Respiratory allergy: Clinical aspects

Human expression of pulmonary disease after exposure to chemicals is highly dependent on the locale and circumstances of the exposure. Most of the information about environmental hazards that is currently available has been obtained from epidemiological investigations. Chemical agents in the workplace have received considerable attention because the workplace is an ideal mini-epidemiological model of air pollution. Many instances of pulmonary immunotoxicology are engendered by adverse reactions to drugs but of necessity these can only be studied on a case-by-case basis. Although the overall expression of pathological processes in the anatomical structures of the respiratory system is limited, many of the clinicopathological features induced by chemicals present with features that are characteristic enough to suggest that several stimulus-response paradigms may be applicable. In this review the immunotoxicological impact of chemicals on the major anatomical components of the lung (the conducting airways, the alveolar, interstitial and capillary compartments, the pleura and the pulmonary vasculature) is considered. The two major classes of hypersensitivity induced in humans by chemicals are those involving IgE humoral and cell-mediated immune responses. Although other isotypic antibodies (IgM, IgG, IgA), as well as complement activation, have been demonstrated after specific types of exposure, the role of these immune components in the pathogenesis of disease does not appear to be of major importance. Chemicals with a special propensity for IgE sensitization and effects on the airways include polyisocyanates, acid anhydrides and platinum salts. Conditions that involve the lung parenchyma are exemplified by hypersensitivity pneumonitis, drug-induced pneumonia and berylliosis.