High efficiency of photon-to-heat conversion with a 6-layered metal/dielectric film structure in the 250-1200 nm wavelength region.

The optical properties and thermal stability of a 6-layered metal/dielectric film structure are investigated in this work. A high optical absorption average of > 98% is achieved in the broad spectral range of 250-1200 nm with experiment results, in good agreement with our simulated results. The samples have a typical layered structure of: SiO(2)(57.3 nm)/Ti(5.7 nm)/SiO(2) (67.1 nm)/Ti(11.6 nm)/SiO(2)(51.4 nm)/Cu(>100 nm), deposited on optically polished Si or K9-glass substrates by magnetron sputtering. The sample of the 6-layered metal/dielectric film structure has an AM1.5G solar absorptance of 95.5% with the features of low thermal emittance of 0.136 at 700K and good thermal stability, and will be potentially suitable for practical application in high-efficiency solar absorber devices in many fields.

Superconducting gap in bi-sr-ca-cu-o by high-resolution angle-resolved photoelectron spectroscopy.

Detailed studies indicate a superconducting gap in the high-temperature superconductor Bi(2)Sr(2)CaCu(2)O(8). Photoemission measurements with high energy and angle resolution isolate the behavior of a single band as it crosses the Fermi level in both the normal and superconducting states, giving support to the Fermi liquid picture. The magnitude of the gap is 24 millielectron volts.

Sister chromatid exchange in chronic ethylene oxide-exposed primates: unexpected effects of in vitro culture duration, incubation temperature, and serum supplementation.

Ethylene oxide (EtO), a potent monofunctional DNA alkylating agent, has been shown to induce sister chromatid exchanges (SCE) in the peripheral blood lymphocytes of animals and workers exposed to it in vivo. We have previously reported that elevations of SCE persist for 6 years after cessation of EtO exposure in cynomolgus monkeys chronically exposed to EtO; the elevation in mean SCE was entirely attributable to a subpopulation of high SCE frequency cells (HFCs). We now report that the detection of persistent HFCs is dependent on the conditions of cell growth, and that EtO exposure increases the replication indices of lymphocytes from the exposed animals when these cells are examined at early cytogenetic harvest times. Culture of lymphocytes in differing serum supplements, changes in cytogenetic harvest times, and alterations in in vitro incubation temperature all markedly affected mean SCE frequency by influencing the detection of HFCs. The frequency of EtO-induced HFCs was independent of 5-bromodeoxyuridine concentration, used for differential staining of sister chromatids. These observations indicate that the detection of persistent alkylation-induced chromosomal changes, observed long after cessation of in vivo chronic exposure of these animals, is highly dependent upon factors affecting cell growth.

Persistently elevated sister chromatid exchanges in ethylene oxide-exposed primates: the role of a subpopulation of high frequency cells.

Ethylene oxide (EtO) is a potent DNA-alkylating agent which has been shown to induce sister chromatid exchanges (SCE) in the peripheral blood lymphocytes of exposed workers. To study further the persistence of EtO-induced SCE, we have examined lymphocytes from a group of cynomolgus monkeys exposed to EtO in control, 50-ppm, and 100-ppm concentrations for 7 h/day, 5 days/week over the years 1979-1981. The data collected in 1987 were compared with those generated immediately prior to the cessation of exposure in 1981. EtO-induced SCE persisted at levels significantly above those of the nonexposed controls. Comparison of the distributions of SCE between 1979 and 1987 shows that, although mean SCE decreased from 1981 to 1987, the mean SCE in the top 10% of the distribution has not diminished over time. Consequently, the increased level of SCE is entirely attributable to a subpopulation of cells with high frequencies of SCE. These findings suggest that long-lived lymphocytes may inefficiently repair EtO-induced lesions which produce SCE. The results also have important implications for the proper use of SCE analytical techniques in the epidemiological study of cytogenetic damage after chronic exposure to DNA-alkylating agents.

Relative ion yields measured with a high-resolution glow discharge mass spectrometer operated with an argon/hydrogen mixture.

Quantitative elemental analysis by glow discharge mass spectrometry (GDMS) requires a calibration factor for each element. The calibration factors used in the present work are called relative ion yields (RIYs). The RIYs of each of 19 elements within samples of four National Institute of Standards and Technology steel reference materials (nos. 661-664) were measured using pure argon and an argon mixture containing 1.0% hydrogen by volume. The RIYs measured using pure argon correlated within a factor of approximately 2-3 to the RIYs calculated by a theoretical model. The RlYs measured for these 19 elements using the argon mixture containing 1.0% hydrogen correlated within a factor of approximately 1.3 to the calculated RIYs. These results may have significant analytical potential with respect to GDMS and may have application to other plasma techniques.

Pneumoconiosis in animals exposed to poly(vinyl chloride) dust.

Rats, guinea pigs and monkeys were exposed by inhalation (6 hr/day, 5 days/week) for up to 22 months to a 13 mg/m3 concentration of PVC dust. Autopsies on rats and guinea pigs were performed after 12 months of exposure and on monkeys after 22 months after 22 months of exposure. Lung function tests were performed on monkeys after 9, 14 and 22 months of exposure. Aggregates of alveolar macrophages containing PVC particles were found in the lungs of all animals. These aggregates were more numerous in the monkey lungs. No fibrosis or significant cellular infiltrates were present in or near these cellular aggregates. No significant effects on pulmonary function could be demonstrated in the monkeys exposed to PVC. Under the conditions of this experiment, inhaled PVC produced a benign pneumoconiosis.

Thirteen-week inhalation toxicity of N,N-dimethylformamide in F344/N rats and B6C3F1 mice.

Male and female F-344 rats and B6C3F1 mice (10/sex/group) were exposed to N,N-dimethylformamide (DMF) by whole body inhalation exposure at 0, 50, 100, 200, 400, or 800 ppm, 6 h/day, 5 days/week, for 13 weeks. A concentration-dependent depression in body weight occurred in rats of both sexes at 400 (6-11%) and 800 ppm (20-22%). In contrast, all weight changes in both sexes of mice were within 10% of controls. No rats died, while 5 mice died from nonexposure-related causes. Relative liver weights were significantly increased at all DMF concentrations in both sexes and both species. Activities of serum sorbitol dehydrogenase (SDH) were statistically increased in male and female rats (200 to 800 ppm) on study days 4, 24, and 91 (13 weeks). Activities of alanine aminotransferase (ALT) and isocitrate dehydrogenase (ICD) were statistically increased in both sexes of rats exposed to 800 ppm DMF at all time points. Cholesterol (CHOL) levels were statistically increased in male and female rats (50-800 ppm) at all sampling time points. Levels of total bile acids (TBA) were statistically increased in both sexes of rats (400-800 ppm) on days 24 and 91. Centrilobular hepatocellular necrosis (minimal to moderate) was seen in rats of both sexes exposed at 400 and 800 ppm, with the lesions more severe in females. Centrilobular hepatocellular hypertrophy (minimal to mild) was found in all groups of DMF-exposed male mice, and in female mice exposed at 100-800 ppm. For male and female rats the no-observed-adverse-effect concentration (NOAEC) for microscopic liver injury was 200 ppm. The NOAEC was 50 ppm for female mice, but an NOAEC based upon the absence of microscopic liver injury was not determined in male mice.

Inhibition of rat heart mitochondrial electron transport in vitro: implications for the cardiotoxic action of allylamine or its primary metabolite, acrolein.

Allylamine (3-aminopropene) is a specific cardiac toxicant that causes aortic, valvular and myocardial lesions in many species. Myocardial necrosis can be observed 24 h after a single dose. Acute toxicity is believed to involve metabolism of allylamine to highly reactive acrolein (2-propenal). Allylamine has been shown to bind to mitochondria from aorta and heart, suggesting that the subcellular site of injury is at or near the mitochondrion. The present investigation compared the effect of allylamine and its primary metabolite, acrolein, on electron transport and oxidative phosphorylation in mitochondria isolated from rat heart (RHM). Both compounds weakly inhibited mitochondrial electron transport with either the combination of glutamate, malate, and malonate (GMM, NADH-linked) or succinate as substrate. Comparisons of the slopes of concentration-effect regression (range of concentrations tested, 0.20-2.0 mM) lines showed acrolein to have significantly greater inhibitory effects than allylamine (range of concentrations tested, 0.22-6.4 mM) on GMM oxidation, while no significant difference in the abilities of the compounds to inhibit succinate oxidation were observed, indicating site preferences for inhibitory action. The addition of an uncoupling agent could not reverse inhibition with either substrate system. These results indicate that both the parent compound and its proposed metabolite primarily inhibit electron transport with little direct effect on the coupling mechanism. The State III EC50 (effective concentrations for 50% inhibition of control mitochondrial enzyme activities) for allylamine (2.29 mM with succinate as substrate and 1.22 mM with GMM) and acrolein (0.80 mM with succinate as substrate and 0.39 mM with GMM) are probably too great to invoke the direct action of either the parent compound or its oxidized metabolite on mitochondrial electron transport as a primary mechanism in the cardiotoxic action of allylamine.

Low glucose under hypoxic conditions induces unfolded protein response and produces reactive oxygen species in lens epithelial cells.

Aging is enhanced by hypoxia and oxidative stress. As the lens is located in the hypoglycemic environment under hypoxia, aging lens with diabetes might aggravate these stresses. This study was designed to examine whether low glucose under hypoxic conditions induces the unfolded protein response (UPR), and also if the UPR then generates the reactive oxygen species (ROS) in lens epithelial cells (LECs). The UPR was activated within 1 h by culturing the human LECs (HLECs) and rat LECs in <1.5 mM glucose under hypoxic conditions. These conditions also induced the Nrf2-dependent antioxidant-protective UPR, production of ROS, and apoptosis. The rat LECs located in the anterior center region were the least susceptible to the UPR, whereas the proliferating LECs in the germinative zone were the most susceptible. Because the cortical lens fiber cells are differentiated from the LECs after the onset of diabetes, we suggest that these newly formed cortical fibers have lower levels of Nrf2, and are then oxidized resulting in cortical cataracts. Thus, low glucose and oxygen conditions induce the UPR, generation of ROS, and expressed the Nrf2 and Nrf2-dependent antioxidant enzymes at normal levels. But these cells eventually lose reduced glutathione (GSH) and induce apoptosis. The results indicate a new link between hypoglycemia under hypoxia and impairment of HLEC functions.

Development of an HPLC-MS procedure for the quantification of N-acetyl-S-(n-propyl)-l-cysteine, the major urinary metabolite of 1-bromopropane in human urine.

An analytical procedure was developed for the detection and quantification of N-acetyl-S-(n-propyl)-l-cysteine (n-propylmercapturic acid, AcPrCys), a metabolite and biomarker for exposure to 1-bromopropane (1-BP). 1-BP is used as an industrial solvent and exposure is a health concern for industrial workers due to its toxicity. It has been associated with neurological disorders in both animals and humans. Urine sample preparation for the determination of AcPrCys consisted of solid phase extraction (SPE). Urine samples on preconditioned SPE (C18) columns were washed with 40% methanol/60% water solution prior to elution with acetone. Quantification was by means of a liquid chromatograph (LC) equipped with a mass spectrometer (MS) using an Aqua 3 microm C18 300A column and [d(7)]-AcPrCys was used as internal standard. Electrospray ionization (ESI) was used with the MS operated in the negative ion mode and selected ion monitoring (SIM) at m/z 204 for AcPrCys and m/z 211 for [d(7)]-AcPrCys. Demonstrated recovery of urine samples fortified at multiple levels (0.625-10 microg/ml) varied between 96 and 103% of theory with relative standard deviations (RSD) of 6.4% or less. The limit of detection (LOD) for the procedure was approximately 0.01 microg/ml AcPrCys in urine. These data will be discussed as well as other factors of the development of this test procedure.

Tantalus, a 240MeV Dedicated Source of Synchrotron Radiation, 1968-1986.

Tantalus was a 240 MeV electron storage ring completed and commissioned in 1968. It was the first storage ring operated exclusively for the production of synchrotron radiation, although it was not designed for that purpose. As such, it influenced the operating pattern for subsequent dedicated sources of synchrotron radiation. Pioneering experiments using synchrotron radiation were carried out on this machine, and innovative instrumentation was produced there. It ceased operation in 1986.

Scanning ellipsometer by rotating polarizer and analyzer.

A new type of scanning photometric ellipsometer with polarizer and analyzer both rotating synchronously at rotation rates of omega(0)/2 and omega(0) (f(0) = 51 Hz), has been designed and constructed. The mechanical and electrical design, alignment, calibration, and error reduction of the system are discussed in detail. Through measuring the amplitudes of the three ac components from the photomultiplier, at frequencies of 51, 102, and 153 Hz, respectively, complex dielectric function spectra have been obtained for test samples of Au and CdTe in the 1.5-5.5-eV range and shown to be in agreement with the results of others.

Urinary 2-thiothiazolidine-4-carboxylic acid (TTCA) as the major urinary marker of carbon disulfide vapor exposure in rats.

Male Sprague-Dawley rats (200-250 g; 60 per exposure group) were exposed to carbon disulfide (CS2) air concentrations of 0, 50, 150, and 500 ppm(v/v) for 6 hr/day, 5 days/week over six months. Following the exposures, nine rats from each exposure group had four sets of cumulated urines collected (between 0-8, 8-16, 16-24, and 24-48 hr). The urinary parameters measured were: 2-thiothiazolidine-4-carboxylic acid (TTCA), total thioethers (TE), and the compounds responsive to the iodine-azide (IA) test. Urinary TTCA elimination obeyed pseudo-first-order, one-compartment model kinetics of half-time (t0.5) 5.2 +/- 0.3 hr up to 16 hr of collection. The elimination of TE within 16 hr had a t0.5 of 8.5 +/- 0.6 hr. TTCA, IA, and TE were correlated highly in the first 16 hr. After 16 hr, the t0.5 for TE lengthened to 13.1 hr. At CS2 concentrations of 50, 150, and 500 ppm, the respective t0.5 for IA-responsive compounds were 12.6, 6.1, and 4.4 hr. TTCA had the highest correlation coefficient and p-value relative to CS2 exposure concentration, and also was the most sensitive, precise, and selective urinary marker.

Evaluation of Drosophila for screening developmental toxicants: test results with eighteen chemicals and presentation of a new Drosophila bioassay.

The objective of this study was to generate a comprehensive data set of chemically induced malformations in Drosophila using a detailed morphological examination of the entire fly (phase one). These data were analyzed, in blind, with the goal of developing a standardized set of criteria which could be used in a new, rapid, and economical Drosophila bioassay useful in the preliminary screening for potential developmental toxicants. After 32 chemicals were tested, formalized criteria were developed to form the basis of a new Drosophila bioassay. These criteria were then applied to the data from the same 32 chemicals (phase two). The data from only 18 of these chemicals met all requirements for evaluation, e.g., statistical significance, minimum fly numbers, sufficient challenge concentration administered, etc. In the new bioassay, rather than the detailed and time-consuming examination of the entire fly for a multitude of morphological defects, only two specific anatomical sites are examined. These sites are the humeral bristle and the wing blade, with focus placed on two structural defects--a bent bristle and a notch in the wing. These defects were the only two external malformations among the multitude of defects observed in flies treated in the first phase with the 32 chemicals which demonstrated the following characteristics: 1) A consistent concentration-response in flies treated with a variety of developmental toxicants; 2) a lack of response with most presumptive non-developmental toxicants; and 3) consistently low-background incidences in control flies. In both phases, developing Drosophila were exposed to the test agents from the egg through three larval stages by incorporating a range of concentrations of each chemical into the culture medium. Emerging adults were examined for an array of defects as part of a detailed morphological examination in the first phase, including bent bristles and wing notches. In the second phase, only bent bristle and wing notch data were evaluated. The incidences of bent humeral bristles and wing notches from flies exposed to each of the 18 chemicals were compared with those of concurrent controls. Of the 18 chemicals that could be evaluated using the new bioassay, 13 were known developmental toxicants while the remaining 5 were presumptive negative agents. Ten of the 13 mammalian developmental toxicants were correctly identified with this test (false negative rate of 23%). Four of five apparent non-developmental toxicants were correctly identified for a false positive rate of 20%.(ABSTRACT TRUNCATED AT 400 WORDS)

Subchronic inhalation toxicity of isobutyl nitrite in BALB/c mice. II. Immunotoxicity studies.

Initial epidemiologic studies of acquired immunodeficiency syndrome (AIDS) occurring in homosexual men identified the use of the inhalants amyl, butyl, and isobutyl nitrite as possible risk factors contributing to the disease. Because of the lack of immunotoxicological data on these chemicals, we studied the effects of subchronic exposure to isobutyl nitrite (IBN) on the immune system. BALB/c mice were exposed to either 50 or 300 ppm IBN for 6.5 h/d, 5 d/wk for up to 18 wk. After 7, 13, or 18 wk of exposure, mice were killed and the following assays were performed. Antibody producing cells were enumerated by a slide plaque assay on animals immunized with sheep red blood cells while still in exposure chambers. The lymphocyte proliferative response to mitogens (phytohemagglutinin, concanavalin A, pokeweed mitogen, and lipopolysaccharide) was tested using several concentrations of each mitogen. Additional mice were immunized with Freund's complete adjuvant 21 d prior to death and were tested for delayed hypersensitivity response to purified protein derivative by a radiometric skin test. Finally, the relative numbers of T cells and T-cell subsets among splenic lymphocytes from exposed and control animals were determined. At the time periods tested there were no discernable immunotoxic effects observed in the exposed animals in any of the assays performed. These results indicate that IBN, at the dosages tested, had no discernable detrimental effect on the immune system of mice.

Subchronic inhalation of diethylamine vapor in Fischer-344 rats: organ system toxicity.

Male and female Fischer 344 (F-344) rats were exposed at 0,25 or 250 ppm diethylamine (DEA) vapor, 6.5 hr per day, 5 days per week, for 24 weeks in order to assess cardiac and other organ system toxicity. Scheduled sacrifices were performed following 30, 60, and 120 days of exposure. During the first 2 weeks of exposure, the rats exposed at 250 ppm DEA did not gain weight. After 2 weeks, however, the rate of weight gain of these rats was greater than that of controls. Nevertheless, mean body weights for both sexes of rats exposed at 250 ppm DEA remained depressed compared to controls throughout the study. Sneezing, tearing, and reddened noses were seen in rats exposed at 250 ppm DEA. Histopathologic examinations revealed lesions of the nasal mucosa of rats exposed at 250 ppm DEA (rats exposed at 25 ppm were not evaluated). These lesions of the respiratory epithelium consisted of squamous metaplasia, suppurative rhinitis, and lymphoid hyperplasia. There were no pronounced treatment-related effects on organ weights, hematology, or clinical chemistry indices except for blood urea nitrogen which was evaluated in rats of both sexes exposed at 250 ppm DEA for 24 weeks. In contrast to the high-dose animals, no treatment-related effects were observed in rats intermittently exposed at 25 ppm DEA for up to 24 weeks. No evidence of cardiotoxicity was seen in rats exposed to either DEA concentration for up to 24 weeks.

Pulmonary effects of acute vanadium pentoxide inhalation in monkeys.

An experimental study was conducted to investigate the hypothesis that changes in pulmonary function induced by vanadium pentoxide (V2O5) inhalation would be accompanied by evidence of pulmonary inflammation. Sixteen adult, male cynomolgus monkeys were acutely exposed by whole-body inhalation of V2O5 dust at aerosol concentrations of 0.5 mg V2O5/m3 and 5.0 mg V2O5/m3, conducted at a 1-wk interval. Comprehensive pulmonary function tests were performed 1 day after each inhalation exposure to detect functional changes in the airways and pulmonary parenchyma. Pulmonary inflammation was assessed by cytologic analysis of respiratory cells recovered from the lower respiratory tract by bronchoalveolar lavage (BAL). Postexposure values for pulmonary function and BAL were compared with the baseline values determined for each monkey prior to V2O5 exposure. Acute V2O5 dust inhalation produced significant air-flow limitation in both central and peripheral airways without producing any detectable changes in parenchymal function. These functional changes were accompanied by a significant increase in the total cell counts recovered from the lungs by BAL. The increase in total cell count occurred through a dramatic increase in absolute number and relative percentage of polymorphonuclear leukocytes (PMN). These findings suggest that pulmonary inflammatory changes involving PMN may play an important role in the occurrence of air-flow limitation after acute inhalation of V2O5 dust.

Subchronic inhalation of triethylamine vapor in Fischer-344 rats: organ system toxicity.

Male and female F-344 rats were exposed at 0, 25, or 247 ppm triethylamine (TEA) vapor, 6 hr per day, 5 days per week for up to 28 weeks in order to characterize the subchronic organ system toxicity. Rats were weighed biweekly and scheduled sacrifices were performed following about 30, 60, and 120 days of exposure. No statistically significant treatment-related effects on organ weights, hematology, clinical chemistry, or electrocardiographic indices were observed. Body weight gain was not affected by TEA treatment. No physiologic or pathologic evidence of cardiotoxicity was seen in rats exposed to either TEA concentration for up to 28 weeks. No gross or histopathologic lesions attributable to TEA exposure were noted in any of the organs examined, including the nasal passages. This latter finding is in marked contrast to previously reported findings from this laboratory in which squamous metaplasia, suppurative rhinitis, and lymphoid hyperplasia were found in the respiratory epithelium of F-344 rats exposed to the structurally related chemical, diethylamine, under the same conditions as this study (Lynch et al., 1986).

Acute toxicity of tetramethylbenzenes: durene, isodurene and prehnitene.

Oral LD50 (rat), primary skin irritation (rabbit), cutaneous sensitization (guinea pig) and eye irritation (rabbit) studies were conducted on the three tetramethylbenzene isomers: durene , isodurene and prehnitene. The order of oral toxicity was isodurene greater than prehnitene greater durene. Durene was not a skin irritant, while isodurene and prehnitene each produced a mild positive skin response (erythema). None of the tetramethylbenzenes were skin sensitizers or eye irritants. Durene, isodurene and prehnitene are only slightly toxic on an acute toxicologic basis and only pose an acute health hazard when injested in excessive quantities.