Article References: Occupational Asthma

OCCUPATIONAL ASTHMA

1.AUTHOR	Brooks-S-M, Weiss-M-A, Bernstein-I-L.
INSTITUTION	Department of Environmental Health, University of Cincinnati College of Medicine 45221.
TITLE	Reactive airways dysfunction syndrome (RADS). Persistent asthma syndrome after high level irritant exposures.
SOURCE	Chest 1985 Sep, VOL: 88 (3), P: 376-84, ISSN: 0012-3692.
Abstract	Ten individuals developed an asthma-like illness after a single exposure to high levels f an irritating vapor, fume, or smoke. In most instances, the high level exposure was the result of an accident occurring in the workplace or a situation where there was poor ventilation and limited air exchange in the area. In all cases, symptoms developed within a few hours and often minutes after exposure. We have designated the illness as reactive airway dysfunction syndrome (RADS) because a consistent physiologic accompaniment was airways hyperreactivity. When tested, all subjects showed positive methacholine challenge tests. No documented preexisting respiratory illness was identified nor did subjects relate past respiratory complaints. In two subjects, atopy was documented, but in all others, no evidence of allergy was identified. In the majority of the cases, there was persistence of respiratory symptoms and continuation of airways hyperreactivity for more than one year and often several years after the incident. The incriminated etiologic agent varied, but all shared a common characteristic of being irritant in nature. In two cases, bronchial biopsy specimens were available, and an airways inflammatory response was noted. This investigation suggests acute high level, uncontrolled irritant exposures may cause an asthma-like syndrome in some individuals which is different from typical occupational asthma. It can lead to long- term sequelae and chronic airways disease. Nonimmunologic mechanisms seem operative in the pathogenesis of this syndrome. Author.

2 .AUTHOR	Meggs-W-J.
INSTITUTION	East Carolina University School of Medicine, Greenville, North Carolina.
TITLE	RADS and RUDS--the toxic induction of asthma and rhinitis.
SOURCE	J-Toxicol-Clin-Toxicol 1994, VOL: 32 (5), P: 487-501, ISSN: 0731-3810 84 Refs.
Abstract	Inhalation exposures can produce asthma and rhinitis by several mechanisms. Sensitization with the production of IgE specific for a substance can lead to symptoms on reexposure via mast cell degranulation and the release of inflammatory mediators. Some substances, known as environmental adjuvants, enhance the immune response to concomitant exposures with the environmental adjuvant. Respiratory irritants can lead to asthma and rhinitis through interaction with chemical irritant receptors in the airway, leading to release of substance P from sensory nerves and neurogenic inflammation. The reactive airways dysfunction syndrome is a chronic asthma-like syndrome resulting from a single acute exposure to a respiratory irritant, while the reactive upper-airways dysfunction syndrome is chronic rhinitis stemming from an irritant exposure. The dysregulation of neurogenic inflammation by chemical exposures may be an important mechanism in the toxic induction of reactive airways dysfunction syndrome and reactive upper-airways dysfunction syndrome and may play a role in understanding the sick building syndrome and the multiple chemical sensitivity syndrome. Author.

3 .AUTHOR	Meggs-W-J, Elsheik-T, Metzger-W-J, Albernaz-M, Bloch-R-M.
INSTITUTION	Department of Emergency Medicine, East Carolina University School of Medicine, Greenville, NC 27858, USA.
TITLE	Nasal pathology and ultrastructure in patients with chronic airway inflammation (RADS and RUDS) following an irritant exposure.
SOURCE	J-Toxicol-Clin-Toxicol 1996, VOL: 34 (4), P: 383-96, ISSN: 0731-3810.
Abstract	BACKGROUND: Reactive airways dysfunction syndrome is a chronic asthma-like condition developing after an acute irritant exposure, and chronic inflammation has been seen on endobronchial biopsy. Reactive upper-airways dysfunction syndrome is chronic rhinitis developing in temporal association with a toxic inhalation exposure, but the pathophysiology is unknown. OBJECTIVES: To study biopsies of the nasal mucosa in patients with reactive upper-airways dysfunction syndrome and in some cases reactive airways dysfunction syndrome developing in temporal association with a chlorine dioxide exposure, to see if a histologic basis for the persistent rhinitis and sensitivity to chemical irritants could be determined. METHODS: Specimens were stained with hematoxylin-eosin and immunoperoxidase stains for substance P, vasointestinal peptide, and S-100 (nerve fibers), and fixed in glutaraldehyde for electron microscopy. Biopsies of three nonexposed subjects were performed for comparison. A pathologist blinded to clinical data interpreted the specimens. RESULTS: Inflammation ratings of exposed individuals were higher than for the nonexposed individuals. The number of nerve fibers stained was greater for patients vs controls. Substance P and vasointestinal peptide staining was nonspecific. Electron microscopy showed desquamation of the epithelium and permeability of epithelial cell junctions. CONCLUSION: This study suggests a mechanism by which ongoing low level exposures perpetuate airway inflammation after an inducing toxic inhalation. A possible overlap between reactive airways dysfunction syndrome, reactive upper-airway dysfunction syndrome and the multiple chemical sensitivity syndrome is suggested. Author.
4. AUTHOR	The Merck Manual
TITLE	Section 4. -Pulmonary Disorders 40. -Occupational Lung Diseases -Diseases Due To Organic Dusts
ABSTRACT	OCCUPATIONAL ASTHMA a. Etiology i. Numerous allergenic and nonallergenic materials in the occupational environment are recognized causes of reversible airways obstruction. Examples include castor bean, grain, proteolytic enzymes used in detergent manufacturing and beer- and leather-making industries, western red cedar wood, isocyanates, formalin, antibiotics (eg, ampicillin, spiramycin), epoxy resins, and tea. The list is continually growing. (For exposure to textile dust, see Byssinosis BYSSINOSIS) b. Pathophysiology i. Although it is tempting to attribute most forms of asthma to either a type I (IgE)-or type III (IgG)-mediated immunologic response, such a simplistic approach is not justified. Thus, isocyanates and western red cedar sometimes cause bronchospasm up to 24 h following exposure, and the response may recur every night for a week or more without further exposure.