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The pathogenesis of byssinosis has been attributed to several different immunopathologic mechanisms, including a type III (immune complex) pulmonary injury. To further examine this type III theory, sera (Monday preshift) from 59 cotton textile workers were examined by gel diffusion and counterimmunoelectrophoresis for precipitating antibodies to aqueous extracts of cotton bract, carpels, stems, leaves, immature cotton bract, carpels, stems, leaves, immature cotton lint, and cardroom cotton dust. Sera were also collected from 35 nonexposed normal volunteers and examined similarly. No true precipitating antibodies to these extracts could be detected in any of the control or worker serum samples. The aqueous extracts of cardroom cotton dust and cotton stems were found to contain naturally occurring components that precipitated (in agarose gel) beta-lipoprotein and gamma-globulins (mostly IgG) in a nonimmunologic manner. Sera from normal human controls and cotton textile workers all produced identical patterns of reaction with these two extracts. Treatment of these extracts with polyvinylpolypyrrolidone, a specific insoluble adsorbent for polyphenolic tannins, eliminated this pseudoimmune reaction. Although the role this pseudoimmune reaction may play in the pathogenesis of byssinosis is still unknown, it demonstrates the problems associated with laboratory-based investigations of the immunologic aspects of byssinosis.

In order to test the hypothesis that the histological changes of extrinsic allergic alveolitis result from non-specific activation of the complement cascade we studied pulmonary reactions to equivalent doses of soluble and particulate activators of complement in rats. A single intratracheal instillation of zymosan, a particulate activator of the complement system, produced a florid granulomatous pneumonitis which was maximal at 5 days. This granulomatous reaction did not appear to be associated with the development of hypersensitivity to zymosan. Complement depletion by cobra venom factor did not suppress the granulomatous reaction. Equivalent doses of soluble activators of complement failed to produce any inflammatory changes in the lung. Large doses of immune complex produced an acute, complement dependent, haemorrhagic alveolitis which was maximal at 8 hr and which resolved completely by 48 hr. We conclude that the late granulomatous pulmonary reaction to intra-tracheally administered zymosan is not due to an immune response, or a consequence of direct activation of the alternative pathway of complement, but is of 'foreign body' type. We urge caution in drawing conclusions regarding the pathogenesis of the allergic alveolitides on histological appearances alone.