Endotoxin has been implicated as a potential causative agent of numerous disorders such as byssinosis, farmers lung, and silo unloaders' syndrome.

As part of our model to investigate the pulmonary effects of inhaled endotoxin, we have previously demonstrated that endotoxin is capable of inducing airway inflammation and altering airway reactivity, although no direct link between these two phenomena was observed.

To understand further the mechanisms involved in endotoxin-induced lung disorders, electron-micrographs of the tracheal, bronchial, and alveolar regions were obtained at various time points following exposure of guinea pigs to an aerosol of endotoxin solution.

In the trachea and bronchi, there was epithelial disruption, focal matting and/or loss of cilia, increased granulocytes, and lumenal erythrocytes, electron dense granules, cellular debris, and increased mucus, following endotoxin exposure. In the trachea maximum damage was observed at 72h. In the bronchi maximum damage was observed at 24h, with recovery by 72h.

Damage of the epithelium also occurred in alveolar tissue. However, endothelial damage was more marked, with complete loss of the endothelium at 72h.

Thus inhaled endotoxin causes significant damage to the pulmonary epithelium and endothelium. However, the changes observed so not explain the differences in reactivity seen with different bronchoconstrictors in previous studies.