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PubMed1993

Proliferation of mouse lung epithelial cells after inhalation exposure to 239PuO2.

The aim of this study was to investigate cell proliferation in mouse lungs up to 12 weeks after exposure to 239PuO2. CBA mice were exposed (nose-only) to 239PuO2 to give an initial alveolar deposit of 500 Bq. The main morphological change observed was hypertrophy of Type II cells. The labeling index (LI) of alveolar cells, which was monitored by immunocytochemical detection of DNA-incorporated 5-bromo-2'-deoxyuridine (BrdU), increased with time after exposure and was eight times that of controls by the end of the study. The LI of the bronchiolar cells was increased markedly after exposure but declined thereafter. The cell proliferation patterns of the alveolar and bronchiolar cells (mainly Type II and Clara cells, respectively) could be related to the distribution and clearance patterns of the deposited particles of 239PuO2 and to the effects of alpha-particle radiation on these cells. This study showed that significant cellular changes, particularly cell proliferation, occurred at early times after exposure of mouse lung to 239PuO2. However, the relevance of these results to the late carcinogenic effects of 239Pu could not be assessed because of the limited duration of this study.

Administration, Inhalation↗
PubMed1992

Distribution to the fetus and major organs of the rat following inhalation exposure to pyrene.

Concentrations of pyrene and total metabolites were determined for individual fetuses and selected maternal organs and tissues immediately and 6 h following a 95-min head-only exposure of pregnant Wistar rats, on gestation day 17, to five levels of pyrene over the range 200-800 mg m-3 as a microcondensation aerosol. The influence of uterine horn, side and position, on distribution to the fetus was assessed. The concentration of both pyrene and its metabolites increased more over the exposure range (eightfold) than did those in the fetus. Concentrations of pyrene or its metabolites in fetal tissues were not found to be related to its position on the uterine horn. There was an unexplained and significant (P less than 0.01) higher concentration of pyrene in fetuses on the right side relative to the left side of the uterine horn for the animals killed immediately following exposure. A comparison of the levels in maternal tissues measured immediately following the exposure and 6 h later showed that there was some redistribution of pyrene and its metabolites to the fat tissues, i.e. levels in the fat increased over the 6 h period following the exposure. Levels in the other tissues diminished during this period. In general, concentrations of pyrene and its metabolites were lowest in the fetal tissues relative to those in the sampled maternal organs and tissues.

Administration, Inhalation↗
PubMed1995

Chronic toxicity/oncogenicity of dimethylacetamide in rats and mice following inhalation exposure.

The potential chronic toxicity and oncogenicity of dimethylacetamide (DMAC) was evaluated by exposing male and female rats and mice to 0, 25, 100, or 350 ppm DMAC for 6 hr/day, 5 days/week for 18 months (mice) or 2 years (rats). Clinical pathology was evaluated at 3, 6, 12, 18, and 24 (rats only) months. An interim euthanization for rats occurred at 12 months and hepatic cell proliferation in rats and mice was examined at 2 weeks and 3 and 12 months. No compound-related effects on survival were observed. Rats exposed to 350 ppm had lower body weight and/or body weight gain. There were no compound-related effects on body weight or weight gain in mice at any concentration. There were no compound-related adverse effects on the incidence of clinical signs of toxicity in rats or mice. No hematologic changes were observed in either species. Serum sorbitol dehydrogenase activity was increased in rats exposed to 350 ppm. Serum cholesterol and glucose concentrations were significantly higher in 100 and 350 ppm female rats. Compound-related morphological changes were observed in the liver. In rats, exposure to 100 or 350 ppm produced increased absolute and/or relative liver weights, hepatic focal cystic degeneration, hepatic peliosis, biliary hyperplasia (350 ppm only), and lipofuscin/hemosiderin accumulation in Kupffer cells. In mice, exposure to 100 or 350 ppm produced increased absolute and relative liver weights (350 ppm females only), accumulation lipofuscin/hemosiderin in Kupffer cells, and centrilobular single cell necrosis. Male rats exposed to 350 ppm also had significantly higher absolute and relative kidney weights which correlated with the gross and microscopic changes resulting from a compound-related increase in severity of chronic progressive nephropathy. Female mice exposed to 350 ppm had an increased incidence of bilateral, diffuse retinal atrophy. No increase in hepatic cell proliferation was seen in mice or rats at any exposure concentration. DMAC was not oncogenic under these experimental conditions in either the rat or mouse. The NOAEL for male and female rats and mice is 25 ppm.

Acetamides↗
PubMed1979

Pulmonary response to glass fiber by inhalation exposure.

Rats, hamsters, and guinea pigs were exposed to airborne glass fiber at a gravimetric concentration of 0.42 mg. per liter for 6 hours per day, 5 days per week for 90 days. The number of dust particles greater than 5 micron. in length was 0.73 x 10(6) per liter with an average diameter of approximately 1.2 micron. Most particles were less than 2 micron. in size and only 15% of the dust particles had a fibrous shape. Few fibers were longer than 10 micron. The pulmonary response was characterized by macrophage reaction with alveolar proteinosis at 90 days of inhalation. The light and ultrastructural alterations were similar to the other experimental or human alveolar proteinosis. The alveolar proteinosis disappeared at 1-year postexposure, but focal dust cell accumulation with proliferating granular pneumocytes persisted throughout the 2-year recovery period. No significant fibrosis or stromal changes were found in the dust-deposited areas. In hamsters and guinea pigs, most ferruginous bodies were developed from fibrous fibers but not from tiny dust particles. The tracheobronchial lymph nodes were markedly swollen and laden with dust cells.

Animals↗
PubMed1990

[Results of a questionnaire survey of pulmonary complaints in dental technicians: effect of inhalation exposure to heavy metal dusts (cobalt-chromium alloys)].

In the course of their working lifetime, dental technicians are exposed to numerous different dusts, some of which also contain toxic substances (Co-Cr alloys), which are employed in the so-called model casting. In order to establish the influence of the nature of the exposure associated with various dental technical procedures on pulmonary symptoms, 24588 questionnaires were sent to 3415 dental laboratories. The return rate was 21.3%. An evaluation of 4328 questionnaires (with account being taken of the influence of smoking, age and sex), revealed a significant relationship between the duration of work on model casting, and the common symptoms "dry cough", "dyspnoea on exertion" and "productive cough". In agreement with other case reports, the results emphasize the significance of the inhalation of heavy metal dusts in the aetiology of pneumoconiosis in dental technicians.

Adult↗
PubMed1977

Effects of lead inhalation exposures alone and in combination with carbon monoxide in nonpregnant and pregnant rats and fetuses. II. Effects on delta-aminolevulinic acid dehydratase activity, hematocrit and body weight.

Pregnant and nonpregnant rats were exposed for 21 days to an aerosol containing 1, 3 and 10 mg lead/m3 air and to a combination of 3 mg Pb/m3 and 500 ppm carbon monoxide (CO). Pregnant and nonpregnant rats exposed to uncontaminated air served as controls. The activity of the fetal delta-aminolevulinic acid dehydratase (ALA-D) was less inhibited by lead than the maternal activity. Furthermore, the degree of inhibition was highly reduced in the fetuses by additional CO-inhalation, whereas in adult animals the depression of the ALA-D was accentuated by additional CO-inhalation in accordance with epidemiological data. Therefore, it is concluded that the mode of plumbic inhibition of the ALA-D activity differs in fetuses from that in adults. Furthermore, the adaptation to the inhibition of the ALA-D by de novo synthesis of this enzyme was less in fetuses than in adult rats. The high lead aerosol concentration reduced hematocrit and body weight of the fetuses, but it did not influence these parameters in adult rats, thus pointing to a higher lead-sensitivity of the fetal than the adult organism. A stronger inhibition of maternal ALA-D activity than of the activity of nonpregnant animals possibly indicates a higher susceptibility to lead in pregnancy.

Air Pollutants↗
PubMed1995

Two weeks inhalation exposure to 4-tert-butyltoluene causes persistent changes in visually evoked potentials in rats.

The effects of repeated exposure to 20 p.p.m. 4-tert-butyltoluene (CAS No. [98-51-1]) 6 hr/day for 14 days on the function of the intact nervous system were examined by measurements of flash evoked potentials in Wistar rats. The exposure to 4-tert-butyltoluene induced changes in the amplitudes of the flash evoked potentials. The changes were significantly different from controls on day 2, 19 and 26 after cessation of the exposure, but not on day 5 and 12. No significant difference in body weight gain between groups was found during the experiment. These results indicate that repeated exposure to 20 p.p.m. 4-tert-butyltoluene causes persistent changes in the function of the central nervous system measured as changes in the flash evoked potential. A reevaluation of the present TLV value of 10 p.p.m. for 4-tert-butyltoluene is suggested.

Administration, Inhalation↗
PubMed1991

[A multi-chamber model of quartz dust kinetics in the pulmonary region during chronic inhalation exposure in rats].

The contributors propose a multichamber model for the assessment of dust particles' concentration, elimination and translocation in deep pulmonary zones. The choice of the model structure is dominated by the following criteria: that dust penetration into the interstitial pulmonary tissues and its translocation to the lymph nodes can be performed by non-phagocytized particle only; that these processes depend on the degree of dust-induced lesions in the macrophages and the growth of compensating neutrophilic phagocytosis; that part of the penetrating particles would continuously return to the free surface of the pulmonary zone together with the mobilized interstitial lung macrophages. The model adequately corresponds to the experimental data obtained in prolonged inhalation experiments, and imitates the kinetic effects related to severe damages and protection of the pulmonary clearance macrophage mechanisms.

Administration, Inhalation↗
PubMedDate not supplied

Regeneration of olfactory mucosa in mice after inhalation exposure to perchloroethylene.

An experimental group of 20 male pure-bred mice was exposed to perchloroethylene gas at 300 ppm for 6 h daily for 5 days. Histopathological study of the nasal mucosa, particularly the olfactory mucosa, was performed sequentially 2 weeks to 3 months after exposure, to clarify the process of regeneration. The tissue damage due to perchloroethylene gas was more persistent in the nasal mucosa of the olfactory region than in the respiratory region. Two weeks after exposure, ciliated epithelial cells, as well as normal pseudostratified nonciliated columnar epithelium, began to appear in the area previously covered by olfactory epithelium and remained for up to 3 months after exposure. A basement membrane was present under the ciliated epithelium, suggesting a possible persistence of basal cells. The olfactory epithelium may thus be replaced by ciliated epithelium. The lamina propria of the olfactory mucosa, however, lost its normal structure with atrophy of the olfactory nerves and Bowman's glands.

Administration, Inhalation↗
PubMed1988

Sensitisation of guinea pigs by inhalation exposure to low molecular weight chemicals.

Guinea pigs could be immunologically sensitised (as shown by the development of antigen-specific homocytotropic antibodies) to toluene diisocyanate by exposing them for 3 h a day for 5 consecutive days to atmospheres containing free chemical. Pulmonary reactions could be elicited in many of the sensitised animals by challenging them with atmospheres containing protein conjugates of the chemical and then measuring changes in respiratory rate. Successful elicitation of pulmonary reactions appeared to depend upon a number of factors, including the quality of the protein conjugate used for the challenge, but possibly also the development of IgE as well as IgG1 antibodies. Antigen-specific homocytotropic antibodies were detected in guinea pigs similarly exposed by inhalation to two non-isocyanate respiratory allergens, trimellitic anhydride and a reactive dye. Although the animals were immunologically sensitised to the chemicals, challenge with atmospheres containing appropriate chemical-protein conjugates failed to stimulate changes in respiratory rate.

Allergens↗
PubMed1980

Dose-related hepatotoxicity of 1,1,2-trichloro-1,2,2-trifluoroethane in short-term intermittent inhalation exposure in rats.

Male Wistar rats were exposed to 200, 1000 or 2000 ppm of 1,1,2-trichloro-1,2,2-trifluoroethane vapor 5 days a week 6 h daily for 1 or 2 weeks. Proliferation and vacuolisation of the smooth endoplasmic reticulum (SER) of the liver was seen electron microscopically after 1 and 2 weeks in the rats exposed to 1000 and 2000 ppm. Among the hepatic drug metabolizing enzymes, NADPH cytochrome c reductase activity showed a dose-related decrease whereas the tightly membrane-bound UDPglucuronosyltransferase exhibited a dose-dependent enhancement in its measurable activity. The overall drug oxidation reaction, 7-ethoxycoumarin O-deethylase was not affected by the 1,1,2-trichloro-1,2,2,-trifluoroethane inhalation at all, either in the liver or in the kidneys. 1,1,2-Trichloro-1,2,2-trifluoroethane binds to cytochrome P-450 with the production of a type I difference spectrum, suggesting that it may act as a substrate for this enzyme. The binding affinity is increased by phenobarbital-treatment of the rats.

Animals↗
PubMedDate not supplied

Olfactory mucosal necrosis in male CD rats following acute inhalation exposure to hydrogen sulfide: reversibility and the possible role of regional metabolism.

Hydrogen sulfide (H2S) is a potent inhibitor of cytochrome oxidase (CO) and is associated with dysosmia and anosmia in humans and nasal lesions in exposed rodents. An improved understanding of the pathogenesis of these lesions is needed to determine their toxicological relevance. We exposed 10-week-old male CD rats to 0, 30, 80, 200, or 400 ppm H2S for 3 hours/day for 1 or 5 days consecutively. The nose was histologically examined 24 hours after H2S exposure, and lesion recovery was assessed at 2 and 6 weeks following the 5-day exposure. A single 3-hour exposure to > or = 80 ppm H2S resulted in regeneration of the respiratory mucosa and full thickness necrosis of the olfactory mucosa localized to the ventral and dorsal meatus, respectively. Repeated exposure to the same concentrations caused necrosis of the olfactory mucosa with early mucosal regeneration that extended from the dorsal medial meatus to the caudal regions of the ethmoid recess. Acute exposure to 400 ppm H2S induced severe mitochondrial swelling in sustentacular cells and olfactory neurons, which progressed to olfactory epithelial necrosis and sloughing. CO immunoreactive cells were more frequently observed in regions of the olfactory mucosa commonly affected by H2S than in regions that were not. These findings demonstrate that acute exposure to >80 ppm H2S resulted in reversible lesions in the respiratory and olfactory mucosae of the CD rat and that CO immunoreactivity may be a susceptibility factor for H2S-induced olfactory toxicity in the rat.

Administration, Inhalation↗
PubMed1991

Two-week, repeated inhalation exposure of F344/N rats and B6C3F1 mice to ferrocene.

Ferrocene (dicyclopentadienyl iron; CAS No. 102-54-5) is a relatively volatile, organometallic compound used as a chemical intermediate, a catalyst, and as an antiknock additive in gasoline. It is of particular interest because of its structural similarities to other metallocenes that have been shown to be carcinogenic. F344/N rats and B6C3F1 mice were exposed to 0, 2.5, 5.0, 10, 20, and 40 mg ferrocene vapor/m3, 6 hr/day for 2 weeks. During these exposures, there were no mortality and no observable clinical signs of ferrocene-related toxicity in any of the animals. At the end of the exposures, male rats exposed to the highest level of ferrocene had decreased body-weight gains relative to the weight gained by filtered air-exposed control rats, while body-weight gains for all groups of both ferrocene- and filtered air-exposed female rats were similar. Male mice exposed to the highest level of ferrocene also had decreased body-weight gains, relative to controls, while female mice had relative decreases in body-weight gains at the three highest exposure levels. Male rats had a slight decrease in relative liver weight at the highest level of exposure, whereas no relative differences in organ weights were seen in female rats. Male mice had exposure-relative decreases in liver and spleen weights, and an increase in thymus weights, relative to controls. For female mice, relative decreases in organ weights were seen for brain, liver, and spleen. No exposure-related gross lesions were seen in any of the rats or mice at necropsy. Histopathological examination was done only on the nasal turbinates, lungs, liver, and spleen.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Inhalation↗
PubMedDate not supplied

Dental pulp infarction in female rats following inhalation exposure to 2-butoxyethanol.

Female Fischer 344 (F344)/N rats (10 per exposure group) were exposed to 2-butoxyethanol (BE) vapors (0, 31, 62.5, 125, 250, or 500 ppm 6 h/d, 5 d/wk, for 13 weeks) to characterize its prechronic toxicity. Dental lesions consisting of bilateral multifocal dental pulp thrombosis, pulp infarction, and odontoblast infarction were noted in the maxillary incisors of 3 of 4 rats from the 500-ppm group that were sacrificed when moribund during the first week of exposure. In addition, 1 rat from the 500-ppm group that was sacrificed on day 32 had similar unilateral incisor lesions but with additional findings consistent with a unilateral maxillary incisor fracture. In contrast, rats sacrificed after 13 weeks of exposure lacked dental lesions. In conclusion, BE has the potential to cause pulp thrombosis and odontoblast infarction in female rats. The apparent variability in response to BE noted in moribund sacrificed vs terminally sacrificed rats was attributed to development of tolerance to BE-induced hemolysis and subsequent incisor regeneration.

Administration, Inhalation↗
PubMed1988

Developmental toxicity in rats after inhalation exposure of di-2-ethylhexylphthalate (DEHP).

Di-2-ethylhexylphthalate (DEHP) was investigated in Wistar rats for developmental toxicity after head-nose exposure to aerosol concentrations of 0, 0.01, 0.05 and 0.3 mg/l for 6 h per day from gestation day 6 through 15. A range finding study revealed peroxisome proliferation in the liver of the dams throughout exposure levels of 0.2, 0.5 and 1.0 mg/l with an increasing trend. 0.3 mg/l was therefore regarded as an exposure level leading to peroxisome proliferation as a marker for maternal effects. All concentrations were tolerated without clinical signs of maternal toxicity. The fetuses of 20 animals per exposure group were investigated for structural defects. Five additional animals per group were allowed to litter and the offsprings were raised and observed for postnatal signs of toxicity. No significant developmental toxicity or changes in the postnatal physical development were observed. DEHP is assumed not to exhibit developmental toxicity under the experimental conditions employed.

Abnormalities, Drug-Induced↗
PubMed1995

Acute effects of inhalation exposure to carbon monoxide on schedule-controlled operant behavior and blood carboxyhemoglobin levels in rats.

The acute effects of carbon monoxide (CO) exposure on a steady-state operant behavior (bar-pressing under a VI 60-sec schedule of food reinforcement) were repeatedly measured in (a) rats exposed to various concentrations of CO (500, 1,000, 1,500 and 2,000 ppm) for 1 h and (b) rats exposed to 1,500 ppm for different periods (1, 2 and 4 h). Measurements were made continuously before, during and after the exposure period. Abrupt cessation of the response was produced by exposure to 1,000 ppm or higher concentrations of CO. Recovery from the effects of CO exposure was observed as sudden resumption of responding during the post-exposure period. The duration of exposure required to produce response inhibition was closely correlated with the exposure concentration. The post-exposure interval required for response recovery was also correlated with the exposure concentration. This post-exposure response recovery interval, however, was constant and independent of the duration of exposure when the concentration was fixed at 1,500 ppm. In order to correlate these behavioral changes with an internal index of CO exposure, blood carboxyhemoglobin (HbCO) levels were determined under several exposure conditions corresponding to those of the behavioral observations. It was found that HbCO levels were within a certain range (33-43%) when response recovery occurred, suggesting the existence of a critical HbCO level (threshold) associated with the drastic behavioral change. Hence, these results support the view that blood HbCO is an important determinant of the acute behavioral effects of CO.

Administration, Inhalation↗
PubMed1999

Effects of continuous inhalation exposure of rats to radon and its progeny at various levels of dose and dose rate: interim results.

Studies of rats at Harwell and CEA [Monchaux et al., Radiat. Res. 152 (Suppl.), S137-S140, 1999] are currently in progress to determine the factors affecting the risk of induction of lung tumors after exposure to radon and radon progeny. Knowledge of the effect of dose, dose rate and characteristics of the aerosol on lung tumor induction in rats may be used to improve estimates of risk from domestic exposure. At Harwell, three studies are in progress, studying the effect of dose, dose rate, and dose rate at low total exposures. Approximately 2000 adult male rats have been exposed. A small number of rats were taken to determine deposition in the respiratory tract and the early effects of exposure on cell proliferation and nuclear aberrations. The remaining animals have been held for their life span. To date 65% of the animals in the first study have been examined. Current results (for 421 rats) suggest that exposure to radon and radon progeny causes elevated incidences of both benign and malignant lung tumors. These findings are based on incomplete tumor incidences. Competing causes of death may affect the results, and full statistical analysis is required before firm conclusions can be drawn about the effect of dose and dose rate.

Administration, Inhalation↗