Occupational Asthma, An Issue of Immunology and Allergy Clinics
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191 pages
English

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Description

This issue of Immunology and Allergy Clinics of North America brings the clinician up to date on essential topics in occupational asthma. Articles cover definition; classification; epidemiology; old and new causes; pathogenesis and disease mechanisms; clinical assessment including differential diagnosis; and management of work-related asthma and related conditions. Other subject matter includes occupational rhinitis; irritant-induced asthma and reactive airways dysfunction; hypersensitivity pneumonitis and related conditions; and evaluation of impairment and disability.

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Publié par
Date de parution 28 août 2011
Nombre de lectures 1
EAN13 9781455712403
Langue English
Poids de l'ouvrage 2 Mo

Informations légales : prix de location à la page 0,6457€. Cette information est donnée uniquement à titre indicatif conformément à la législation en vigueur.

Extrait

Immunology and Allergy Clinics of North America , Vol. 31, No. 4, November 2011
ISSN: 0889-8561
doi: 10.1016/S0889-8561(11)00095-6

Contributors
Immunology and Allergy Clinics of North America
Occupational Asthma
GUEST EDITOR: David I. Bernstein, MD
Division of Immunology, Allergy and Rheumatology, University of Cincinnati College of Medicine, 3255 Eden Avenue, Cincinnati, OH 45267-0563, USA
CONSULTING EDITOR: Rafeul Alam. MD, PhD
ISSN  0889-8561
Volume 31 • Number 4 • November 2011

Contents
Cover
Contributors
Forthcoming Issues
When the Workplace Air Makes Me Wheeze—Occupational Asthma
Preface
Definitions and Classification of Work-Related Asthma
The Epidemiology of Work-Related Asthma
Old and New Causes of Occupational Asthma
Pathogenesis and Disease Mechanisms of Occupational Asthma
Clinical Assessment of Occupational Asthma and its Differential Diagnosis
Work-Related Asthma: A Case-Based Approach to Management
Irritant-Induced Airway Disorders
Hypersensitivity Pneumonitis and Related Conditions in the Work Environment
Occupational Rhinitis
Index
Immunology and Allergy Clinics of North America , Vol. 31, No. 4, November 2011
ISSN: 0889-8561
doi: 10.1016/S0889-8561(11)00097-X

Forthcoming Issues
Immunology and Allergy Clinics of North America , Vol. 31, No. 4, November 2011
ISSN: 0889-8561
doi: 10.1016/j.iac.2011.08.002

Foreword
When the Workplace Air Makes Me Wheeze—Occupational Asthma

Rafeul Alam, MD, PhD
Division of Allergy and Immunology, National Jewish Health and, University of Colorado Denver Health Sciences Center, 1400 Jackson Street, Denver, CO 80206, USA
E-mail address: AlamR@NJHealth.org


Rafeul Alam, MD, PhD, Consulting Editor
First recognized by Hippocrates, fully described by Bernardino Ramazzini, and scientifically researched by Jack Pepys, occupational asthma remains the most prevalent occupational lung disease despite the implementation of governmental regulatory processes at the workplace. Its incidence remains largely unchanged. This is likely due to the introduction of an increasing number of novel chemicals into the workplace. Occupational asthma distinguishes itself from other forms of asthma in a number of important aspects. There is a well-defined exposure to an offending agent and duration of the exposure. The chemical nature of the offending agent is usually known. Further, the time of onset of asthma is known. These attributes make occupational asthma a highly desirable subject for research.
The induction of asthma by occupational agents with and without a latency period has challenged the classic immunologic dogma of sensitization for many years. Immunological sensitization usually requires a latency period. Another challenge has been the mechanism of T-cell sensitization to small molecular weight compounds. Until recently, we believed that immunological sensitization to non-protein chemicals primarily relied on haptenization of endogenous proteins. This is likely true in some, but not all, cases. Our understanding of immunological sensitization to non-protein chemicals has been undergoing dramatic changes. New immunological paradigms have been established that allow direct recognition of and sensitization to non-protein chemicals such as lipids, glycolipids, and inorganic small molecules. 1, 2 These novel paradigms will help us understand the immunological basis of asthma with many occupational agents.
We have invited leading experts and scholars to update us on the latest in occupational asthma. This effort is led by Dr David Bernstein, an internationally recognized leader in occupational asthma. I hope you will enjoy this issue.

References

   1. D.I. Godfrey, J. Rossjohn, J. McCluskey. The fidelity, occasional promiscuity, and versatility of T cell receptor recognition. Immunity . 2008;28:304-314.
   2. D. Chessman, L. Kostenko, T. Lethborg, et al. Human leukocyte antigen class I-restricted activation of CD8+ T cells provides the immunogenetic basis of a systemic drug hypersensitivity. Immunity . 2008;28(6):822-832.

Supported by NIH grants R01AI091614, R56AI077535, PPG HL 36577, and N01 HHSN272200700048C.
Immunology and Allergy Clinics of North America , Vol. 31, No. 4, November 2011
ISSN: 0889-8561
doi: 10.1016/j.iac.2011.08.001

Preface

David I. Bernstein, MD
Division of Immunology, Allergy and Rheumatology, University of Cincinnati College of Medicine, 3255 Eden Avenue, Cincinnati, OH 45267-0563, USA
E-mail address: bernstdd@ucmail.uc.edu


David I. Bernstein, MD, Guest Editor
Work-related asthma is the most common form of occupational lung disease, affecting 10–25% of the adult population. These conditions take on greater importance in industrialized countries but are even more significant in the developing world, which has seen tremendous growth in manufacturing of all kinds. Patients and workers with increased asthma symptoms at work may present to occupational physicians, allergists, or pulmonologists. This monograph, authored by a renowned group of experts, has been written for all physicians with special interests in occupational lung disease, although it is not intended as a comprehensive review. Rather the aim of this issue of Immunology and Allergy Clinics of North America is to update selected and timely topics in this field.
Agreement over common definitions for the various work-related asthma syndromes is an essential requisite for evaluating very complicated patients or investigation of these disorders. Drs Malo and Vandenplas introduce this monograph by delineating current definitions work-related asthma and carefully differentiate “work-aggravated asthma” from occupational asthma induced at work. Occupational asthma is very familiar to most clinicians and is now subclassified as: 1) asthma induced by workplace sensitizers; and 2) irritant-induced asthma beginning after acute work-related exposure to high levels of an irritating substance (aka, Reactive Airways Dysfunction Syndrome). New knowledge pertaining to irritant-induced airways disorders is comprehensively addressed by Drs Brooks and Bernstein. In others articles, authoritative authors provide up-to-date reviews of epidemiology, well-recognized and novel etiologic agents, pathogenesis, work-related hypersensitivity pneumonitis, and occupational rhinitis. In their respective articles, Drs Cartier, Sastre, Pacheco, and Tarlo provide practical and rational approaches for the clinician consultant on the clinical assessment and management of work-related asthma.
I would like to acknowledge and thank the esteemed group of authors represented in this monograph for their contributions. Finally, we must recognize the small cadre of researchers all over the globe whose scientific contributions during the past 50 years continue to build our knowledge of occupational lung disorders and improve the health of workers at risk.
Immunology and Allergy Clinics of North America , Vol. 31, No. 4, November 2011
ISSN: 0889-8561
doi: 10.1016/j.iac.2011.07.003

Definitions and Classification of Work-Related Asthma

Jean-Luc Malo, MD a , * , Olivier Vandenplas, MD, PhD b
a Department of Chest Medicine, Hôpital du Sacré-Cœur, Université de Montréal, 5400 West Gouin Boulevard, Montreal H4J 1C5, Canada
b Department of Chest Medicine, Cliniques de Mont-Godinne, Université Catholique de Louvain, 1 Avenue G. Therasse, B5530 Yvoir, Belgium
* Corresponding author.
E-mail address: malojl@meddir.umontreal.ca

Abstract
The workplace can trigger or induce asthma and cause the onset of different types of work-related asthma (WRA). Based on current knowledge of clinical features, pathophysiologic mechanisms, and evidence supporting a causal relationship, the following conditions should be distinguished in the spectrum of WRA: (1) immunologic occupational asthma (OA), (2) nonimmunologic OA, (3) work-exacerbated asthma, and (4) variant syndromes, including eosinophilic bronchitis, potroom asthma, and asthmalike disorders caused by organic dusts. The rationale, issues, and controversies relating to this approach are critically reviewed to stimulate the development of a consensus on operational definitions of the various phenotypes of WRA.

Keywords
• Asthma • Bronchial hyperresponsiveness • Occupational disease • Irritant-induced asthma • Reactive airways dysfunction syndrome
The expression occupational asthma (OA) was originally the only term used to describe the link, most often causal, between asthma and the workplace. Moreover, OA then included only the form that occurred after a latency period and the onset of sensitization. However, in recent years, a more general approach that encompasses all conditions that link asthma to the workplace, not only having a causal relationship but also playing a role in asthma exacerbations, has been proposed and is being labeled work-related asthma (WRA) ( Fig. 1 ). Another type of OA has also been recognized, the type caused by inhalational accidents and causing acute irritation of the airways. Variants have also been described, especially occupational eosinophilic bronchitis. In the same way as the existence of a consensus definition of asthma 1 has improved its recognition and management, precise and workable definitions of OA and other types of WRA are required to improve the investigation and management of these conditions.

Fig. 1 Definition of WRA.
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