Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Inhalation Exposure”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

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

At least 667 records · Page 37Linked to original sources
PubMed1977

Biochemical and behavioural effects of inhalation exposure to tetrachlorethylene and dichlormethane.

The exposure of adult male rats to 200 ppm of tetrachlorethylene t hours daily for 4 days resulted in a marked sequestration of solvent in perirenal fat 17 hours after the last exposure period. Similar exposure of similar rats to 500 ppm of dichlormethane led to a lesser accumulation of the solvent in fat as studied at the same time. Further exposures on the fifth day increased promptly the solvent contents of various organs. The exposure to tetrachlorethylene caused a diminished brain RNA content on the fifth day with simultaneous increase in the activity of non-specific cholinesterase. Similar changes in the RNA content were not seen in experiments with dichlormethane while the activity of acid proteinase increased above the control level in brain. Observations on the performance of the same animals in an open-field situation revealed that ambulation was affected in experiments with tetrachlorethylene immediately after exposure while preening pattern was changed after exposure to dichlormethane. Analysis on liver microsomal cytochrome P-450 content displayed slight increases in the hemochrome content in both experiments. The present data indicated that a rather modest exposure to both solvents could cause significant solvent accumulation in the fat and brain with marked effects on rat behaviour and protein metabolism in brain while changes in liver cytochrome P-450 content might not reflect the magnitude of these changes.

Adipose Tissue↗
PubMed1980

Behavioural and glial cell effects of inhalation exposure to styrene vapour with special reference to interactions of simultaneous peroral ethanol intake.

Male Wistar rats were exposed to 300 p.p.m. of styrene vapour with simultaneous ethanol ingestion for 4 to 17 weeks. The effects on behaviour were analyzed after 4, 9 and 13 weeks of the experiment. The most manifest behavioural effects were found in rats exposed to the combination, and the changes included increased preening time at the 4th week and increased ambulation and rearing at the end of the exposure. The ethanol ingestion affected also the accumulation of the solvent burden by delaying the peak solvent concentration in the perirenal fat to the 8th week of exposure. The fat solvent concentration did not differ from each other in the two groups at the end of the experiment, and they were similar as compared the concentration found in phenobarbital-pretreated rats exposed for reference. The styrene exposure had almost no effects on cerebral glial cells whereas ethanol induced unexpectedly increased protein destruction in them throughout the experiment. Co-exposure to ethanol and styrene decreased the magnitude of protein destruction in the glial cells. Withdrawal of the rats after an 8-week exposure showed that the styrene effects were largely abolished in two weeks of exposure-free period as analyzed by the determination of brain RNA and acid proteinase activity. Brain RNA was lower than control after two weeks of ethanol deprivation. The present data indicate that marked metabolic interactions between ethanol and styrene take place in agreement with experience on other similar solvent combinations.

Adipose Tissue↗
PubMed1985

Blood and brain n-pentanol in inhalation exposure.

Male Wistar rats exposed to 100, 300 or 600 p.p.m. n-pentanol vapour for 7 to 14 weeks during five days weekly and 6 hrs daily showed a dose-dependent blood n-pentanol concentration. The brain n-pentanol content was linearly related to the blood pentanol concentrations although this relationship changed after 14 weeks because the brain n-pentanol was significantly smaller than the respective values at 7 weeks. Valeraldehyde, the primary metabolite of n-pentanol, was only found in the brain at the highest vapour dose level. The liver n-pentanol dehydrogenase and 7-ethoxycoumarin O-deethylase activities remained unchanged while kidney ethoxycoumarin deethylase activity was enhanced in a dose-dependent manner at both time points. Brain and muscle acetylcholinesterase activities were increased by the exposure dose-dependently after 7 weeks although this effect ameliorated after 14 weeks. Moderate n-pentanol vapour exposure seems to cause metabolic and functional adaptation in its target organs.

Acetylcholinesterase↗
PubMed1985

Multiple organ carcinogenicity of 1,3-butadiene in B6C3F1 mice after 60 weeks of inhalation exposure.

Groups of 50 male and 50 female B6C3F1 mice were exposed 6 hours per day, 5 days per week, for 60 to 61 weeks to air containing 0, 625, or 1250 parts per million 1,3-butadiene. These concentrations are somewhat below and slightly above the Occupational Safety and Health Administration standard of 1000 parts per million for butadiene. The study was designed for 104-week exposures but had to be ended early due to cancer-related mortality in both sexes at both exposure concentrations. There were early induction and significantly increased incidences of hemangiosarcomas of the heart, malignant lymphomas, alveolar-bronchiolar neoplasms, squamous cell neoplasms of the forestomach in males and females and acinar cell carcinomas of the mammary gland, granulosa cell neoplasms of the ovary, and hepatocellular neoplasms in females. Current workplace standards for exposure to butadiene should be reexamined in view of these findings.

Air Pollutants, Occupational↗
PubMed1989

Asbestosis occurring after brief inhalational exposure: usefulness of bronchoalveolar lavage in diagnosis.

A case of clinically and radiologically typical asbestosis manifesting in a 55 year old man occurred 36 years after a brief exposure period of less than one year. A transbronchial lung biopsy was performed but the samples were considered non-diagnostic. The diagnosis was supported by the use of bronchoalveolar lavage to obtain alveolar samples and scanning electron microscopy-energy dispersive x ray analysis of fibres found in the bronchoalveolar lavage fluid which showed a predominance of amosite.

Asbestos↗
PubMed1994

Prediction of the comparative intensity of pneumoconiotic changes caused by chronic inhalation exposure to dusts of different cytotoxicity by means of a mathematical model.

A multicompartmental mathematical model has been used to simulate variations in the cytotoxicity of dusts in the kinetics of the retention, in the pulmonary region and tracheobronchial lymph nodes, of practically insoluble quartzite and titanium dioxide dust particles deposited on the free surfaces of the acini from alveolar air. Experiments with these dusts were conducted on rats exposed to virtually the same dust concentrations in the air for an experimental period of 20 weeks and a period of 10 weeks after exposure. Satisfactory approximation to the experimental data on the retention of these dusts is obtained by using the model parameters that depend either on damage to lung macrophages by phagocytosed particles or on the response of the host organism to this damage by enhanced recruitment of neutrophilic leucocytes; all the other variables of the model being unchanged. The values of the "action integral" computed from this model and multiplied by the index of comparative cytotoxicity of particles in vitro satisfactorily approximate to quantitative differences in the intensity of pneumoconioses caused by the dusts under study by the end of the experimental period. On the whole, the results of the mathematical model agree with the hypothesis that the cytotoxicity of particles plays a key part in both the process of retention of dust in the lung parenchyma and lung associated lymph nodes, and the pathological process caused by the retained dust. Thus given the factors and conditions on which the deposition of practically insoluble dusts in the pulmonary region depends, it is necessary to take into account the multiplicative nature of these two effects of cytotoxicity when predicting the comparative risk of pneumoconiosis.

Animals↗
PubMed1984

Developmental effects after inhalation exposure of gravid rabbits and rats to ethylene glycol monoethyl ether.

The effects of ethylene glycol monoethyl ether (EGEE) were determined on development in utero. Pregnant New Zealand White rabbits were exposed to air or 160 or 617 ppm EGEE for 7 hr/day from 1 to 18 days of gestation (dg). Virgin Wistar rats were exposed to 150 or 649 ppm EGEE or air 5 days/week for the 3 weeks immediately preceding their breeding. Sperm-positive rats were subsequently exposed to air or 202 or 767 ppm EGEE for 7 hr/day from 1 to 19 dg. Group sizes were 29 to 38 per concentration for both species. Pregestational exposure of rats had no effect on mating success, and there was no effect of EGEE exposure on establishment of pregnancy in either species. Rabbits exposed to the both concentrations had decreased food intake and depressed weight gain. Exposure-related mortality occurred in the 617 ppm EGEE group of rabbits. The only toxic sign seen in rats was reduced weight gain after exposure to 767 ppm EGEE. Exposure induced high embryomortality at maternal toxic concentrations in rats and rabbits, while lower levels induced fetal growth retardation in rats but not in rabbits. Gestational exposure increased the incidence of anomalies and variations; these were primarily of soft tissues in rabbits and of skeleton in rats. Thus, significant evidence of terata, fetal growth retardation and embryomortality were induced in rabbits and rats at levels that were below or similar to those that induced maternal manifestation of toxicity. These data implicate EGEE as a teratogen.

Abnormalities, Drug-Induced↗
PubMed1987

Functional evidence of persistent airway obstruction in rats following a two-hour inhalation exposure to methyl isocyanate.

Pulmonary function was assessed in male, F344 rats 1,2,4,7, and 13 weeks after a single 2-hr exposure to 0, 3, 10, or 30 ppm methyl isocyanate. No significant changes were observed in the rats exposed to 3 ppm through 13 weeks. Diffusing capacity (DLco), quasistatic lung compliance, and homogeneity of ventilation, as determined by multibreath nitrogen washout, were depressed in the rats exposed to 10 and 30 ppm by 1 week after exposure. None of the rats exposed to 30 ppm survived beyond 1 week. By 13 weeks, dramatic increases in lung volumes were observed in the rats exposed to 10 ppm, while DLco and lung compliance were only mildly affected. However, volume-specific DLco and compliance were depressed in the rats exposed to 10 ppm, suggesting that lung hyperinflation or other compensatory means of increasing lung size occurred in response to the methyl isocyanate-induced lung lesion. This group also exhibited increased expiratory times during tidal breathing and severely impaired distribution of ventilated air. Collectively, these results suggest the development and likely progression of a severe, obstructive airway lesion with associated gas trapping, and the existence of a pronounced concentration-response relationship between 3 and 10 ppm methyl isocyanate exposures.

Airway Obstruction↗
PubMed1994

Accumulation of alveolar macrophages induced by inhalation exposure of coal fly ash in golden hamster lungs.

To investigate the possible mechanisms of the accumulation of particle-laden alveolar macrophages (AMs) in alveoli, male golden hamsters were exposed to coal fly ash (FA) at the concentration of 0 or 2 mg/m3 for 6 months (20 hr/day, 7 days/week) in the first series of experiments, and at 0, 1, 2, or 20 mg/m3 of FA for 3 months in the subsequent experiments. Particle-laden AMs accumulated dose- and time-dependently in alveoli. In the lungs of 1 and 2 mg/m3-exposed groups. AMs first appeared in a cluster in alveoli at the alveolar-bronchiole junctions proximal to the lobar bronchus. Agglomerated AMs in these regions were generally larger in size and ingested more particles than those in the peripheral regions. These results indicate that the accumulation of AMs is closely related to the amount of particles deposited in alveoli and that ingested by AMs. Histochemical analysis revealed that AMs with small amount of particles showed the positive activity of acid phosphatase. On the other hand, heavily particle-laden AMs showed no such activity. Scanning electron microscopic observations revealed the time-related formation of small blebs and loss of surface features on the cell surface of AMs. These results suggest that the accumulation of particle-laden AMs might be caused by the decrease and/or loss of their activities, especially their mobility during migration toward terminal bronchioles from alveoli, due to the increase of ingested particles in parallel with the prolongation of exposure time.

Animals↗
PubMed1994

Effect of subchronic inhalation exposure to low-level trichloroethylene on heart rate and wakefulness-sleep in freely moving rats.

Electroencephalographic (EEG) and heart rate (HR) responses to repeated 8-h exposure for 6 weeks to trichloroethylene (TRI) vapor of 50, 100 and 300 ppm were examined in freely moving rats with chronically implanted electrodes for polygraphic recordings. Exposure to all the TRI levels significantly decreased amount of time spent in wakefulness (W) during the exposure period. Exposure to 100 ppm and higher levels significantly decreased the time-averaged HR during the post-exposure period. The HRs during the stages of slow-wave sleep (SWS) and paradoxical sleep (PS) were significantly lowered after cessation of exposure to 50 ppm. When compared with the previously reported responses to short-term exposure to TRI (Arito H, et al. Arch Toxicol 1993; 67: 193-199), significant changes in wakefulness-sleep and HR elicited by the long-term exposure appeared at lower exposure levels. The EEG and HR effects of long-term exposure to TRI of 50 ppm or higher levels are discussed for their causative factors on the basis of the reported findings and for validity of the ongoing biological exposure limit value of TRI with reference to documentations enlisted for ACGIH's TLV of 50 ppm (ACGIH. Documentation of the threshold limit values and biological exposure indices, 5th ed. 1986: 595-597).

Animals↗
PubMed1985

Metabolism of ethylbenzene in the rat during long-term intermittent inhalation exposure.

After exposure of rats to atmospheres of 50, 300 or 600 p.p.m. ethylbenzene six hours/day, five days/week, for a max. of 16 weeks, the concn. of ethylbenzene in perirenal fat and the urinary excretion of 1-phenylethanol, omega-hydroxyacetophenone, mandelic, phenylglyoxylic, hippuric and phenaceturic acids were measured at the second, fifth and ninth weeks. Excretion of metabolites into urine increased in a dose-related manner, but less than linearly. The level of exposure, but not the duration of exposure, markedly affected the pattern of the metabolites in the urine. The concn. of ethylbenzene in perirenal fat was low at 50 p.p.m., high at 300 p.p.m. and higher still at 600 p.p.m., but not in proportion to the increased dose.

Adipose Tissue↗