Treatment of inhalational exposure to hydrofluoric acid with nebulized calcium gluconate.
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Administration, Inhalation↗
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Effects of chronic inhalation exposure to diesel exhaust on the development of lung tumors in di-isopropanol-nitrosamine-treated F344 rats and newborn C57BL and ICR mice.
Long-term exposure to diesel exhaust from a small diesel engine was carried out in order to elucidate the effects of exhaust on the development of lung tumors in F344 rats and newborn ICR and C57BL mice. The deposition of inhaled particles progressed in accordance with duration of exposure in both sets of the animals. No evidence of lung tumor formation was detected following exposure to diesel exhaust alone in rats. However, the combined treatment with DIPN and diesel exhaust led to an overadditive effect in the development of lung tumors. There was a tendency for the diesel-exposed mice to have higher incidences of lung tumors compared with non-exposed mice. The results obtained in the present study suggest that diesel exhaust may act as a factor relating to human respiratory carcinogenesis.
Adenocarcinoma↗
Distribution of benzo[a]pyrene in pregnant rats following inhalation exposure and a comparison with similar data obtained with pyrene.
Eight pregnant rats were exposed, on the 17th day of gestation, for 95 min to a microcondensation aerosol of benzo[a]pyrene at five different atmospheric concentrations between 200 and 800 mg m-3 in a 'head-only' inhalation chamber. Five rats were killed immediately following the exposure and three were killed at 6 h post-dosing. Concentrations of the radiolabel and 'free' benzo[a]pyrene were measured in the individual fetuses and in the maternal blood, fat, kidney, liver and lung. Distribution to the fetus did not appear to be related to its position on the uterine horn and the uptake of benzo[a]pyrene was non-linear with increasing exposure concentrations, which was similar to the observations previously reported for pyrene. The levels of benzo[a]pyrene were much higher in the fetus and, especially, the lung than those observed in the pyrene study; so also were the levels of total metabolites in these tissues, which might, in part, account for the carcinogenic potency of benzo[a] pyrene.
Administration, Inhalation↗
The toxicity of dimethylamine in F-344 rats and B6C3F1 mice following a 1-year inhalation exposure.
Dimethylamine is a widely used commodity chemical, for which there are few chronic toxicity data. Male and female F-344 rats and B6C3F1 mice were exposed by inhalation to 0, 10, 50, or 175 ppm dimethylamine (DMA) for 6 hr/day, 5 days/week for 12 months. Groups of 9-10 male and female rats and mice were necropsied after 6 and 12 months of exposure. No male mice were sacrificed at 12 months due to a high incidence of early deaths in that group. The mean body weight gain of rats and mice exposed to 175 ppm DMA was depressed to approximately 90% of control after 3 weeks of exposure. The only other treatment-related changes were concentration-related lesions in the nasal passages. Two distinct locations in the nose were affected: the respiratory epithelium in the anterior nasal passages, and the olfactory epithelium, especially that lining the anterior dorsal meatus. There was focal destruction of the anterior nasoturbinate and nasal septum, local inflammation, and focal squamous metaplasia of the respiratory epithelium in rats and mice. Mild goblet cell hyperplasia was observed only in rats. The olfactory epithelium exhibited extensive loss of sensory cells with less damage to sustentacular cells. There was also loss of olfactory nerves, hypertrophy of Bowman's glands, and distension of the ducts of these glands by serocellular debris in regions underlying degenerating olfactory epithelium. At the 175-ppm exposure level, rats had more extensive olfactory lesions than mice, with hyperplasia of small basophilic cells adjacent to the basement membrane being present in rats but not mice. After 12 months of exposure to 10 ppm DMA, minimal loss of olfactory sensory cells and their axons in olfactory nerve bundles was observed in the nasal passages of a few rats and mice. These results indicate that the olfactory sensory cell is highly sensitive to the toxic effects of DMA, with minor lesions being produced in rodents even at the current threshold limit value of 10 ppm.
Air Pollutants↗
Effects of short-term inhalation exposure to 1-nitropropane and 2-nitropropane on rat liver enzymes.
Male Sprague-Dawley rats were exposed to vapors of 1-nitropropane (1-NP) and 2-nitropropane (2-NP) at air concentrations of 100 ppm for 7 hours per day on four consecutive days. Livers were analyzed for enzymatic activities after 1-, 2-, and 4-day inhalation periods. Liver microsomal cytochrome P450 was depressed by 2-NP and elevated following exposure to 1-NP. Levels of cytochrome b5 were slightly increased in rats exposed to 1-NP and remained unchanged after inhalation of 2-NP. Total glutathione (GSH), GSH S-transferase, and UDP-glucuronosyltransferase activities were enhanced by 2-NP. 1-NP induced GSH peroxidase while 2-NP did not. Glutathione reductase was not altered after exposure to either isomer. No changes in the microsomal malondialdehyde content as a measure of lipid peroxidation and in the levels of serum aspartate transferase and serum glutamic oxaloacetic transaminase were observed during a 4-day exposure period in either of the exposed groups compared to control animals.
Animals↗
[The cytopathic and cytogenetic sequelae of chronic inhalational exposure to formaldehyde on female germ cells and bone marrow cells in rats].
A study was made of cytopathological and cytogenetic effects of formaldehyde chronic inhalation, in doses 0.5 and 1.5 mg/m3, on the female rat's germ and marrow cells. The harmful effect of formaldehyde on germ cells (according to the patterns of early embryogenesis) is noted under the dose 1.5 mg/m3 only, while the reliable clastogenic and cytogenetic effects on the marrow cells were revealed even in the dose 0.5 mg/m3. It is concluded that the differences between effects of small doses of formaldehyde on different cell systems were evidently caused by the specific cell dynamics of these systems.
Administration, Inhalation↗
Effects of a 13-week chloropentafluorobenzene inhalation exposure of Fischer 344 rats and B6C3F1 mice.
Chloropentafluorobenzene (CPFB) has been identified as a candidate simulant for nonpersistent chemical warfare agents. Acute toxicity studies have shown that CPFB has limited adverse effects on laboratory animals. A 21-day inhalation study of rats and mice to 2.5, 0.8, and 0.25 mg CPFB/liter resulted in reduced weight gain in male and female rats exposed at the high concentration only and identified the liver as a potential target organ. This multiconcentration inhalation study was designed to detect a no-observable-effect level associated with repeated exposure to CPFB. Male and female rats and mice were exposed to 250, 50, or 10 mg CPFB/m3 (0.25, 0.05, or 0.01 mg CPFB/liter) for 13 weeks. No treatment-related effects on body weight, clinical chemistries, mortality, absolute or relative organ weight or histopathology were noted.
Administration, Inhalation↗
The toxicity of microcystin LR in mice following 7 days of inhalation exposure.
Microcystins, a family of cyclic heptapeptides produced by the cyanobacteria, Microcystis aeruginosa, have documented hepatotoxic and tumor promoting activities. The purpose of this study was to evaluate the toxicity of inhaled microcystin LR (microcystin). Male BALB/c mice were exposed by nose-only inhalation to 260-265 microg microcystin/m(3) for 7 days. The low-, mid- and high-dose groups were exposed for 0.5, 1, and 2h, respectively. Control animals were sham exposed to aerosolized vehicle. Treatment-related microscopic lesions were observed only in the nasal cavity of the mid- and high-dose groups. These lesions consisted of minimal to moderate multifocal degeneration and necrosis of the respiratory epithelium, with variable neutrophilic inflammation and minimal to marked degeneration, necrosis, and atrophy of the olfactory epithelium. The no-adverse-effect dose for the nasal lesions was approximately 3 microg/kg body weight, or 20 ng/cm(2) of nasal epithelium. In serum, only two protein peaks, occurring at m/zs of 11,688 and 11,829 Da, exhibited decreases in intensity that were microcystin dose-dependent. While these proteins have not been positively identified, they may be useful in the future as biomarkers of microcystin exposure in humans.
Administration, Inhalation↗
Effects of inhalation exposure to carbon disulfide and its combination with hydrogen sulfide on embryonal and fetal development in rats.
Pregnant rats were exposed to 0, 100, 200, 400 or 800 ppm of carbon disulfide (CS2), 100 ppm of hydrogen sulfide (H2S) alone or in combination with 400 and 800 ppm CS2, 6 h/d during days 6-20 of gestation. Maternal reproduction and fetal parameters were evaluated on gestational day 21. Treatment with 100 or 200 ppm CS2 or with 100 ppm H2S caused no maternal toxicity or adverse effects on the developing embryo or fetus. Exposure to 400 or 800 ppm CS2 resulted in a low incidence of club foot and in a significant reduction of maternal weight gain. Significant increases in unossified sternebrae occurred at 800 ppm CS2 and reduction of fetal body weight at 400 and 800 ppm CS2. The latter effect was enhanced by combination with 100 ppm H2S. These results support the conclusion that, at levels of exposure associated with maternal toxicity, CS2 leads to an increase in incidence of club foot and to fetal toxicity which is enhanced by simultaneous exposure to H2S.
Administration, Inhalation↗
Pulmonary function changes in rats after chronic and subchronic inhalation exposure to various particulate matter.
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Administration, Inhalation↗
Effects of repeated inhalation exposures to 1-nitropyrene, benzo[a]pyrene, Ga2O3 particles, and SO2 alone and in combinations on particle clearance, bronchoalveolar lavage fluid composition, and histopathology.
The toxicities of 1-nitropyrene (NP) and benzo[a]pyrene (BaP), inhaled alone and in combination with particles and an irritant gas, were examined to evaluate synergisms among the organic compounds, particles, and gas. Groups of F344 rats were exposed 2 h/d, 5 d/wk for 4 wk to atmospheres of pure NP aerosol (7.5 mg/m3), and to these same compounds adsorbed to Ga2O3 particles (27 mg/m3) both with and without coexposure to 5 ppm SO2. Rats were also exposed to Ga2O3 and SO2 alone. Measurements were made of lung burdens of Ga2O3 particles and retention of radiolabeled tracer particles after the cessation of exposure to evaluate effects on particle clearance. Bronchoalveolar lavage fluid was analyzed to assess inflammation and cytotoxicity. Histopathology was examined to assess the nature and extent of lung injury. Particle clearance was significantly impaired (p less than .05) in all groups whose exposure atmosphere included Ga2O3, but was not significantly changed in the other exposure groups.
Administration, Inhalation↗
Effect of inhalation exposure regimen on DNA binding potency of 1,2-dichloroethane in the rat.
1,2-Dichloroethane (DCE) was reported to be carcinogenic in rats in a long-term bioassay using gavage in corn oil (24 and 48 mg/kg/day), but not by inhalation (up to 150-250 ppm, 7 h/day, 5 days/week). The daily dose metabolized was similar in the two experiments. In order to address this discrepancy, the genotoxicity of DCE was investigated in vivo under different exposure conditions. Female F-344 rats (183-188 g) were exposed to [1.2-14C]-DCE in a closed inhalation chamber to either a low, constant concentration (0.3 mg/l = 80 ppm for 4 h) or to a peak concentration (0.3 mg/l = 80 ppm for 4 h) or to a peak concentration (up to 18 mg/l = 4400 ppm) for a few minutes. After 12 h in the chamber, the dose metabolized under the two conditions was 34 mg/kg and 140 mg/kg. DNA was isolated from liver and lung and was purified to constant specific radioactivity. DNA was enzymatically hydrolyzed to the 3'-nucleotides which were separated by reverse phase HPLC. Most radioactivity eluted without detectable or with little optical density, indicating that the major part of the DNA radioactivity was due to covalent binding of the test compound. The level of DNA adducts was expressed in the dose-normalized units of the Covalent Binding Index, CBI = mumol adduct per mol DNA nucleotide/mmol DCE per kg body wt.(ABSTRACT TRUNCATED AT 250 WORDS)
Administration, Inhalation↗
Lung response to test toner upon 2-year inhalation exposure in rats.
SPF F-344 rats were exposed 6 h/day 5 days/wk for up to 24 months to a special test toner at 0, 1, 4 and 16 mg/m3 or TiO2 at 5 mg/m3, or SiO2 at 1 mg/m3, by the inhalation route. The animals were kept for an additional 6 weeks in filtered air. Surviving animals were sacrificed at 25.5 months after start of exposure. Life-span and causes of death were independent of treatment and in accordance with published values. No evidence for systemic toxicity or any upper-respiratory system effects were found in the toner-exposed groups. The incidence of lung tumors was comparable in the control, 3 toner and TiO2-exposed groups. An incidence of 18%, combined benign and malignant tumors was observed in the quartz-treated rats. A slight to moderate degree of fibrosis was observed at the toner high exposure level in all animals, while a very slight degree of fibrosis was noted in 20% of the animals at the toner middle (4 mg/m3) exposure level. The fibrogenic potency of the test toner was calculated to be comparable to TiO2. No pulmonary changes were seen at the toner low (1 mg/m3) and environmentally most relevant exposure level.
Administration, Inhalation↗
Effect of equilibration zones on stability, uniformity, and homogeneity profiles of vapors and aerosols in the ADG nose-only inhalation exposure system.
A commercially available, inexpensive, nose-only exposure chamber was modified to include removable equilibration zones, and the effect of these zones on chamber performance was determined. Since limited performance data were available concerning this unit, a more extensive characterization was performed. EPA limit concentrations (greater than or equal to 5 mg/liter) of toluene vapor or corn oil aerosol, and relatively low concentrations of uranine aerosol (less than or equal to 50 micrograms/liter) were produced by standard techniques. The presence or absence of equilibration zones did not affect the stability or uniformity of toluene vapor atmospheres, with the coefficient of variation (CV) not exceeding 3.33% in all experiments. In contrast, the presence of two equilibration zones was found to progressively enhance the uniformity of the inhalable test aerosols in the animal exposure zone (CV less than or equal to 3.16%). Matrix sampling revealed that in both uranine and corn oil experiments, the center matrix point concentration was consistently lower than samples taken in the actual animal breathing zone. Equilibration zones markedly reduced the difference between breathing zone and center point concentrations. These performance data indicated that the modified ADG nose-only exposure system performed exceptionally well with the materials that were studied. Results were comparable to those describing whole-body chamber performance. The ready availability of this inexpensive prototype lends itself to standardization of techniques between laboratories.
Aerosols↗
1,2-Dichloropropane hepatotoxicity in rats after inhalation exposure.
The hepatic effects of 1,2-dichloropropane (DCP) were investigated in male Wistar rats exposed to 15, 50, 100, 250, 450, 1000, 1300, 1800 or 4900 mg DCP m-3. At the end of a 4-h period of exposure, average blood DCP levels were 0.025 and 5.38 micrograms ml-1 in animals treated with 15 and 1300 mg m-3, respectively. Blood DCP concentrations were correlated with the air DCP concentrations in the inhalation chamber. At DCP concentrations of 100 mg m-3 or higher, the liver non-protein thiol (NPT) content was significantly reduced. Assays performed 20 h after 4-h DCP exposure showed that exposure to 100-1000 mg DCP m-3 had no effect on hepatic NPT levels. The NPT content increased only in the liver of rats exposed to higher (1300-4900 mg m-3) DCP concentrations. Treatment with DCP did not cause hepatic lipid peroxidation and did not modify total protein content. The observed changes in liver cell thiol homeostasis are likely to reflect the action of reactive intermediates formed during DCP metabolism. These changes can occur in rats following exposure to considerably low levels of DCP vapour.
Administration, Inhalation↗
Gas chromatographic identification of urinary metabolites of insect repellent N,N-diethylphenylacetamide on inhalation exposure in rats.
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Acetamides↗
Molecular analysis of lacI mutants from bone marrow of B6C3F1 transgenic mice following inhalation exposure to 1,3-butadiene.
Chronic exposure to 1,3-butadiene (BD) results in early occurrence and high incidence of lethal lymphomas in male B6C3F1 mice. Male B6C3F1 lacI transgenic mice (BigBlue) were exposed by inhalation to 0, 62.5, 625 or 1250 p.p.m. BD for 4 weeks (6 h/day, 5 days/week). The lacI- mutant frequency and mutational spectrum were evaluated in DNA isolated from bone marrow cells. Two weeks after exposure the lacI- mutant frequency in bone marrow from BD-exposed mice had increased 2- to 3.5-fold over air control mice. DNA sequence analysis of 56 and 54 lacI- mutants from the air control and butadiene-exposed groups, respectively, demonstrated that there was a shift in the spectrum of base substitution mutations at A:T sites in BD-exposed mice (6/26) compared to the air control mice (2/45). A:T-->T:A transversions were found only in BD-exposed animals. Sequence data also indicate that clonal expansion, a natural process in hematopoiesis, can contribute to the lacI- mutant frequency from bone marrow cells such that mutant frequency and mutation frequency are not equivalent. This study shows that BD is mutagenic in B6C3F1 transgenic mouse bone marrow, causing a shift in the mutation spectrum at A:T base pairs in BD-exposed mice compared to air control mice. Sequencing DNA from lacI- mutants from transgenic animals, to determine mutant/mutation frequency and mutational spectra after subchronic bioassay-like exposure conditions, will aid in linking exposure, dose and biological response for genetic risk assessment of BD.
Administration, Inhalation↗
Mutagenicity at the Hprt locus in T cells of female mice following inhalation exposures to low levels of 1,3-butadiene.
A study was conducted to test the hypothesis that repeated low level exposures to 1,3-butadiene (BD), approaching the OSHA occupational threshold for this chemical, produce a significant mutagenic response in mice. Female B6C3F1 mice (4-5 weeks of age) were exposed by inhalation for 2 weeks (6 h/day, 5 days/week) to 0 or 3 ppm BD, and then necropsied at 4 weeks after the cessation of exposures to measure the frequency of mutations (MF) at the Hprt locus using the T-lymphocyte clonal assay. At necropsy, T cells were isolated from spleen and cultured in the presence of mitogen, growth factors, and a selection agent. Cells were scored for growth on days 8-9 after plating to determine cloning efficiencies (CEs) and Hprt MFs. There was a marginal but significant reduction in the growth of splenic T cells from mice exposed to 3 ppm (n=27) compared with control mice (n=24) (P=0.004), suggesting the occurrence of BD-induced cytotoxicity at this low exposure concentration. In addition, the average Hprt MF in mice exposed to 3 ppm BD [1.54+/-0.82 (S.D.)x10(-6)] was significantly increased by 1.6-fold over the average control value of 0.96+/-0.51 (S.D.)x10(-6) (P=0.004). Comparisons of these data to earlier Hprt mutagenicity studies of mice exposed to high concentrations of BD (where significant mutagenic but not cytotoxic effects were observed) indicate that the ability to detect the cytotoxic and mutagenic responses of T cells to low levels of BD was enhanced by using a much larger sample size than usual for both the control and treatment groups. Additional analyses of the quantitative relationships between CE and MF demonstrated that CE had no significant effect upon MF values in sham-exposed control mice or mice exposed to low-level BD. Furthermore, the approaches for assessing the impact of CE and clonality on Hprt MFs in these control and BD-exposed mice were applied with the same rigor as in in vivo Hprt mutagenicity studies in human children. The overall study results support the conclusion that short-term low-level BD exposure is mutagenic in the mouse.
Administration, Inhalation↗