Workplace irritant exposures: do they produce true occupational asthma?

Department of Medicine, University of Toronto, Toronto Western Hospital, Gage Occupational and Environmental Health Unit, Toronto, Ontario, Canada.
Annals of allergy, asthma & immunology: official publication of the American College of Allergy, Asthma, & Immunology (Impact Factor: 2.75). 06/2003; 90(5 Suppl 2):19-23. DOI: 10.1016/S1081-1206(10)61643-2
Source: PubMed

ABSTRACT To describe the features of irritant-induced asthma and discuss the diagnosis in relation to differing workplace irritant exposures and symptomatic responses.
A review of MEDLINE articles on this topic from January 1, 1985, through December 31, 2001 was performed.
The author selected relevant articles for inclusion in the review.
Many reports indicate that unintentional high-level respiratory irritant exposures can induce the new onset of asthma. Cases that meet strict criteria for a syndrome of irritant-induced asthma, termed reactive airways dysfunction syndrome, can be diagnosed with relative certainty. Several reports of irritant-induced asthma, especially prevalence studies, have relied on historical data or have otherwise modified the reactive airways dysfunction syndrome criteria for diagnosis (eg, expanding the definition to include the symptom onset several days after exposure). Such modifications, or inclusion of cases with incomplete documentation, likely increase diagnostic sensitivity but may reduce the certainty of diagnosis for individual cases. Expanding exposure criteria to moderate or long-term low-level irritant exposures causes difficulty in excluding transient irritant exacerbation of underlying asthma or coincidental onset of asthma during working life. Although recent population studies suggest a greater relative risk of asthma in occupations with expected low-to-moderate respiratory irritant exposures, currently no objective laboratory tests exist to exclude coincidental asthma in such patients.
Irritant-induced asthma can be produced by high-level unintentional respiratory irritant exposures at work or outside the workplace. Lower levels of exposure to respiratory irritants at work are more common, and additional studies are needed to determine the airway effects of such exposures.

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    ABSTRACT: The term irritant-induced (occupational) asthma (IIA) has been used to denote various clinical forms of asthma related to irritant exposure at work. The causal relationship between irritant exposure(s) and the development of asthma can be substantiated by the temporal association between the onset of asthma symptoms and a single or multiple high-level exposure(s) to irritants, whereas this relationship can only be inferred from epidemiological data for workers chronically exposed to moderate levels of irritants. Accordingly, the following clinical phenotypes should be distinguished within the wide spectrum of irritant-related asthma: 1) definite IIA, i.e. acute-onset IIA characterized by the rapid onset of asthma within a few hours after a single exposure to very high levels of irritant substances; 2) probable IIA, i.e. asthma that develops in workers with multiple symptomatic high-level exposures to irritants; and 3) possible IIA, i.e. asthma occurring with a delayed onset after chronic exposure to moderate levels of irritants. This document prepared by a panel of experts summarizes our current knowledge on the diagnostic approach, epidemiology, pathophysiology, and management of the various phenotypes of IIA. This article is protected by copyright. All rights reserved.
    Allergy 05/2014; 69(9). DOI:10.1111/all.12448 · 6.00 Impact Factor
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    ABSTRACT: Introduction Since persulfate salts are an important cause of occupational asthma (OA), we aimed to study the persistence of respiratory symptoms after a single exposure to ammonium persulfate (AP) in AP-sensitized mice. Material and Methods BALB/c mice received dermal applications of AP or dimethylsulfoxide (DMSO) on days 1 and 8. On day 15, they received a single nasal instillation of AP or saline. Airway hyperresponsiveness (AHR) was assessed using methacholine provocation, while pulmonary inflammation was evaluated in bronchoalveolar lavage (BAL), and total serum immunoglobulin E (IgE), IgG1 and IgG2a were measured in blood at 1, 4, 8, 24 hours and 4, 8, 15 days after the single exposure to the causal agent. Histological studies of lungs were assessed. Results AP-treated mice showed a sustained increase in AHR, lasting up to 4 days after the challenge. There was a significant increase in the percentage of neutrophils 8 hours after the challenge, which persisted for 24 hours in AP-treated mice. The extent of airway inflammation was also seen in the histological analysis of the lungs from challenged mice. Slight increases in total serum IgE 4 days after the challenge were found, while IgG gradually increased further 4 to 15 days after the AP challenge in AP-sensitized mice. Conclusions In AP-sensitized mice, an Ig-independent response is induced after AP challenge. AHR appears immediately, but airway neutrophil inflammation appears later. This response decreases in time; at early stages only respiratory and inflammatory responses decrease, but later on immunological response decreases as well.
    PLoS ONE 10/2014; 9(10):e109000. DOI:10.1371/journal.pone.0109000 · 3.53 Impact Factor
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