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The Spectrum of Irritant-Induced Asthma : Sudden and Not-So-Sudden Onset and the Role of Allergy

Stuart M. Brooks; Yahia Hammad; Ira Richards; Joette Giovinco-Barbas; Kathleen Jenkins
Author and Funding Information

Affiliations: From the Department of Environmental and Occupational Health, College of Public Health, and the Division of Pulmonary, Critical Care and Occupational Medicine and Division of Allergy and Clinical Immunology, Department of Internal Medicine, College of Medicine, University of South Florida, Tampa,  From the Department of Environmental and Occupational Health, College of Public Health, College of Medicine, University of South Florida, Tampa

Affiliations: From the Department of Environmental and Occupational Health, College of Public Health, and the Division of Pulmonary, Critical Care and Occupational Medicine and Division of Allergy and Clinical Immunology, Department of Internal Medicine, College of Medicine, University of South Florida, Tampa,  From the Department of Environmental and Occupational Health, College of Public Health, College of Medicine, University of South Florida, Tampa


1998 by the American College of Chest Physicians


Chest. 1998;113(1):42-49. doi:10.1378/chest.113.1.42
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Abstract

A retrospective investigation of 86 asthmatic subjects defined clinical features of irritant-induced asthma and assessed the contributory role of an allergic predisposition. Three categories of asthma were evaluated: (1) occupational asthma due to a sensitizer (11 subjects, 13%); (2) irritant-induced asthma (54 persons, 63%); and (3) not occupational/environmental exposure-related asthma (21 subjects, 24%). Two distinct clinical presentations of irritant-induced asthma emerged: the first was sudden onset (29 subjects) and the second was not so sudden in onset (25 subjects). Sudden-onset, irritant-induced asthma was analogous to the reactive airways dysfunction syndrome. Clinical manifestations began immediately or within a few hours (always within 24 h) following an accidental, brief, and massive exposure. In contrast, for the not-so-sudden-onset asthma subjects, the causative irritant exposure was not brief, usually not massive, continued for >24 h, and the initiation of asthma took longer to evolve. Eighty-eight percent of individuals with not-so-sudden irritant-induced asthma displayed an atopy/allergy status (p<0.01). Some of the atopy/allergy subjects with presumed new-onset asthma were found to have suffered preexisting asthma that had been clinically quiescent for at least 1 year before the triggering exposure (16 persons). We conclude that preexisting allergic/atopy and/or preexisting asthma were significant contributors to the pathogenesis of not-so-sudden, irritant-induced asthma and emphasizes a critical interaction between environmental and host factors in the pathogenesis of asthma.


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