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At least 19 recordsLinked to original sources

Neurochemical effects on rats of n-heptane inhalation exposure.

Inhalation exposure of male rats at three dose levels (4.2, 21, 62 mol/L) to n-heptane vapor caused a dose-dependent brain and body solvent burden, which increased during two weeks of exposure. Initial neurochemical effects included reduced RNA concentration and increased NADPH-diaphorase in brain at the lowest dose. Increased proteolysis was detected in the cerebral samples in the second week at all doses, and the NADPH-diaphorase returned to the control range. Brain RNA content tended to be larger than in the controls. All biochemical effects were abolished after two weeks of withdrawal from the two-week exposure, with the exception of reduced glutathione at the lowest dose. None of the rats presented clinical signs of neuropathy, which indicates that heptane and its metabolites do not share the specific neurotoxicity of hexane and its metabolites.

Adipose Tissue↗

Subchronic toxicity of cyclohexane in rats and mice by inhalation exposure.

Inhalation studies were conducted to determine the potential toxicity and/or potential neurotoxicity of cyclohexane. Groups of rats and mice were exposed to 0, 500, 2000, or 7000 ppm concentrations of cyclohexane vapor 6 hr/day, 5 days/week for 14 weeks. Subgroups of rats and mice were further observed during a 1-month recovery period. Functional observational battery (FOB) and motor activity (MA) behavioral tests were conducted on rats. These tests were conducted prior to the exposure series and during weeks 4, 8, and 13 on non-exposure days. Clinical pathology evaluations were conducted after approximately 7, 13, and 18 weeks. Approximately 14 and 18 weeks after study initiation, tissues from rats and mice were histologically processed and evaluated by light microscopy. During exposure to 2000 or 7000 ppm, rats and mice had a diminished response or an absent response to delivery of a punctate auditory alerting stimulus. Immediately following removal of rats from the inhalation chambers, 7000 ppm males and females and 2000 ppm females displayed a compound-related increase in the incidence of wet and/or stained fur (which occurred in the areas of the mouth, chin, and/or perineum). These signs were transient, were not observed during exposure or prior to exposure the following day, and were not associated with any behavioral or morphological changes. During exposure sessions, mice exposed to 7000 ppm exhibited clinical signs of toxicity which included hyperactivity, circling, jumping/hopping, excessive grooming, kicking of rear legs, standing on front legs, and occasional flipping behavior. Clinical signs of toxicity observed in 7000 ppm mice immediately after exposure included hyperactivity, hyperreactivity, ruffled fur (females only), gait abnormalities, spasms in both rear legs, and excessive grooming (males only). The clinical signs observed in mice during and immediately after exposure were transient, and were not present prior to the subsequent exposure. A few mice exposed to 2000 ppm appeared hyperactive during exposure in the latter portion of the study. There were no compound-related changes in mean body weights, body weight gains, food consumption, food efficiency, or mortality; and there were no ophthalmological abnormalities in rats or mice. In addition, there were no compound-related effects on 37 different behavioral parameters assessed during the FOB or during motor activity tests in rats. Male and female mice exposed to 7000 ppm had slight increases in measures of circulating erythrocyte mass (red blood cells, hemoglobin, hematocrit) and plasma protein concentration (males only). Male rats and male and female mice exposed to 7000 ppm had significantly increased relative liver weights, and 7000 ppm male mice also had significantly increased absolute liver weights at the end of the exposure period. At the end of the 1-month recovery period, absolute and relative liver weights of male and female mice were similar to control. However, relative liver weights of 7000 ppm male rats continued to be significantly higher at the end of the recovery period. Male and female rats exposed to 7000 ppm had a significantly increased incidence of hepatic centrilobular hypertrophy at the end of the exposure period, which was not observed at the conclusion of the 1-month recovery period. No microscopic changes were observed in mice. In rats, the no-observed-effect level (NOEL) for acute, transient effects was 500 ppm based on a diminished/absent response to an auditory alerting stimulus at 2000 ppm and above. The NOEL for subchronic toxicity in rats was 7000 ppm based on the lack of adverse effects on body weight, clinical chemistry, tissue morphology, and neurobehavioral parameters. In mice, the NOEL for acute, transient effects was 500 ppm based on behavioral changes during exposure at 2000 ppm and above. The NOEL for subchronic toxicity in mice is 2000 ppm based on hematological changes at 7000 ppm.

Animals↗

Time-course of effects of toluene on microsomal enzymes in rat liver, kidney and lung during and after inhalation exposure.

Inhalation of toluene vapour of 2000 ppm increased the activities of aniline hydroxylase, aminopyrine N-demethylase, aryl hydrocarbon hydroxylase and NADPH-cytochrome c reductase and the concentrations of cytochromes P-450 and b5 in liver microsomes of adult male rats after an exposure period of 1 day or less. Repeated treatments, 8 h daily for 1-16 days, had only a slight further effect. In lung microsomes, the activities of monooxygenases and the concentration of cytochrome P-450 decreased after 6-24 h toluene exposure, but those of cytochrome b5 and NADPH-cytochrome c reductase did not change. In kidney microsomes the changes were mostly insignificant. After discontinuation of exposure the activities of enzymes and the concentrations of cytochromes returned to the control level in 1-4 days. The results obtained resemble the time-courses for the induction of monooxygenases by other inducers. The tissue differences suggest the unequal distribution of various cytochrome P-450 forms and their individual responsiveness to induction in liver, kidneys and lungs.

Animals↗

Repeated exposure inhalation study of pentane in rats.

Pentane (CAS No. 109-66-0) is a chemical being used as a co-solvent in a polymer production facility with potential for inhalation exposure in humans. To assess the toxicity of pentane, groups of 10 male rats each were exposed by inhalation, 6 hr/day, 5 days/week for 2 weeks to either 0 (control), 1,000, 3,000 or 10,000 ppm. Five rats per group were killed following the 10th exposure; the remaining 5/group were killed after a 14-day post-exposure recovery period. Parameters investigated were clinical signs of toxicity, functional behavior, body weights, clinical pathology, and gross and microscopic pathology including organ weights. No unusual clinical observations were seen in the pentane-treated rats, and body weights were not altered. Test rats generally exhibited normal behavioral responses in the functional observational battery. Increases in serum calcium and phosphorus concentrations were seen in rats exposed to either 3,000 or 10,000 ppm. These were reversible during the 2-week recovery period. No other clinical pathology changes were observed and no pentane-related tissue pathology was seen in any of the groups. The no-observed-adverse-effect level was 1,000 ppm with reversible clinical pathology changes produced at 3,000 and 10,000 ppm.

Administration, Inhalation↗

US EPA's acute reference exposure methodology for acute inhalation exposures.

The US Environmental Protection Agency (EPA) National Center for Environmental Assessment is engaged in the development of a methodology for Agency use to perform risk assessments for non-cancer effects due to acute inhalation exposures. The methodology will provide general guidance for deriving chemical-specific acute exposure benchmarks called acute reference exposures (AREs). Chemical-specific AREs are analogous to reference concentra tions (RfCs) for chronic non-cancer effects and will be incorporated in chemical-specific files in the US EPA's Integrated Risk Information System (IRIS) as they are developed and reviewed. AREs will have wide applicability in assessing the potential health risks of accidental and routine acute releases of chemicals to the environment. The proposed methodology for ARE development provides a framework for choosing an optimal derivation approach, depending on the type of data available, from the no-observed-adverse-effect level (NOAEL), benchmark concentration (BMC), or categorical regression approaches. Uncertainty factors are applied to the point of departure, determined by one of the recommended approaches, to derive the ARE. Due to the capability to use more exposure-response information than the NOAEL approach allows, exposure-response analyses such as BMC and categorical regression are favored as methods to develop the point of departure when the available database will support such analyses. The NOAEL approach is suitable when the data are insufficient to support exposure-response modeling. Applications of the proposed ARE methodology are illustrated by the derivation of example AREs for hydrogen sulfide and hexachlorocyclopentadiene, which showcase the categorical regression and NOAEL approaches, respectively. In addition, a recent review of the proposed ARE methodology by the US EPA Risk Assessment Forum is discussed.

Air Pollutants↗

Nose-only exposure system for inhalation exposures of rodents to large particles.

A large-particle exposure system for small animals was designed, constructed and evaluated. The system was designed by incorporating a fluidized bed aerosol generator (FBG) and a nose-only exposure device to accommodate 40 small animals into a single unit. The system has four levels of exposure ports, each level having ten exposure ports radially positioned around the aerosol delivery components of the system. The aerosol generator produces aerosols that travel to the top of the system then downwards in order to be drawn past each animal's nose via vacuum ports immediately above the exposure ports. Nearly monodisperse polystyrene latex aerosols with nominal sizes of 3.0, 9.0 and 15.0 micron were generated as dry powders in an FBG with an inside diameter of 5 cm. During 60-min test runs, average aerosol mass concentrations up to 37 mg/m3 were achieved with less than 10% variation in mass concentration distribution throughout the unit.

Administration, Inhalation↗

A new inhalation exposure system for the determination of inhaled doses in laboratory rats.

A new inhalation exposure system has been developed which allows the determination of inhaled doses of vapors and gases by laboratory rats. The system consists of saran bags connected to head-only exposure cylinders via one-way valves. One bag serves as the source of contaminant and another receives expired air. The exposure cylinders also serve as whole body plethysmographs. Up to three rats can be exposed concurrently to the same concentration of test material. The construction of the system and its use for inhalation exposures to a direct-acting radiolabeled carcinogen are described.

Administration, Inhalation↗

Binding of ethylene oxide in spermiogenic germ cell stages of the mouse after low-level inhalation exposure.

Mice received inhalation exposures of 3H-labeled ethylene oxide (EtO) gas at levels from 0.65 to 3.2 parts per million-hours (ppm-hr), which are below the exposure limits currently allowed for humans. Subsequently, spermatozoa were recovered from the reproductive tracts of the animals over a two-week period and assayed for the amount of bound EtO. A strong increase in the level of EtO binding occurred in late spermatid stages; these stages are also genetically sensitive to the action of EtO. The maximum binding of EtO in late spermatids amounted to 6 X 10(3) alkylations/sperm head/ppm-hr of exposure. Alkylation of the DNA within the sperm accounted for a very small fraction of the total sperm head alkylation, averaging about 20 DNA alkylations per sperm per ppm-hr of exposure over the two-week period. However, alkylation of protamine, a protein unique to sperm cells, was found to be correlated with total sperm head alkylation and accounted for nearly all of the EtO binding. Protamine alkylation appears to be a significant cause of EtO-induced genetic damage in spermiogenic cells of the mammal.

Administration, Inhalation↗

Effects of chelating on organ distribution and excretion of manganese after inhalation exposure to 54MnCl2. II: Inhalation of chelating agents.

The effect of 1, 2-cyclohexylene-aminetetraacetic acid (CDTA) and diethylenetriaminepentaacetic acid (DTPA) on Min distribution and excretion in rats was examined after 1 hr exposure to 54MnCl2 (0.3 micrograms Mn/m3). Both chelating agents were inhaled independently, by nose only, for 30 min for the four following days, starting immediately after cessation of Mn exposure. During the experiment, the mean concentrations of CDTA and DTPA aerosols were 508 mg/cm3 and 517 mg/cm3, respectively. The activity of 54Mn was determined in lung, liver, kidney and brain 24 hrs after the last treatment, and in urine and faeces collected for 24 hrs on days 1-4 after Mn exposure. The CDTA inhalation appeared to be more effective than DTPA in mobilizing the inhaled manganese: about a twofold decrease of 54Mn was observed in all excised organs: lung, liver, kidney and brain, as compared to the controls. The DTPA inhalation resulted in about a twofold decrease of 54Mn in the lung, but was not effective in removing the metal from the liver, kidney and brain. As it can be seen from the comparison of these results with our previous data (6), the CDTA inhalations were more effective than its i.p. injections mobilizing manganese additionally also from the lung; but generally less effective in the case of DTPA, which decreased 54Mn levels in the lung only. On the first day after 54Mn exposure, manganese levels in the urine of rats inhaling CDTA and DTPA were respectively more than 200 and 30 times higher than in the control group. Excretion of Mn in faeces was not affected significantly in this experiment. Our data show that the effectiveness of removing inhaled Mn depends not only on the chelating agent, the time of its administration (see Part I) but also on the method of its administration.

Animals↗

Kinetics of benzene metabolism in rats in inhalation exposure.

Rats inhaling benzene concentrations 400, 800, 2,000, or 4,000 mg m-3 for 6 h excreted similar amounts of phenol in urine; hence benzene metabolism was already capacity-limited at 400 mg m-3. The rate of phenol elimination in the course of 12 h inhalation of benzene, 2,000 mg m-3, was increasing; the in vitro rate of hepatic microsomal benzene metabolism was increasing accordingly. Phenobarbital (PB) pretreatment significantly increased phenol excretion in rats exposed to benzene at 800 mg m-3 and higher concentrations. This effect disappeared during 12 h benzene inhalation, although the in vitro hepatic microsomal benzene metabolism in PB rats was significantly higher than in the controls.

Aerosols↗

Construction of an exposure chamber for animals and its use for inhalation exposure to welding fumes and gases.

An inhalation exposure system, consisting of an inhalation chamber and an generating and feeding device for welding fumes and gases with a welding robot, was constructed and examined for its application to experimental toxicology for ventilatory responses of conscious rats to welding fumes and gases. The exposure system allowed an inhalation of fresh welding fumes and gases, and could supply airflow containing stable concentrations of fumes and ozone even the levels exceeding those corresponding occupational exposure limit values were supplied into the exposure chamber. The air temperature in the chamber was kept constant under rat's physiological conditions. Rats were exposed to fresh welding fumes and gases and examined for their ventilatory responses with a body plethysmograph in the chamber. A transient increase in breathing frequency with a concomitant decrease in the tidal volume was observed within several minutes immediately after the start of welding operation. The rapid, shallow breathing response disappears after repeated exposures, indicating rapid adaptation of this ventilatory response to inhalation of welding fumes and gases.

Adaptation, Physiological↗

Toxicity of gallium oxide particles following a 4-week inhalation exposure.

To evaluate the inhalation toxicity of Ga2O3, F344 rats were exposed nose-only to 0.2 micron Ga2O3 particles 2 h/day, 5 days/week for 4 weeks. The exposure concentration was 23 +/- 5 mg/m3 (mean +/- SD) resulting in lung burdens of 0.8 +/- 0.1 mg Ga2O3/lung (mean +/- SE) at the end of 4 weeks of exposure. Analysis of bronchoalveolar lavage fluid of exposed rats showed marked responses. One day after termination of exposure, lactate dehydrogenase was increased 6-fold, and the lysosomal enzyme, beta-glucuronidase, was increased 38-fold in rats exposed to Ga2O3 compared to sham exposed controls. Alkaline phosphatase, glutathione reductase, glutathione peroxidase, white blood cells, acid proteinase, and protein were increased 3- to 4-fold. Responses remained elevated 6 and 12 months after exposure. Lung clearance of radiolabeled tracer particles was evaluated 4 days and 6 months after the end of 4 weeks of Ga2O3 exposures. Long-term clearance half-times were significantly longer (3-4 fold, P less than 0.01) in rats exposed to Ga2O3 than in the sham-exposed control rats at both 4 days and 6 months, indicating persistent impairment of particle clearance. Histopathological lesions consisted primarily of alveolar proteinosis 1 day after 4 weeks exposure, progressing in severity to large focal lesions of alveolar histiocytosis and septal fibrosis 6 and 12 months after exposure. Inhaled Ga2O3 produced cytotoxic, inflammatory, and fibrogenic responses of comparable or greater magnitude than those seen after similar exposures of rats to inhaled quartz particles in other studies. These data show that inhaled Ga2O3 particles produce considerable toxicity and exposures in the work place should be limited.

Administration, Inhalation↗

Inhalation exposure to isobutyl nitrite inhibits macrophage tumoricidal activity and modulates inducible nitric oxide.

Abuse of nitrite inhalants is common among male homosexuals and a history of abuse has been correlated with seropositivity to HIV and with the incidence of Kaposi's sarcoma among AIDS patients. The present study shows that inhalation exposure of mice to 900 ppm isobutyl nitrite for 45 min/day for 14 days compromised macrophage tumoricidal activity by up to 40% and it remained compromised for at least 7 days after terminating exposures. The inhalation exposures did not affect tumor cell binding but did inhibit inducible nitric oxide (NO zero). The NO zero synthase inhibitor NG-methyl-L-arginine totally inhibited both NO zero production and cytotoxicity, suggesting that reductions in NO zero due to inhalant exposure may be responsible for the reduced cytotoxic activity. Exposure to the inhalant increased constitutive production of tumor necrosis factor-alpha (TNF-alpha). TNF-alpha has been reported to stimulate the replication of HIV and the proliferation of Kaposi's sarcoma cells in vitro.

Administration, Inhalation↗

Effects of NiCl2 and NiO in Wistar rats after oral uptake and inhalation exposure respectively.

The effects of NiCl2 and NiO after oral uptake and after inhalation exposure respectively were investigated in three experiments, using clinical and clinico-chemical methods. I. Oral application of NiCl2 in male rats over a period of 28 days. The NiCl2 concentrations were 2.5; 5.0 and 10.0 microgram/ml in drinking water. II. Inhalation exposure of male rats with NiO-aerosols (0.2; 0.4 and 0.8 mg/m3) over a period of 28 days. III. Inhalation exposure of non-pregnant and pregnant rats with NiO-aerosols (0.8; 1.6 and 3.2 mg/m3) over a period of 21 days. After oral application of NiCl2 and inhalation exposure of NiO in male rats a significant dose-dependent hyperglycaemia occurred. In contrast of these findings the serum glucose content in non-pregnant rats exposed to Ni-concentrations of 0.8 and 1.6 mg/m3 were content in non-pregnant rats exposed to Ni-concentrations of 0.8 and 1.6 mg/m3 were significantly reduced. After NiO inhalation (1.6 and 3.2 mg/m3), exposure signs of a marked macrocytosis occurred in pregnant and non-pregnant rats. The oral application of NiCl2 in drinking water in male rats induced a significant decrease of urea in serum and a significant increase of urea in urine. The activity of alkaline phosphatase in serum was inhibited in male rats exposed to 0.4 and 0.8 mg/m3 NiO-aerosols. No significant difference in serum protein pattern and no 'nickeloplasmin' was detected by serumelectrophoresis and tandem-crossed immunoelectrophoresis after oral inhalation exposure in male rats. Fetuses of exposed dams showed in the groups receiving 1.6 and 3.2 mg/m3 significantly reduced body weights.

Administration, Oral↗

Evaluation of a multitiered inhalation exposure chamber.

A multitiered inhalation exposure chamber was evaluated for use in aerosol toxicity studies by determining the uniformity of pulmonary deposition in 144 rats simultaneously exposed to 99mTc-CsCl aerosols. The activity median aerodynamic diameter and geometric standard deviation were 1.7-2.1 micron and 1.8 respectively. In one experiment, lung deposition of 99mTc in male and female rats was 728 and 544 nCi, respectively, after 130 min exposure to an aerosol concentration of 173 nCi/L. Analysis of variance revealed a significant effect of several factors on lung deposition. Animals housed on one side of the chamber had lung burdens 8-11% greater than those on the opposite side. Because an animal's location within the chamber had a slight effect on its lung burden of inhaled aerosol we recommend the rotation of animals among the chamber's six tiers during chronic aerosol toxicity studies. The overall coefficient of variation in lung burden was only 21% which is less than the variability reported in small rodents given a nose-only aerosol exposure.

Aerosols↗

Inhalation exposure of cadmium workers: effects of respirator usage.

The objective of this study was to determine the average reduction in inhalation exposures produced by intermittent use of filter cartridge respirators by cadmium workers. Inhalation exposure was estimated by measuring the cadmium concentration inside the respirator while it was worn or hanging around the worker's neck. Air concentrations of cadmium were measured simultaneously inside the respirator and at the worker's lapel with a dual sampling system. Each of nine workers were measured on three consecutive days for a full work shift. The average inhalation exposures ranged from 3 to 67 micrograms/m3 while the TWA lapel concentrations ranged from 19 to 3600 micrograms/m3; respirator use produced a substantial reduction in inhalation exposures when lapel concentrations were above 100 micrograms/m3. On the average, the inhalation exposure was 26% of the lapel concentration, but the effective protection varied widely between individuals and from day to day. If used cautiously, this relationship may be useful for estimating the approximate average inhalation exposure of a group of workers routinely using half mask respirators.

Air Pollutants↗

Inhalation exposure to THMs from drinking water in south Taiwan.

Trihalomethanes (THMs) are important disinfection byproducts (DBPs) in drinking water. To understand the magnitude of exposure to THMs for the people in southern Taiwan, models are used to estimate the inhalation exposure associated with drinking water based on raw water quality. Two parts of models are used in this study, one for estimating THM concentration from raw water quality, and one for estimating inhalation exposure to people. Important raw water quality and operational parameters, including TOC, UV254, pH, temperature, chlorine dosage, and water residence time of a major water treatment plant in south Taiwan were collected. An empirical THM formation model was then employed to predict the THM concentration at consumers' dwellings based on the parameters collected. Differences between the predicted results and experimental data were found to be small, indicating that the model is appropriate. The predicted THM concentration distribution was served as input parameters for the exposure models. Three major scenarios associated with probable inhalation exposure of THMs, including shower, pre- and post-cooking activities, and cooking processes, were considered in the exposure models. The model results show that the mean inhalation exposure of THMs for shower, pre- and post-cooking activities, and cooking processes are 26.4, 1.56, 3.29 micrograms/day, respectively. The total inhalation exposure (summation of the three scenarios) was found to be comparable with that for direct ingestion, indicating that inhalation is an important pathway for THM exposure from drinking water.

Activities of Daily Living↗

Assessment of human inhalation exposure to polycyclic aromatic hydrocarbons.

The aim of the investigation was to find a suitable approach for assessing inhalation exposure of urban inhabitants to polycyclic aromatic hydrocarbons (PAHs) in air. Personal exposure to PAHs of fifteen subjects, Zagreb inhabitants, was measured over a week in summer and again in winter. All subjects kept a diary of motion and activities and filled in a questionnaire on the characteristics of their fiat and household members. PAHs concentrations inside and outside subject's homes were simultaneously measured as were those in the working environment and in transport. Using an exposure model which takes into account the time spent by the subjects in each microenvironment and the respective concentrations measured, the inhalation exposure of each subject was calculated and compared with the directly measured personal exposure for the winter season only the summer concentrations being negligible. For a few subjects the calculated inhalation exposure deviated considerably from the one measured directly. This could be attributed to the fact that the subject spent some time in a microenvironment with significantly different PAH levels which were not included in the calculation. However, if the average results for the whole group are considered, there was no statistically significant difference between the directly measured and calculated PAH inhalation exposures. Therefore the described approach could be used for calculating average inhalation exposure to PAHs of population groups with common characteristics.

Air Pollution↗