Creation of High-Fluence Precursors by 351-nm Laser Exposure on SiO2 substrates
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Ultra-thin film coatings are used to protect semiconductor photoelectrodes from the harsh chemical environments common to photoelectrochemical energy conversion. These layers add contact transfer resistance to the interface that can result in a reduction of photoelectrochemical energy conversion efficiency of the photoelectrode. Here, we describe the concept of a partial protection layer, which allows for direct chemical access to a small fraction of the semiconductor underlayer for further functionalization by an electrocatalyst. The rest of the interface remains protected by a stable, inert protection layer. CuO is used as a model system for this scheme. Atomic layer deposition (ALD)-prepared TiO 2 layers on CuO thin films prepared from electrodeposited Cu 2 O allow for the control of interfacial morphology to intentionally expose the CuO underlayer. The ALD-TiO 2 overlayer shrinks during crystallization, while Cu 2 O in the underlayer expands during oxidation. As a result, the TiO 2 protection layer cracks to expose the oxidized underlying CuO layer, which can be controlled by preceding thermal oxidation. Furthermore, this work demonstrates a potentially promising strategy for the parallel optimization of photoelectrochemical interfaces for chemical stability and high performance.
X-ray diffraction, electron probe microanalysis, and scanning transmission electron microscopy with focused ion beam lift-out sample preparation techniques were used to study corrosion products in a 304L (UNS S30403) stainless steel fluidized-bed reactor segment from Iowa State University’s Pyrolysis Process Development Unit Facility. This reactor segment is particularly valuable because a detailed history of operation time, temperature, and biomass feedstock was available. As previously reported for a range of stainless steel pyrolysis-related equipment, external scaling and internal attack along alloy grain boundaries were observed. Here, the scaling was primarily associated with O, although S, Ca, K, Si, Mg, and P were also detected in the outer scale regions. However, unlike those other recent advanced characterization analyses, in this instance the internal alloy grain boundary attack was not directly related to S. Rather, only internal oxidation and localized nanoporosity were observed along the alloy grain boundaries, with associated local nanoscale Cr depletion and Ni enrichment. Mechanistic implications of this finding are discussed.
Sodium exposure tests were conducted on the first commercial heat, H58776 of A709 steel. Six different processing and heat treatment conditions were investigated, including three processing conditions, namely, Argon-Oxygen-Decarburization (AOD), Electro-slag Remelting (ESR), and Electro-slag Remelting with subsequent homogenization (HOMO), and two heat treatment conditions, i.e. solution annealing at 1100°C (SA1100°C) or 1150°C (SA1150°C). Specimens of AOD-SA1100°C, AOD-SA1150°C, ESR-SA1100°C, ESR-SA1150°C, HOMO-SA1100°C, and HOMO-SA1150°C were tested in sodium at 650°C and for times up to 10,152 h. Specimens in the AOD-SA1100°C and AOD-SA1150°C conditions were also tested in sodium at 550 and 600°C. Parallel thermal aging experiments were carried out for comparison with sodium exposure tests to separate the thermal and sodium effects. It was found that A709 H58776 generally showed a weight loss after sodium exposures at 650°C except a few data points of the ESR-SA1100°C specimens. The corrosion rate showed large variations in the initial stage and decreased with increasing exposure time. Long-term exposure tests are needed to determine its steady-state corrosion rate. The AOD-SA1100°C and HOMO-SA1100°C specimens showed similar tensile responses after thermal or sodium exposures at 650°C. The yield stress increased, the ultimate tensile strength decreased, and the uniform and total elongations were reduced after thermal or sodium exposures. A longer exposure time had a minimal effect on the tensile strength but further reduced the tensile ductility. The sodium-exposed specimens had higher tensile strength than the thermally-aged specimens. In contrast, the ESR-SA1100°C specimens showed an increase in the yield stress and the ultimate tensile strength after thermal or sodium exposures at 650°C and ~10,000 h. The AOD-SA1150°C and ESR-SA1150°C specimens showed similar tensile behavior after thermal or sodium exposures at 650°C.Thermal or sodium exposures at 650°C increased the yield stress, decreased the ultimate tensile strength, and reduced uniform and total elongations. There were minimal differences in tensile properties between the sodium-exposed and thermally-aged specimens after an ~3000 h exposure. After an exposure for ~10,000 h the sodium-exposed specimens showed higher yield stress and ultimate tensile strength and lower uniform and total elongations than the thermally-aged specimens. For the HOMO-SA1150°C specimens, thermal or sodium exposures at 650°C significantly increased the yield stress but had a minimal effect on the ultimate tensile strength. Both uniform and total elongations were significantly reduced at an exposure time of ~3,000 h, and they were further reduced after an exposure of ~10,000 h. The sodium-exposed specimens had lower tensile ductility than the thermally-aged specimens. Before exposure, the stress-strain curves of the specimens in all six processing-heat treatment conditions showed serrations indicating the dynamic aging effect at 650°C. Thermal aging or sodium exposures at 650°C after ~10,000 h completely removed the serrations of the flow curves in A709 H58776, indicating strong precipitation during thermal or sodium exposures. Longer-term sodium exposure tests are needed to determine the steady-state corrosion rates in sodium for A709 H58776 and fully understand the influence of sodium exposures on its mechanical performance.
Highlights: • The environmental context affects people's mental health. • Environmental exposure assessments are frequently restricted to the neighborhoods in which people currently live. • Dynamic exposures along people's daily paths may trigger mental disorders. • Exposures over people's residential history might affect mental health later in life. • Only dynamic exposure assessments enable the inclusion of the duration and sequence of exposures and risk accumulation over time. It is increasingly recognized that mental disorders are affected by both personal characteristics and environmental exposures. The built, natural, and social environments can either contribute to or buffer against metal disorders. Environmental exposure assessments related to mental health typically rely on neighborhoods within which people currently live. In this article, I call into question such neighborhood-based exposure assessments at one point in time, because human life unfolds over space and across time. To circumvent inappropriate exposure assessments and to better grasp the etiologies of mental disease, I argue that people are exposed to multiple health-supporting and harmful exposures not only during their daily lives, but also over the course of their lives. This article aims to lay a theoretical foundation elucidating the impact of dynamic environmental exposures on mental health outcomes. I examine, first, the possibilities and challenges for mental health research to integrate people's environmental exposures along their daily paths and, second, how exposures over people's residential history might affect mental health later in life. To push the borders of scientific inquiries, I stress that only such mobility-based approaches facilitate an exploration of exposure duration, exposure sequences, and exposure accumulation.
Adequate information on external exposure is often a limiting factor in ecological risk assessments because of a lack of exposure data for free-ranging animals as they interact with a heterogeneous distribution of contaminants. Instead, most wildlife exposure data are estimated from model simulations. However, empirical exposure data are rarely available to verify model results, or to test fundamental assumptions inherent in exposure assessments. We used novel, GPS-coupled radiation dosimeters on reindeer (Rangifer tarandus) to quantify their external exposure for five months in a Chernobyl fallout affected mountainous area of Norway. The exposure data were then used to test a fundamental assumption in screening-level risk assessments: Mean soil contaminant concentrations can be used to conservatively estimate chronic external exposures to representative animals. External exposure and GPS coordinates were obtained hourly and compared to model simulations of exposure based on airborne surveys of 137 Cs soil contamination. Our objectives were to determine 1) if modelled dose estimates based on mean 137 Cs soil concentrations were conservative, and 2) if modelled dose estimates could be improved by adjusting for spatial–temporal heterogeneity of contaminants using 137 Cs concentrations within reindeers’ GPS-defined home ranges and core areas. We found that external exposure modelled from mean soil contaminant concentrations underestimated exposure by 70% compared to empirical measurements from GPS-dosimeter collars worn on individual animals. Using area-weighted mean contaminant levels within the animals’ home range improved the model estimates, but still underestimated the field dosimeter data by 53%. The best estimate of external exposure was obtained when high-use areas within their home range, along with spatial heterogeneity of the contaminant, was accounted for by using area-weighted mean soil contaminant levels within GPS-derived core areas. Accounting for temporal use of core areas within animals’ home range provided a 24% improvement. Here, a comparison of our analyses to similar work performed on Chernobyl wolves found the two studies concur that risk assessors should be cautious in relying on the paradigm of using averaged soil contaminant levels to provide conservative estimates of external exposure to representative individuals. Results of modelled external exposure based on mean soil contaminant concentrations could misguide assessors and cause inappropriate management decisions.
Digital technology has wider exposure latitude and post-processing algorithms which can mask the evidence of underexposure and overexposure. Underexposure produces noisy, grainy images which can impede diagnosis and overexposure results in a greater radiation dose to the patient. These exposure errors can result from inaccurate adjustment of exposure factors in response to changes in patient thickness. This study aims to identify all published radiographic exposure adaptation systems which have been, or are being, used in general radiography and discuss their applicability to digital systems. Studies in EMBASE, MEDLINE, CINAHL and SCOPUS were systematically reviewed. Some of the search terms used were exposure adaptation, exposure selection, exposure technique, 25% rule, 15% rule, DuPont™ Bit System and radiography. A manual journal-specific search was also conducted in The Radiographer and Radiologic Technology. Studies were included if they demonstrated a system of altering exposure factors to compensate for variations in patients for general radiography. Studies were excluded if they focused on finding optimal exposures for an ‘average’ patient or focused on the relationship between exposure factors and dose. The database search uncovered 11 articles and the journal-specific search uncovered 13 articles discussing systems of exposure adaptation. They can be categorised as simple one-step guidelines, comprehensive charts and computer programs. Only two papers assessed the efficacy of exposure adjustment systems. No literature compares the efficacy of exposure adaptations system for film/screen radiography with digital radiography technology nor is there literature on a digital specific exposure adaptation system.
Currently, there are two main scan patterns, including the continuous exposure scan pattern and the point exposure scan pattern, during the selective laser melting (SLM) process. The point exposure scan pattern allows a three-dimensional (3-D) printer to build finer detail features as a static molten pool that is more stable than a dynamic one. However, there has been limited theoretical research on the thermal behavior characteristics during the process in the point exposure scan pattern. Therefore, in this study, the simulation of thermal behavior during SLM of Ti-6Al-4V powder in the point exposure scan pattern was performed. The temperature evolution behavior of different positions and the effects of exposure time on the temperature evolution behavior of different positions, temperature distributions, and dimensions of the molten pool were investigated. The results showed that the direct exposure position and unexposed position had significantly different temperature evolution behaviors under a given condition, and the changed exposure time had the greatest influence on the direct exposure position compared with unexposed position. Moreover, the thermal accumulation effect of a former exposure point on a later one decreased with increasing exposure time. In addition, with the increase of exposure time, the maximum temperature of the molten pool was enhanced and the surface morphology of the molten pool changed from an approximate ellipse to an approximate circle. Besides, the molten pool dimensions were found to increase with exposure time, which indicated that the exposure time played an important role in the stability of the molten pool and the metallurgical bonding in the process. Furthermore, the dimensions of the molten pool and metallurgical bonding in the cross-sectional view were obtained through experiments. Good agreement was obtained when comparing the simulated results with the experimental ones.
Ethyl-N-(2-hydroxyethyl)-perfluorooctanesulfonamide (EtFOSE) was one of the key building blocks for many of the perfluorooctanesulfonyl-based chemistry and laboratory studies have shown that EtFOSE can metabolically degrade to perfluorooctanesulfonate (PFOS). Non-occupational contribution sources to PFOS are thought to occur in general population via diets, drinking water, air and dust. For workers, however, the exposure route was mostly airborne and the exposure source was predominantly to precursor compounds such as EtFOSE. We undertook this study to investigate how much EtFOSE was converted to PFOS in the serum for male rats after 6 h of exposure to EtFOSE vapor (whole body) at ambient temperature, which simulated a work place exposure scenario. There were no abnormal clinical observations and all rats gained weight during study. Interim tail-vein blood samples, collected up to 21 days after exposure, were analyzed for Et-FOSE and PFOS concentrations by LC-MS/MS. Upon inhalation exposure, the biotransformation of EtFOSE to PFOS in serum in the male rats was rapid and very little EtFOSE was detected in the serum within 24 h after EtFOSE exposure. The highest conversion to PFOS in serum after exposure to EtFOSE vapor appeared to occur between Day 8−14 post exposure. Considering the potential surface and fur adsorption of test compound in the whole-body exposure system, our data would support that at least 10% of the inhaled EtFOSE was biotransformed to PFOS in the serum based on the range of lower 95% CI (confidence interval) values. This information is valuable because it quantitatively translates EtFOSE exposure into serum PFOS concentration, which serves as a matrix for internal dosimetry (of PFOS exposure) that can be used as an anchor across species as well as between different exposure routes. - Highlights: • First inhalation study reported in rats that investigates the conversion of a major precursor compound (EtFOSE) to form PFOS. • Systemic absorption of EtFOSE in rats can occur upon inhalation exposure. • Our data suggest that at least 10% of the inhaled EtFOSE can be biotransformed to PFOS in the serum.
Alcohol abuse increases the risk for pancreatitis. The pattern of alcohol drinking may impact its effect. We tested a hypothesis that chronic ethanol consumption in combination with binge exposure imposes more severe damage to the pancreas. C57BL/6 mice were divided into four groups: control, chronic ethanol exposure, binge ethanol exposure and chronic plus binge ethanol exposure. For the control group, mice were fed with a liquid diet for two weeks. For the chronic ethanol exposure group, mice were fed with a liquid diet containing 5% ethanol for two weeks. In the binge ethanol exposure group, mice were treated with ethanol by gavage (5 g/kg, 25% ethanol w/v) daily for 3 days. For the chronic plus binge exposure group, mice were fed with a liquid diet containing 5% ethanol for two weeks and exposed to ethanol by gavage during the last 3 days. Chronic and binge exposure alone caused minimal pancreatic injury. However, chronic plus binge ethanol exposure induced significant apoptotic cell death. Chronic plus binge ethanol exposure altered the levels of alpha-amylase, glucose and insulin. Chronic plus binge ethanol exposure caused pancreatic inflammation which was shown by the macrophages infiltration and the increase of cytokines and chemokines. Chronic plus binge ethanol exposure increased the expression of ADH1 and CYP2E1. It also induced endoplasmic reticulum stress which was demonstrated by the unfolded protein response. In addition, chronic plus binge ethanol exposure increased protein oxidation and lipid peroxidation, indicating oxidative stress. Therefore, chronic plus binge ethanol exposure is more detrimental to the pancreas. - Highlights: • Chronic plus binge alcohol drinking causes more pancreatic injury. • Chronic plus binge alcohol drinking induces more pancreatic inflammation. • Chronic plus binge alcohol causes more endoplasmic reticulum stress and oxidative stress.
INTRODUCTION: Repeated altitude exposures in a single day occur during special operations parachute training, hypobaric chamber training, unpressurized flight, and extravehicular space activity. Inconsistent and contradictory information exists regarding the risk of decompression sickness (DCS) during such hypobaric exposures. HYPOTHESIS: We hypothesized that four short exposures to altitude with and without ground intervals would result in a lower incidence of DCS than a single exposure of equal duration. METHODS: The 32 subjects were exposed to 3 different hypobaric exposures--condition A: 2 h continuous exposure (control); condition B: four 30-min exposures with descent/ascent but no ground interval between the exposures; condition C: four 30-min exposures with descent/ascent and 60 min of ground interval breathing air between exposures. All exposures were to 25,000 ft with 100% oxygen breathing. Subjects were observed for symptoms of DCS, and precordial monitoring of venous gas emboli (VGE) was accomplished with a SONOS 1000 echo-imaging system. RESULTS: DCS occurred in 19 subjects during A (mean onset 70+/-29 min), 7 subjects in B (60+/-34 min), and 2 subjects in C (40+/-18 min). There was a significant difference in DCS incidence between B and A (p = 0.0015) and C and A (p = 0.0002), but no significant difference between B and C. There were 28 cases of VGE in A (mean onset 30+/-23 min), 21 in B (41+/-35 min), and 21 in C (41+/-32 min) with a significant onset curve difference between B and A and between C and A, but not between B and C. Exposure A resulted in four cases of serious respiratory/neurological symptoms, while B had one and C had none. All symptoms resolved during recompression to ground level. CONCLUSION: Data indicate that repeated simulated altitude exposures to 25,000 ft significantly reduce DCS and VGE incidence compared with a single continuous altitude exposure.
Carbon dioxide (CO2) originates from human metabolism and typically remains about 10-fold higher in concentration on the International Space Station (ISS) than at the earth's surface. There have been recurring complaints by crew members of episodes of "mental viscosity" adversely affecting their performance, and there is evidence from the ISS that associates CO2 levels with reports of headaches by crewmembers. Consequently, flight rules have been employed to control CO2 below 3 mm Hg, which is well below the existing Spacecraft Maximum Allowable Concentration (SMAC) of 10 mm Hg for 24-hour exposures, and 5.3 mm Hg for exposures of 7 to 180 days. Headaches, while sometime debilitating themselves, are also symptoms that can provide evidence that physiological defense mechanisms have been breached, and there is evidence that CO2 has effects at levels below the threshold for headaches. This concern appears to be substantiated in reports that CO2 at concentrations below 2 mm Hg substantially reduced some cognitive functions that are associated with the ability to make complex decisions in conditions that are characterized by volatility, uncertainty, complexity, ambiguity, and delayed feedback. These are conditions that could be encountered by crews in off-nominal situations or during the first missions beyond low earth orbit. Therefore, we set out to determine if decision-making under volatile, uncertain, confusing and ambiguous circumstances, where feedback is delayed or absent, is correlated with low levels of CO2 during acute exposures (several hours) in crew-like subjects and to determine if additional cognitive domains are sensitive to concentrations of CO2 at, or below, current ISS levels by using a test battery that is currently available onboard ISS. We enrolled 22 volunteers (8 females, 14 males) between the ages of 30-55 (38.8 +/- 7.0) years whose training and professional experience reflect that of the astronaut corps. Subjects were divided among 4 study groups. Exposures occurred in the 20-foot environmental chamber in Bldg 7 at JSC. Each group was exposed to each of four concentrations of CO2 (600, 1200, 2500, and 5000 ppm), and the exposure order was balanced across the groups which were randomly assigned to 4 possible complete exposure orders. Study participants and investigators were blinded to the exposure order. Each exposure lasted 4 hours and occurred on the same day each week for 4 consecutive weeks. Testing included the Strategic Management Simulation (SMS) methodology and the Cognition battery of psychometric measures that are being utilized aboard the ISS. Subjects participated in a familiarization session one week prior to the start of exposure sessions. Each exposure session followed the schedule noted in Figure 1 below. On the morning of each exposure, subjects completed the Cognition battery in a conference room at indoor ambient CO2 levels. Subjects then entered the exposure chamber and were acclimated to the environment for 15 minutes before completing another round of the Cognition battery. After a 20 minute rest, subject completed the approx.80 minute SMS. Subjects were allowed another 20 minute rest period before completing the final Cognition test battery in the exposure chamber. Subjects then returned to the conference room where they completed one final round of Cognition. Data from both testing methodologies are currently being analyzed and will be presented. Study investigators have not yet been unblinded to the coded exposure concentrations, but preliminary results suggest differences.
Highlights: • Comparing dietary and non-dietary prenatal exposure to BPA and DEHP. • PBPK model predict the fetus’ toxicokinetic profile based on mother exposure. • Non-diet sources exposure contribution is smaller than diet sources. • First-pass metabolism is lacking in dermal and inhalation exposure. • More unconjugated BPA is expected due to a lack of the first-pass metabolism. Bisphenol A (BPA) and Di-(2-ethylhexyl) phthalate (DEHP) are two wide spread chemicals classified as endocrine disruptors (ED). The present study aims to estimate the non-dietary (dermal, non-dietary ingestion and inhalation) exposure to BPA and DEHP for a pregnant women cohort. In addition, to assess the prenatal exposure for the fetus, a physiologically based pharmacokinetic (PBPK) model was used. It was adapted for pregnancy in order to assess the internal dosimetry levels of EDs (BPA and DEHP) in the fetus. Estimates of exposure to BPA and DEHP from all pathways along with their relative importance were provided in order to establish which proportion of the total exposure came from diet and which came from non-dietary exposures. In this study, the different oral dosing scenarios (dietary and non-dietary) were considered keeping inhalation as a continuous exposure case. Total non-dietary mean values were 0.002 µg/kg{sub bw}/day (0.000; 0.004 µg/kg{sub bw}/day for 5th and 95th percentile, respectively) for BPA and 0.597 µg/kg{sub bw}/day (0.116 µg/kg{sub bw}/day and 1.506 µg/kg{sub bw}/day for 5th and 95th percentile, respectively) for DEHP. Indoor environments and especially dust ingestion were the main non-dietary contributors to the total exposure of BPA and DEHP with 60% and 81%. However, as expected, diet showed the higher contribution to total exposure with > 99.9% for BPA and 63% for DEHP. Although diet was considered the primary source of exposure to BPA and phthalates, it must be taken into account that with non-dietary sources the first-pass metabolism is lacking, so these may be of equal or even higher toxicological relevance than dietary sources. The present study is in the framework of “Health and environmental-wide associations based on large population surveys” (HEALS) project (FP7–603946).
The aim of this review was to develop a radiographic optimisation strategy to make use of digital radiography (DR) and needle phosphor computerised radiography (CR) detectors, in order to lower radiation dose and improve image quality for paediatrics. This review was based on evidence-based practice, of which a component was a review of the relevant literature. The resulting exposure chart was developed with two distinct groups of exposure optimisation strategies – body exposures (for head, trunk, humerus, femur) and distal extremity exposures (elbow to finger, knee to toe). Exposure variables manipulated included kilovoltage peak (kVp), target detector exposure and milli-ampere-seconds (mAs), automatic exposure control (AEC), additional beam filtration, and use of antiscatter grid. Mean dose area product (DAP) reductions of up to 83% for anterior–posterior (AP)/posterior–anterior (PA) abdomen projections were recorded postoptimisation due to manipulation of multiple-exposure variables. For body exposures, the target EI and detector exposure, and thus the required mAs were typically 20% less postoptimisation. Image quality for some distal extremity exposures was improved by lowering kVp and increasing mAs around constant entrance skin dose. It is recommended that purchasing digital X-ray equipment with high detective quantum efficiency detectors, and then optimising the exposure chart for use with these detectors is of high importance for sites performing paediatric imaging. Multiple-exposure variables may need to be manipulated to achieve optimal outcomes.
Exposure to solar ultraviolet (UV) radiation is the main causative factor for skin cancer. UV exposure depends on environmental and individual factors, but individual exposure data remain scarce. While ground UV irradiance is monitored via different techniques, it is difficult to translate such observations into human UV exposure or dose because of confounding factors. A multi-disciplinary collaboration developed a model predicting the dose and distribution of UV exposure on the basis of ground irradiation and morphological data. Standard 3D computer graphics techniques were adapted to develop a simulation tool that estimates solar exposure of a virtual manikin depicted as a triangle mesh surface. The amount of solar energy received by various body locations is computed for direct, diffuse and reflected radiation separately. Dosimetric measurements obtained in field conditions were used to assess the model performance. The model predicted exposure to solar UV adequately with a symmetric mean absolute percentage error of 13% and half of the predictions within 17% range of the measurements. Using this tool, solar UV exposure patterns were investigated with respect to the relative contribution of the direct, diffuse and reflected radiation. Exposure doses for various body parts and exposure scenarios of a standing individual were assessed using erythemally-weighted UV ground irradiance data measured in 2009 at Payerne, Switzerland as input. For most anatomical sites, mean daily doses were high (typically 6.2-14.6 Standard Erythemal Dose, SED) and exceeded recommended exposure values. Direct exposure was important during specific periods (e.g. midday during summer), but contributed moderately to the annual dose, ranging from 15 to 24% for vertical and horizontal body parts, respectively. Diffuse irradiation explained about 80% of the cumulative annual exposure dose.
Purpose: To investigate the kVp dependence of the transmitted exposure for a radiography x-ray unit. Methods: The study used a GE DiscoveryTM XR656 DR unit, a 30 (L) × 30 (W) × 25 cm thick Lucite phantom, two anthropomorphic phantoms (an Alderson RS-310 chest phantom and a 3M skull phantom), an Unfors detector, and a Radcal 10x9-6 ion chamber. We measured the entrance exposure and transmitted exposure of each phantom at 60, 70, 80, 90, 100, 110, 120 kVp for mAs range from 2.5 to 200 mAs, without any additional filter. The FOV is 30×30 cm for the Lucite and chest phantom (AP view), and 20×20 cm for skull phantom (Lateral view). The transmitted exposure was measured at the phantom center of the x-ray exit side. For chest phantom, the transmitted exposures at 3 inch upper right and upper left from the center were also measured. We also checked the reproducibility and accuracy of the DR unit. Results: For each phantom, at every kVp and mAs setting, the transmitted exposure per mAs was calculated and normalized by the relative entrance exposure; the averaged transmitted exposure per mAs at each specific kVp was then determined. For chest phantom, the mean transmitted exposure per mAs was the average of three exit locations. The averaged transmitted exposure per mAs was fit as a power function of kVp. The result showed the transmitted exposure per mAs was approximately proportional to third power of the kVp for two anthropomorphic phantoms and forth power of the kVp for the Lucite phantom. Conclusion: The traditional assumption of fifth power kVp dependence to the transmitted exposure is inaccurate. At the normal radiography kVp range, the transmitted exposure is approximately proportional to third power of the kVp for a typical patient and up to forth power of the kVp for a large patient.
Acute ozone exposure induces a classical stress response with elevated circulating stress hormones along with changes in glucose, protein and lipid metabolism in rats, with similar alterations in ozone-exposed humans. These stress-mediated changes over time have been linked to insulin resistance. We hypothesized that acute ozone-induced stress response and metabolic impairment would persist during subchronic episodic exposure and induce peripheral insulin resistance. Male Wistar Kyoto rats were exposed to air or 0.25 ppm or 1.00 ppm ozone, 5 h/day, 3 consecutive days/week (wk) for 13 wks. Pulmonary, metabolic, insulin signaling and stress endpoints were determined immediately after 13 wk or following a 1 wk recovery period (13 wk + 1 wk recovery). We show that episodic ozone exposure is associated with persistent pulmonary injury and inflammation, fasting hyperglycemia, glucose intolerance, as well as, elevated circulating adrenaline and cholesterol when measured at 13 wk, however, these responses were largely reversible following a 1 wk recovery. Moreover, the increases noted acutely after ozone exposure in non-esterified fatty acids and branched chain amino acid levels were not apparent following a subchronic exposure. Neither peripheral or tissue specific insulin resistance nor increased hepatic gluconeogenesis were present after subchronic ozone exposure. Instead, long-term ozone exposure lowered circulating insulin and severely impaired glucose-stimulated beta-cell insulin secretion. Thus, our findings in young-adult rats provide potential insights into epidemiological studies that show a positive association between ozone exposures and type 1 diabetes. Ozone-induced beta-cell dysfunction may secondarily contribute to other tissue-specific metabolic alterations following chronic exposure due to impaired regulation of glucose, lipid, and protein metabolism. - Highlights: • Subchronic episodic ozone exposure caused pulmonary and metabolic effects. • These effects were largely reversible upon one week recovery. • Ozone exposure did not cause liver or muscle insulin resistance. • Subchronic ozone exposure led to decrease in serum insulin. • Ozone severely impaired beta cell insulin secretion in response to glucose.