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1. |
Introduction |
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Journal of Toxicology and Environmental Health,
Volume 17,
Issue 2-3,
1986,
Page 3-4
DonaldE. Gardner,
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ISSN:0098-4108
DOI:10.1080/15287398609530812
出版商:Taylor & Francis Group
年代:1986
数据来源: Taylor
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2. |
Comparative anatomy of mammalian respiratory tracts: The nasopharyngeal region and the tracheobronchial region |
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Journal of Toxicology and Environmental Health,
Volume 17,
Issue 2-3,
1986,
Page 163-174
AmitL. Patra,
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摘要:
Silicone rubber casts of the respiratory tract were used in morphological studies of the human, baboon, rhesus monkey, dog, rabbit, guinea pig, rat, hamster, and mouse. In these studies, the trachea of the specimen was opened by tracheotomy, and silicone rubber (734 RTV) was introduced through the trachea to form nasopha‐ryngeal and tracheobronchial casts. Measurements were made on the nasal structures, and the lungs were observed for species variation in branching pattern and number of lobes per lung. While species differences in respiratory tract anatomy are known to exist, the present study provides a focus for toxicologists when extrapolating toxicological results from one species to another.
ISSN:0098-4108
DOI:10.1080/15287398609530813
出版商:Taylor & Francis Group
年代:1986
数据来源: Taylor
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3. |
Pulmonary changes resulting from subchronic exposure to cadmium chloride aerosol |
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Journal of Toxicology and Environmental Health,
Volume 17,
Issue 2-3,
1986,
Page 175-189
R. S. Kutzman,
R. T. Drew,
R. N. Shiotsuka,
B. Y. Cockrell,
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摘要:
Fischer‐344 rats were exposed to 0.0, 0.3, 1.0, or 2.0 mg Cd/m3as CdCI2aerosol for 6 h/d, 5 d/wk, for 62 exposure days. Exposure to 2.0 mg Cd/m3resulted in rapid weight loss, and all of the animals died within the first 45 exposure days. As a group, female rats survived significantly longer than the males. Exposure to Cd resulted in dose‐dependent increases in lung weight. The increased weight was the result of additional tissue mass rather than edema. Both connective‐tissue components, elastin and collagen, were significantly increased in the 1.0‐mg/m3group when these components were expressed on the basis of dry weight. Dose‐dependent changes at the terminal bronchioles consisted of hyperplasia and flattening of type II cells, inflammation, and the proliferation of fibroblasts. Exposure to Cd also resulted in the development of intralymphatic microgranulomas in the perivascular and peribronchiolar lymphoid tissues.
ISSN:0098-4108
DOI:10.1080/15287398609530814
出版商:Taylor & Francis Group
年代:1986
数据来源: Taylor
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4. |
Effects of cadmium inhalation on mitochondrial enzymes in rat tissues |
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Journal of Toxicology and Environmental Health,
Volume 17,
Issue 2-3,
1986,
Page 191-199
P. V. V. Prasada Rao,
D. E. Gardner,
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摘要:
Pulmonary and extrapulmonary effects from a 2‐h inhalation exposure to cadmium (850 μg Cd/m3) were studied in male rats. The effect of this chemical on mitochondrial enzyme activity in the lung, liver, kidney, and testis were investigated immediately after exposure and at 48, 144, and 336 h postexposure. In all tissues studied, mitochondrial citrate synthase activity was significantly increased immediately after the cessation of the exposure. This activity level began to decrease at 48 h postexposure. Succinic dehydrogenase activity was significantly decreased in the lungs and kidney at all periods tested, but increased activity was seen in the liver and testis. Cytochrome c oxidase activity in lungs and testis mictochondria was inhibited at all time periods studied. In the liver and kidney this activity was significantly increased immediately after the exposure ceased, and then a significant reduction began to appear at 48 h postexposure. This study demonstrates that inhaled cadmium, after deposition in the lungs, may alter various enzyme activities in other organs.
ISSN:0098-4108
DOI:10.1080/15287398609530815
出版商:Taylor & Francis Group
年代:1986
数据来源: Taylor
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5. |
Pulmonary clearance of soluble and insoluble forms of manganese |
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Journal of Toxicology and Environmental Health,
Volume 17,
Issue 2-3,
1986,
Page 201-212
D. B. Drown,
S. G. Oberg,
R. P. Sharma,
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摘要:
Manganese is an essential metal of toxicologic concern primarily because of exposure via inhalation. Environmental forms of Mn exist mainly as insoluble oxides, yet much of the research information available relates to the soluble salts. In the present study, adult male Sprague‐Dawley rats were intratracheally instilled with either soluble MnCI2or insoluble Mn3O4labeled with54Mn. Lungs and other major organs were sampled over a span of 3 mo after dosing with the respective chemicals, which were equivalent to 8 μ‐Ci and 1 μmol of manganese in 0.2 ml of buffer. There was rapid clearance of Mn from the lungs in the case of both chemicals; the chloride cleared at an initial rate of nearly four times that of the oxide. Despite this early difference, the amount of54Mn remaining in the lungs after 2 wk was similar for both compounds. The level of54Mn in the liver, kidney, spleen, and testes peaked at the 3‐d sampling point in the case of the oxide, whereas the chloride peaked in these organs within 4 h. At 1 wk after administration, however, the54Mn activity was comparable for both compounds in most organs sampled. Mn uptake in the brain was also more rapid with the chloride form, but both compounds remained at high levels for several weeks.
ISSN:0098-4108
DOI:10.1080/15287398609530816
出版商:Taylor & Francis Group
年代:1986
数据来源: Taylor
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6. |
Early alveolar clearance in rabbits intermittently exposed to sulfuric acid mist |
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Journal of Toxicology and Environmental Health,
Volume 17,
Issue 2-3,
1986,
Page 213-220
RichardB. Schlesinger,
JefferyM. Gearhart,
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摘要:
During the course of 1‐h/d, 5‐dlwk exposure to submicrometer sulfuric acid mist at 250 μg/m3, rabbits were exposed to a radioactively tagged polystyrene latex tracer aerosol to assess clearance from the alveolar region during the period 2–14 d after tracer exposure. The latex was administered on d 1, 57, and 240 following the start of the H2SO4exposures. Early alveolar clearance was found to be accelerated during the first test, and this acceleration was maintained throughout the 8‐mo monitoring period.
ISSN:0098-4108
DOI:10.1080/15287398609530817
出版商:Taylor & Francis Group
年代:1986
数据来源: Taylor
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7. |
Effects of low‐yield‐cigarette smoke inhalation on rat lung macrophages |
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Journal of Toxicology and Environmental Health,
Volume 17,
Issue 2-3,
1986,
Page 221-228
RicardoJ. Gonzalez‐Rothi,
J. Ocie Harris,
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摘要:
It has been suggested that low‐yield cigarettes (LYC) may be less hazardous and that smokers of these cigarettes are exposed to less tar, nicotine, and carbon monoxide. Recent studies have challenged this and question the analysis techniques for measuring yields of these cigarettes. Because published LYC contents may not reflect tissue toxicity and because compensatory puffing behaviors may alter smoke delivery to end‐organ tissues, we studied the effect of smoke from a typical LYC on phagoly‐sosome fusion and phagocytosis in alveolar macrophages of rats that chronically inhaled the smoke generated by an intermittently puffing apparatus. Alveolar macrophages were obtained by lung lavage and established in monolayers. Phagolysosome fusion and phagocytosis were assessed using the acridine orange fluorochrome assay. After 8 wk of exposure, there was no difference in phagolysosome fusion between controls and smokers. Carboxyhemoglobin levels in controls versus smokers were 1.36 ± 0.09% versus 2.13 ± 0.32% (mean ± SE) (p = 0.06). A group of animals was similarly exposed, but the side pores of the cigarette filters were sealed with tape to simulate the compensatory behaviors often used by LYC smokers of occluding filter pores with their lips or fingertips. This significantly increased smoke exposure, and the carboxyhemoglobin level of the smokers increased to 7.0 ± 1.4% (versus controls,p≤ 0.01). Cells from these rats showed alterations in phagocytosis and in phagolysosome fusion compared with alveolar macrophages of control rats. These data suggest that the tobacco in LYC may have toxic effects similar to those of high‐yield cigarettes and that LYC are likely to be less hazardous only if smoked in a fashion similar to that of a smoke‐generating apparatus.
ISSN:0098-4108
DOI:10.1080/15287398609530818
出版商:Taylor & Francis Group
年代:1986
数据来源: Taylor
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8. |
Activation and increment of alveolar macrophages induced by nitrogen dioxide |
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Journal of Toxicology and Environmental Health,
Volume 17,
Issue 2-3,
1986,
Page 229-239
Katsumi Mochitate,
Yuji Takahashi,
Takumi Ohsumi,
Takashi Miura,
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摘要:
Male Wistar rats were exposed to 4 ppm nitrogen dioxide (NO2) for 10 d, and at intervals alveolar macrophages were collected by pulmonary lavage. A metabolic enhancement of alveolar macrophages was observed on d 4 of exposure. The specific activities of glucose‐6‐phosphate dehydrogenase and glutathione peroxidase of the peroxidative metabolic pathway increased to 1.29‐fold (p< 0.001) and 1.17‐fold (p< 0.05) those of the control values, respectively. The specific activities of succinate‐cy‐tochrome c reductase of the mitochondrial respiratory system and pyruvate kinase of the glycolytic pathway also increased to 1.17‐fold (p< 0.01) and 1.20‐fold (p< 0.01) those of the control values, respectively. In addition, the incorporation of [3H]Ieucine and [14C]thymidine into alveolar macrophages were elevated to 1.77‐fold (p< 0.001) and 1.84‐fold (p< 0.01) those of the control values, respectively. The activities of all enzymes tested decreased to control levels by d 10.
ISSN:0098-4108
DOI:10.1080/15287398609530819
出版商:Taylor & Francis Group
年代:1986
数据来源: Taylor
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9. |
Effects of No2on immune responses |
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Journal of Toxicology and Environmental Health,
Volume 17,
Issue 2-3,
1986,
Page 241-248
S. S. Lefkowitz,
J. J. McGrath,
D. L. Lefkowitz,
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摘要:
The effects of NO2on immune reponses of mice were investigated. Mice were exposed to various concentrations of NO2in inhalation chambers. After exposure the following parameters were measured: phagocytosis of polystyrene beads by both peritoneal and alveolar macrophages, production of antibody‐forming cells from mice immunized with sheep erythrocytes, lymphocyte blastogenesis of splenic cells, and susceptibility to influenza virus. The production of antibody‐forming cells was reduced in mice that were exposed to 5 ppm NO2. The serum antibody titers, phagocytosis, and other immune parameters measured were not affected. Exposure to NO2did not affect mortality to influenza virus. These data indicate that certain immune parameters were altered by exposure to NO2however, NO2does not appear to be a major immunosuppressive factor at the concentrations tested.
ISSN:0098-4108
DOI:10.1080/15287398609530820
出版商:Taylor & Francis Group
年代:1986
数据来源: Taylor
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10. |
Nitrogen dioxide exposure and development of pulmonary emphysema |
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Journal of Toxicology and Environmental Health,
Volume 17,
Issue 2-3,
1986,
Page 249-267
D. M. Stavert,
D. C. Archuleta,
L. M. Holland,
B. E. Lehnert,
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摘要:
This study assessed the relationship between nitrogen dioxide inhalation and the development of pulmonary emphysema and investigated how the severity of preexisting emphysema brought about by protease (elastase) instillation into the lung may be augmented by a subchronic exposure to a relatively high concentration of nitrogen dioxide. Lungs of adult Fischer‐344 rats were evaluated for emphysematous changes after (1) a single intratracheal instillation of elastase (E), (2) a 25‐d exposure to 35 ppm nitrogen dioxide (NO2), and (3) elastase instillation followed by 25‐d exposure to 35 ppm NO2(E + NO2). Rats instilled with sterile normal saline and subsequently exposed to filtered air served as a control group (NS). Residual volumes (RV) of the NO2and NS groups were virtually identical, whereas the RV of the E and E + NO2lungs (2.3 and 2.3 ml, respectively) were significantly greater than those of the NS and NO2lungs (1.3 and 1.4 ml, respectively). Directionally similar changes in the excised lung volumes and total lung capacities were obtained with the E and E + NO2groups; NO2alone, however, did not alter these volumetric parameters. No differences in arterial blood gases and pH values, minute ventilation, or breathing frequencies were found among the experimental groups. The mean linear intercept values (MLI) obtained with the NS and NO2exposed lungs were essentially identical with average values of ∼62 μm. This morphometric parameter was substantially increased in the E‐ and E + NO2‐exposed lungs; no significant differences, however, were found between the MLI values obtained with the E and E + NO2lungs (∼95 and ∼97 μm, respectively). From these data, as well as histologic examinations of lung sections for evidence of emphysema, we conclude that (1) a subchronic, moderately high level of NO2exposure does not produce an irreversible emphysematous lesion in the rat model and (2) exposure of rats to 35 ppm for 25 d after elastase instillation into the lungs does not potentiate protease‐induced emphysema or bring about a progression in preexisting emphysema.
ISSN:0098-4108
DOI:10.1080/15287398609530821
出版商:Taylor & Francis Group
年代:1986
数据来源: Taylor
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