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Search indexed NASA NTRS and DOE OSTI research on propulsion, heat transfer, battery materials and energy systems. Follow report and document links to the original sources.

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At least 19 records
All sourcesNASA NTRSDOE OSTI
NASA NTRS2015

Heat-Related Mortality Projections for Cardiovascular and Respiratory Disease Under the Changing Climate in Beijing, China

Because heat-related health effects tend to become more serious at higher temperatures, there is an urgent need to determine the mortality projection of specific heat-sensitive diseases to provide more detailed information regarding the variation of the sensitivity of such diseases. In this study, the specific mortality of cardiovascular and respiratory disease in Beijing was initially projected under five different global-scale General Circulation Models (GCMs) and two Representative Concentration Pathways scenarios (RCPs) in the 2020s, 2050s, and 2080s compared to the 1980s. Multi-model ensembles indicated cardiovascular mortality could increase by an average percentage of 18.4 percent, 47.8 percent, and 69.0 percent in the 2020s, 2050s, and 2080s under RCP 4.5, respectively, and by 16.6 percent, 73.8 percent and 134 percent in different decades respectively, under RCP 8.5 compared to the baseline range. The same increasing pattern was also observed in respiratory mortality. The heat-related deaths under the RCP 8.5 scenario were found to reach a higher number and to increase more rapidly during the 21st century compared to the RCP4.5 scenario, especially in the 2050s and the 2080s. The projection results show potential trends in cause-specific mortality in the context of climate change, and provide support for public health interventions tailored to specific climate-related future health risks.

health↗
DOE OSTI2024

Generalizability of heat-related health risk associations observed in a large healthcare claims database of patients with commercial health insurance

Extreme ambient heat is unambiguously associated with higher risk of illness and death. The Optum Labs Data Warehouse (OLDW), a database of medical claims from US-based patients with commercial or Medicare Advantage health insurance, has been used to quantify heat-related health impacts. Whether results for the insured sub-population are generalizable to the broader population has to our knowledge not been documented. We sought to address this question, for the US population in California from 2012 to 2019. We examined changes in daily rates of emergency department (ED) encounters and in-patient hospitalization encounters for all-causes, heat-related outcomes, renal disease, mental/behavioral disorders, cardiovascular disease, and respiratory disease. OLDW was the source for health data for insured individuals in California, and health data for the broader population were gathered from the California Department of Health Care Access and Information (HCAI). We defined extreme heat exposure as any day in a group of 2 or more days with maximum temperatures exceeding the county-specific 97.5 th percentile and used a space-time-stratified case–crossover design to assess and compare the impacts of heat on health. Average incidence rates of medical encounters differed by dataset. However, rate ratios for ED encounters were similar across datasets for all causes (ratio of incidence rate ratios (rIRR) = 0.989; 95% confidence interval (CI) = 0.973, 1.011), heat-related causes (rIRR = 1.080; 95% CI = 0.999, 1.168), renal disease (rIRR = 0.963; 95% CI = 0.718, 1.292), and mental health disorders (rIRR = 1.098; 95% CI = 1.004, 1.201). Rate ratios for inpatient encounters were also similar. This work presents evidence that OLDW can continue to be a resource for estimating the health impacts of extreme heat.

54 ENVIRONMENTAL SCIENCES↗
NASA NTRS2012

Paramyxovirus Infection Mimics In Vivo Cellular Dynamics in Three-Demensional Human Bronchio-Epithelial Tissue-Like Assemblies

Respiratory syncytial virus and parainfluenza virus cause severe respiratory disease, especially in infants, children and the elderly. An in vitro model that accurately mimics infection of the human respiratory epithelium (HRE) would facilitate vaccine development greatly. Monolayer cultures traditionally used to study these viruses do not accurately and precisely differentiate the replication efficiencies of wild type and attenuated viruses. Therefore, we engineered novel three-dimensional (3D) tissue-like assemblies (TLAs) of human broncho-epithelial (HBE) cells to produce a more physiologically relevant in vitro model of the HRE. TLAs resemble HRE structurally and by expression of differentiated epithelial cell markers. Most significantly, wild type viruses exhibited a clear growth advantage over attenuated strains in TLAs unlike monolayer cultures. In addition, the TLAs responded to virus infection by secreting pro-inflammatory mediators similar to the respiratory epithelia of infected children. These characteristics make the TLA model a valuable platform technology to develop and evaluate live, attenuated respiratory virus vaccine candidates for human use. Respiratory virus diseases, the most frequent and least preventable of all infectious diseases, range in severity from the common cold to severe bronchiolitis and pneumonia . Two paramyxoviruses, respiratory syncytial virus (RSV) and parainfluenza virus type 3 (PIV3), are responsible for a majority of the most severe respiratory diseases of infants and young children. RSV causes 70% of all bronchiolitis cases and is a major cause of morbidity and mortality worldwide, especially in infants. PIV3 causes 10-15% of bronchiolitis and pneumonia during infancy, second only to RSV, and 40% of croup in infants To date, licensed vaccines are not available to prevent these respiratory diseases. At present, traditional monkey kidney (Vero and LLC-MK2) and human (HEp-2) tissue culture cells and small animal models (mouse, cotton rat, guinea pig, ferret, and hamster) fail to accurately imitate viral replication and human disease states (8). Lacking an authentic model has impeded the development and evaluation of live, attenuated vaccine candidates. Development of a physiologically relevant in vitro tissue culture model that reproduces characteristics of the HRE, the primary target of RSV and PIV3, would aid in predicting clinical attenuation and safety of vaccine candidates. Successful tissue engineering of a 3D human intestinal model using novel NASA technology inspired the development of a tri-culture 3D model for the HRE. Sequential layering of primary mesenchymal cells (comprised of normal human fibroblasts and endothelial cells) followed by BEAS-2B epithelial cells derived from human bronchi and tracheae were recapitulated on Cultisphere and/or cytodex3 microcarriers in cylindrical vessels that rotate horizontally creating an organized epithelial structure. Horizontal rotation randomizes the gravity vector modeling aspects of microgravity. Mesenchymal and epithelial cells grown under these conditions reproduce the structural organization, multi-cellular complexity, and differentiation state of the HRE. The opportunity to study respiratory viruses in a nasal epithelium model is invaluable because the most promising respiratory virus vaccine candidates are live attenuated viruses for intranasal administration. Here we characterize the interactions of respiratory viruses and epithelial cells grown under modeled microgravity in comparison to gravity-ladened monolayers. 3D HBE TLAs and traditional monolayers (2D) are infected at 35 C, the upper temperature of the upper HRE, to simulate in vivo infection conditions. Growth kinetics of wild type (wt) RSV and PIV3 viruses were compared in 2D and 3D cells to that of strains attenuated in humans or rhesus macaques. This novel 3D HBE model also offers an opportunity to study whether the epithelial cell function, especially in host defenses recapitulated by mimicking the structural organization of the HRE. In vivo, airway epithelial cells play a significant and dynamic role in host defense by blocking paracellular permeability and modulating airway function through cellular interactions or tight junctions. As regulators of the innate immune response, epithelial cells constitutively express cytokines, chemokines, and colony stimulating factors including RANTES, IL-8, IL-6, GM-CSF, and G-CSF for proactive host defense. In response to viral infection, epithelial cells induce potent immuno-modulatory and pro-inflammatory cytokines that recruit phagocytic and inflammatory cells to clear the virus and enhance protection. Although disease pathogenesis is classically attributed to the cytopathic effects of the pathogen, severe disease states associated with RSV and PIV3 are attributed to the inflammatory response, especially in infants. RSV is a potent inducer of cytokines and pro-inflammatory mediators in epithelial cells in vivo. A differentiated human epithelial model independent of the complete functional immune system will help elucidate the role of epithelial cells in respiratory disease. We reported here, virus and host cell interactions in 3D HBE TLAs are similar to that in vivo. Because the epithelial cell organization of the TLAs impacts not only the expression of airway epithelial characteristics, but also cellular communication, the TLAs represent a more physiologically relevant model of the HRE than BEAS-2B or other non-tumour monolayer models of respiratory disease. As a result, wild type respiratory viruses have a clear growth advantage over attenuated viruses in TLAs unlike traditional monolayers. In addition, the TLAs respond to wild type virus infection by secreting pro-inflammatory mediators characteristic of infected HRE. TLAs expressing microbial defense mechanisms provide an excellent model to study the interactions of respiratory pathogens with their host and to identify the innate immunity mediators. Therefore, 3D HBE TLAs offer advantages for the study of respiratory viruses and the development of viral vaccine candidates.

Deatly, Anne M.↗
NASA NTRS2003

Land Use and Land Cover Change, Urban Heat Island Phenomenon, and Health Implications: A Remote Sensing Approach

Land use and land cover maps of Atlanta Metropolitan Area in Georgia were produced from Landsat MSS and TM images for 1973,1979,1983,1987,1992, and 1997, spanning a period of 25 years. Dramatic changes in land use and land cover have occurred with loss of forest and cropland to urban use. In particular, low-density urban use, which includes largely residential use, has increased by over 119% between 1973 and 1997. These land use and land cover changes have drastically altered the land surface characteristics. An analysis of Landsat images revealed an increase in surface temperature and a decline in NDVI from 1973 to 1997. These changes have forced the development of a significant urban heat island effect and an increase in ground level ozone production to such an extent, that Atlanta has violated EPA's ozone level standard in recent years. The urban heat island initiated precipitation events that were identified between 1996 and 2000 tended to occur near high-density urban areas but outside the I-285 loop that traverses around the Central Business District, i.e. not in the inner city area, but some in close proximity to the highways. The health implications were investigated by comparing the spatial patterns of volatile organic compounds (VOC) and nitrogen oxides (NOx) emissions, the two ingredients that form ozone by reacting with sunlight, with those of rates of cardiovascular and chronic lower respiratory diseases. A clear core-periphery pattern was revealed for both VOC and NOx emissions, but the spatial pattern was more random in the cases of rates of cardiovascular and chronic lower respiratory diseases. Clearly, factors other than ozone pollution were involved in explaining the rates of these diseases. Further research is therefore needed to understand the health geography and its relationship to land use and land cover change as well as urban heat island effect. This paper illustrates the usefulness of a remote sensing approach for this purpose.

Lo, C. P.↗
DOE OSTI2025

Dysregulation of lung epithelial cell homeostasis and immunity contributes to Middle East respiratory syndrome coronavirus disease severity

Coronaviruses (CoV) emerge suddenly from animal reservoirs to cause novel diseases in new hosts. Discovered in 2012, the Middle East respiratory syndrome coronavirus (MERS-CoV) is endemic in camels in the Middle East and is continually causing local outbreaks and epidemics. While all three newly emerging human CoVs from the past 20 years (SARS-CoV, SARS-CoV-2, and MERS-CoV) cause respiratory disease, each CoV has unique host interactions that drive differential pathogeneses. To better understand the virus and host interactions driving lethal MERS-CoV infection, we performed a longitudinal multi-omics analysis of sublethal and lethal MERS-CoV infection in mice. Significant differences were observed in body weight loss, virus titers, and acute lung injury among lethal and sub-lethal virus doses. Virus-induced apoptosis of type I and II alveolar epithelial cells suggests that loss or dysregulation of these key cell populations was a major driver of severe disease. Omics analysis suggested differential pathogenesis was multi-factorial with clear differences among innate and adaptive immune pathways as well as those that regulate lung epithelial homeostasis. Infection of mice lacking functional T and B cells showed that adaptive immunity was important in controlling viral replication but also increased pathogenesis. In summary, we provide a high-resolution host response atlas for MERS-CoV infection and disease severity. Multi-omics studies of viral pathogenesis offer a unique opportunity to not only better understand the molecular mechanisms of disease but also to identify genes and pathways that can be exploited for therapeutic intervention all of which is important for our future pandemic preparedness.

MERS-CoV↗
DOE OSTI2024

Characterization of Histophilus somni sialic acid uptake mutant (Δ nanP -Δ nanU ) using a mouse septicemia and mortality model

Histophilus somni is an important pathogen of the bovine respiratory disease complex, yet the mechanisms underlying its virulence remain poorly understood. It is known that H. somni can incorporate sialic acid into lipooligosaccharide (LOS), and sialylated H. somni is more resistant to phagocytosis and complement-mediated killing by serum compared to non-sialylated bacteria in vitro. However, the virulence of non-sialylated H. somni has not been evaluated in vivo using an animal model. In this study, we investigated the contribution of sialic acid to virulence by constructing an H. somni sialic acid uptake mutant (ΔnanP-ΔnanU) and comparing the parent and mutant strains in a mouse septicemia and mortality model. Intraperitoneal challenge of mice with wildtype H. somni (1 × 10 8 colony forming units/mouse, CFU) was lethal to all animals. Mice challenged with three different doses (1, 2, or 5 × 108 CFU/mouse) of an H. somni ΔnanP-ΔnanU sialic acid uptake mutant exhibited survival rates of 90 %, 60 %, and 0 % respectively. High-performance anion exchange chromatography analyses revealed that LOS prepared from both parent and the ΔnanP-ΔnanU mutant strains of H. somni were sialylated. These findings suggest the presence of de novo sialic acid synthesis pathway, although the genes associated with de novo sialic acid synthesis (neuB and neuC) were not identified by genomic analysis. The lower attenuation in mice is most likely attributed to the sialylated LOS of H. somni nanPU mutant.

59 BASIC BIOLOGICAL SCIENCES↗
DOE OSTI2024

Misclassification of causes of death among a small all-autopsied group of former nuclear workers: Death certificates vs. autopsy reports

The U.S. Transuranium and Uranium Registries performs autopsies on each of its deceased Registrants as a part of its mission to follow up occupationally-exposed individuals. This provides a unique opportunity to explore death certificate misclassification errors, and the factors that influence them, among this small population of former nuclear workers. Underlying causes of death from death certificates and autopsy reports were coded using the 10 th revision of the International Classification of Diseases (ICD-10). These codes were then used to quantify misclassification rates among 268 individuals for whom both full autopsy reports and death certificates with legible underlying causes of death were available. When underlying causes of death were compared between death certificates and autopsy reports, death certificates correctly identified the underlying cause of death’s ICD-10 disease chapter in 74.6% of cases. The remaining 25.4% of misclassified cases resulted in over-classification rates that ranged from 1.2% for external causes of mortality to 12.2% for circulatory disease, and under-classification rates that ranged from 7.7% for external causes of mortality to 47.4% for respiratory disease. Neoplasms had generally lower misclassification rates with 4.3% over-classification and 13.3% under-classification. A logistic regression revealed that the odds of a match were 2.8 times higher when clinical history was mentioned on the autopsy report than when it was not. Similarly, the odds of a match were 3.4 times higher when death certificates were completed using autopsy findings than when autopsy findings were not used. This analysis excluded cases where it could not be determined if autopsy findings were used to complete death certificates. The findings of this study are useful to investigate the impact of death certificate misclassification errors on radiation risk estimates and, therefore, improve the reliability of epidemiological studies.

63 RADIATION, THERMAL, AND OTHER ENVIRON. POLLUTAN↗
NASA NTRS2012

Use of Giovanni System in Public Health Application

The role of environment and climate in propagating infectious disease has long been recognized since the 5th century. The effect is particularly evident in vector-borne diseases such as malaria where temperature, precipitation and humidity influence the lifecycle of the pathogens and mosquitoes. Likewise, the transmission of respiratory diseases is also often associated with climatic factors. For example, a recent study showed that low humidity and temperature provides efficient condition for seasonal influenza transmission. Understanding of how environment and climate affect infectious diseases would essentially provide guides to prevent and control the spread of disease. Toward this end, our group has developed models for infectious disease risk such as for malaria, dengue and influenza that are driven by climatic and environmental inputs. Results will be presented, especially those that used TRMM data from GIOVANNI.

Soebiyanto, Radina↗
DOE OSTI2024

Emergency department visits in California associated with wildfire PM 2.5 : differing risk across individuals and communities

The threats to human health from wildfires and wildfire smoke (WFS) in the United States (US) are increasing due to continued climate change. A growing body of literature has documented important adverse health effects of WFS exposure, but there is insufficient evidence regarding how risk related to WFS exposure varies across individual or community level characteristics. To address this evidence gap, we utilized a large nationwide database of healthcare utilization claims for emergency department (ED) visits in California across multiple wildfire seasons (May through November, 2012–2019) and quantified the health impacts of fine particulate matter <2.5 μm (PM 2.5 ) air pollution attributable to WFS, overall and among subgroups of the population. We aggregated daily counts of ED visits to the level of the Zip Code Tabulation Area (ZCTA) and used a time-stratified case-crossover design and distributed lag non-linear models to estimate the association between WFS and relative risk of ED visits. We further assessed how the association with WFS varied across subgroups defined by age, race, social vulnerability, and residential air conditioning (AC) prevalence. Over a 7 day period, PM 2.5 from WFS was associated with elevated risk of ED visits for all causes (1.04% (0.32%, 1.71%)), non-accidental causes (2.93% (2.16%, 3.70%)), and respiratory disease (15.17% (12.86%, 17.52%)), but not with ED visits for cardiovascular diseases (1.06% (–1.88%, 4.08%)). Analysis across subgroups revealed potential differences in susceptibility by age, race, and AC prevalence, but not across subgroups defined by ZCTA-level Social Vulnerability Index scores. These results suggest that PM 2.5 from WFS is associated with higher rates of all cause, non-accidental, and respiratory ED visits with important heterogeneity across certain subgroups. Notably, lower availability of residential AC was associated with higher health risks related to wildfire activity.

54 ENVIRONMENTAL SCIENCES↗
NASA NTRS1974

Studies on disease transmission in spacecraft environments

The effects of the Skylab gas mixtures on general health and immunocompetence of mice and ferrets subjected to the Skylab space cabin environment (SCE) were initially studied in a stainless steel low pressure facility which was maintained at gas ratios of 30% nitrogen and 70% oxygen under 5 psia, and which consisted of two subchambers, that permitted mutual isolation of experimental groups and/or selective removal of animals without return of the entire cabin to ambient pressure was developed. The studies demonstrated that ferrets immunized with Brucella Strain 19 prior to being housed in SCE had decreased synthesis of IgG compared to their respective controls. The possibility of latent infections being responsible for stress-induced upper respiratory diseases of astronauts required that the role of neutralizing antibody as a function of antibody affinity/avidity be investigated. The model consisted of Aleutian disease virus (ADV) which infects ferrets and mink resulting in nonneutralized immune complexes. These studies demonstrated that early antibody to ADV had lower affinity/avidity than late antibody with respect to chronicity. These studies culminated in a description of antibody affinity, first isolation of ADV and its cultivation in vitro.

Kenyon, A. J.↗
NASA NTRS2010

Benefits of Using Remote Sensing for Health Alerts and Chronic Respiratory Exposures

Respiratory diseases such as asthma can be triggered by environmental conditions that can be monitored using Earth observing data and environmental forecast models. Frequent dust storms in the southwestern United States, the annual cycle of juniper pollen events in the spring, and increased aerosol and ozone concentrations in summer, are health concerns shared by the community at large. Being able to forecast the occurrence of these events would help the health care community prepare for increased visits to emergency rooms, as well as allow public health officials to issue alerts to affected persons. This information also is important to epidemiologists for analyzing long-term trends and impacts of these events on the health and well-being of the community. Earth observing data collected by remote sensing platforms are important for improving the performance of models that can forecast these events, and in turn, improve products and information for decision-making by public health authorities. This presentation will discuss the benefits of using remote sensing data for forecasting environmental events that can adversely affect individuals with respiratory ailments. The presentations will include a brief discussion on relevant Earth observing data, the forecast models used, and societal benefits of the resulting products and information. Several NASA-funded projects will be highlighted as examples

Luvall, J. C.↗
DOE OSTI2025

Acute Exposure to Aerosolized Nanoplastics Modulates Redox-Linked Immune Responses in Human Airway Epithelium

Micro- and nanoplastics (MPs and NPs) are pervasive environmental pollutants detected in aquatic ecosystems, with emerging evidence suggesting their presence in airborne particles generated by water body motion. Inhalation exposure to airborne MPs and NPs remains understudied despite documented links between occupational exposure to these particles and adverse respiratory outcomes, including airway inflammation, oxidative stress, and chronic respiratory diseases. This study explored the effects of acute NP exposure on a fully differentiated 3D human airway epithelial model derived from 14 healthy donors. Airway epithelium was exposed to aerosolized 50 nm polystyrene NPs at concentrations ranging from 2.5 to 2500 µg/mL for three minutes per day over three days. Functional assays revealed no significant alterations in tissue integrity, cell survival, mucociliary clearance, or cilia beat frequency, suggesting intact epithelial function post-exposure. However, cytokine and chemokine profiling identified a significant five-fold increase in CCL3 (MIP-1α), a neutrophilic chemoattractant, in NP-exposed samples compared to controls. This was corroborated by increased neutrophil chemotaxis in response to conditioned media from NP-exposed tissues, indicating a pro-inflammatory neutrophilic response. Conversely, levels of interleukins (IL-21, IL-2, IL-15), CXCL10, and TGF-β were significantly reduced, suggesting immunomodulatory effects that may impair adaptive immune responses and tissue repair mechanisms. These findings demonstrate that short-term exposure to NP-containing aerosols induces a distinct pro-inflammatory response in airway epithelium, characterized by enhanced neutrophil recruitment and reduced secretion of key immune modulators. These findings underscore the potential for aerosolized NPs to induce oxidative and inflammatory stress, raising concerns about their long-term impact on respiratory health and redox regulation.

Biochemistry & Molecular Biology↗
DOE OSTI2024

A review of antimicrobial implications for improving indoor air quality

The frequent outbreak of infectious respiratory diseases, such as the recent COVID-19 epidemic, raised the importance of indoor air quality. Removing microorganisms from indoor air is critical to improve indoor air quality. Numerous studies in recent years have been published on developing antimicrobial materials and technologies for antibacterial and antiviral applications. Further, this study critically reviews the recent antimicrobial advances for improving indoor air quality. This paper provides a comprehensive analysis of the antimicrobial mechanisms, development of materials, and deployment strategies, as well as a performance evaluation of the antimicrobial implication for indoor air quality. Furthermore, the challenges and opportunities of future research directions are also highlighted.

59 BASIC BIOLOGICAL SCIENCES↗
DOE OSTI2024

The Exoproteome and Surfaceome of Toxigenic Corynebacterium diphtheriae 1737 and Its Response to Iron Restriction and Growth on Human Hemoglobin

Toxin-producing Corynebacterium diphtheriae strains are the etiological agents of the severe upper respiratory disease, diphtheria. A global phylogenetic analysis revealed that biotype gravis is particularly lethal as it produces diphtheria toxin and a range of other virulence factors, particularly when it encounters low levels of iron at sites of infection. Here, to gain insight into how it colonizes its host, we have identified iron-dependent changes in the exoproteome and surfaceome of C. diphtheriae strain 1737 using a combination of whole-cell fractionation, intact cell surface proteolysis, and quantitative proteomics. In total, we identified 1414 of the predicted 2265 proteins (62%) encoded by its reference genome. For each protein, we quantified its degree of secretion and surface exposure, revealing that exoproteases and hydrolases predominate in the exoproteome, while the surfaceome is enriched with adhesins, particularly DIP2093. Our analysis provides insight into how components in the heme-acquisition system are positioned, showing pronounced surface exposure of the strain-specific ChtA/ChtC paralogues and high secretion of the species-conserved heme-binding HtaA protein, suggesting it functions as a hemophore. Profiling the response of the exoproteome and surfaceome after microbial exposure to human hemoglobin and iron limitation reveals potential virulence factors that may be expressed at sites of infection. Data are available via ProteomeXchange with identifier PXD051674.

cell envelope↗
DOE OSTI2024

Molecular basis of hemoglobin binding and heme removal in Corynebacterium diphtheriae

To successfully mount infections, nearly all bacterial pathogens must acquire iron, a key metal cofactor that primarily resides within human hemoglobin. Corynebacterium diphtheriae causes the life-threatening respiratory disease diphtheria and captures hemoglobin for iron scavenging using the surface-displayed receptor HbpA. Here, we show using X-ray crystallography, NMR, and in situ binding measurements that C. diphtheriae selectively captures iron-loaded hemoglobin by partially ensconcing the heme molecules of its α subunits. Quantitative growth and heme release measurements are compatible with C. diphtheriae acquiring heme passively released from hemoglobin’s β subunits. We propose a model in which HbpA and heme-binding receptors collectively function on the C. diphtheriae surface to capture hemoglobin and its spontaneously released heme. Acquisition mechanisms that exploit the propensity of hemoglobin’s β subunit to release heme likely represent a common strategy used by bacterial pathogens to obtain iron during infections.

NMR↗