Experimental infection of the respiratory tract with Mycoplasma pneumoniae.

M. pneumoniae, a common human respiratory pathogen, has been studied experimentally for years using intranasal inoculation of the golden Syrian hamster. Because of recent evidence outlining the role in pulmonary immune development of particle size and depth of mycoplasma deposition in the hamster lung, we developed an aerosol chamber for the reproducible aerosolization of radiolabeled M. pneumoniae. Organisms were labeled to high specific activity by the incorporation of 3H-oleic acid and aerosolized under airflow and humidity conditions creating a mean particle diameter of 2.0 micrometers. Under these conditions, viable mycoplasmas were reproducibly and evenly distributed to all major lobes of the lung. Examination of radioactive clearance and organism viability within the lung during the first 48 hr after aerosolization have suggested a minimal role for macrophage mycoplasmacidal activity and a more prominent role for ciliary clearance. Data from aerosol infections of hamsters with radio-labeled M. pneumoniae should provide a unique opportunity to examine in a highly controlled manner the effects of air pollutants on the initial stages of infection as well as effects on the development of pulmonary immunity and histologic alterations.

Nasopharyngeal removal of ozone in rabbits and guinea pigs.

In estimating pollutant concentrations responsible for observed pulmonary effects, nasopharyngeal removal of the pollutant plays an important role. The nasopharyngeal removal of ozone (O3) in anesthetized male guinea pigs and male and female rabbits was determined by drawing O3 through the isolated upper airways at a constant flow rate which approximated the animal's respiratory minute volume. The tracheal O3 concentration in rabbits and guinea pigs was markedly similar and was linearly related to the chamber concentration of O3 over a range of 196--3920 micrograms/m3 (0.1--2.0 ppm O3). Regression analyses showed that O3 removal in the nasopharyngeal region is approximately 50% in both species. Both rabbit sexes responded similarly over the concentration range studied. Exposures of guinea pigs to O3 concentrations between 3920 and 5880 micrograms/m3 (2.0 and 3.0 ppm) showed that, at these higher concentrations, relatively more O3 is removed by the upper airways.

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.