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.
D000336:Aerosols; D000818:Animals; D002104:Cadmium / Q000494:pharmacology* / Q000633:toxicity; D008168:Lung / Q000187:drug effects / Q000276:immunology*; D008214:Lymphocytes / Q000187:drug effects; D008264:Macrophages / Q000187:drug effects*; D051379:Mice; D009026:Mortality; D010587:Phagocytosis / Q000187:drug effects*; D011650:Pulmonary Alveoli / Q000166:cytology; D012141:Respiratory Tract Infections / Q000276:immunology*; D013297:Streptococcus pyogenes
D000336:Aerosols; D002104:Cadmium