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Work-Related Asthma ACOEM PRACTICE GUIDELINES Work-Related Asthma Athena T. Jolly, MD, MPH, Julia E. Klees, MD, MPH, Karin A. Pacheco, MD, MSPH, Tee L. Guidotti, MD, MPH, DABT, Howard M. Kipen, MD, MPH, Jeremy J. Biggs, MD, MSPH, Mark H. Hyman, MD, Bruce K. Bohnker, MD, MPH, Matthew S. Thiese, PhD, MSPH, Kurt T. Hegmann, MD, MPH, and Philip Harber, MD, MPH Objective: Summarize developed evidence- includes sensitizer-induced asthma, result- questions developed by the Evidence-based based diagnostic and treatment guidelines ing from sensitization to an antigen in the Work-related Asthma Panel: for work-related asthma (WRA). Methods: workplace, and irritant-induced asthma, Comprehensive literature reviews conducted induced by workplace exposures to irritants 1. Is there evidence on how to identify with article critiquing and grading. Guidelines (Table 1). Each condition has the potential workers who are at higher risk of devel- developed by a multidisciplinary expert panel for considerable acute morbidity, long-term oping occupational asthma? and peer-reviewed. Results: Evidence supports disability, and adverse impact on income 2. What evidence is there for the diagnosis spirometric testing as an essential early test. and quality of life.6–12 of occupational asthma? Serial peak expiratory flow rates measurement The most common form of occu- 3. Is there evidence that different diagnos- is moderately recommended for employees diag- pational lung disease in many industrialized tic modalities are needed for workers nosed with asthma to establish work-relatedness. countries, with approximately 10% to 15% with new onset of symptoms or worsen- Bronchial provocation testing is moderately of all prevalent adult cases attributed to ing of previous asthma symptoms? recommended. IgE and skin prick testing for occupational factors,6–8,10,12–14 OA is fur- 4. Are there diagnostic tests that can specific high-molecular weight (HMW) antigens ther classified into OA with latency or OA assist in differentiating occupationally are highly recommended. IgG testing for HMW without latency. OA without latency is less related asthma from nonoccupational antigens, IgE testing for low-molecular weight common, and is believed to represent 5% to asthma? antigens, and nitric oxide testing for diagnosis are 15% of all OA cases.1,15 The percentage of 5. Is there evidence on treatment options not recommended. Removal from exposure is new-onset adult asthma attributable to that differ for occupationally related associated with the highest probability of occupational causes is considered to be asthma from nonoccupational asthma? improvement, but may not lead to complete much higher, up to a third of all cases.16,17 6. What management options are available recovery. Conclusion: Quality evidence sup- The frequency of WEA, defined as preex- for occupational asthma? ports these clinical practice recommendations. isting reactive airways disease that is made 7. Is removal from work necessary in all The guidelines may be useful to providers who temporarily or permanently worse due to cases of occupationally related asthma? diagnose and/or treat WRA. occupational exposures, is substantially The primary target population is more common than OA.18 working-age adults, although the literature The predisposing factors for devel- searches included articles addressing all INTRODUCTION oping OA with latency are not well known. adults. Thus, it is recognized that the prin- sthma is a common, chronic disorder Atopy is the primary established risk factor, ciples may apply more broadly. A of the airways that involves a com- operating largely with respect to high mol- plex interaction of airflow obstruction, ecular weight (HMW) antigens such as GUIDELINE DEVELOPMENT bronchial hyperresponsiveness, and under- animal proteins. It has been proposed that lying inflammation with increased airway PROCESS human leukocyte antigen class-2 alleles A detailed methodology document responsiveness to a variety of stimuli being may be a risk factor for the development typical.1–5 Work-related asthma (WRA) specified evidence selection, scoring, of OA resulting from low molecular weight incorporation of cost considerations, and includes both asthma of an occupational 11,19,20 agents. Medical management and formulation of recommendations.22,23 The origin (occupational asthma [OA]) and compensation decisions require a thorough work-exacerbated asthma (WEA). OA aim was to identify the highest quality assessment of suspected OA, which may be evidence on any given topic. Guidance mistaken for non-OA unless a detailed was drafted using tables that abstracted The ACOEM Practice Guidelines, including the history, including occupational history, the evidence and which were forwarded Work-related Asthma Guideline, is published and appropriate medical tests are performed 21 to the multidisciplinary Panel that reviewed by Reed Group, Ltd. Excerpts from the ACOEM to support an association with work. the evidence and finalized the text and Work-related Asthma Guideline, MDGuide- lines, reproduced with permission from Reed recommendations. Group, Ltd. All rights reserved. The Evidence- GUIDELINE FOCUS/TARGET based Practice Work-related Asthma Panel and POPULATION EVIDENCE REVIEW AND the Research Team have complete editorial independence from ACOEM and Reed Group, The American College of Occu- GRADING neither of which have influenced the recommen- pational and Environmental Medicine All evidence related to WRA in dations contained in this guideline. (ACOEM) created its evidence-based searching four databases (PubMed, Excerpts from the ACOEM Work-related Asthma EBSCO Cochrane Library Scopus Guideline, MDGuidelines, reproduced with per- Work-related Asthma Guideline to primar- , , and ) mission from Reed Group, Ltd. All rights ily address diagnostic options to help deter- was included in this guideline. The com- reserved. mine whether an employee has asthma, and prehensive searches for evidence were The authors declare no conflicts of interest. whether the asthma is related to workplace performed through September 2012 for Address correspondence to: Kurt T. Hegmann, MD, MPH, University of Utah Rocky Mountain exposures (Fig. 1). It was designed to diagnostic studies and February 2014 for Center for Occupational and Environmental present health care providers—who are management studies to help ensure Health, 391 Chipeta Way, Suite C, Salt Lake the primary target users—with evidence- complete study capture. The search strat- City, UT 84108-1294 (Kurt.Hegmann@hsc. based guidance on the evaluation and egies retrieved a total of 10,598 articles that utah.edu). treatment of WRA. This report summarizes were screened, with all potentially appro- Copyright ß 2015 American College of Occu- pational and Environmental Medicine findings from that Guideline (138 pages, priate study abstracts reviewed and eval- DOI: 10.1097/JOM.0000000000000572 497 references) and addresses the following uated against specified inclusion and JOEM Volume 57, Number 10, October 2015 e121 Copyright © 2015 American College of Occupational and Environmental Medicine. Unauthorized reproduction of this article is prohibited Jolly et al JOEM Volume 57, Number 10, October 2015 TABLE 1. Types of Work-Related Asthma Nomenclature Term Defining Features Sensitizer-induced OA OA with latency of allergic or presumed Immunological/hypersensitivity component and diagnostic tests include immunological mechanism: not measures of specific sensitization (eg, skin-prick test, serum specific IgE, necessarily IgE circulating IgC against the antigen or skin sensitization) Irritant-induced OA OA without latency No allergic component and worker is not sensitized to an agent; rather, the agent causes inflammatory responses through irritant mechanisms WEA or aggravated WEA or aggravated asthma Worker has prior or concurrent history of asthma not induced by that asthma (no latency period) workplace. The worker is not sensitized to an agent at work, but is irritated by a ‘‘non-massive’’ exposure (eg, cold, exercise, non-sensitizing dust, fumes, or sprays) that provokes an asthmatic reaction IgE, immunoglobulin E; OA, occupational asthma; WEA, work-exacerbated asthma. Adapted from the American College of Chest Physicians. exclusion criteria. Searches were supple- synthesis of the evidence plus expert con- by other methods. Six moderate-quality mented with articles from personal files and sensus. These recommendations are for studies support the use of peak expiratory reference reviews. A total of 497 articles practitioners, and decisions to adopt a flow rate for the diagnosis of OA and WRA; were retrieved of which 157 met the particular course of action must be made however, peak expiratory flow rate is heav- inclusion criteria. Of those, 114 were by trained practitioners on the basis of avail- ily dependent upon the worker’s efforts and included as high- or moderate-quality stud- able resources and the particular circum- assumes worker honesty in performing and ies in evidence-based guideline develop- stances presented by the individual patient. recording the test results.33–40 ment. The remaining 43 studies were deemed low-quality and excluded. CLINICAL All included studies were scored for RECOMMENDATIONS NONSPECIFIC BRONCHIAL quality. Recommendations were graded Sixteen diagnostic recommendations PROVOCATION TESTING from (A) to (C) in favor and against the were formulated for diagnostic testing, of Nonspecific bronchial provocation specific diagnostic test or treatment, with which 11 were
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