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Biomedical subjects

J W Illing

Publications and source records attributed to J W Illing.

14 recordsLinked to original sources
PubMed1988

Evaluation of effects of ozone exposure on influenza infection in mice using several indicators of susceptibility.

Mice were exposed to 1 ppm O3, 3 hr/day, for 5 consecutive days. Separate groups of mice were infected with influenza following each of the individual exposures. A twofold increase in the incidence of mortality and a 3-day decrease in mean survival time were observed in mice infected after the second exposure. There were no effects on percentage mortality or mean survival time due to exposure to 1 ppm O3 in mice infected after the first, third, fourth, or fifth exposure. When the exposure concentration was lowered to 0.5 ppm, there were no effects on mortality in mice infected after the second exposure. Five, daily, 3-hr exposures to 1 ppm O3 had no effect on virus titers in the lungs of mice infected after either the second or fifth exposure. In contrast, wet lung weights were significantly enhanced over infected air controls in mice infected after the second O3 exposure at both 1 and 0.5 ppm but not at 0.25 ppm exposure concentrations. This effect on lung wet weight was observed in mice infected with a dose of virus which produced 7-33% mortality in controls as well as in mice infected with a sublethal dose of virus. Histopathologic changes due to sublethal influenza infection, including nonsuppurative pneumonitis and necrosis, squamous metaplasia and hyperplasia of the epithelium lining the bronchi and bronchioles, were more severe in mice infected after the second of five, 1 ppm O3 exposure than in comparable air controls. Sublethal infection caused a loss of lung volume with secondary reduction in diffusing capability and homogenity of ventilation distribution. These latter two effects were also exacerbated in mice infected after the second of five, 1 ppm O3 exposures as compared to air controls. When mice were infected after the fifth, 1 ppm O3 exposure, there was no effect due to ozone on either lung wet weight or histopathology. The data indicate that O3 has little if any effect on antiviral defense mechanisms since virus titers in the lungs were not affected by O3 exposure. However, mortality and morbidity, as indicated by lung wet weights, histopathology, and pulmonary function changes, were enhanced by O3 exposure in mice infected after the second of five exposures suggesting that symptoms due to infection can be enhanced in the absence of enhanced virus replication, possibly due to synergistic effects of O3 and virus in production of lung pathology.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1987

Evaluating the toxicity of urban patterns of oxidant gases. II. Effects in mice from chronic exposure to nitrogen dioxide.

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-background-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 NO2 may have induced a subtle lesion. The chronic study results indicate that the presence of spikes of NO2 is contributing significantly to effects on antibacterial lung defenses and pulmonary function of mice.

Administration, Inhalation↗
PubMed1987

Pulmonary effects due to short-term exposure to oil fog.

Rats were exposed to an oil fog generated by flash vaporation and subsequent condensation of lightweight lubricating oil. Exposures were for 3.5 h/d, 4 d/wk, for 4 wk, at concentrations of 1.5, 0.5, or 0.0 mg/l and a particle size of approximately 1 micron. Samples of respiratory tissues were taken for histopathologic analyses, lavage fluid samples were collected, and pulmonary function measurements were made the day after the last exposure. An accumulation of macrophages within the alveolar lumen, an increase in lavage fluid protein content, and an increase in total cell content in lavage fluid due to an influx of polymorphonuclear leukocytes was noted in rats exposed at the 1.5-mg level. Also, for this exposure group there was an increase in lung wet and dry weight and an increase in end-expiratory volume, and pneumonitis was observed histopathologically in 4 of 10 male rats exposed. Pneumonitis was not observed among six female rats examined. Oil fog had no effect on total lung capacity, residual volume, vital capacity, lung compliance, or the distribution of ventilated air within the lung. Effects following exposure to 0.5 mg/l were limited to slight accumulation of macrophages in the alveolar lumen and an increase in the total cells in lavage fluid, which could not be attributed to an increase in any particular cell type.

Air Pollutants↗
PubMed1985

Inhalation studies of Mt. St. Helens volcanic ash in animals. III. Host defense mechanisms.

The effects of inhalation exposure of mice or rats to 9.4 mg/m3 volcanic ash, 2.5 mg/m3 SO2, or both on host defense mechanisms were assessed. Cytologic changes in pulmonary lavage fluid included an increase in percentage polymorphonuclear leukocytes due to SO2 exposure and an increase in eosinophils due to ash. SO2 and ash also produced decreases in percentage alveolar macrophages. In the case of ash-exposed animals, this decrease was offset by an increase in lymphocytes. Total cell counts and viability were not affected by any of the exposures. Pulmonary clearance mechanisms were affected in that there were both decreased alveolar macrophage phagocytic capability following ash and ash + SO2 exposures and depressed ciliary beat frequency attributable to ash exposure. None of the inhalation exposures caused increases in susceptibility to an immediate or 24 hr postexposure aerosol challenge with Streptococcus. However, intratracheal instillation of both fine- and coarse-mode volcanic ash caused slight but significant increases in mortality due to bacterial challenge 24 hr after the instillation. The phytohemagglutinin-induced blastogenic response of splenic lymphocytes from exposed animals did not differ significantly from that of control lymphocytes, although the lipopolysaccharide-induced blastogenic response was enhanced. Ash exposure had no effect on susceptibility to murine cytomegalovirus. In summary, volcanic ash alone or in combination with SO2 had only minimal effects on certain host defense mechanisms.

Air Pollutants↗
PubMed1984

Increased susceptibility to parathion poisoning following murine cytomegalovirus infection.

In mice treated with ordinarily sublethal doses of parathion 2 to 5 days postinfection with murine cytomegalovirus (MCMV) 50 to 100% mortality was observed. These mortalities appeared to be due to a decrease in the ability of infected mice to detoxify parathion. Pentobarbital-induced sleeping time was also enhanced 3 and 6 days postinfection and cytochrome P-450 concentrations were markedly depressed in mice tested 3 days after infection. MCMV-induced effects on sensitivity to parathion and pentobarbital did not appear to be directly attributable to liver infection since concentrations of virus in the liver persisted at maximum concentrations well beyond the time when sensitivity to these compounds returned to normal. The time frame during which enhanced sensitivity to parathion and pentobarbital was observed suggests that this sensitivity may have been caused by viral-induced interferon-mediated depression of cytochrome P-450.

Analysis of Variance↗
PubMed1982

Pulmonary host defense responses to inhalation of sulfuric acid and ozone.

The effects of simultaneous exposure to ozone (O3) and sulfuric acid [H2SO4, 0.23 microns volume median diameter (VMD)] and a single exposure to ultrafine (less than 0.1 micron VMD) H2SO4 under various conditions were studied using the infectivity/mortality and the ciliary beating frequency model systems. A 3-h exposure to a combined aerosol of 196 micrograms O3/m3 and 483 or 241 micrograms H2SO4/m3 significantly increased the susceptibility of mice to a laboratory-induced respiratory infection. However, exposure to 543 micrograms ultrafine H2SO4/m3 for 2 h or 365 micrograms/m3 2 h/d for 5 d did not significantly affect this parameter. Upper airway response, as measured by changes in hamster tracheal ciliary beating frequency, was not affected by either a 3-h combined exposure to 196 micrograms O3/m3 and 847 micrograms H2SO4/m3 or a 2-h exposure to 458 micrograms ultrafine H2SO4/m3.

Aerosols↗
PubMed1980

Extrapulmonary effects of NO2 as reflected by pentobarbital-induced sleeping time in mice.

The influence of nitrogen dioxide (NO2) on pentobarbital (PEN)-induced sleeping time (S.T.) was investigated in mice. Acute exposure to concentractions as low as 470 microgram NO2/m3 (0.25 ppm) caused a significant increase in PEN-induced S.T. No significant effects on PEN-induced S.T. were detected after 1 or 2 days (3 h/day) exposure to 235 microgram NO2/m3 (0.125 ppm). None of the exposure regimens affected the time required for the drug to induce sleep. When the effects of repeated daily exposures (3 h/day) to 9400 microgram NO2/m3 (5 ppm) were compared in male and female mice, the females had a significantly increased PEN-induced S.T. after 1 and 2 days of exposure. However, an increase in PEN-induced S.T. was not observed in males until the 3rd day of exposure. Since the duration of PEN-induced S.T. is primarily determined by hepatic mixed function oxidase activity, it is possible that NO2 may alter some aspects of xenobiotic metabolism.

Animals↗
PubMed1980

Decreased resistance to infection in exercised mice exposed to NO2 and O3.

A mechanized wheel was constructed for use in evaluating the interaction of exercise and gaseous pollutants such as O3 and NO2. Immediately after the pollutant exposure, both exercised and nonexercised female mice (CD-1) were combined with controls, challenged with an aerosol of viable Streptococcus pyogenes (group C), and then observed over a 15-d period for incidence of mortality. Exposure to O3 at 196 micrograms/m3 (0.1 ppm) or 590 micrograms/m3 (0.3 ppm) while exercising yielded mortality rates that were significantly higher than those observed in the O3 groups that were not exercised. With exposure to NO2 at 5640 micrograms/m3 (3 ppm), exercise produced a significant enhancement in mortality over the other treatment groups. These studies show that exercise can affect the mortality observed in this model system and indicate the need for establishing safe exposure levels of pollutants as a function of the activity level of the exposed population.

Air Pollutants↗
PubMed1975

Motorized exercise wheel for exposure of small animals to environmental pollutants.

For environmental inhalation studies a motorized exercise wheel was designed for small laboratory animals. Mice or hamsters were separated in individual enclosures, and each animal was required to perform the same exercise. The wheel was driven by a common barbecue spit motor, the speed of which may be varied by a standard variable transformer, from 1-6 revolutions per min. This unit can be adapted for a variety of laboratory applications.

Animals↗
PubMed1973

Technique for differentiating particles that are cell-associated or ingested by macrophages.

Phagocytosis is a two-step process involving attachment and ingestion of particulate material. It is often difficult to determine under a light microscope whether the particles are actually ingested or are merely attached to the cell. A more accurate, easy to perform technique with the use of xylene has been developed for determining the difference between the attachment and ingestion of polystyrene latex spheres. The xylene treatment dissolves the extracellular spheres, leaving only the intracellular spheres to be counted by the experimenter to obtain a more accurate phagocytic index. This technique also allows an investigator to get an ingestion index, an attachment index, or both.

Animals↗
PubMedDate not supplied

Alterations in bacterial defense mechanisms of the lung induced by inhalation of cadmium.

Exposure to an aerosol of CdCl2 has a marked proclivity to reduce the ability of the lung to defined itself against microbial insults. A significant enhancement of mortality was observed in mice exposed to CdCl2 concentrations ranging from 80 to 1600 mug/m3 prior to being challenged with viable streptococci. The increase in percent mortality above control varied from 15% at the lowest CdCl2 concentration to approximately 70% at the highest concentration. In order to determine the various mechanistic factors which may explain the observed effect of reduced host resistance to infection, a variety of pulmonary defense systems was studied. There was a significant decrease in the total number of alveolar macrophages recoverable from rat lungs immediately after completion of the exposure regimen. The number of macrophages returned to normal (about 5.5 million) within 24 hours after cessation of the exposure. However, total polymorphonuclear leucocytes increased 1.5 million immediately after completion of the exposure and 13 million within 24 hours after cessation of the exposure. Lymphocyte numbers were not affected by these exposure levels. Data concerning clearance of streptococci from the lung following CdCl2 exposure closely correlated with the observed mortality pattern.

Aerosols↗