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PubMed1987

Effects of subchronic inhalation exposure of mice to a high-boiling coal liquid.

Mice (CD-1) were exposed to aerosol concentrations of 0.0, 0.03, 0.14, or 0.69 mg/liter of heavy distillate (HD), a high-boiling coal liquid from the solvent-refined coal (SRC)-II process. Exposures were for 6 hr/day, 5 days/week for 13 weeks. Particle sizes ranged between 1.6 and 1.8 micron, mass median aerodynamic diameter, with a geometric standard deviation range of 1.9-2.5. Growth for high-dose males was significantly less than that of the control group. Compared to controls, weights of liver were significantly higher and those of ovaries and thymus significantly lower; these changes were significant on both absolute and relative weight bases. The number of red blood cells, volume of packed red cells, and hemoglobin concentration for animals from the high-dose group were significantly lower than those of controls. Microscopic examination of organ sections showed focal hepatic necrosis and nonspecific hepatopathy. Additionally, olfactory epithelial degeneration occurred in a dose-dependent manner. Results from this study indicated that exposure to HD caused adverse effects at the high dose and that these changes were either less severe or absent in middle-dose group mice. Comparison of these results with those for rats indicated that with rats the biological effects were more severe and present at lower doses than was observed for mice.

Administration, Inhalation↗
PubMed1992

Evaluation of the potential for developmental toxicity in rats and mice following inhalation exposure to tetrahydrofuran.

Sprague-Dawley rats and Swiss (CD-1) mice were exposed to 0, 600, 1800, or 5000 ppm THF (a four-carbon cyclic ether, widely used as an industrial solvent) vapors, 6 hr/day, 7 days/week (6-19 days of gestation (DG) for rats; 6-17 DG for mice). Body weights of pregnant rats in the 5000 ppm group were reduced at euthanization. There were no effects on the percentage of live rat fetuses/litter or on the fetal sex ratio. Fetal body weight was significantly reduced for the 5000 ppm group, but the incidence of abnormalities was not increased. Mice in the 1800 and 5000 ppm groups were sedated during exposure; approximately 27% of the mice in the 5000 ppm group died. Mean body and uterine weights of mice were reduced for the 1800 and 5000 ppm groups at euthanization (18 DG), but adjusted maternal weight gain was not affected at 1800 ppm. There was a reduction in the percentage of live fetuses/litter for the mice in 1800 and 5000 ppm groups (95% resorptions in the 5000 ppm group). Fetal weight and sex ratio in mice were not affected. An increase in the incidence of reduced sternebral ossifications was correlated to THF concentration, although differences between groups were not statistically significant. There were no increases in the incidences of other malformations or variations. These results suggest that THF may be embryotoxic in mice, but if the conceptus survives, development as assessed by this experimental design continues in a normal fashion. The no-observable-adverse-effect level (NOAEL) for maternal toxicity was 1800 ppm in both rats and mice. The NOAEL for developmental toxicity was 1800 ppm in rats and 600 ppm in mice.

Abnormalities, Drug-Induced↗
PubMed1984

Behavioral and neurochemical alterations in the offspring of rats after maternal or paternal inhalation exposure to the industrial solvent 2-methoxyethanol.

The industrial solvent 2-methoxyethanol (2ME) has antifertility effects in male rats at 300 ppm and is teratogenic in rats and rabbits at 50 ppm. The present research investigated if exposure of paternal or maternal animals to 25 ppm 2ME, the current U.S. permissible occupational exposure limit, would produce detectable effects in the offspring. Eighteen male young-adult Sprague-Dawley rats were exposed to 25 ppm 2ME 7 hr/day, 7 days/week for 6 weeks; they were then mated with untreated females which were allowed to deliver and rear their young. In addition, groups of 15 pregnant rats were exposed 7 hr/day on gestation days 7-13 or 14-20 and allowed to deliver and rear their young. At birth, litters were culled to 4 females and 4 males for behavioral testing of neuromotor function, activity, and simple learning ability on days 10 through 90. In addition, brains from newborn and 21-day-old offspring were analyzed for neurochemical deviations from controls. No effects on paternal or maternal animals, nor on the number or weight of live offspring, were noted. Behavioral testing revealed significant differences from controls only in avoidance conditioning of offspring of mothers exposed on days 7-13. In contrast, neurochemical deviations were observed in brains from 21-day-old offspring from the paternally exposed group as well as from both maternally exposed groups; changes were numerous in the brainstem and cerebrum but were fewer in the cerebellum and midbrain. Thus it appears that both paternal and maternal inhalation of 25 ppm 2ME produces some effect which is reflected in neurochemical deviations in the offspring.

Acetylcholine↗
PubMedDate not supplied

[The characteristics of the behavior and brain lipid peroxidation function of rats in acute inhalation exposure to a hydrogen sulfide-containing gas condensate].

As a result of the effect of the gas condensate containing hydrogen sulfide a depression takes place of orienting-investigatory activity of Wistar male rats in conditions of open field, disturbance of elaboration and reproduction of conditioned reflex of two-way avoidance, surplus accumulation in the cerebral cortex tissue of products of peroxide lipids oxidation and depression of catalase. The changes were of cyclic character and returned to the level of the control animals in 48 h after the finishing of the effect.

Administration, Inhalation↗
PubMed1995

Chronic inhalation exposure and phospholipids in lung surfactant and tissue.

Golden hamsters were exposed to 2 mg/m3 coal fly ash for 180 days. The exposure raised the phospholipid level in the tissue, whereas no such elevation was observed in the surfactant. Increased phospholipid in the tissue is thought to reflect the accumulated surfactant in type II cells. Fatty acid composition analysis indicated an increase of arachidonic acid in the surfactant and increases of palmitic acid and arachidonic acid in the tissue. In conclusion, the pulmonary surfactant high in fluidity was stored in the lung tissue more than control, and the surfactant was secreted into the alveoli normally.

Administration, Inhalation↗
PubMed1994

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

The potential chronic toxicity and oncogenicity of dimethyl-formamide (DMF) was evaluated by exposing male and female rats and mice to 0, 25, 100, or 400 ppm DMF 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 euthanasia for rats occurred at 12 months and hepatic cell proliferation in rats and mice was examined at 2 weeks, 3 months, and 12 months. No compound-related effects on clinical observations or survival were observed. Body weights of rats exposed to 100 (males only) and 400 ppm were reduced. Conversely, body weights were increased in 400 ppm mice. No hematologic changes were observed in either species. Serum sorbitol dehydrogenase activity was increased in rats exposed to 100 or 400 ppm. There were no compound-related effects on the estrous cycle of rats or mice at any concentration. Compound-related morphological changes were observed only in the liver. In rats, exposure to 100 and 400 ppm produced increased relative liver weights, centrilobular hepatocellular hypertrophy, lipofuscin/hemosiderin accumulation in Kupffer cells, and centrilobular single cell necrosis (400 ppm only). In mice, increased liver weights (100 ppm males, 400 ppm both sexes), centrilobular hepatocellular hypertrophy, accumulation of lipofuscin/hemosiderin in Kupffer cells, and centrilobular single cell necrosis were observed in all exposure groups. These observations occurred in a dose-response fashion and were minimal at 25 ppm. No increase in hepatic cell proliferation was seen in mice or female rats. Slightly higher proliferation was seen in male rats exposed to 400 ppm at 2 weeks and 3 months but not at 12 months. Dimethylformamide was not oncogenic under these experimental conditions in either the rat or mouse.

Administration, Inhalation↗
PubMed1996

Inhalation exposure of rats and mice to 1,3-butadiene induces N6-adenine adducts of epoxybutene detected by 32P-postlabeling and HPLC.

In this paper we report DNA binding of butadiene monoepoxide, a first metabolite of 1,3-butadiene catalyzed by monooxygenases. We prepared alkylated purines as marker compounds for 32-P-postlabeling and electrochemical analysis and developed methods to measure the corresponding products. The traditional postlabeling assay was modified by incorporating a solid phase extraction column and high-performance liquid chromatography (HPLC) enrichment steps to the assay prior to labeling. The final analysis of adducted N6 adenines is based on two dimensional thin-layer chromatography (TLC) and an on-line HPLC/radioactivity analysis. The qualitative and quantitative results are based on positively identified marker compounds. Alkylated N7 guanines were released from DNA by neutral thermal hydrolysis, prepurified by HPLC, and analyzed by HPLC with a sensitive electrochemical detection procedure. By using these methods, we found alkylation of calf thymus DNA exposed to butadiene monoepoxide in vitro at adenine N6 and guanine N7 sites. Analysis of lung DNA samples from mice and rats exposed to butadiene through inhalation showed that adenine N6 adducts were formed in vivo in a dose responsive manner.

Adenine↗
PubMed1998

Chronic toxicity/oncogenicity study of styrene in CD rats by inhalation exposure for 104 weeks.

Groups of 70 male and 70 female Charles River CD (Sprague-Dawley-derived) rats were exposed whole body to styrene vapor at 0, 50, 200, 500, or 1000 ppm 6 h/day 5 days/week for 104 weeks. The rats were observed daily, body weights and food and water consumption were measured periodically, and a battery of hematologic and clinical pathology examinations was conducted at weeks 13, 26, 52, 78, and 104. Nine or 10 rats per sex per group were necropsied after 52 weeks of exposure and the remaining survivors were necropsied after 104 weeks. Control and high-exposure rats received a complete histopathologic examination, while target organs, gross lesions, and all masses were examined in the lower exposure groups. Styrene had no effect on survival in males, but females exposed to 500 or 1000 ppm had a dose-related increase in survival. Levels of styrene in the blood at the end of a 6-h exposure during week 95 were proportional to exposure concentration. Levels of styrene oxide in the blood of rats exposed to 200 ppm or greater styrene were proportional to styrene exposure concentration. There were no changes of toxicologic significance in hematology, clinical chemistry, urinalysis, or organ weights. Males exposed to 500 or 1000 ppm gained less weight than the controls during the first year and maintained the difference during the second year. Females exposed to 200, 500, or 1000 ppm gained less weight during the first year; those exposed to 500 or 1000 ppm continued to gain less during months 13-18. Styrene-related non-neoplastic histopathologic changes were confined to the olfactory epithelium of the nasal mucosa. There was no evidence that styrene exposure caused treatment-related increases of any tumor type in males or females or in the number of tumor-bearing rats in the exposed groups compared to controls. In females, there were treatment-related decreases in pituitary adenomas and mammary adenocarcinomas. Based on an overall evaluation of eight oncogenicity studies, there is clear evidence that styrene does not induce cancer in rats.

Administration, Inhalation↗
PubMed1995

Four weeks inhalation exposure to n-heptane causes loss of auditory sensitivity in rats.

The effects of exposure to 800 or 4000 p.p.m. of n-heptane, CAS No. [142-82-5]) 6 hr per day during a period of 28 days, on the function of the auditory system were examined by measurements of auditory brain stem response (ABR) in Long Evans rats. The ABR was measured simultaneously with both needle electrodes and implanted electrodes. The wave forms recorded with the two types of electrodes were similar, but the amplitudes were largest on the recordings with implanted electrodes. The overall ratio between the amplitudes obtained with implanted electrodes and with needle electrodes was 1.4 for peak Ia and 2.5 for peak IV of the ABR. The exposure to n-heptane (4000 p.p.m.) reduced the amplitudes of components Ia and IV of the ABR. The reduction was most consistent for component IV and most pronounced at higher frequencies and intensities. The reduction in ABR corresponds to an increase in the auditory threshold of approximately 10 dB at all frequencies. Neither the latencies nor the interpeak latencies of components Ia and IV were changed. No significant changes in ABR were observed in the group exposed to 800 p.p.m. The mechanism behind the ototoxicity of organic solvents is discussed.

Administration, Inhalation↗
PubMed1993

Effects of six months' white spirit inhalation exposure in adult and old rats.

In two separate experiments in rats the irreversible effects of six months' exposure to white spirit (0, 400 p.p.m., and 800 p.p.m.) were studied. In one experiment the exposure started at the age of three months, in the other the rats were 15 months at the beginning of the exposure. After an exposure-free period of several months neurobehavioural, pathological, and neurochemical examinations were performed. A marked difference in motor activity between young and aged animals was found. A slight effect on kidney function was seen at 800 p.p.m. No macroscopic or histopathological changes related to dosing were found. The concentrations of noradrenaline, dopamine, and 5-hydroxytryptamine in various brain regions and in whole brain were irreversibly changed. In conclusion, the study revealed different changes within the CNS, but failed to demonstrate neurobehavioural white spirit-induced neurotoxicity.

Administration, Inhalation↗
PubMed1993

Thirteen-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 compound used as a chemical intermediate, a catalyst, and an antiknock additive in gasoline. This organometallic chemical is of particular interest because of its structural similarities to other metallocenes, some of which are carcinogenic. F344/N rats and B6C3F1 mice were exposed to 0, 3.0, 10, and 30 mg ferrocene vapor/m3, 6 hr/day, 5 days/week, for 13 weeks. During these exposures, no rats or mice died, nor were any clinical signs of ferrocene-related toxicity observed. At the end of the exposures, male rats exposed to the lowest and highest level of ferrocene had decreased body weight gains compared to filtered-air-exposed control male rats, while body weight gains for all groups of both ferrocene- and filtered-air-exposed female rats were similar. Male mice exposed to ferrocene had no differences in body weight gains, compared to controls, but female mice had decreases in body weight gains at the 10 and 30 mg/m3 exposure levels. There were exposure concentration- and exposure-time-related increases in lung burdens of iron. The mean iron lung burden in rats exposed to 30 mg ferrocene vapor/m3 for 90 days was four times greater than the burden in control rats. No exposure-related changes in respiratory function, lung biochemistry, bronchoalveolar lavage cytology, total lung collagen, clinical chemistry, and hematology parameters were observed. This suggests that the accumulations of iron in lung did not cause an inflammatory response nor any functional impairment of the lung. There were no indications of developing pulmonary fibrosis nor of any hematologic toxicity. No exposure-related gross lesions were seen in any of the rats or mice at necropsy. Exposure-related histopathologic alterations, primarily pigment accumulations, were observed in the nose, larynx, trachea, lung, and liver of both species, and in the kidneys of mice. Lesions were most severe in the nasal olfactory epithelium where pigment accumulation, necrotizing inflammation, metaplasia, and epithelial regeneration occurred. Nasal lesions were observed in all ferrocene-exposed animals and differed only in severity, which was dependent on the exposure concentration. Histochemical stains of these target tissues showed the presence of iron ions. The results suggest that the mechanism of ferrocene toxicity may be the intracellular release of ferrous ion through ferrocene metabolism, followed by either iron-catalyzed lipid peroxidation of cellular membranes or the iron-catalyzed Fenton reaction to form hydroxyl radicals that directly react with other key cellular components, such as protein or DNA.

Administration, Inhalation↗
PubMed1992

Localization of mercury in CNS of the rat. V. Inhalation exposure to metallic mercury.

The autometallographical technique has been used to determine the distribution and cellular localization of mercury deposits in the Wistar rat CNS after exposure to elemental mercury vapor (50-550 micrograms Hg/m3 of air for 4-24 h). In animals exposed to 50 micrograms Hg/m3 for 8 h, silver-enhanced mercury grains were confined to the capillary walls. Increasing the concentration of mercury to 500 micrograms Hg/m3 caused mercury staining to appear in neurons in the corpus striatum, mesencephalic nucleus of the trigeminal nerve and cerebellar deep nuclei. In the spinal cord, mercury appeared primarily in the motoneurons of lamina IX. Following exposure to 550 micrograms Hg/m3 for 12 h mercury was additionally detected in the ependyma. Animal exposure to 550 micrograms Hg/m3 for 24 h resulted in visible mercury deposits in the cerebellar and cerebral cortices. In the cerebral cortex, mercury was present in neurons populating lamina III in the isocortex. No mercury was detected in the allocortex. In the cerebellar cortex, mercury staining was limited to the Purkinje cells. Neurons in the thalamus contained heavy accumulations of mercury. Heavy staining for mercury was detected in lung alveolar macrophages in sections prepared from animals exposed to 550 micrograms Hg/m3 for 24 h. In animals exposed to 500 micrograms Hg/m3 or more, the primary target cells were the neurons, but glia cells also contained scattered mercury deposits. Ultrastructurally, mercury deposits were detected in the lysosomes.

Administration, Inhalation↗
PubMed1991

Irreversible effects in rats of toluene (inhalation) exposure for six months.

The irreversible CNS effects of six months' exposure to toluene (0, 500, and 1500 p.p.m.) in rats was studied applying a multi-disciplinary approach. After an exposure-free period, neurobehavioural, morphometric, pathological, and biochemical examinations were performed. No neurobehavioural or gross pathological changes were found. Morphometric measurements did not show loss of neurones. At 500 p.p.m. the mean nuclear volume and mean perikaryonal volume and the variation of the values of these parameters was increased in the exposed groups compared to the controls. Noradrenaline (NA), dopamine (DA), and 5-hydroxytryptamine (5-HT) levels were significantly changed in various brain regions. It is concluded that this investigation failed to reveal overt toluene-induced CNS-neurotoxicity, however, certain irreversible effects were found which further add to the accumulating evidence of the chronic CNS-neurotoxicity of toluene.

Administration, Inhalation↗
PubMed1996

Effects of the structure of a toxicokinetic model of butadiene inhalation exposure on computed production of carcinogenic intermediates.

A flow-limited physiologically based toxicokinetic model was constructed for uptake, metabolism, and clearance of butadiene (BD) and its principal metabolite 1,2-epoxy-3-butene (EB), using physiological and biochemical parameters from the literature where available. The model includes compartments for blood, liver, lung, fat, GI tract, other rapidly perfused tissues, and slowly perfused tissues. The blood was distributed among compartments for arterial plus venous blood and subcompartments for vascular spaces associated with each of the tissue compartments. The lung contained a subcompartment for the alveolar space. Metabolic activation of BD by cytochrome P450-catalyzed epoxidation was modeled as occurring in liver, lung, and the rapidly perfused tissue compartments. The detoxication of EB catalyzed by epoxide hydrolase and glutathione S-transferase (GST) was modeled as occurring in liver, lung, and the rapidly perfused tissues compartments and by blood GST activity. The model also includes depletion of glutathione (GSH) by GST-catalyzed conjugation of EB and 3-butene-1,2-diol and resynthesis of GSH from cysteine. Values of biochemical parameters that were unavailable in the literature were estimated by iteratively reweighted least squares optimization to reproduce data for uptake of BD and EB by rats and mice in closed chambers. The resulting model also reproduced the depletion of GSH in liver and lung in flow-through systems. It reproduced the concentrations of expired EB produced from BD in closed chambers but overpredicted separately measured blood EB concentrations in flow-through systems, indicating an inconsistency between these two experiments that cannot be resolved by this model or an inadequacy in the model. Equilibration of chamber gases with the alveolar space and alveolar gas with lung capillary blood results in much less dilution of the inhaled gas in the blood compared with the predictions of models in which chamber gas equilibrates directly with the total circulation. The production of EB predicted by the present model was found to be sensitive to a number of physiological and biochemical parameters. A valid and useful toxicokinetic model must have reliable physiological and enzymological data for BD biotransformation before it can be credibly used for human risk assessment.

Administration, Inhalation↗
PubMed1989

Thirteen-week toxicity study of n-hexane in B6C3F1 mice after inhalation exposure.

B6C3F1 mice were exposed to n-hexane 6 h/day, 5 days/week for 13 weeks at concentrations of 0, 500, 1000, 4000, and 10,000 ppm and at 1000 ppm 22 h/day, 5 days/week for 13 weeks (1000C group). Toxicological endpoints assessed included clinical signs, body and organ weight changes, gross and histopathology, neuropathology, and a battery of neurobehavioral tests. All mice survived the treatment. Exposure-related effects of n-hexane included sneezing at 10,000 ppm and body weight gain depression at 1000C and 10,000 ppm. Histopathologic changes included mild inflammatory, erosive and regenerative lesions in the olfactory and respiratory epithelium of the nasal cavity at 1000C, 4000, and 10,000 ppm. The only neurobehavioral parameter affected was a decrease in locomotor activity in female mice at 1000C and 10,000 ppm. In teased fiber preparations of tibial nerve, paranodal axonal swellings were observed at 1000C or at 10,000 ppm, but not in the control groups. The severity of the peripheral nerve lesion was mild. These studies show that n-hexane has minimal toxicity to the nervous system and respiratory system of mice.

Administration, Inhalation↗
PubMed1993

The toxicologic and oncogenic potential of JP-4 jet fuel vapors in rats and mice: 12-month intermittent inhalation exposures.

Three-hundred Fischer 344 rats and 300 C57BL/6 mice of each sex were divided into three treatment groups and exposed intermittently (6 hr/day, 5 days/week) to JP-4 jet fuel vapors at concentrations of 0, 1000, and 5000 mg/m3 for 12 months. At exposure termination, 10% of the animals were killed and those remaining were held for a 12-month postexposure tumorigenesis observation period. Pathologic findings in male rats revealed treatment-related renal toxicity and neoplasia consistent with the male rat unique alpha 2 mu-globulin nephropathy syndrome. Distinct JP-4-induced respiratory toxicity was not observed, and pulmonary neoplasms were not significantly increased in any treatment group. Benign hepatocellular adenomas were slightly increased in high-dose female mice, but the trend was reversed in male mice. Other pathologic findings were regarded as equivocal or compatible with expected biologic variation. The study did not demonstrate target organ toxicity or carcinogenesis which could be extrapolated to other species.

Administration, Inhalation↗
PubMed2000

1-Bromopropane, an alternative to ozone layer depleting solvents, is dose-dependently neurotoxic to rats in long-term inhalation exposure.

1-Bromopropane has been newly introduced as an alternative to ozone layer-depleting solvents. We aimed to clarify the dose-dependent effects of 1-bromopropane on the nervous system. Forty-four Wistar male rats were randomly divided into 4 groups of 11 each. The groups were exposed to 200, 400, or 800 ppm of 1-bromopropane or only fresh air 8 h per day for 12 weeks. Grip strength of forelimbs and hind limbs, maximum motor nerve conduction velocity (MCV), and distal latency (DL) of the tail nerve were measured in 9 rats of each group every 4 weeks. The other 2 rats of each group were perfused at the end of the experiment for morphological examinations. The rats of the 800-ppm group showed poor kicking and were not able to stand still on the slope. After a 12-week exposure, forelimb grip strength decreased significantly at 800 ppm and hind limb grip strength decreased significantly at both 400 and 800 ppm or after a 12-week exposure. MCV and DL of the tail nerve deteriorated significantly at 800 ppm. Ovoid or bubble-like debris of myelin sheaths was prominent in the unraveled muscular branch of the posterior tibial nerve in the 800-ppm group. Swelling of preterminal axons in the gracile nucleus increased in a dose-dependent manner. Plasma creatine phosphokinase (CPK) decreased dose-dependently with significant changes at 400 and 800 ppm. 1-Bromopropane induced weakness in the muscle strength of rat limbs and deterioration of MCV and DL in a dose-dependent manner, with morphological changes in peripheral nerve and preterminal axon in the gracile nucleus. 1-Bromopropane may be seriously neurotoxic to humans and should thus be used carefully in the workplace.

Administration, Inhalation↗
PubMed1992

The pulmonary response and clearance of Ludox colloidal silica after a 4-week inhalation exposure in rats.

Rats were exposed to Ludox colloidal silica (CS) at concentrations of 0, 10, 50, and 150 mg/m3 for 6 hr/day, 5 days/week for 4 weeks. Rats were killed after 4 weeks of exposure and 10 days or 3 months postexposure (PE). The exposure concentration of 10 mg/m3 Ludox CS is considered to be the no-effect concentration. There were no exposure-related clinical signs in any group. After 4 weeks exposure, lung weights were increased significantly in rats exposed to 50 and 150 mg/m3 Ludox CS, but lung weights were similar to those of controls at 3 months PE. After 4 weeks exposure to 50 mg/m3 Ludox CS, a slight alveolar macrophage response, polymorphonuclear leukocytic infiltration, and Type II pneumocyte hyperplasia in alveolar duct regions were present. After 3 months PE, these pulmonary lesions had almost disappeared with removal of most dust-laden alveolar macrophages (AMs). The pulmonary response to 150 mg/m3 Ludox CS was similar in character but increased in magnitude from that seen at 50 mg/m3. At 3 months PE, most particle-laden AMs had disappeared and the remaining AMs were aggregated and sharply demarcated. A few aggregates of particle-laden AMs appeared to transform into silicotic nodules comprising macrophages, epithelioid cells, and lymphocytic infiltration in some animals. Some silicotic nodules showed reticular fiber networks with minute collagen fiber deposition. Tracheobronchial lymph nodes were enlarged with aggregates of particle-laden AMs and hyperplastic histiocytic cells. Lung-deposited Ludox cleared rapidly from the lungs with half-times of approximately 40 and 50 days for the 50 and 150 mg/m3 groups, respectively.

Administration, Inhalation↗