Inhalation exposure to acrolein induced a dose-dependent impairment of pulmonary antibacterial defenses in mice. Animals exposed to 3 or 6 ppm of acrolein were increasinglless effective in inactivation of aerogenic challenges of 32P-labeled Staphylococcus aureus. Acrolein concentrations greater than 6 ppm caused increased sensory irritations, but no additional impairment of lung antibacterial resistance. Influenza A viral pneumonia in mice also suppressed pulmonary bactericidal activity. Mice convalescing from moderate viral pneumonia became severely deficient in antibacterial defenses when exposed to acrolein. Whether the viral-induced impairment in pulmonary defense delayed the inactivation or allowed the proliferation of bacteria was dependent upon the dose of acrolein. The present study demonstrated that an underlying infectious disease process compounded the pulmonary toxicity of acrolein such that normally moderate toxicity was elevated to a virtual abolition of antibacterial defense mechanisms.
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