OCCUPATIONAL ASTHMA AND RELATED RESPIRATORY DISORDERS - FOREWORD

Authors
Citation
Rc. Bone, OCCUPATIONAL ASTHMA AND RELATED RESPIRATORY DISORDERS - FOREWORD, Disease-a-month, 41(3), 1995, pp. 144-199
Citations number
174
Categorie Soggetti
Medicine, General & Internal
Journal title
ISSN journal
00115029
Volume
41
Issue
3
Year of publication
1995
Pages
144 - 199
Database
ISI
SICI code
0011-5029(1995)41:3<144:OAARRD>2.0.ZU;2-V
Abstract
Occupational rhinitis is a common but generally underreported entity. Although it may occur alone, it is frequently associated with occupati onal asthma. Occupational asthma may have one of several presentations that are difficult to distinguish from nonwork conditions. The respir atory tract acts as the final common pathway for all inhaled environme ntal pollutants, whether encountered in the home or at work. More than 200 chemicals have been incriminated as a cause of work-related asthm a. It is said that about 2% of the 10 million Americans who have asthm a acquired it as a result of some chemical irritant or immunogen in th eir work environment. A number of predisposing factors facilitate the development of work-related asthma. These include industrial condition s, climatic factors, atopic predisposition, smoking, recreational drug use, viral infection, nonspecific bronchial hyperreactivity, and a va riety of miscellaneous factors. Pathogenetically, occupational asthma may be immunologic or nonimmunologic in nature. The immunologic varian ts involve sensitization to a variety of large-molecular-weight consti tuents. The major nonimmune variant is referred to as inflammatory bro nchoconstriction or reactive airways dysfunction syndrome (RADS). Ther e are well-defined criteria for the diagnosis of immunologic and nonim munologic asthma. The several clinical variations of occupational asth ma can be difficult to distinguish from nonindustrial disorders. The m ost common presentation in practice involves the worker with preexiste nt asthma who has been adversely affected by work exposures. Occasiona lly these industrial exposures precipitate permanent impairment. It is clear, however, that occupational asthma is not a single, simple, or homogeneous entity, even when a single specific causal factor can be i dentified in the workplace. Therefore the physician must be aware of t he patient's entire medical history and the precise occupational expos ures and must have convincing physiologic evidence that demonstrates a cause-and-effect relationship before making a definitive diagnosis of work-related asthma. Once the diagnosis is established, the worker sh ould be removed from the workplace. If the diagnosis is made in a time ly fashion, the patient should experience a significant improvement. T he major factor in determining a poor prognosis in occupational asthma is the duration of exposure before the diagnosis is established. Prev ention of the disorder is the best therapeutic intervention.