Current trends in research on the etiology and pathogenesis of byssinosis

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Abstract
The features of the cotton dust syndrome which need to be considered when formulating a hypothesis on mechanism(s) are: 1) the presence of fever, 2) the “Monday effect,” 3) the slow onset of forced expiratory volume in 1 second (FEV1) changes, and 4) the presence of bronchitis in chronic sufferers but the absence of emphysema or fibrosis. The main hypotheses concerning the mechanisms are direct release of histamine triggered by cotton dust components, immune reactions (principally antibody mediated) to cotton dust antigens, and inflammatory response(s) triggered by endotoxins released from bacterial contaminants on the dust. While histamine release and immune reactions may occur as a result of cotton dust inhalation, it is suggested that they are of secondary importance in comparison to inflammation. Evidence is reviewed that implicates bacterial lipopolysaccharide (LPS) present in the dust as the principal etiologic agent in this process. It is postulated that LPS inhalation stimulates a secretory response by lung macrophages, involving the release of effector molecules which trigger coagulation, bronchoconstriction, fever, and mucus production. LPS‐induced macrophage secretory products also promote the local sequestration and activation of both neutrophils and platelets, which serve to amplify the inflammatory response. Evidence is presented implicating both interstitial and alveolar macrophages in this process. The problems associated with the identification of “high risk” groups of cotton workers will be discussed, from a number of viewpoints; consideration will be given to the role of a variety of environmental factors (including tobacco smoking) in this context, as well as possible genetic factors. Regarding genetic predisposition, preliminary evidence will be presented from ongoing studies on the presence of high and low responders to LPS.