IMMUNOLOGIC AND CLINICAL FEATURES OF TOXIC INHALATIONS

Abstract

Irritant gases and dusts can cause intense damage to the airway. Some authors have speculated that the irritant effects of these gases in the airway are the mechanism for the development of bronchial hyper-responsiveness and occupational asthma in patients exposed to sensitizing chemicals. Others have postulated that toxic inhalation produces airway damage that increases the susceptibility to antigen entrance into the subepithelial layer of the bronchial mucosa, which, in some unexplained way, increases the risk for subsequent hypersensitivity to that antigen. Other toxic gases, such as chlorine, produce airway damage that may take months or years to develop through unknown mechanisms. Toxic dusts may produce an atypical form of hypersensitivity pneumonitis, most likely nonimmunologically mediated, related to the effects of high concentrations of microbial and mycotoxins. The role of immunologic mechanisms in a variety of toxic inhalation syndromes is unclear.