摘要:

A system to simultaneously measure the total deposition of four different sizes of monodisperse microspheres in normal and damaged lungs of rats was developed and tested. The system reproducibly measured the deposition of microspheres in control rats, and the procedure was shown to be sufficiently sensitive to measure ozone‐induced changes in deposition rates. Rats exposed to 1.2 ppm ozone 6 h/d for 2 consecutive days showed greater deposition of the 1.09‐μm‐, 2.02‐μm‐, and 2.99‐μm‐ but not of the 0.48‐μm‐diameter microspheres when compared to controls. After 8 consecutive days of exposure to the same concentration of ozone, there were no differences in deposition rates between control and ozone‐exposed rats. Respiratory physiology and lung histopathology data provided evidence that subtle changes in the airway architecture and/or aerodynamics were likely to be responsible for the differential deposition rates as a function of the duration of ozone exposure.

ISSN:0098-4108    

DOI:10.1080/15287398709530998

出版商:Taylor & Francis Group    

年代:1987

数据来源: Taylor

ISSN:0098-4108    

DOI:10.1080/15287398709530997

出版商:Taylor & Francis Group    

年代:1987

数据来源: Taylor

摘要:

An increase in the number of pulmonary alveolar macrophages (AM) can be induced by a number of toxic insults to the lung, including ozone, an important photochemical oxidant air pollutant. This increase could arise from an influx of monocytes from the vascular or interstitial compartments, or from proliferation of AM in situ. While proliferation of alveolar type II cells after oxidant exposure has been well documented, it is not clear whether AM are also capable of this response. Rats were exposed to air or to 0.12, 0.25, or 0.50 ppm ozone for 1, 2, 3, 7, or 14 d, 20 hid. The labeling index in both AM and type II cells increased about 10‐fold after 2 d of exposure to 0.25 and 0.50 ppm of ozone, but returned to control levels by the end of 1 wk of exposure. These changes closely paralleled the temporal and dose‐response characteristics of changes in total lung DNA synthesis. α‐Difluoromethylornithine (DFMO) administered to rats during a 2‐d exposure to 0.50 ppm ozone did not inhibit the ozone‐induced increase in labeling index in AM or type II cells, although evidence of inhibition of lung ornithine decarboxylase activity was obtained, and the ozone‐induced increase in total lung DNA synthesis was inhibited by 23%. These results suggest that, like type II cells, AM are capable of entering the cell cycle and synthesizing new DNA in situ in response to short‐term exposure to environmentally relevant doses of ozone, and that the ozone‐induced stimulation of DNA synthesis in these cell types was refractory to inhibition by DFMO.

ISSN:0098-4108    

DOI:10.1080/15287398709530999

出版商:Taylor & Francis Group    

年代:1987

数据来源: Taylor

摘要:

Ozone is a potent oxidant gas and a common constituent of photochemical smog. This investigation evaluated the numbers and functional capabilities of alveolar macrophages (AM) recovered from rabbits undergoing acute and subchronic ozone exposure. Bronchoalveolar lavage was performed immediately, 24 h, and 7 d after acute (2‐h) exposure to 0.1 or 1.2 ppm ozone, and on d 3, 7, and 14 during subchronic (2 h/d × 13 d) exposure to 0.1 ppm ozone. After acute exposure to 1.2 ppm, a marked increase in lavaged neutrophils was observed at 24 h. A single exposure to 0.1 ppm resulted in increased AM at 7 d, while repeated exposures resulted in an increase in AM and neutrophils on d 7 and 14. AM phagocytosis was depressed immediately and 24 h after acute exposure to 0.1 ppm, and at all time points after exposure to 1.2 ppm. Repeated exposures to 0.1 ppm produced reductions in the numbers of phagocyt‐ically active AM on d 3 and 7, with a return to control levels by d 14. Substrate attachment by AM was impaired immediately after exposure to 1.2 ppm; AM mobility was not altered by any of the ozone exposures. The results of these studies demonstrated significant alterations in the numbers and functional properties of AM as a result of single or repeated exposure to 0.1 ppm ozone, a level below the current National Ambient Air Quality Standard. These findings indicate that levels of ozone frequently encountered in areas of high photochemical air pollution can elicit a pulmonary inflammatory response and can impair pulmonary defense capabilities.

ISSN:0098-4108    

DOI:10.1080/15287398709531000

出版商:Taylor & Francis Group    

年代:1987

数据来源: Taylor

摘要:

The phospholipid polyunsaturated fatty acid (PUFA) content and the membrane fluidity of rat alveolar macrophages were modified dose‐dependently and in different ways. This was done to study the importance of both membrane characteristics for the cellular sensitivity toward ozone and nitrogen dioxide. Cells preincubated with arachidonic acid (20:4) complexed to bovine serum albumin (BSA) demonstrated an increased in vitro sensitivity versus ozone and nitrogen dioxide. The phenomenon was only observed at the highest 20:4 concentrations tested, whereas the membrane fluidity of the 20:4‐treated cells already showed a maximum increase at lower prein‐cubation concentrations.

ISSN:0098-4108    

DOI:10.1080/15287398709531001

出版商:Taylor & Francis Group    

年代:1987

数据来源: Taylor

摘要:

The number, appearance, and functional reactivity of T‐lymphocytes of mediastinal lymph nodes are altered during experimental ozone inhalation. The purpose of the present work is to determine how the lymph nodes and lungs of a mutant strain of animal, which lacks this type of cell, differ in their response to ozone exposure when compared with animals that possess a normal complement of lymphocytes. We exposed athymic nude fnu/nuj mice or heterozygous (nu/ +) euthymic mice to 0.7ppm ozone for 20 h/d for 7 or 14 d while maintaining control groups in clean air. At 7 d the lymph‐node hyperplastic response normally seen in euthymic, ozone‐exposed animals was greatly reduced in exposed athymic animals. By both 7 and 14 d, greater damage had occurred in the lungs of ozone‐exposed, athymic animals than in similarly exposed euthymic animals. Lung wet weight divided by body weight, which was used as a general indicator of lung damage, increased by substantially more in athymic animals than in conventional animals. In a parallel manner, quantitative microscopic analysis, a more sensitive indicator, revealed a marked increase in the lung lesion volumes. Qualitative histologic analysis showed that the change in the response in the athymic animal was most prominent in the peripheral region of the lung extending from the alveolar duct to the alveoli, and was characterized by a greater acute inflammatory cell reaction. Possible mechanisms by which the T‐cell could produce the observed effect include secretion of factors that enhance inherent resistance of the lung's target cells, or alterations in the way the inflammatory response to ozone‐mediated damage occurs. The results support the idea that the mediastinal lymph node lymphocyte response is adaptive in nature and aids in protecting the lung from ozone‐mediated effects.

ISSN:0098-4108    

DOI:10.1080/15287398709531002

出版商:Taylor & Francis Group    

年代:1987

数据来源: Taylor

摘要:

Measurements of pulmonary epithelial permeability were made in rats exposed for 2 h to either purified air or ozone (O3) at concentrations of 0.8 or 2 ppm. [99mTc]Dieth‐ylenetriaminepentaacetate ([99mTc]DTPA) (492 daltons) and125l‐labeled bovine serum albumin (T125/]BSA) (69,000 daltons) were injected intravenously, and the lungs were lavaged 6 min later. In rats exposed to air, transfer of the larger tracer molecule (BSA) from blood to the lavage fluid was less than that of the smaller molecule (DTPA) when the amount of tracer in the lavage fluid was calculated as percent of the counts in femoral artery blood 5 min after injection, i.e., 1 min prior to lavage. In rats exposed to O3, alveolar permeability increased in a dose‐related fashion, the increase under all exposure conditions was greater for the smaller molecule than for the larger one, and the permeability was reversible with time. The increase in permeability from blood to air was comparable to the increase from air to blood reported earlier (Bhalla et al., 1986). The increased permeability provided an early and reliable indicator of short‐term O3exposure effect in rats. Autoradiography by electron microscopy identified multiple pathways for BSA transfer from blood to the alveolar space. Crains produced by [125/]BSA were localized over endothelial and epithelial cell surfaces, were associated with cytoplasmic vesicles, were over cell surface invaginations, and were found in the cytoplasm of apparently degenerating cells. Although defects in tight junctions of alveolar type I cells were observed in lungs of rats exposed to O3, auto‐radiographic grains also appeared in intercellular spaces, with the intercellular junctions remaining intact.

ISSN:0098-4108    

DOI:10.1080/15287398709531003

出版商:Taylor & Francis Group    

年代:1987

数据来源: Taylor

摘要:

An automated animal inhalation exposure facility was designed to conduct chronic exposures of rodents to gaseous pollutants. The facility consisted of 3 walk‐in chambers with modular cages to allow for exposure of up to a maximum of 480 mice or 240 adult rats. Critical parameters of operation, such as relative humidity, pollutant concentration, and temperature, were monitored continuously. Failure of the system to maintain parameters within specified limits activated the alarm system. Distribution of test gases in the chambers was evaluated for homogeneity, and the standard deviation was determined to be within ±5% of the target concentrations throughout the chamber. The exposure facility was successfully used to expose 720 rats to diurnal patterns of O3(baseline of 0.06ppm for 13 h with an exposure peak to 0.25 ppm over 9 h) and NO2(baseline of 0.5 ppm for 16 h with an exposure peak to 1.5 ppm over 6 h) for a period of 18 mo.

ISSN:0098-4108    

DOI:10.1080/15287398709531004

出版商:Taylor & Francis Group    

年代:1987

数据来源: Taylor

摘要:

The study reported herein evaluates the influence of a chronic exposure to an urban pattern of NO2(continuous baseline exposure of 0.2 ppm, on which were superimposed two 1‐h spikes of 0.8 ppm NO2, 5 d/wk) as compared to the baseline exposure to determine the contribution of the spikes to toxicity. Mice were exposed for up to 52 wk with interim examinations. Multivariate analysis of variance revealed a statistically significant treatment effect on infectivity (p = 0.05) and pulmonary function (p = 0.03) parameters. Infectivity mortality of mice in the spiked exposure regimen was significantly greater than that in either the NO2‐backgmund‐exposed mice or in control mice. Four of the pulmonary function variables exhibited the greatest differences among the treatment groups: end expiratory volume, vital capacity, respiratory‐system compliance, and multiple‐breath nitrogen washout. Results from the pulmonary‐function analyses indicate that the spiked exposures to 0.8 ppm NO2may have induced a subtle lesion. The chronic study results indicate that the presence of spikes of NO2is contributing significantly to effects on antibacterial lung defenses and pulmonary function of mice.

ISSN:0098-4108    

DOI:10.1080/15287398709531005

出版商:Taylor & Francis Group    

年代:1987

数据来源: Taylor

摘要:

The nitrogen dioxide (NO2) diurnal cycle found in urban communities usually consists of a low basal concentration upon which are superimposed higher concentration peaks or spikes of short duration. Various components of this environmental exposure mode were examined to assess effects of urban exposure profiles on susceptibility to infectious pulmonary disease. Mice were exposed to NO2peaks of 4.5 ppm for 1, 3.5, or 7 h, challenged with Streptococcus sp. either immediately or 18 h postex‐posure, and then observed for mortality. When the streptococcal challenges were immediately after NO2exposure, the mortality rate was directly related to the length of peak exposure, whether or not a basal exposure was used, and all peak lengths significantly increased mortality. When the challenge was delayed for 18 h after the peak exposure, spiked exposures of 3.5 and 7 h increased mortality to the same degree. If a 1‐h peak exposure to 4.5 ppm was superimposed twice daily upon a continuous basal NO2concentration of 1.5 ppm, there was a suggestive trend toward increased mortality near the end of the second week of exposure when challenge occurred immediately after the morning spike. Studies were also conducted to examine interactions with ozone (O3) and NO2, since urban air typically contains both of these oxidants. Using various combinations of basal and spiked exposure levels of NO2and O3, synergistic results were obtained for streptococcal‐induced mortality.

ISSN:0098-4108    

DOI:10.1080/15287398709531006

出版商:Taylor & Francis Group    

年代:1987

数据来源: Taylor