Engineering Papers⌕ Search

SEARCH · Engineering Papers

Results for “LUNGS”

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.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 199 records · Page 11

Space Radiation Cancer, Circulatory Disease and CNS Risks for Near Earth Asteroid and Mars Missions: Uncertainty Estimates for Never-Smokers

The uncertainties in estimating the health risks from galactic cosmic rays (GCR) and solar particle events (SPE) are a major limitation to the length of space missions and the evaluation of potential risk mitigation approaches. NASA limits astronaut exposures to a 3% risk of exposure induced cancer death (REID), and protects against uncertainties in risks projections using an assessment of 95% confidence intervals after propagating the error from all model factors (environment and organ exposure, risk coefficients, dose-rate modifiers, and quality factors). Because there are potentially significant late mortality risks from diseases of the circulatory system and central nervous system (CNS) which are less well defined than cancer risks, the cancer REID limit is not necessarily conservative. In this report, we discuss estimates of lifetime risks from space radiation and new estimates of model uncertainties are described. The key updates to the NASA risk projection model are: 1) Revised values for low LET risk coefficients for tissue specific cancer incidence, with incidence rates transported to an average U.S. population to estimate the probability of Risk of Exposure Induced Cancer (REIC) and REID. 2) An analysis of smoking attributable cancer risks for never-smokers that shows significantly reduced lung cancer risk as well as overall cancer risks from radiation compared to risk estimated for the average U.S. population. 3) Derivation of track structure based quality functions depends on particle fluence, charge number, Z and kinetic energy, E. 4) The assignment of a smaller maximum in quality function for leukemia than for solid cancers. 5) The use of the ICRP tissue weights is shown to over-estimate cancer risks from SPEs by a factor of 2 or more. Summing cancer risks for each tissue is recommended as a more accurate approach to estimate SPE cancer risks. 6) Additional considerations on circulatory and CNS disease risks. Our analysis shows that an individual s history of smoking exposure has a larger impact on GCR risk estimates than amounts of radiation shielding or age at exposure (amongst adults). Risks for never-smokers compared to the average U.S. population are estimated to be reduced between 30% and 60% dependent on model assumptions. Lung cancer is the major contributor to the reduction for never-smokers, with additional contributions from circulatory diseases and cancers of the stomach, liver, bladder, oral cavity and esophagus, and leukemia. The relative contribution of CNS risks to the overall space radiation detriment is potentially increased for never-smokers such as most astronauts. Problems in estimating risks for former smokers and the influence of second-hand smoke are discussed. Compared to the LET approximation, the new track structure derived radiation quality functions lead to a reduced risk for relativistic energy particles and increased risks for intermediate energy particles. Revised estimates for the number of safe days in space at solar minimum for heavy shielding conditions are described for never-smokers and the average U.S. population. Results show that missions to near Earth asteroids (NEA) or Mars violate NASA's radiation safety standards with the current levels of uncertainties. Greater improvements in risk estimates for never-smokers are possible, and would be dependent on improved understanding of risk transfer models, and elucidating the role of space radiation on the various stages of disease formation (e.g. initiation, promotion, and progression).

Cucinotta, Francis A.↗

The Next Generation of Cold Immersion Dry Suit Design Evolution for Hypothermia Prevention

This new utility patent is an active design that relies on the lung's role as an organic heat exchanger for providing deep body core heating of air. It is based on the fact that the greatest heat loss mechanism for an insulated human body immersed in a cold water environment is due to heat loss through respiration. This innovation successfully merges two existing technologies (cold immersion suit and existing valve technologies) to produce a new product that helps prevent against the onset of hypothermia at sea. During normal operations, a human maintains an approximate body temperature of [98.6 F (37 C)]. A mechanism was developed to recover the warm temperature from the body and reticulate it in a survival suit. The primary intention is to develop an encompassing systems design that can both easily and cost effectively be integrated in all existing currently manufactured cold water survival suits, and as such, it should be noted that the cold water immersion suit is only used as a framework or tool for laying out the required design elements. At the heart of the suit is the Warm Air Recovery (WAR) system, which relies on a single, large Main Purge Valve (MPV) and secondary Purge Valves (PV) to operate. The main purge valve has a thin membrane, which is normally closed, and acts as a one-way check valve. When warm air is expelled from the lungs, it causes the main purge valve to open. Air forced from the MPV is dumped directly into the suit, thereby providing warmth to the torso, legs, and arms. A slight positive over-pressure in the suit causes warm waste air (or water if the suit is punctured) to be safely vented into the sea through large PVs located at the bottom of each arm and leg. The secondary purge valves act to prevent the buildup of large concentrations of CO2 gas and help guard against asphyxia. It is noted that the MPV causes the inhalation and exhalation cycles to be completely isolated from one another in the current suit design.

Galofaro, Joel↗

Pulmonary and Systemic Immune Response to Chronic Lunar Dust Inhalation

Background: Due to millennia of meteorite impact with virtually no erosive effects, the surface of the Moon is covered by a layer of ultra‐fine, reactive Lunar dust. Very little is known regarding the toxicity of Lunar dust on human physiology. Given the size and electrostatic characteristics of Lunar dust, countermeasures to ensure non‐exposure of astronauts will be difficult. To ensure astronaut safety during any future prolonged Lunar missions, it is necessary to establish the effect of chronic pulmonary Lunar dust exposure on all physiological systems. Methods: This study assessed the toxicity of airborne lunar dust exposure in rats on pulmonary and system immune system parameters. Rats were exposed to 0, 20.8, or 60.8 mg/m3 of lunar dust (6h/d; 5d/wk) for up to 13 weeks. Sacrifices occurred after exposure durations of 1day, 7 days, 4 weeks and 13 weeks post‐exposure, when both blood and lung lavage fluid were collected for analysis. Lavage and blood assays included leukocyte distribution by flow cytometry, electron/fluorescent microscopy, and cytokine concentration. Cytokine production profiles following mitogenic stimulation were performed on whole blood only. Results: Untreated lavage fluid was comprised primarily of pulmonary macrophages. Lunar dust inhalation resulted in an influx of neutrophils and lymphocytes. Although the percentage of lymphocytes increased, the T cell CD4:CD8 ratio was unchanged. Cytokine analysis of the lavage fluid showed increased levels of IL‐1b and TNFa. These alterations generally persisted through the 13 week sampling. Blood analysis showed few systemic effects from the lunar dust inhalation. By week 4, the peripheral granulocyte percentage was elevated in the treated rats. Plasma cytokine levels were unchanged in all treated rats compared to controls. Peripheral blood analysis showed an increased granulocyte percentage and altered cytokine production profiles consisting of increased in IL‐1b and IL‐6, and decreased IL‐2 production. Conclusion: Lunar dust inhalation results in significant lung inflammation, and some systemic effects, that does not resolve through 13 weeks. Lunar dust may therefore represent a crew health risk during sortie or long‐duration Lunar missions.

Crucian, Brian↗

Characterization of Particulate Matter Profiling and Alveolar Deposition from Biomass Burning in Northern Thailand: The 7-SEAS Study

Biomass burning (BB) frequently occurs in SouthEast Asia (SEA), which significantly affects the air quality and could consequently lead to adverse health effects. The aim of this study was to characterize particulate matter (PM) and black carbon (BC) emitted from BB source regions in SEA and their potential of deposition in the alveolar region of human lungs. A 31-day characterization of PM profiling was conducted at the Doi Ang Khang (DAK) meteorology station in northern Thailand in March 2013. Substantial numbers of PM (10147 +/- 5800 # per cubic centimeter) with a geometric mean diameter (GMD) of 114.4 +/- 9.2 nm were found at the study site. The PM of less than 2.5 micron in aerodynamic diameter (PM sub 2.5) hourly-average mass concentration was 78.0 +/- 34.5 per cubic microgram whereas the black carbon (BC) mass concentration was 4.4 +/- 2.6 micrograms per cubic meter. Notably, high concentrations of nanoparticle surface area (100.5 +/- 54.6 square micrometers per cubic centimeter) emitted from biomass burning can be inhaled into the human alveolar region. Significant correlations with fire counts within different ranges around DAK were found for particle number, the surface area concentration of alveolar deposition, and BC. In conclusion, biomass burning is an important PM source in SEA, particularly nanoparticles, which has high potency to be inhaled into the lung environment and interact with alveolar cells, leading to adverse respiratory effects. The fire counts within 100 to 150 km shows the highest Pearson's r for particle number and surface area concentration. It suggests 12 to 24 hr could be a fair time scale for initial aging process of BB aerosols. Importantly, the people lives in this region could have higher risk for PM exposure.

biomass burning↗

GEOS-CF Model Assessment of PM2.5 During Wildfires: Inferring the Impact of PM2.5 Exposure on Adverse Respiratory & Cardiovascular Conditions

Exposure to fine particulate matter (PM2.5) can aggravate pre-existing respiratory and cardiovascular conditions. When PM2.5 is inhaled it can cause damage to the lungs such as reduced lung function and shortness of breath. After being inhaled PM2.5 can enter the bloodstream and cause harm to the heart. One major natural source of PM2.5 exposure is from wildfire smoke. The particulates within the smoke from the wildfires can spread from the initial source region, potentially impacting communities both near and far. During and after wildfire events, PM2.5 levels can exceed the WHO air quality guidelines (10 gm^3 annual mean; 25 gm^3 daily mean), becoming hazardous to an individual's health. Global models can be used to simulate the emission and transport of these particulates and subsequently they can be valuable to air quality forecasting in highly polluted areas. The NASA Goddard Earth Observing System (GEOS) version 5 Composition Forecast (GEOS-CF) system has been used to produce near-real time air quality forecasts of atmospheric composition at a high global resolution of 25 km. The GEOS-CF system utilizes the GEOS weather forecast model coupled with GEOS-Chem (version 11) chemistry module to provide analyses and forecasts of various toxic air pollutants, including PM2.5. The GEOS-CF simulated high levels of PM2.5 (40 gm^3 to 250 gm^3 ), exceeding the WHO guidelines, during multiple recent regional and global wildfire seasons, including the 2017 Seattle, WA and Los Angeles, CA wildfire seasons, and biomass burning events in India. Furthermore, the GEOS-CF simulated PM2.5 applied to a human health assessment model, BenMAP (The Environmental Benefits Mapping and Analysis Program, version 1.3), estimates the impact on adverse respiratory health conditions due to PM2.5 exposure from wildfires. The GEOS-CF predicted PM2.5 during the wildfire season with the corresponding BenMAP results provides an assessment of the human health impact of PM2.5 exposure.

Saunders, Emily↗

NASA's GEOS Composition Model Assessment of PM2.5 During Wildfires: Inferring the Impact of PM2.5 Exposure on Adverse Respiratory & Cardiovascular Conditions

Particulate matter pollution is a mixture of solid and liquid droplets floating in the air that can lead to reduced air quality and increased adverse health impact. Fine particulate matter (PM2.5) can be emitted into the air from anthropogenic sources such as the burning of fossil fuels, motor vehicles, and powerplant emissions. Exposure to PM2.5 can aggravate pre-existing respiratory and cardiovascular conditions. When PM2.5 is inhaled it can cause damage to the lungs such as reduced lung function and shortness of breath. After being inhaled PM2.5 can enter the bloodstream and cause harm to the heart. One major natural source of PM2.5 exposure is from wildfire smoke. The particulates within the smoke from the wildfires can spread from the initial source region, potentially impacting communities both near and far. During and after wildfire events, PM2.5 levels can exceed the WHO air quality guidelines (10 m.g/m^3 annual mean; 25 m.g/m^3 daily mean), becoming hazardous to an individual's health. Global models can be used to simulate the emission and transport of these particulates and subsequently they can be valuable to air quality forecasting in highly polluted areas. The NASA Goddard Earth Observing System (GEOS) Composition Forecast (GEOS-CF) system has been used to produce near-real time air quality forecasts of atmospheric composition at a high global resolution of 25x25 km2. The GEOS-CF system utilizes the GEOS weather forecast model coupled with GEOS-Chem (version 11) chemistry module to provide analyses and forecasts of various toxic air pollutants, including PM2.5. The GEOS-CF simulated high levels of PM2.5 (40 m.g/m^3 to 250 m.g/m^3 ), exceeding the WHO guidelines, during multiple recent regional and global wildfire seasons, including the 2017 Washington State and Northern and Southern California wildfire seasons. Furthermore, the GEOS-CF simulated PM2.5 applied to a human health assessment model, BenMAP (The Environmental Benefits Mapping and Analysis Program, version 1.3), estimates the impact on adverse respiratory health conditions due to PM2.5 exposure from wildfires. The GEOS-CF predicted PM2.5 during the wildfire season with the corresponding BenMAP results provides an assessment of the human health impact of PM2.5 exposure.

Saunders, Emily↗

Bayesian estimation of dose thresholds

An example is described of Bayesian estimation of radiation absorbed dose thresholds (subsequently simply referred to as dose thresholds) using a specific parametric model applied to a data set on mice exposed to 60Co gamma rays and fission neutrons. A Weibull based relative risk model with a dose threshold parameter was used to analyse, as an example, lung cancer mortality and determine the posterior density for the threshold dose after single exposures to 60Co gamma rays or fission neutrons from the JANUS reactor at Argonne National Laboratory. The data consisted of survival, censoring times and cause of death information for male B6CF1 unexposed and exposed mice. The 60Co gamma whole-body doses for the two exposed groups were 0.86 and 1.37 Gy. The neutron whole-body doses were 0.19 and 0.38 Gy. Marginal posterior densities for the dose thresholds for neutron and gamma radiation were calculated with numerical integration and found to have quite different shapes. The density of the threshold for 60Co is unimodal with a mode at about 0.50 Gy. The threshold density for fission neutrons declines monotonically from a maximum value at zero with increasing doses. The posterior densities for all other parameters were similar for the two radiation types.

NASA Discipline Radiation Health↗

Association of particulate air pollution and acute mortality: involvement of ultrafine particles?

Recent epidemiological studies show an association between particulate air pollution and acute mortality and morbidity down to ambient particle concentrations below 100 micrograms/m3. Whether this association also implies a causality between acute health effects and particle exposure at these low levels is unclear at this time; no mechanism is known that would explain such dramatic effects of low ambient particle concentrations. Based on results of our past and most recent inhalation studies with ultrafine particles in rats, we propose that such particles, that is, particles below approximately 50 nm in diameter, may contribute to the observed increased mortality and morbidity In the past we demonstrated that inhalation of highly insoluble particles of low intrinsic toxicity, such as TiO2, results in significantly increased pulmonary inflammatory responses when their size is in the ultrafine particle range, approximately 20 nm in diameter. However, these effects were not of an acute nature and occurred only after prolonged inhalation exposure of the aggregated ultrafine particles at concentrations in the milligrams per cubic meter range. In contrast, in the course of our most recent studies with thermodegradation products of polytetrafluoroethylene (PTFE) we found that freshly generated PTFE fumes containing singlet ultrafine particles (median diameter 26 nm) were highly toxic to rats at inhaled concentrations of 0.7-1.0 x 10(6) particles/cm3, resulting in acute hemorrhagic pulmonary inflammation and death after 10-30 min of exposure. We also found that work performance of the rats in a running wheel was severely affected by PTFE fume exposure. These results confirm reports from other laboratories of the highly toxic nature of PTFE fumes, which cannot be attributed to gas-phase components of these fumes such as HF, carbonylfluoride, or perfluoroisobutylene, or to reactive radicals. The calculated mass concentration of the inhaled ultrafine PTFE particles in our studies was less than 60 micrograms/m3, a very low value to cause mortality in healthy rats. Aging of the fumes with concomitant aggregation of the ultrafine particles significantly decreases their toxicity. Since ultrafine particles are always present in the urban atmosphere, we suggest that they play a role in causing acute lung injury in sensitive parts of the population.

NASA Discipline Environmental Health↗

Alterations of p53 in tumorigenic human bronchial epithelial cells correlate with metastatic potential

The cellular and molecular mechanisms of radiation-induced lung cancer are not known. In the present study, alterations of p53 in tumorigenic human papillomavirus-immortalized human bronchial epithelial (BEP2D) cells induced by a single low dose of either alpha-particles or 1 GeV/nucleon (56)Fe were analyzed by PCR-single-stranded conformation polymorphism (SSCP) coupled with sequencing analysis and immunoprecipitation assay. A total of nine primary and four secondary tumor cell lines, three of which were metastatic, together with the parental BEP2D and primary human bronchial epithelial (NHBE) cells were studied. The immunoprecipitation assay showed overexpression of mutant p53 proteins in all the tumor lines but not in NHBE and BEP2D cells. PCR-SSCP and sequencing analysis found band shifts and gene mutations in all four of the secondary tumors. A G-->T transversion in codon 139 in exon 5 that replaced Lys with Asn was detected in two tumor lines. One mutation each, involving a G-->T transversion in codon 215 in exon 6 (Ser-->lle) and a G-->A transition in codon 373 in exon 8 (Arg-->His), was identified in the remaining two secondary tumors. These results suggest that p53 alterations correlate with tumorigenesis in the BEP2D cell model and that mutations in the p53 gene may be indicative of metastatic potential.

Non-NASA Center↗

System identification of closed-loop cardiovascular control mechanisms: diabetic autonomic neuropathy

We applied cardiovascular system identification (CSI) to characterize closed-loop cardiovascular regulation in patients with diabetic autonomic neuropathy (DAN). The CSI method quantitatively analyzes beat-to-beat fluctuations in noninvasively measured heart rate, arterial blood pressure (ABP), and instantaneous lung volume (ILV) to characterize four physiological coupling mechanisms, two of which are autonomically mediated (the heart rate baroreflex and the coupling of respiration, measured in terms of ILV, to heart rate) and two of which are mechanically mediated (the coupling of ventricular contraction to the generation of the ABP wavelet and the coupling of respiration to ABP). We studied 37 control and 60 diabetic subjects who were classified as having minimal, moderate, or severe DAN on the basis of standard autonomic tests. The autonomically mediated couplings progressively decreased with increasing severity of DAN, whereas the mechanically mediated couplings were essentially unchanged. CSI identified differences between the minimal DAN and control groups, which were indistinguishable based on the standard autonomic tests. CSI may provide a powerful tool for assessing DAN.

Non-NASA Center↗

Human heart rate variability relation is unchanged during motion sickness

In a study of 18 human subjects, we applied a new technique, estimation of the transfer function between instantaneous lung volume (ILV) and instantaneous heart rate (HR), to assess autonomic activity during motion sickness. Two control recordings of ILV and electrocardiogram (ECG) were made prior to the development of motion sickness. During the first, subjects were seated motionless, and during the second they were seated rotating sinusoidally about an earth vertical axis. Subjects then wore prism goggles that reverse the left-right visual field and performed manual tasks until they developed moderate motion sickness. Finally, ILV and ECG were recorded while subjects maintained a relatively constant level of sickness by intermittent eye closure during rotation with the goggles. Based on analyses of ILV to HR transfer functions from the three conditions, we were unable to demonstrate a change in autonomic control of heart rate due to rotation alone or due to motion sickness. These findings do not support the notion that moderate motion sickness is manifested as a generalized autonomic response.

NASA Discipline Neuroscience↗

Linear and nonlinear ARMA model parameter estimation using an artificial neural network

This paper addresses parametric system identification of linear and nonlinear dynamic systems by analysis of the input and output signals. Specifically, we investigate the relationship between estimation of the system using a feedforward neural network model and estimation of the system by use of linear and nonlinear autoregressive moving-average (ARMA) models. By utilizing a neural network model incorporating a polynomial activation function, we show the equivalence of the artificial neural network to the linear and nonlinear ARMA models. We compare the parameterization of the estimated system using the neural network and ARMA approaches by utilizing data generated by means of computer simulations. Specifically, we show that the parameters of a simulated ARMA system can be obtained from the neural network analysis of the simulated data or by conventional least squares ARMA analysis. The feasibility of applying neural networks with polynomial activation functions to the analysis of experimental data is explored by application to measurements of heart rate (HR) and instantaneous lung volume (ILV) fluctuations.

NASA Discipline Regulatory Physiology↗

Alveolar ventilation to perfusion heterogeneity and diffusion impairment in a mathematical model of gas exchange

This study describes a two-compartment model of pulmonary gas exchange in which alveolar ventilation to perfusion (VA/Q) heterogeneity and impairment of pulmonary diffusing capacity (D) are simultaneously taken into account. The mathematical model uses as input data measurements usually obtained in the lung function laboratory. It consists of two compartments and an anatomical shunt. Each compartment receives fractions of alveolar ventilation and blood flow. Mass balance equations and integration of Fick's law of diffusion are used to compute alveolar and blood O2 and CO2 values compatible with input O2 uptake and CO2 elimination. Two applications are presented. The first is a method to partition O2 and CO2 alveolar-arterial gradients into VA/Q and D components. The technique is evaluated in data of patients with chronic obstructive pulmonary disease (COPD). The second is a theoretical analysis of the effects of blood flow variation in alveolar and blood O2 partial pressures. The results show the importance of simultaneous consideration of D to estimate VA/Q heterogeneity in patients with diffusion impairment. This factor plays an increasing role in gas alveolar-arterial gradients as severity of COPD increases. Association of VA/Q heterogeneity and D may produce an increase of O2 arterial pressure with decreasing QT which would not be observed if only D were considered. We conclude that the presented computer model is a useful tool for description and interpretation of data from COPD patients and for performing theoretical analysis of variables involved in the gas exchange process.

NASA Discipline Environmental Health↗