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PubMed1996

Embryotoxicity study of monomeric 4,4'-methylenediphenyl diisocyanate (MDI) aerosol after inhalation exposure in Wistar rats.

One of the uses of MDI is as an alternative to formaldehyde in the manufacture of furniture, its main route of exposure to humans being by inhalation. There have been no previous studies on the potential prenatal toxic effects of this compound. To close this gap in information, gravid Wistar rats, Crl:(WI)BR, were exposed by whole-body inhalation to clean air (control) and to 1, 3, and 9 mg/m3 MDI, respectively, for 6 hr per day from Days 6 to 15 post conception (p.c.). Rats were killed on Day 20 p.c. and the following results were obtained: Treatment caused a dose-dependent decrease in food consumption in all substance-treated groups during exposure, returning to normal values after cessation of treatment. The lung weights in the high-dose group were significantly increased compared to the sham-treated control animals. Treatment did not influence any other material and/or fetal parameters investigated (maternal weight gain, number of corpora lutea, implantation sites, pre- and postimplantation loss, fetal and placental weights, gross and visceral anomalies, degree of ossification), although a slight but significant increase in litters with fetuses displaying asymmetric sternebra(e) was observed after treatment with the highest dose of 9 mg/m3. Although the relevance of an increase of this minor anomaly in doses which cause toxic effects in dams (reduced food consumption, increased lung weights) is limited and the number observed is within the limits of biological variability, a substance-induced effect in the high-dose group cannot be excluded with certainty. Consequently, a no embryotoxic effect level of 3 mg/m3 was determined.

Administration, Inhalation↗
PubMed1996

Acute inhalation exposure to isobutyl nitrite causes nonspecific blood cell destruction.

Abuse of nitrite inhalants is widespread among male homosexuals and has been epidemiologically correlated with seropositivity to human immunodeficiency virus (HIV) and to Kaposi's sarcoma. These drugs may act as cofactors in AIDS if they compromise the ability to resist infection or tumor growth. We have previously reported that 14 daily 45-minute exposure to 900 ppm isobutyl nitrite in an inhalation chamber did compromise the immunocompetence of mice. We now report that a single 45-minute exposure produced a transient anemia. Erythrocyte counts, hemoglobin, and hematocrit levels were reduced by 7% but rebounded to above-normal levels 24 hours later. In vitro exposure of blood to isobutyl nitrite vapors did not lyse the cells but did induce Heinz body formation and increase their binding to macrophages. Thus, it is likely that the red cells were removed by phagocytic clearance not by direct lysis. Blood leukocyte numbers were also reduced following a single exposure to the inhalant, but the cell loss was delayed until 24 hours after exposure. Recovery of peripheral blood leukocytes 72 hours after exposure coincided with a reduction in spleen cellularity, suggesting that spleen cells were mobilized to replace lost blood leukocytes.

Animals↗
PubMed2002

Maternal-fetal distribution of cadmium in the guinea pig following a low dose inhalation exposure.

Pregnant guinea pigs in their last trimester of gestation were exposed by inhalation to cadmium (Cd) chloride level (50 microg/m3 Cd) for 1 and 5 days. Cd content was evaluated by atomic absorption spectrophotometry. Maternal blood Cd concentration increased by 127 and 223% of control for 1 and 5 days of exposure. Maternal lung Cd concentration increased significantly by 11.66- and by 48.24-fold after 1 and 5 days of treatment, while maternal liver showed an increase of 188 and 227% for 1 and 5 days of exposure. Also, fetal Cd concentration significantly increased in brain (156 and 192%), liver (159 and 174%) and heart (201 and 157%) after 1 and 5 days of exposure, compared to unexposed females. Placental calcium content decreased significantly by 16% of control after 5 days of exposure. These results suggest that low-level inhalation of Cd may pass through the guinea pig placenta and accumulate in fetal brain, liver and heart.

Administration, Inhalation↗
PubMed1977

A pharmacokinetic model to study the excretion of trichloroethylene and its metabolites after an inhalation exposure.

For a better understanding of absorption, distribution, excretion, and metabolism of trichloroethylene the time-course of blood concentration of the vapour and urinary excretion of its metabolites was examined using a pharmacokinetic model. After a single experimental exposure in which four men inhaled 100 parts per million (ppm) of trichloroethylene for four hours an elimination curve showed three exponential components, that is, X=1-0005e(-16.71t)+0-449e(-1.710t)+0-255e(-0.2027t), where X is that blood concentration in mg/l and t the time in hours from 0 to 10. The overall rate constant for the disappearance of trichloroethylene was found to a agree with the theoretical one, estimated by means of a mathematical model for the blood concentration data. A D8- XD plot, developed from a mathematical model for urinary excretion, could also give a good estimate of rate constant for the transfer of trichloroethylene in the body. The rate constant thus estimated from urinary excretion was consistent with data on the blood concentration.

Adult↗
PubMed1999

Histomorphological and histochemical alterations following short-term inhalation exposure to sulfur mustard on visceral organs of mice.

Toxic effects of inhaled sulfur mustard (SM) on the histology of visceral organs was investigated by exposing mice to 84.6 mg/m3 for 1 h duration, using controlled single exposure conditions. A progressive fall in body weight from third day onwards was noticed. Light microscopic examination of the pulmonary tissue of these animals at 6 h post exposure revealed that the tracheobronchial epithelium remained intact, but was infiltrated by inflammatory cells. By 24 h post exposure, the mucosecretory cells were destroyed. The inflammatory reaction was maximum at 48 h. By 7th day post exposure there was swelling and vacuolation of lung parenchymal cells and thrombi formation. In addition SM caused congestion and hemorrhage at alveolar level. SM also caused granulovacuolar degeneration with perinuclear clumping of the cytoplasm of hepatocytes and renal parenchymal cells. Renal lesions were characterized by congestion and hemorrhage. Among visceral tissues, maximum atrophy was observed in spleen. Distribution of lesions increased with post exposure period. The maximum lesions were observed at 7th day post-exposure.

Animals↗
PubMed2003

Effect of asphalt fume inhalation exposure at simulated road paving conditions prior to bacterial infection on lung defense responses in rats.

Asphalt fume inhalation has been suspected of affecting immune function in exposed workers. The objective of this study was to evaluate the effect of asphalt exposure on lung immune responses in rats using a bacterial infectivity model. Pathogen-free male Sprague-Dawley rats were exposed by inhalation to asphalt fumes (72.6 +/- 4.95 mg/m3) or filtered air for 6 h/day for 5 days. One day after the final asphalt exposure, rats were intratracheally inoculated with 5 x 10(5) Listeria monocytogenes. At 0 (prior to bacterial inoculation), 3, and 7 days after L. monocytogenes instillation, the lungs of each animal were divided. Bronchoalveolar lavage (BAL) was performed on right lungs. The recovered BAL cells were then differentiated and counted, and alveolar macrophage (AM) function was determined. Albumin and lactate dehydrogenase (LDH), two indices of lung injury, were measured in the acellular BAL fluid. To assess bacterial clearance, the left lungs were removed, homogenized, and bacterial colony-forming units (CFUs) were counted. In addition, lung-draining lymph nodes were removed, and lymphocyte phenotype and lymphocyte-induced cytokine production were examined. Asphalt fume exposure did not cause lung injury or inflammation in rats in the absence of infection. Infection induced elevations in AMs, neutrophils (PMNs), albumin, and LDH. Importantly, no significant differences were seen when comparing the asphalt group with the air and nonexposed naive groups at any time before or after infection. Also, asphalt fume inhalation exposure did not affect the rate of pulmonary clearance of L. monocytogenes or AM production of reactive oxygen and nitrogen species. However, asphalt-related increases in lymphocyte secretion of interferon (IFN)-gamma, interleukin (IL)-6, and IL-10 were observed at different times after bacterial infection, whereas the total number of lymph-node cells and the percentage of CD4+ and CD8+ cells were not significantly different among the treatment groups. Despite the asphalt-induced changes observed in lymphokine secretion, adaptive immune function seemed to function properly in lung defense against bacterial infection. Because innate nonspecific lung responses and pulmonary clearance of L. monocytogenes were unaffected by asphalt fume exposure, lung defenses were sufficient to control the infection. It was concluded that acute inhalation of asphalt fumes at a high concentration had a minimal effect on lung immune responses to infection in rats.

Animals↗
PubMedDate not supplied

Behavioural effects of prenatal metallic mercury inhalation exposure in rats.

The effects of administration by inhalation of metallic mercury vapour (Hg0) to pregnant rats, approximately corresponding to doses of 0.2 mg Hg0/kg/day (high dose) or 0.07 mg Hg0/kg/day (low dose), on the developmental and behavioural repertoire of the offspring were studied. Exposure occurred during days 11-14 plus 17-20 of gestation. The dose levels were selected so as not to induce maternal toxicity. Maturation variables such as surface righting, negative geotaxis, pinna unfolding, and tooth eruption revealed no differences between Hg0-treated offspring and controls. Tests of spontaneous motor activity showed that the Hg0-treated offspring were hypoactive at 3 months of age but hyperactive at 14 months. In spatial learning tasks the prenatally exposed offspring showed retarded acquisition in the radial arm maze but no differences in circular swim maze. A simple test of learning, habituation to a novel environment (activity chambers), indicated a reduced ability to adapt. These data suggest that prenatal exposure to Hg0 vapour results in similar behaviour changes in the offspring as reported for methylmercury.

Administration, Inhalation↗
PubMed1997

Assessment of the in vivo mutagenicity of ethylene oxide in the tissues of B6C3F1 lacI transgenic mice following inhalation exposure.

In the present study, the lacI mutant frequency was determined in the tissues of B6C3F1 lacI transgenic mice exposed by inhalation to ethylene oxide (EO). Groups of 15 male transgenic lacI B6C3F1 mice were exposed to either 0, 50, 100, or 200 ppm EO for 4 weeks (6 h/day, 5 days/week) and were sacrificed at 0, 2, or 8 weeks after the last EO exposure. The lacI transgene was recovered from lung, bone marrow, spleen, and germ cells for determination of the lacI mutant frequency. The tissues selected for analysis were tumor target site tissues in chronic bioassays (lung tumors and lymphomas) and germ cells. The lacI mutant frequency in lung was significantly increased at 8 weeks post exposure to 200 ppm EO (6.2 +/- 2.2 vs. 9.1 +/- 1.5. p = 0.046). In contrast, the lacI mutant frequency in spleen and bone marrow at 2 and 8 weeks was not significantly increased in mice exposed to 200 ppm EO. The lacI mutant frequencies in male germ cells for 200 ppm EO-exposed mice were not increased compared to air controls at 2 and 8 weeks post-exposure. In a spleen cell fraction two of three EO-exposed mice at the 200 ppm exposure level demonstrated an elevated lacI mutant frequency. The increased lacI mutant frequency in these animals was likely due to mutant siblings that contained background G:C --> A:T transitions at CpG sites. These results demonstrate that a 4-week inhalation exposure to EO is mutagenic in lung. However, EO did not increase the frequency of mutations recovered at the lacI transgene in other tissues examined under the conditions used in the present studies. Since the mutational spectrum for EO in other systems consists of an increased proportion of large deletions, the lack of a mutagenic response in the tissues examined is likely due to the lack of recovery of large deletions in lambda-based shuttle vector systems. These data indicate that a primary mechanism of EO-induced mutagenicity in vivo is likely through the induction of deletions, not specific point mutations.

Administration, Inhalation↗
PubMed1984

The effect of 3-methylfuran inhalation exposure on the rat nasal cavity.

The acute inhalation toxicity of 3-methylfuran (3MF) was investigated in female CD/CR rats. Animals were killed 1, 3, 6, 9, 12, 15 and 30 days following a 1-h exposure to 148 mumol 3MF/1. Relatively selective 3MF-induced necrosis of the olfactory epithelium was seen at day 1 post exposure. Subsequent resolution of the acute olfactory necrosis was not complete and resulted in partial occlusive fibrosis of the nasal cavity as seen at 30 days. Pretreatment of the animals with piperonyl butoxide (PB) did not block 3MF-induced olfactory epithelial necrosis although it prevented Clara cell necrosis when given at a dose of 800 mg/kg intraperitoneally 1 h before exposure to 3MF.

Animals↗
PubMed2005

Inhalation exposure to isocyanates of car body repair shop workers and industrial spray painters.

As part of a large-scale epidemiological study, occupational isocyanate exposure was assessed in spray-painting environments. The aim was to assess which compounds contribute to isocyanate exposure in car body repair shops and industrial painting companies, and to identify tasks with high risk of isocyanate exposure. Mainly personal task-based samples (n = 566) were collected from 24 car body repair shops and five industrial painting companies using impingers with DBA in toluene. Samples were analysed by LC-MS for isocyanate monomers, oligomers and products of thermal degradation. From the 23 analysed compounds, 20 were detected. Exploratory factor analysis resulted in a HDI, TDI and MDI factor with the thermal degradation products divided over the TDI and MDI factors. The HDI factor mainly consisted of HDI oligomers and was dominant in frequency and exposure levels in both industries. Spray painting of PU lacquers resulted in the highest exposures for the HDI factor (<LOD-2643 microg/m(3) NCO), with no significant difference between the industries. Exposure variability during PU spray painting was large with a variability over time of (ww)S(2) = 9.1 compared with between-worker variability of (bw)S(2) = 1.6. Lower level exposure to the HDI factor was found during other painting-related tasks and even tasks without direct exposure to paint. Exposure to the TDI factor was found more regularly in car body repair shops than in industrial painting companies. Exposure levels were low (<LOD-5 microg/m(3) NCO) compared with the HDI factor and no clear contrast in levels between the tasks was observed. Exposure to the MDI factor was found incidentally during spraying and welding in car body repair shops (<LOD-0.5 microg/m(3) NCO). The results indicate that paint is the most important source and major contributor of isocyanate exposure in both industries with highest exposures during PU spraying. However, since respiratory protection is less extensively used during other tasks, lower level exposure during these other tasks may significantly contribute to the internal dose.

Air Pollutants, Occupational↗
PubMed2005

Hardwood smoke alters murine splenic T cell responses to mitogens following a 6-month whole body inhalation exposure.

The purpose of these studies was to assess the effects of hardwood smoke (HWS) inhalation (30-1000 microg/m3) on the systemic immune responses of A/J mice evaluated after 6 months of daily exposures. Spleen cells obtained from mice were assessed for changes in cell number, cell surface marker expression [B, T, macrophage, and natural killer (NK) cells], and responses to B cell (LPS, endotoxin) and T cell (Con A) mitogens. Results showed that HWS smoke increased T cell proliferation in the 100 microg/m3 exposure group and produced a concentration-dependent suppression of T cell proliferation at concentrations >300 microg/m3. There were no effects on B cell proliferation or in spleen cell surface marker expression. Analyses of the exposure atmospheres revealed the presence of significant levels of naphthalene and methylated napthalenes, fluorene, phenanthrene, and anthracene in the exposure chambers, as well as low concentrations of several metals (K, Ca, and Fe). Our results demonstrate that environmentally relevant concentrations of HWS may be immunosuppressive to the immune system of mice exposed during a 6-month period.

Animals↗
PubMedDate not supplied

[Proteolytic system in lungs upon inhalation exposure to low doses of lead salts].

Changes in proteinase--antiproteinase activities in lungs as a result of short-term (for 1 week) inhalation of rats with 0.01% (CH3COO)2 Pb have wholly compensative patterns, but it have been found increased cathepsine B activity as a negative prognostic factor. Chronic (for 2 month) toxicant inhalation caused considerable activation of both trypsine and cathepsine B under decreasing alpha 1-antitrypsine and alpha 2-macroglobuline activities. Cathepsine L activity was not affected. Disorders in the proteolysis system were evaluated as desadaptation situation in lung tissue under chronic toxic influence.

Animals↗
PubMed1981

Pulmonary response and transmigration of inorganic fibers by inhalation exposure.

Rats, hamsters, and guinea pigs were exposed by inhalation to different concentrations of potassium octatitanate fibers. Following 3 months of exposure, the animals were sacrificed between the 15th and 24th month. The exposed animals showed dose-related dust deposition and pulmonary fibrosis mainly in the respiratory bronchiolar region. Most short fibers (less than 5 micrograms) were phagocytized by alveolar macrophages, but long fibers (greater than 10 micrograms) were phagocytized by foreign body giant cells. Dust-laden macrophages (dust cells) entered into the lumen of bronchial lymphatic or pulmonary blood vessels. Numerous dust cells were transported from the lung to the tracheobronchial and mediastinal lymph nodes where some dust cells penetrated into the blood or lymphatic circulation. Massive direct cell migration of the mediastinal adipose tissue from the lymph nodes occurred occasionally. Dust-laden giant cells were found only occasionally in the liver, and there was widespread migration of the fibers into other vital organs and tissues without any significant responses.

Animals↗
PubMedDate not supplied

Morphology of nasal lesions in F344/N rats following chronic inhalation exposure to naphthalene vapors.

Naphthalene (CAS No. 91-20-3) administered by inhalation at concentrations of 10, 30, or 60 ppm for 6 hours per day, 5 days per week for 105 weeks caused nonneoplastic and neoplastic effects in nasal respiratory and olfactory regions of male and female F344/N rats. Non-neoplastic nasal effects were characterized by an increase in the incidence and severity of a complex group of lesions, including atypical hyperplasia, atrophy, chronic inflammation, and hyaline degeneration of olfactory epithelium; hyperplasia, squamous metaplasia, hyaline degeneration, and goblet cell hyperplasia of the respiratory epithelium; and hyperplasia and squamous metaplasia of mucosal glands. Neoplastic effects were characterized by the induction of two types of rare primary nasal tumors, olfactory neuroblastomas and respiratory epithelial adenomas. The incidences of olfactory neuroblastomas in males at 0 ppm, 10 ppm, 30 ppm, and 60 ppm were, respectively, 0%, 0%, 8%, and 6%, whereas in females they were 0%, 4%, 6%, and 24%. The incidences of respiratory epithelial adenomas in males at 0 ppm, 10 ppm, 30 ppm, and 60 ppm were, respectively, 0%, 12%, 17%, and 31% and in females 0%, 0%, 8%, and 4%. The olfactory neuroblastomas and respiratory epithelial adenomas were considered carcinogenic effects related to naphthalene exposure based on their relatively high incidence in exposed rats, their absence in concurrent control rats and NTP historical controls, and their rare spontaneous occurrence in rats of any strain.

Adenoma↗