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Pathogenesis of occupational asthma

¹ Servicio de Alergia, Fundación Jiménez Díaz, Universidad Autónoma de Madrid, Madrid, Spain. ² Service de Pneumologie, Cliniques de Mont-Godinne, Université catholique de Louvain, Yvoir, Belgium. ³ Dept of Allergy and Clinical Immunology, Ajou University School of Medicine, Suwon, Korea

CORRESPONDENCE: J. Sastre, Fundación Jiménez Díaz, Servicio de Alergia, Av Reyes Católicos 2, 28040 Madrid, Spain. Fax: 34 915499498. E-mail: jsastre@fjd.es

Keywords: asthma, eosinophils, immunoglobulin E, immunoglobulin G, leukocytes, occupational disease

Received: April 22, 2003
Accepted April 28, 2003

Abstract

The development of occupational asthma (OA) is likely to result from the complex interaction of environmental and host factors. This article addresses a series of issues relating to the multiple environmental factors that could affect the initiation of OA, including the intrinsic characteristics of causative agents, as well as the influence of the level, mode and route of exposure.

Although the clinical and pathological features of OA caused by low molecular weight agents resemble those of immunoglobulin (Ig)E-mediated asthma, the failure to detect specific IgE antibodies against most of these agents and/or poor association with disease status have resulted in intense speculation about alternative or complementary physiopathological mechanisms leading to airway sensitisation.

In this contribution, the roles of specific immunoglobulin E and G antibodies, cell-mediated immunity and inflammatory effector cells are critically reviewed. Recent advances in the characterisation of the molecular interactions between chemical sensitisers and human airway proteins provide promising avenues for elucidating the immunological basis of occupational asthma caused by low molecular weight agents.

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