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At least 685 records · Page 38Linked to original sources
PubMed1985

Biochemical and morphological effects of long-term inhalation exposure of rats to ethylbenzene.

Male Wistar rats were exposed (six hours/day, five days/week) to 0, 50, 300 or 600 p.p.m. of ethylbenzene vapour in the air, and killed after 2, 5, 9 or 16 weeks of exposure. After 600 p.p.m., liver-microsomal protein but not cytochrome P-450 concn. was slightly increased; NADPH-cytochrome c reductase was increased maximally by 30% (1.3-fold), 7-ethoxycoumarin O-deethylase (1.8-fold) and UDPG-transferase (2.3-fold). The increase in liver-cytosolic D-glucuronolactone dehydrogenase paralleled the glucuronidation activity (less than or equal to 2-fold). In the kidneys, only 7-ethoxycoumarin O-deethylase (less than or equal to 3.5-fold) and UDPG-transferase (less than or equal to 1.8-fold) showed dose-related increases. Ethylbenzene exposure did not deplete hepatic glutathione (GSH); kidney GSH was slightly increased (less than or equal to 1.3-fold) according to dose. Urine excretion of thioethers was increased with dose, and at 600 p.p.m. was eight times control levels. At 600 p.p.m. there was no increase in serum alanine aminotransferase activity, and liver cells showed slight proliferation of smooth endoplasmic reticulum, slight degranulation and splitting of rough endoplasmic reticulum and enlarged mitochondria, but no necrosis.

Air Pollutants, Occupational↗
PubMed1982

Distribution and elimination of 2-[14C]-acetone in mice after inhalation exposure.

This study was undertaken to determine the tissue distribution and elimination of acetone and its metabolic radioactive fragments in mice after exposure to about 1,200 mg/m3 (500 ppm) of 2-[14C]-acetone vapor. The tissue concentrations of acetone seemed to reach steady state plateaus within 6 h of exposure. In the adipose tissue the maximal concentration was about one-third of that in the highly perfused nonadipose tissues, in which acetone was rather evenly distributed. The contents of radioactivity also reached a plateau within 6 h of exposure in all tissues except the liver and brown adipose tissue. In these tissues the radioactivity increased during exposures up to 24 h. Prolonging the exposure time from 6 h to 6 h/d for three and five consecutive days gave no or only a small additional accumulation of radioactivity in all tissues except adipose tissue. The half-times of acetone after 6 h of exposure were between 2 and 5 h in all tissues. Almost equal amounts of acetone were excreted via the lungs unmetabolized or metabolized to carbon dioxide. In all tissues endogenous levels of acetone were reached within 24 h after exposure. Thus, acetone did not accumulate after prolonged or repeated exposure to concentrations of 1,200 mg/m3.

Acetone↗
PubMed1975

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

Male CF-1 mice (24 to 34 gm.) were exposed to either 250 p.p.m. or 1000 p.p.m. of 1,1,1-trichloroethane in air continuously for 14 weeks. Control mice were exposed to room air. Serial sacrifice of exposed and control mice from 1 to 14 weeks demonstrated significant changes in the centrilobular hepatocytes of animals in the 1000 p.p.m. group. Moderate liver triglyceride accumulation was evident in the 1000 p.p.m. group and peaked at 40 mg. per gm. of tissue (wet weight) after 7 weeks of exposure. Partial recovery was indicated by a decrease in the hepatic triglyceride level of 16 mg. per gm. by 14 weeks of exposure to 1000 p.p.m. Electron microscopic evaluation revealed that cytoplasmic altertions were most severe in centrilobular hepatocytes in the 1000 p.p.m. group and were mild to minimal in the 250 p.p.m. group. These alterations consisted of vesiculation of the rough endoplasmic reticulum, with loss of attached polyribosomes, increased smooth endoplasmic reticulum, microbodies, and triglyceride droplets. Some cells had ballooned cisternae of the rough endoplasmic reticulum. Necrosis of individual hepatocytes occurred in 40 per cent of the mice exposed to 1000 p.p.m. for 12 weeks. This necrosis was associated with an acute inflammatory infiltrate and hypertrophy of Kupffer cells. Comparison of these findings to the results obtained by other investigators studying dichloromethane indicates that the pathologic alterations observed with 1,1,1-trichloroethane were similar to those observed with dichloromethane, except for different time courses of the effects and different degrees of recovery. The toxic effects of 1,1,1-trichloroethane were of a type similar to those produced by carbon tetrachloride, but they appeared to be much less severe.

Animals↗
PubMed1992

Repeated inhalation exposure of rats to aerosols of 144CeO2. II. Effects on survival and lung, liver, and skeletal neoplasms.

Groups of 94-day-old F344/Crl rats were exposed repeatedly to aerosols of 144CeO2 to reestablish desired lung burdens of 1.9, 9.2, 46, or 230 kBq of 144Ce every 60 days for 1 year (seven exposures). Other 94-day-old rats were exposed once to achieve similar desired initial lung burdens of 144Ce. Older rats were exposed once to achieve desired initial lung burdens of 46 or 230 kBq when 500 days of age, the same age at which rats had the last of the repeated exposures. Control rats were either unexposed, sham-exposed once or repeatedly, or exposed once or repeatedly to stable CeO2. Approximately equal numbers of male and female rats were used. The median survival time and cumulative percentage survival curves were significantly decreased only in male and female rats exposed repeatedly to reestablish a 230-kBq lung burden and among the 94-day-old male rats exposed once to achieve a 230-kBq lung burden of 144Ce. The crude incidences of primary lung cancers (well described by a single Weibull distribution function), time to death with lung tumors, and risk of lung cancer per unit of beta-radiation dose to the lungs were correlated with the cumulative beta-radiation dose rather than the rate at which the dose was accumulated. A linear function, 70 (+/- 7.3) + -0.15 (+/- 0.056) x dose (+/- SD), adequately described the excess numbers of rats with lung cancers over a beta-radiation dose range to the lungs of 6.8 to 250 Gy for two groups of rats with the highest doses to the lungs after a single exposure and for two groups with the highest doses after repeated exposure.

Aerosols↗
PubMed2003

Health effects of inhalation exposure to organic dust in hops farmers.

Medical examinations were performed in a group of 23 hops farmers exposed to organic dust from hop (Humulus lupulus). The examinations took place in individual farms during harvesting, sorting and transporting of hop cones. As a reference group, 50 urban dwellers not exposed to organic dust were examined. There were conducted physical examinations, interviews concerning the occurrence of respiratory disorders and work-related symptoms, lung function tests, determination of cytokines concentrations, and allergological tests comprising skin prick test with 4 microbial antigens associated with organic dust, precipitin test with 12 microbial antigens, and a test for inhibition of leukocyte migration. Five farmers (21.7%) reported occurrence of work-related symptoms, including dry cough and dyspnoea. Eight farmers (34.8%) reported symptoms of chronic bronchitis. Mean spirometric values were within normal ranges. The farmers showed positive responses in precipitin test and test for inhibition of leukocyte migration to antigens of environmental microbes, mainly to the antigen of Gram-negative bacterium Pantoea agglomerans. The results showed a potential risk of occupational respiratory diseases in the population of hops farmers.

Adult↗
PubMed1986

[Inhalational exposure to rapidly eliminated substances: possibility and strategies for biological monitoring. A proposal for the use of biological limits equivalent to environmental limits].

Some advantages of biological compared with environmental monitoring and some preparatory steps and difficulties to be overcome during the planning of a biological monitoring program are firstly discussed. Then the biological compartments, their peculiarities and their use in the field of biological monitoring are described. The problem concerning the biological thresholds of the reference normal values and the biological limits corresponding to environmental limits (biological equivalent limits, BEL) is the next topic, followed by the description of the methods for measuring the BELs (in case of linear regression between biological and environmental values) and of the methods for the upper and lower confidence limits (UCL, LCL) of a biological value. They are to be used for a decision of compliance or noncompliance biological exposure. Finally some ways of using biological UCL-LCL and variation coefficients during cross-sectional and longitudinal studies (biological monitoring strategies) are shown.

Air Pollutants, Occupational↗
PubMed1985

[Kinetic study of phthalate accumulation and elimination in a model of inhalational exposure in volunteers].

Studies were performed on volunteers exposed to 0.5 and 2 mg/m3 diethylhexyl phthalate for a period of 5 days. The accumulation of diethylhexyl phthalate in blood and its elimination with urine was traced. Accumulation of phthalates in the organism was established even in lower MAC concentration of 0.5 mg/m3, which puts the problem of reevaluation of this norm (1 mg/m3).

Diethylhexyl Phthalate↗
PubMed1985

An ultrastructural study of lesions induced in the cerebellum of mice by inhalation exposure to methyl chloride.

Female C57BL/6 mice were exposed for 6 h/day, 5 day/wk for 2 weeks, to 1,500 ppm methyl chloride. Focal and diffuse malacia, involving the cerebellar inner granular layer was found while renal lesions were minimal or absent. The cerebellar lesions were most frequently found in the ventral paraflocculus, and less often in other regions of the cerebellum. The earliest ultrastructural changes were seen in the nuclei of scattered cerebellar granule cells, with progression from slight confluence of heterochromatin, to complete nuclear condensation or karyorrhexis. More severely affected areas exhibited severe watery swelling and disruption of granule cell perikarya with less severe changes in other cell types. Blood vessels appeared normal, even in areas of severe malacia. It was concluded that the lesions in the mouse cerebellum closely resemble methyl chloride induced brain lesions previously described in guinea pigs, and that these lesions are not secondary to the renal toxicity of methyl chloride.

Air Pollutants↗
PubMed1985

Brain tumors in F344 rats associated with chronic inhalation exposure to ethylene oxide.

Groups of F344 rats of each sex were exposed to either ethylene oxide (ETO) vapor (concentrations of 100, 33 or 10 ppm) or to room air for 6 hours daily, 5 days per week, for up to 2 years. Three representative sections of the brain from each rat were evaluated. Twenty-three primary brain tumors were found, two of which were in control animals. Increased numbers of brain tumors were seen in 100 ppm and 33 ppm ETO exposed male and female rats. Significant trend analyses were found for both males and females, indicating that, under the conditions of this study, ETO exposure above 10 ppm was related to the development of these brain tumors.

Air Pollutants↗
PubMed1979

[Changes in lipid metabolism in pregnant white rats and their fetuses in inhalational exposure to carbon disulfide].

It is known from the literature that carbon bisulphide affects lipid metabolism, but observations in this field are quite controversial. In the present work the authors studied the influence of carbon bisulphide on some parameters of lipid metabolism in pregnant albino rats, following inhalatory exposure to carbon bisulphide concentrations of 50, 100 and 200 mg/m3, 8 hours daily throughout the whole gestation period. The lipid metabolism changes were followed up both in two subsequent generations. The offsprings were examined at birth and after they had reached sexual maturity, at the end of gestation. Part of the animals of the basic generation were subjected to repeated carbon bisulphide treatment in the same concentrations. The following parameters were studied: total lipids, triglycerides, phospholipids, cholesterol and free fatty acids in the liver. Correlation dependencies were found between exposure carbon bisulphide concentrations and the parameters of lipid metabolism. The degree and nature of the changes depended on the concentration and type of exposure (antenatal, postnatal and combined). A distinct rise in free fatty acid levels was associated with a mild decrease in the triglyceride and phospholipid content.

Animals↗