)
. However, ...it remains unclear whether fibroblast subclasses with non-overlapping functions also exist and are responsible for the wide variety of tissue-driven processes observed in IMIDs, such as inflammation and damage
. Here we identify and describe the biology of distinct subsets of fibroblasts responsible for mediating either inflammation or tissue damage in arthritis. We show that deletion of fibroblast activation protein-α (FAPα)
fibroblasts suppressed both inflammation and bone erosions in mouse models of resolving and persistent arthritis. Single-cell transcriptional analysis identified two distinct fibroblast subsets within the FAPα
population: FAPα
THY1
immune effector fibroblasts located in the synovial sub-lining, and FAPα
THY1
destructive fibroblasts restricted to the synovial lining layer. When adoptively transferred into the joint, FAPα
THY1
fibroblasts selectively mediate bone and cartilage damage with little effect on inflammation, whereas transfer of FAPα
THY1
fibroblasts resulted in a more severe and persistent inflammatory arthritis, with minimal effect on bone and cartilage. Our findings describing anatomically discrete, functionally distinct fibroblast subsets with non-overlapping functions have important implications for cell-based therapies aimed at modulating inflammation and tissue damage.
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EMUNI, FIS, FZAB, GEOZS, GIS, IJS, IMTLJ, KILJ, KISLJ, MFDPS, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, SBMB, SBNM, UKNU, UL, UM, UPUK, VKSCE, ZAGLJ
The association between hearing impairment and dementia has emerged as a major public health challenge, with significant opportunities for earlier diagnosis, treatment and prevention. However, the ...nature of this association has not been defined. We hear with our brains, particularly within the complex soundscapes of everyday life: neurodegenerative pathologies target the auditory brain, and are therefore predicted to damage hearing function early and profoundly. Here we present evidence for this proposition, based on structural and functional features of auditory brain organization that confer vulnerability to neurodegeneration, the extensive, reciprocal interplay between 'peripheral' and 'central' hearing dysfunction, and recently characterized auditory signatures of canonical neurodegenerative dementias (Alzheimer's disease, Lewy body disease and frontotemporal dementia). Moving beyond any simple dichotomy of ear and brain, we argue for a reappraisal of the role of auditory cognitive dysfunction and the critical coupling of brain to peripheral organs of hearing in the dementias. We call for a clinical assessment of real-world hearing in these diseases that moves beyond pure tone perception to the development of novel auditory 'cognitive stress tests' and proximity markers for the early diagnosis of dementia and management strategies that harness retained auditory plasticity.
Increases in thermal variability elevate metabolic rate due to Jensen's inequality, and increased metabolic rate decreases the fitness of dormant ectotherms by increasing consumption of stored energy ...reserves. Theory predicts that ectotherms should respond to increased thermal variability by lowering the thermal sensitivity of metabolism, which will reduce the impact of the warm portion of thermal variability. We examined the thermal sensitivity of metabolic rate of overwintering Erynnis propertius (Lepidoptera: Hesperiidae) larvae from a stable or variable environment reared in the laboratory in a reciprocal common garden design, and used these data to model energy use during the winters of 1973-2010 using meteorological data to predict the energetic outcomes of metabolic compensation and phenological shifts. Larvae that experienced variable temperatures had decreased thermal sensitivity of metabolic rate, and were larger than those reared at stable temperatures, which could partially compensate for the increased energetic demands. Even with depressed thermal sensitivity, the variable environment was more energy-demanding than the stable, with the majority of this demand occurring in autumn. Autumn phenology changes thus had disproportionate influence on energy consumption in variable environments, and variable-reared larvae were most susceptible to overwinter energy drain. Therefore the energetic impacts of the timing of entry into winter dormancy will strongly influence ectotherm fitness in northern temperate environments. We conclude that thermal variability drives the expression of metabolic suppression in this species; that phenological shifts will have a greater impact on ectotherms in variable thermal environments; and that E. propertius will be more sensitive to shifts in phenology in autumn than in spring. This suggests that increases in overwinter thermal variability and/or extended, warm autumns, will negatively impact all non-feeding dormant ectotherms which lack the ability to suppress their overwinter metabolic thermal sensitivity.
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