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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 NTRS1976

Mathematical modeling of inhalation exposure

The paper presents a mathematical model of inhalation exposure in which uptake, distribution and excretion are described by exponential functions, while rate constants are determined by tissue volumes, blood perfusion and by the solubility of vapors (partition coefficients). In the model, tissues are grouped into four pharmokinetic compartments. The model is used to study continuous and interrupted chronic exposures and is applied to the inhalation of Forane and methylene chloride.

Fiserova-Bergerova, V.↗
NASA NTRS1974

A study of the biological effect of continuous inhalation exposure of 1, 1, 1-trichloroethene (methyl chloroform) on animals

The effects of continuous exposure to 1,1,1-trichloroethane on hepatic morphology and function are evaluated and compared with those produced by methylene chloride (dichloromethane) to determine environmental concentrations of each compound that would produce a similar biological response, i.e., a comparable increase in liver triglycerides over control levels. Experimental findings on mice, rats, dogs, and monkeys indicate that the pathological alternations observed with 1,1,1-trichloroethane are similar to those observed with dichloromethane except for different time courses of the effects and different degrees of recovery. A ten fold greater atmospheric concentration of 1,1,1-trichloroethane is required to produce the minimal liver changes found at 100 ppm dichloromethane.

Macewen, J. D.↗
NASA NTRS1974

Hepatic pathology in mice after continuous inhalation exposure to 1, 1, 1-trichloroethane

Mice exposed to either 250ppm or 1,000ppm 1,1,1-trichloroethane in air continuously for 14 weeks demonstrated significant changes in the centrilobular hepatocytes for the 1,000ppm group. Moderate liver triglyceride accumulation was evident in the 1,000ppm group and peaked at 40mg/gm of tissue after 7 weeks of exposure. Focal hepatocyte necrosis occurred in 40% of the mice exposed to 1,000ppm for 12 weeks. This necrosis was associated with an acute inflammatory infiltrate and hypertrophy of Kupffer cells. These findings indicate that the pathological alternations observed with 1,1,1-trichloroethane are similar to those observed with dichloromethane except for different time courses of the effects and different degrees of recovery. The toxic effects of 1,1,1-trichloroethane are of a similar type to those produced by carbon tetrachloride but appear much less severe.

Mcnutt, N. S.↗
NASA NTRS2000

Comparative Study in Laboratory Rats to Validate Sperm Quality Methods and Endpoints

Abstract The Naval Health Research Center, Detachment (Toxicology) performs toxicity studies in laboratory animals to characterize the risk of exposure to chemicals of Navy interest. Research was conducted at the Toxicology Detachment at WPAFB, OH in collaboration with Wright State University, Department of Biological Sciences for the validation of new bioassay methods for evaluating reproductive toxicity. The Hamilton Thorne sperm analyzer was used to evaluate sperm damage produced by exposure to a known testicular toxic agent, methoxyacetic acid and by inhalation exposure to JP-8 and JP-5 in laboratory rats. Sperm quality parameters were evaluated (sperm concentration, motility, and morphology) to provide evidence of sperm damage. The Hamilton Thorne sperm analyzer utilizes a DNA specific fluorescent stain (similar to flow cytometry) and digitized optical computer analysis to detect sperm cell damage. The computer assisted sperm analysis (CASA) is a more rapid, robust, predictive and sensitive method for characterizing reproductive toxicity. The results presented in this poster report validation information showing exposure to methoxyacetic acid causes reproductive toxicity and inhalation exposure to JP-8 and JP-5 had no significant effects. The CASA method detects early changes that result in reproductive deficits and these data will be used in a continuing program to characterize the toxicity of chemicals, and combinations of chemicals, of military interest to formulate permissible exposure limits.

Price, W. A.↗
DOE OSTI2024

Systemic immunological responses are dependent on sex and ovarian hormone presence following acute inhaled woodsmoke exposure

Background: Rural regions of the western United States have experienced a noticeable surge in both the frequency and severity of acute wildfire events, which brings significant challenges to both public safety and environmental conservation efforts, with impacts felt globally. Identifying factors contributing to immune dysfunction, including endocrinological phenotypes, is essential to understanding how hormones may influence toxicological susceptibility. Methods: This exploratory study utilized male and female C57BL/6 mice as in vivo models to investigate distinct responses to acute woodsmoke (WS) exposure with a focus on sex-based differences. In a second set of investigations, two groups were established within the female mouse cohort. In one group, mice experienced ovariectomy (OVX) to simulate an ovarian hormone-deficient state similar to surgical menopause, while the other group received Sham surgery as controls, to investigate the mechanistic role of ovarian hormone presence in driving immune dysregulation following acute WS exposure. Each experimental cohort followed a consecutive 2-day protocol with daily 4-h exposure intervals under two conditions: control HEPA-filtered air (FA) and acute WS to simulate an acute wildfire episode. Results: Metals analysis of WS particulate matter (PM) revealed significantly increased levels of 63 Cu, 182 W, 208 Pb, and 238 U, compared to filtered air (FA) controls, providing insights into the specific metal components most impacted by the changing dynamics of wildfire occurrences in the region. Male and female mice exhibited diverse patterns in lung mRNA cytokine expression following WS exposure, with males showing downregulation and females displaying upregulation, notably for IL-1β, TNF-α, CXCL-1, CCL-5, TGF-β, and IL-6. After acute WS exposure, there were notable differences in the responses of macrophages, neutrophils, and bronchoalveolar lavage (BAL) cytokines IL-10, IL-6, IL-1β, and TNF-α. Significant diverse alterations were observed in BAL cytokines, specifically IL-1β, IL-10, IL-6, and TNF-α, as well as in the populations of immune cells, such as macrophages and polymorphonuclear leukocytes, in both Sham and OVX mice, following acute WS exposure. These findings elucidated the profound influence of hormonal changes on inflammatory outcomes, delineating substantial sex-related differences in immune activation and revealing altered immune responses in OVX mice due to ovarian hormone deficiency. In addition, the flow cytometry analysis highlighted the complex interaction between OVX surgery, acute WS exposure, and their collective impact on immune cell populations within the hematopoietic bone marrow niche. Conclusions: In summary, both male and female mice, alongside females subjected to OVX and those who had sham surgery, exhibit significant variations in the expression of proinflammatory cytokines, chemokines, lung mRNA gene expression, and related functional networks linked to signaling pathways. These differences potentially act as mediators of sex-specific and hormonal influences in the systemic inflammatory response to acute WS exposure during a wildfire event. Understanding the regulatory roles of genes expressed differentially under environmental stressors holds considerable implications, aiding in identifying sex-specific therapeutic targets for addressing acute lung inflammation and injury.

59 BASIC BIOLOGICAL SCIENCES↗
DOE OSTI2024

Systemic immunological responses are dependent on sex and ovarian hormone presence following acute inhaled woodsmoke exposure

Rural regions of the western United States have experienced a noticeable surge in both the frequency and severity of acute wildfire events, which brings significant challenges to both public safety and environmental conservation efforts, with impacts felt globally. Identifying factors contributing to immune dysfunction, including endocrinological phenotypes, is essential to understanding how hormones may influence toxicological susceptibility.

59 BASIC BIOLOGICAL SCIENCES↗
DOE OSTI2026

Statistical Uncertainty of Inhalation Dose Coefficients: Impact of Particle Deposition in ICRP 66 Human Respiratory Tract Model

Inhaled radioactive materials can pose a long-term health concern, as the material can be incorporated into the body’s metabolic pathways and remain in organs and tissues for extended durations. During the retention period, the radioactive material may localize in a source organ and irradiate adjacent target organs and tissues. Distribution of these materials changes over time, requiring biokinetic modeling to evaluate their movement through various tissues and organs. The evolving distribution depends on multiple inputs characterizing the inhaled material, such as particle size and size distribution, particle density, aspect ratio, specific radionuclide, the chemical form, and solubility. In addition, biological parameters such as breathing rate, breathing type (nasal or nasal/oral), respiratory system morphometry, tidal volume, functional residual capacity, and anatomical dead space all influence material transport. These aerosol properties and physiological characteristics of the respiratory tract jointly define a range of initial conditions that influence the time-dependent distribution of radioactive material. To evaluate both uncertainty in the initial conditions of inhalation exposure and the final output (committed effective dose) from biokinetic models, a Python-based software tool, Radiological Exposure Dose Calculator (REDCAL), was developed to propagate uncertainty within the human respiratory tract model. Focusing on deposition fraction uncertainty, the primary objective was to characterize the initial activity distribution across respiratory regions as a function of anticipated particle sizes and distributions. The impact of the deposition fraction uncertainty was propagated to committed effective dose coefficients for selected radionuclides in a companion publication. For each particle size, a lognormal distribution, characterized by its geometric mean as defined within ICRP Publication 66, serves as the basis for introducing uncertainty into the physical processes governing deposition in various lung regions. Finally, this study addresses the deposition process and examines how uncertainty in deposition mechanisms affects activity distribution in the airways, ultimately presenting the expected range and standard deviation of deposited activity as a function of particle size.

International Commission on Radiological Protectio↗
NASA NTRS2004

Pulmonary toxicity of single-wall carbon nanotubes in mice 7 and 90 days after intratracheal instillation

Nanomaterials are part of an industrial revolution to develop lightweight but strong materials for a variety of purposes. Single-wall carbon nanotubes are an important member of this class of materials. They structurally resemble rolled-up graphite sheets, usually with one end capped; individually they are about 1 nm in diameter and several microns long, but they often pack tightly together to form rods or ropes of microscopic sizes. Carbon nanotubes possess unique electrical, mechanical, and thermal properties and have many potential applications in the electronics, computer, and aerospace industries. Unprocessed nanotubes are very light and could become airborne and potentially reach the lungs. Because the toxicity of nanotubes in the lung is not known, their pulmonary toxicity was investigated. The three products studied were made by different methods and contained different types and amounts of residual catalytic metals. Mice were intratracheally instilled with 0, 0.1, or 0.5 mg of carbon nanotubes, a carbon black negative control, or a quartz positive control and euthanized 7 d or 90 d after the single treatment for histopathological study of the lungs. All nanotube products induced dose-dependent epithelioid granulomas and, in some cases, interstitial inflammation in the animals of the 7-d groups. These lesions persisted and were more pronounced in the 90-d groups; the lungs of some animals also revealed peribronchial inflammation and necrosis that had extended into the alveolar septa. The lungs of mice treated with carbon black were normal, whereas those treated with high-dose quartz revealed mild to moderate inflammation. These results show that, for the test conditions described here and on an equal-weight basis, if carbon nanotubes reach the lungs, they are much more toxic than carbon black and can be more toxic than quartz, which is considered a serious occupational health hazard in chronic inhalation exposures.

Nanotubes, Carbon/adverse effects↗
NASA NTRS1992

Occupational safety considerations with hydrazine fuels

A simple pharmacokinetic model and a specially designed dermal vapor exposure chamber which provides respiratory protection were used to determine the rate of penetration of hydrazine and 1,1-dimethylhydrazine (UDMH) vapor through the skin of rats. Parameters for the pharmacokinetic model were determined from intravenous and inhalation exposure data. The model was then used to estimate the skin permeation coefficient for hydrazine or UDMH vapor from the dermal-vapor exposure data. This analysis indicates that UDMH vapor has a relatively high permeability through skin (0.7 cm/hr), a value somewhat higher than was obtained for hydrazine by the same procedure (0.09 cm/hr). Based on these skin permeability results, a skin-only vapor exposure limit giving protection equivalent to the inhalation Threshold Limit Value (TLV) could be calculated. The current TLV's for UDMH and hydrazine are 0.5 and 0.1 ppm, respectively. The corresponding skin-only TLV equivalents, for personnel wearing respiratory protection, are 32 ppm for UDMH and 48 ppm for hydrazine. Should the proposed lowering to the TLV's for these compounds to 0.01 ppm be adopted, the equivalent skin-only TLV's would become 0.64 ppm for UDMH and 4.8 for hydrazine.

Clewell, H. J.↗
NASA NTRS1991

Potential health risks from postulated accidents involving the Pu-238 RTG on the Ulysses solar exploration mission

Potential radiation impacts from launch of the Ulysses solar exploration experiment were evaluated using eight postulated accident scenarios. Lifetime individual dose estimates rarely exceeded 1 mrem. Most of the potential health effects would come from inhalation exposures immediately after an accident, rather than from ingestion of contaminated food or water, or from inhalation of resuspended plutonium from contaminated ground. For local Florida accidents (that is, during the first minute after launch), an average source term accident was estimated to cause a total added cancer risk of up to 0.2 deaths. For accidents at later time after launch, a worldwide cancer risk of up to three cases was calculated (with a four in a million probability). Upper bound estimates were calculated to be about 10 times higher.

Goldman, Marvin↗
DOE OSTI2023

Characterization of 3D printing filaments containing metal additives and their particulate emissions

Polylactic acid (PLA) filaments are widely used in fused filament fabrication (FFF) processes (3D printing). Filament additives such as metallic particles incorporated into PLA to modify functional and aesthetic features of print objects are becoming increasingly popular. However, the identities and concentrations of low percentage and trace metals in these filaments have not been well described in either the literature or product safety information included with the product. Here, we report the structures and concentrations of metals in selected Copperfill, Bronzefill and Steelfill filaments. We also report size-weighted number concentrations and size-weighted mass concentrations of particulate emissions as a function of print temperature for each filament. Particulate emissions were heterogenous in shape and size with airborne particles below 50 nm diameter dominating the size-weighted particle concentrations and larger particles (approximately 300 nm) dominating the mass weighted particle concentration. Results indicate that potential exposure to particles in the nano-size range increase when using print temperatures above 200o C. Because inhalation exposure to nanoparticles has been linked to adverse health outcomes, we suggest that using lower print temperatures for specific metal-fill filaments may reduce their operational hazard.

36 MATERIALS SCIENCE↗
NASA NTRS1992

Occupational safety considerations with hydrazine

Hydrazine is a reducing agent that is most commonly used as a propellant and as an oxygen scavenger in boilers. Hydrazine is extremely irritating and has been demonstrated to produce both acute and chronic toxicity. As a result, the established permissible inhalation exposure limits are very low, and respiration protection is required whenever vapors are present. Liquid hydrazine penetrates the skin and produces a chemical burn; therefore, some protective measures must also be taken to protect the skin from liquid contact. Often, however, a cumbersome, whole-body protective suit is worn to protect against skin contact with vapor as well. To what extent it is actually necessary to protect skin from vapor penetration had not previously been demonstrated. In an attempt to answer this question, we conducted a study with rats to compare the dermal penetration of hydrazine vapor with inhalation. Pharmacokinetic modeling was used to compare body burdens resulting from these different routes of exposure. The analysis concluded that the vapor concentration during a skin-only exposure would have to be at least 200 times higher than that during inhalation to achieve the same body burden. This type of estimation illustrates the use of predictive toxicology in occupational exposures.

Clewell, Harvey J., III↗
NASA NTRS1995

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↗
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↗
NASA NTRS1994

Acute, 2-week, and 13-week inhalation toxicity studies on dimethylethoxysilane vapor in Fischer 344 rats

Dimethylethoxysilane (DMES), a volatile liquid, is used by NASA to waterproof the heat-protective silica tiles and blankets on the Space Shuttle. Acute, 2-wk, and 13-wk inhalation exposures to DMES vapor were conducted in male and female Fischer 344 rats. In the acute study, rats were exposed to 4000, 2000, 1000, 500, or 0 (control) ppm DMES for 4 h and observed for 14 days. There were no deaths. Narcosis and ataxia were observed in rats of the two highest concentrations only. These signs disappeared within 1 h following exposure. There were no DMES-related gross or microscopic tissue lesions in rats of all exposure groups. In the 2-wk study, rats were exposed for 6 h/day, 5 days/wk to 3000, 1000, 300, 100, or 0 ppm DMES. During exposure, narcosis was observed in rats of the 3000 and 1000 ppm groups. There was a mild decrease in body weight gain in rats of the 3000 ppm group. A decrease in platelet count, an increase in bile acids, and reduced weights of the thymus, testis, and liver were observed in rats of the 3000 ppm group. Microscopically, hypospermatogenesis and spermatid giant cells were observed in the seminiferous tubules of the testes of rats exposed to 3000 ppm DMES. In the 13-wk study, rats were exposed 6 h/day, 5 days/wk to 2000, 600, 160, 40, or 0 ppm DMES. During exposure, rats of the 2000 ppm group exhibited mild narcosis and loss of startle reflex. Recovery from these central nervous system signs was rapid. Body weights were mildly decreased for rats of the 2000 ppm group. There were no exposure-related effects in hematology, serum chemistry, or urinalysis. Female rats of the 2000 ppm group had delayed estrous cycles (6 days compared to 5 days in control rats). Noteworthy organ weight changes in rats of the 2000 ppm group included decreases in thymus, liver, and testicular weights; however, pathologic lesions were observed in the testes only. Sperm motility, epididymal sperm count, and testicular spermatid count were dramatically reduced. Microscopic lesions included degeneration of the seminiferous tubular cells, pyknosis or absence of germ cells, and hypospermia in the epididymis. Rats of the 600 ppm group had a slight decrease in thymic weight and a transient decrease in body weight. Results of the acute, 2-wk, and 13-wk inhalation studies indicate DMES concentrations of 1000 ppm and higher produce narcosis that rapidly disappears following exposure. Repeated exposure of rats to DMES at either 3000 ppm for 2 wk or 2000 ppm for 13 wk caused testicular atrophy and hypospermia in male rats. Female rats exposed to 2000 ppm for 13 wk had delayed estrous cycles. Toxicological effects in rats of the 600 ppm group were minimal and equivocal. The 160 ppm concentration was a no-observable-effect level (NOEL) for 13 wk of exposure to DMES.

NASA Discipline Number 04-10↗
DOE OSTI2026

Adverse Neurological Effects of Wildfire Smoke

The respiratory and cardiovascular effects of smoke exposure are well documented from cigarette smoking and particulate matter (PM) associated with air-pollution studies, but epidemiological data also suggests exposure to high levels of woodsmoke correlate with central-nervous-system (CNS) dysfunction, including elevated rates of Alzheimer’s disease (AD) and dementia. Neuro-inflammation is believed to initiate the majority of Alzheimer’s and other neurodegenerative diseases attributed to environmental factors. We investigated whether inhaled PM and specific classes of compounds in wildfire smoke condensate extract (WSE) reach the brain and cause neuro-inflammation that can lead to progressive neurological degeneration, using isotope tracing of labeled particulate matter and major compound classes, biomarkers of blood-brain barrier (BBB) integrity, and biomarkers of neuro-inflammation. This project showed that inhalation exposure to PM and major compound classes present in WSE reached the brain through absorption in the nasal cavity and systemic circulation across the BBB. Twenty-four exposures of WSE to brain endothelial cells that form the main physical barrier of the BBB produced dose-dependent increases in biomarkers of inflammation and decreases in tight junction markers between cells. Intranasal exposure to WSE caused inflammatory disfunction in lung and brain. Biomarkers of inflammation increased and an enzyme inhibiting inflammation decreased. Similar patterns of chemical-induced changes in the lung and brain suggest either: (1) chemicals may act through shared molecular pathways upon entering lung and brain, or (2) that mediators originating in the lung circulate systemically to the brain and drive neuroinflammation. These findings warrant further mechanistic studies to delineate the temporal sequence of events to establish the lung-brain axis.

54 ENVIRONMENTAL SCIENCES↗
NASA NTRS2014

Persistent Expression Changes of Fibrosis-Related Genes in the Lung Tissues of Rats Exposed to Lunar Dust Particles

The Moon's surface is covered by a layer of fine, potential reactive dust. Lunar dust contain about 1‐2% of very fine respirable dust (less than 3 micrometers). The habitable area of any lunar landing vehicle and outpost would inevitably be contaminated with lunar dust that could pose a health risk. The purpose of the study is to evaluate the toxicity of Apollo moon dust in rodents to assess the health risk of dust exposures to humans. One of the particular interests in the study is to evaluate dust‐induced changes of the expression of fibrosis‐related genes, and to identify specific signaling pathways involved in lunar dustinduced toxicity. F344 rats were exposed for 4 weeks (6h/d; 5d/wk) in nose‐only inhalation chambers to concentrations of 0 (control air), 2.1, 6.8, 21, and 61 milligrams per cubic meters of lunar dust. Five rats per group were euthanized at 1 day, 1 week, 1 month, and 3 months after the last inhalation exposure. The bronchoalveolar lavage fluid (BALF) was collected by lavaging with phosphate‐buffered saline (PBS). A zymosan‐induced luminolbased chemiluminescence assay was used to assess the activity of BAL cells. The lavaged lung tissue was snap frozen in LN2 and total RNA was isolated using the Qigen RNeasy kit. The expression of 84 fibrosisrelated genes were analyzed using the RT2 Profiler PCR Array technique. The expression of 18 genes of interest were further measured using real‐time PCR technique in all the samples. 10 out of 18 genes of interest showed persistently significant expression changes in the local lung tissue exposed to lunar dust, indicating a prolonged proinflammatory response. The expressions of several of these genes were dose‐ and time‐dependent and were significantly correlated with other pathological parameters. The potential signaling pathways and upstream regulators were further analyzed using IPA pathway analysis tool based on the gene expression data. The data presented in this study, for the first time, explore the molecular mechanisms of lunar dust induced toxicity, contributing not only the risk assessment for future space exploration, but also understandings of the dust‐induced toxicity in humans on earth.

Zhang, Ye↗