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Diagnosis and Management of Work-Related Asthma: ACCP Consenus Statement: DIAGNOSIS AND MANAGEMENT OF WORK-RELATED ASTHMA: ACCP CONSENSUS STATEMENT |

Diagnosis and Management of Work-Related Asthma: American College of Chest Physicians Consensus Statement FREE TO VIEW

Susan M. Tarlo, MBBS, FCCP; John Balmes, MD, FCCP; Ronald Balkissoon, MD; Jeremy Beach, MD; William Beckett, MD, MPH, FCCP; David Bernstein, MD; Paul D. Blanc, MD, FCCP; Stuart M. Brooks, MD; Clayton T. Cowl, MD, MS, FCCP; Feroza Daroowalla, MD, MPH, FCCP; Philip Harber, MD, MPH; Catherine Lemiere, MD, MSc; Gary M. Liss, MD, MS; Karin A. Pacheco, MD, MSPH; Carrie A. Redlich, MD, MPH, FCCP; Brian Rowe, MD, FCCP; Julia Heitzer, MS
Author and Funding Information

*From the University of Toronto (Drs. Tarlo and Liss), Toronto, ON, Canada; the University of California San Francisco (Drs. Balmes and Blanc), San Francisco, CA; National Jewish Medical and Research Center (Drs. Balkissoon and Pacheco), Denver, CO; the University of Alberta (Drs. Beach and Rowe), Calgary, AB, Canada; the University of Rochester School of Medicine and Dentistry (Dr. Beckett), Rochester, NY; the University of Cincinnati (Dr. Bernstein), Cincinnati, OH; the University of South Florida (Dr. Brooks), Tampa, FL; Mayo Clinic (Dr. Cowl), Rochester, MN; the State University of New York (Dr. Daroowalla), Stony Brook, NY; the University of California, Los Angeles (Dr. Harber), Los Angeles, CA; the Université de Montréal (Dr. Lemiere), Montréal, QC, Canada; the Yale University School of Medicine (Dr. Redlich), New Haven, CT; and the American College of Chest Physicians (Ms. Heitzer), Northbrook, IL.

Correspondence to: Susan M. Tarlo, MBBS, FCCP, Toronto Western Hospital EW7-449, 399 Bathurst St, Toronto, ON, Canada M5T 2S8; e-mail: susan.tarlo@utoronto.ca


As part of the practice of occupational pulmonary medicine, most of the panel members have served as consultants or medical experts in workers' compensation or other cases of suspected work-related asthma, and/or have provided other consulting services involving possible work-related asthma. In addition, Dr. Tarlo has received research funding for studies in work-related asthma from the Ontario Thoracic Society, and both Drs. Tarlo and Liss have received research funding from the Ontario Workplace Safety and Insurance Board Research Advisory Council for studies including work-related asthma. Dr. Tarlo has also served the following organizations with a direct interest in occupational asthma: the American Thoracic Society (Committee on Work-Exacerbated Asthma); the American Academy of Asthma, Allergy and Immunology Occupational Disease Committee; and the Canadian Thoracic Society Asthma Committee. Dr. Balmes has served organizations with a direct interest in occupational asthma, including the American Thoracic Society (Committee on Asthma Impairment and Committee on Occupational Contribution to the Burden of Obstructive Airway Disease) and the Centers for Disease Control and Prevention (CDC)-NIOSH (Study Section). Dr. Beckett has received funding from the Association for Occupational and Environmental Clinics and NIOSH to review the literature and provide written reports on issues related to occupational lung diseases, including occupational asthma. Dr. Beach has received research funding from the Alberta Workers' Compensation Board Research Program. Dr. Bernstein has received CDC-NIOSH research funding. Dr. Blanc has served organizations with a direct interest in occupational asthma, including the American Thoracic Society (Committee on Occupational Contribution to the Burden of Obstructive Airway Disease) and the Institute of Medicine committee reviewing respiratory disease programs at CDC-NIOSH. Dr. Brooks has received CDC-NIOSH research funding. Dr. Harber has served the following organizations with a direct interest in occupational asthma: the American College of Occupational and Environmental Medicine (Board of Directors, Pulmonary Committee, and Treatment Guidelines Committee); the American Thoracic Society (the Asthma Impairment Committee and the Committee on Work Exacerbated Asthma); the American Medical Association (guidelines reviewer); and CDC-NIOSH (the Committee on Work Exacerbated Asthma, Study Section). He has received research funding from CDC-NIOSH for projects related to the recognition and prevention of occupational lung diseases such as asthma. Dr. Lemiere has received research funds from the Institut de Recherche en Sante et Sécurité au Travail (or IRSST) Robert Sauve and from CDC-NIOSH, and is a member of the American Thoracic Society Committee on Work Exacerbated Asthma and Canadian Thoracic Society Asthma Committee. Dr. Pacheco has received research funding from the National Institutes of Health (NIH) for projects related to occupational asthma, and is also a member of the American Academy of Asthma, Allergy, and Immunology Occupational Disease Committee. Dr. Redlich has received research funding from the NIH and CDC-NIOSH for projects related to occupational asthma, and has also served organizations with a direct interest in occupational asthma, including the American Thoracic Society (Committee on Work Exacerbated Asthma), American Medical Association (guidelines reviewer) and CDC-NIOSH (grant reviewer). Dr. Rowe is supported by a 21st Century Research Chair from the Government of Canada (Ottawa, ON, Canada) and has received funding for work-related asthma research from the Agency for Healthcare Quality and Research (Bethesda, MD). Drs. Balkissoon, Cowl, and Daroowalla have reported to the ACCP that no significant conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article. None of the authors has received funding from tobacco companies.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (www.chestjournal.org/misc/reprints.shtml).


Chest. 2008;134(3_suppl):1S-41S. doi:10.1378/chest.08-0201
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Background:  A previous American College of Chest Physicians Consensus Statement on asthma in the workplace was published in 1995. The current Consensus Statement updates the previous one based on additional research that has been published since then, including findings relevant to preventive measures and work-exacerbated asthma (WEA).

Methods:  A panel of experts, including allergists, pulmonologists, and occupational medicine physicians, was convened to develop this Consensus Document on the diagnosis and management of work-related asthma (WRA), based in part on a systematic review, that was performed by the University of Alberta/Capital Health Evidence-Based Practice and was supplemented by additional published studies to 2007.

Results:  The Consensus Document defined WRA to include occupational asthma (ie, asthma induced by sensitizer or irritant work exposures) and WEA (ie, preexisting or concurrent asthma worsened by work factors). The Consensus Document focuses on the diagnosis and management of WRA (including diagnostic tests, and work and compensation issues), as well as preventive measures. WRA should be considered in all individuals with new-onset or worsening asthma, and a careful occupational history should be obtained. Diagnostic tests such as serial peak flow recordings, methacholine challenge tests, immunologic tests, and specific inhalation challenge tests (if available), can increase diagnostic certainty. Since the prognosis is better with early diagnosis and appropriate intervention, effective preventive measures for other workers with exposure should be addressed.

Conclusions:  The substantial prevalence of WRA supports consideration of the diagnosis in all who present with new-onset or worsening asthma, followed by appropriate investigations and intervention including consideration of other exposed workers.

Figures in this Article

This Consensus Statement on the diagnosis and management of work-related asthma (WRA) has been developed by an expert panel of specialists in allergy, pulmonary medicine, and occupational medicine, which was impaneled at the request of the American College of Chest Physicians (ACCP) Health and Science Policy Committee, with the endorsement of the ACCP Board of Regents to update the earlier 1995 ACCP Consensus Statement: Assessment of Asthma in the Workplace.1 The initial aim was to develop formal recommendations using an evidence-based approach and including greater consideration of work-exacerbated asthma (WEA) than that in the previous Consensus Statement. However, by the nature of the topic, the citations captured through systematic review were limited in scope and number. Randomized controlled trials (RCTs) relevant to the diagnosis and treatment of WRA are not available and are not likely to be performed. A limited number of studies have compared various diagnostic tests for sensitizer-induced occupational asthma to the selected reference standard test, a specific inhalation challenge (SIC). Most of the published literature consists of clinical studies of patients in whom occupational asthma (OA) was diagnosed rather than cross-sectional or longitudinal cohort studies of exposed workers. The panel also considered additional studies, which were not included in the formal Agency for Healthcare Quality and Research (AHRQ) analysis, as well as later literature identified by an additional review of the literature into 2007. Therefore, due to the evidence considered for this document, this statement does not use the ACCP grading system (which relies heavily on RCT data),2 but rather is based on the best available evidence and has been arrived at by consensus among the panel members. This Consensus Document addresses WRA (Fig 1), which the panel defined as including OA (caused by work) as well as WEA (preexisting or concurrent asthma that is worsened by work factors). In addition to addressing the diagnosis and management of patients with WRA, this Consensus Statement also covers several other important topics, including the physician's role in promoting safer employment options and access to worker's compensation or other benefit systems, as well as the prevention of WRA. It is hoped that this document will assist health-care providers in the diagnosis and management of WRA. The advised approach is summarized in Figure 2. Since WRA is potentially largely preventable and is best diagnosed early in its course, this Consensus Document also addresses primary, secondary, and tertiary preventive measures for WRA. Additional practical materials are provided on the CHEST Web site (www.chestjournal.org). Consistent with the ACCP requirements for consensus statements, the panel does not use the term recommendation but instead “suggests” approaches based on panel consensus in light of the best available evidence.

Figure Jump LinkFigure 1 Relationships of asthma to the workplace.Grahic Jump Location
Figure Jump LinkFigure 2 Summary flow chart of clinical evaluation and management of WRA.Grahic Jump Location

The panel reached consensus (organized around 12 main topics), on the following, as summarized below:

  1. In all individuals with new-onset or worsening asthma, take a history to screen for WRA (OA and WEA). Then confirm the diagnosis of asthma and investigate to determine whether the patient has WRA, performing these tests, whenever possible, prior to advising the patient to change jobs.

  2. In all individuals with suspected WRA, obtain a history of job duties, exposures, industry, use of protective devices/equipment, and the presence of respiratory disease in coworkers, and consult material safety data sheets (MSDSs), which list many recognized hazardous agents. Document the onset and timing of symptoms, medication use, and lung function, and their temporal relationship to periods at and away from work.

  3. In individuals who have asthma not caused by work but that subsequently worsens while working, consider the diagnosis of WEA, which is usually based on changes in symptoms, medication use, and/or lung function temporally related to work.

  4. In individuals with suspected sensitizer-induced OA, in addition to carefully documenting the occupational history, perform additional objective tests when feasible (eg, serial peak flow recordings, serial methacholine challenges, immunologic assessments, induced sputum testing, and SICs) to improve the diagnostic probability.

  5. In individuals with suspected WRA who are currently working at the job in question, record serial measurements of peak flow as part of the diagnostic evaluation and ask the patient to record these optimally a minimum of four times daily, for at least 2 weeks at work and 2 weeks off work.

  6. In individuals with suspected sensitizer-induced OA, working at the job in question, perform a methacholine challenge test or obtain comparable measurements of nonspecific airway responsiveness during a working period, and repeat it during a period (optimally, at least 2 weeks) away from the work exposure to identify work-related changes.

  7. In individuals with suspected sensitizer-induced OA, perform immunologic tests (skin prick testing or in vitro specific IgE assays) to identify sensitization to specific work allergens when these tests are technically reliable and available.

  8. In individuals with suspected sensitizer-induced OA, conducting an SIC (where available) is suggested when the diagnosis or causative agent remains equivocal; however, this testing should only be performed in specialized facilities, with medical supervision throughout the testing.

  9. For all individuals with WRA, attempt better control of exposures. Remove patients with sensitizer-induced OA from further exposure to the causative agent in addition to providing other asthma management.

  10. In individuals with irritant-induced asthma or WEA, the panel advises optimizing asthma treatment and reducing the exposure to relevant workplace triggers. If not successful, change to a workplace with fewer triggers is suggested in order to control asthma.

  11. For workers who are potentially exposed to sensitizers or uncontrolled levels of irritants, the panel advises primary prevention through the control of exposures (eg, elimination, substitution, process modification, respirator use, and engineering control).

  12. An individual diagnosis of OA represents a potential sentinel health event:

    • Evaluate the workplace to identify and prevent other cases of OA in the same setting; and

    • For work environments with potential exposure to sensitizers, the Panel advises secondary preventive measures including medical surveillance using tools such as questionnaires, spirometry, and, where available, immunologic tests.

WRA, which includes OA and WEA, presents a major health challenge with significant potential for acute morbidity, long-term disability, and adverse social and economic impacts.3 Since the 18th century, medical writers have noted links between certain trades and respiratory symptoms recognizable today as asthma. In the 20th century, the number of work-related causes of asthma (sensitizers) expanded substantially. By the mid-1980s, recognition grew4 that acute irritant exposure could cause asthma in an etiologic process that is distinct from that of sensitizers. Currently, hundreds of distinct causes of OA have been recognized.1,57 WEA has received less systematic study, yet has been recognized as a priority area for further research.8,9

The prevalence of WRA has not been well defined due in part to variable definitions, diagnostic criteria, and work settings, as well as limited surveillance data. It has become clear that WRA is a far more substantive component of adult asthma than has been appreciated from clinical case series, or from studies of individual worksites or single industries. Approximately 10 to 15% of cases of adult asthma are attributable to occupational factors, which is consistent with a role for work in initiating asthma.1013 The incidence of OA has been difficult to measure with precision. OA surveillance data vary widely in case capture, underestimating the true extent of the problem. As much as 25% of adult asthmatic patients are estimated to have WRA, which would include WEA as well as OA.14 Consistent with this, in other studies3,1517 of patients in whom WRA has been diagnosed, the proportion of patients with WEA ranges from about 10 to 50% of cases of WRA, although this may be as reflective of compensation practices as of true prevalence.

The magnitude of WRA is matched by the important opportunities for the primary prevention of new cases and the secondary and tertiary prevention of disease progression and disability. Prevention is intimately linked both to the diagnosis and treatment of disease. The diagnosis of a single case of OA among a group sharing similar exposures offers the possibility of preventing new asthma (ie, primary prevention) or the progression of subclinical illness to frank disease (ie, secondary prevention) in other workers. Moreover, the appropriate management of WRA involves the control of the specific factors responsible for disease onset or exacerbation/aggravation, thus avoiding a situation in which ongoing exposure causes disease progression (ie, tertiary prevention).

Clinical practice in the diagnosis and management of WRA differs from standard asthma care in several important ways. In addition, critical aspects of this subject can be unfamiliar or daunting, even to practitioners who are well versed in standard clinical asthma care. The goal of this review is to provide guidance to health-care providers, including those who treat adult asthma patients in primary care practice, those approaching this question from a pulmonary or allergy care perspective, and clinicians working in occupational health settings.

To meet this ambitious goal, we include topics that have not typically been emphasized in standard practice guidelines, such as WEA and preventive measures. A thorough occupational history is essential to the diagnosis of WRA, including the delineation of work-related exposures. General issues of evidence-based medicine and the diagnostic process have been well described.18 Because of the limitations to diagnostic testing, the pretest probability of WRA based on symptoms and the occupational history (and the related Bayesian analysis of posttest likelihood) warrants particular consideration. Bayesian issues are especially relevant here because the diagnosis of occupational disease often demands a different level of diagnostic certainty than that used in other fields of practice. In occupational practice, the attribution of etiology is frequently benchmarked against a “more-likely-than-not” (ie, > 50% likelihood) standard (eg, for workers compensation and medicolegal determinations) rather than achieving a higher level of certainty, as is typically desired in standard clinical practice.

We will also address a combination approach based on the results of several diagnostic modalities used together, as opposed to a linear algorithm restricted to a stepwise series of tests. Although such an integrative approach is not typically emphasized in practice guidelines, it is especially relevant to the evaluation of WRA because testing choices are often limited by factors such as occupational status, access to the workplace, and logistical access to certain diagnostic modalities.

Despite limitations in the relevant literature and in the accuracy of the diagnostic modalities available, there is a tremendous need for guidance on how to diagnose and manage patients with WRA. It is important to remember that the goal of this Consensus Document is to assist clinicians along a management pathway, rather than to prescribe a specific checklist that must be fulfilled in order to achieve a valid clinical decision. Keeping these limitations in mind, we believe that this document based on published literature and supplemented with clinical expert guidance will assist clinicians to diagnose and treat WRA.

In 1995, the ACCP published ACCP Consensus Statement: Assessment of Asthma in the Workplace.1 In 2005, the Health and Science Policy Committee of the ACCP chose to reexamine this topic. This new publication is intended to update and expand the previous review. The University of Alberta/Capital Health Evidence-Based Practice Center was commissioned to review the evidence in the areas of diagnosis and treatment of OA. An international panel of experts was convened to provide a document, synthesized from this evidence review and supplemented by an additional literature review, to inform pulmonary, occupational, allergy/immunology, and primary care practitioners on the diagnosis and management of WRA. Although initially intended to develop formal “evidence-based” guidelines, a Consensus Document has been developed as more fitting to the available published studies on WRA.

Susan Tarlo, MBBS, FCCP, of the Department of Medicine at the University of Toronto (Toronto, ON, Canada) served as the Chair of this international panel of experts, representing a variety of specialties including pulmonary, occupational medicine, allergy, and clinical immunology. Many were members of ACCP; however, members of other organizations (eg, the American Thoracic Society; the Canadian Thoracic Society; the American Academy of Allergy, Asthma, & Immunology; the American College of Allergy, Asthma, & Immunology; and the Occupational and Environmental Medicine Association of Canada) were also invited to participate. The expert panel first met in August 2005 in Chicago, at which time they selected the final scope of the topics. Teleconference and e-mail communication supplemented that initial work.

Authors volunteered to draft sections of the document. The assignments were made by the steering committee based on known expertise and interest in the area; however, all committee participants reviewed the entire document, and contributed to discussion and consensus on the document and made suggestions. The proposals and suggestions in this document should not be used for performance measurement or for competency purposes, since they are not evidence based, as outlined by the ACCP Health and Science Policy Committee. This Consensus Document has been endorsed by the Canadian Thoracic Society and the Canadian Society of Allergy and Clinical Immunology.

Funding for the development of this document was supported by an educational grant from the Schering-Plough Corporation. No representatives from this company were granted the right of review nor were they allowed participation in any portion of the document development including participation on any conference calls or attendance at any meetings. The document authors were unaware of the origin of the funding and were not paid for their contributions.

The very stringent approach of the ACCP to the issue of potential or perceived conflicts of interest has created many firewalls to ensure that there are no influences from industry or other sources. This policy is available on the ACCP Web site (www.chestnet.org). All conflicts of interest within the preceding 5 years were required to be disclosed by all panelists, at all face-to-face meetings, the final conference, and prior to submission of the Consensus Document for publication. The most recent of these are documented in this published Consensus Document. Furthermore, the panel was instructed in this matter, verbally and in writing, prior to the deliberations of the final conference. Any disclosed memberships on speaker's bureaus; consultant fees, grants, and other research monies; and any fiduciary responsibilities to industry were provided to the full panel in writing at the beginning of the conference and at the time of submission of the Consensus Document for publication.

For the purposes of this document, we consider WRA to include asthma initiated by workplace exposures (ie, OA) as well as preexisting asthma made worse by work exposures (ie, WEA). Other respiratory conditions, such as industrial bronchitis, work-related chronic obstructive disease and emphysema, or “asthma-like” syndromes associated with certain occupational exposures, will not be subsumed within this document, even though they may share characteristics with WRA. Most of the published literature has addressed OA rather than WEA. Nonetheless, the panel determined that it should be included in the present document since WEA is considered to be a type of WRA, can be difficult to distinguish from OA, and does have an important impact on morbidity, work time loss, and job efficiency.

The evidence review for this clinical practice guideline included a systematic review commissioned by ACCP through the AHRQ on the diagnosis and treatment of OA, as well as topic specific searches following the completion of the systematic review.11 In addition, the authors of specific sections of this document were encouraged to conduct searches and to supplement the evidence from knowledge of their topic area.

Formal systematic reviews performed by The University of Alberta/Capital Health Evidence-based Practice Center were focused on the diagnosis and management of OA. The diagnosis review focused on evidence from studies that reported an acceptable reference standard (usually an SIC19 or clinical consensus) compared to a single diagnostic test or some combination thereof. The management review focused on evidence from studies that included patients in whom OA had been diagnosed, and for whom clinical outcomes had been reported at follow-up. A detailed description of the methods used can be found at www.ahrq.gov. For the ACCP document, additional and updated information was obtained regarding the domains of clinical history, and primary and secondary prevention.

The Consensus Panel also derived supplemental data from peer-reviewed publications up to 2007 (identified through searches of standard databases, including the National Library of Medicine PubMed database). When available data were limited, inconclusive, or conflicting, the panel relied on a consensus-reaching process in order to develop its final suggestions.

High-quality evidence is particularly problem ridden in WRA. First, for diagnostic tests there is no “gold standard” against which to determine sensitivity and specificity. Although SIC served as a “reference standard” for OA in the initial evidence-based literature review that we utilized,11 our Consensus Document is circumspect in comparing SIC testing to other diagnostic approaches for several reasons. OA is not a single disease, and diagnostic tests evaluated in one clinical setting, such as bakers' asthma, may not be applicable to other conditions, such as diisocyanate-induced asthma or irritant-induced OA. Additionally, several diagnostic approaches depend on the worker still being at the job in question, as well as the ability to remove the worker from work exposures for days to weeks during testing followed by a return to work, which is difficult to achieve in many real-world situations. Second, for treatment and management issues in patients with WRA, there have been few controlled clinical trials (as noted previously), and such trials are unlikely to be performed in the future. Thus, ecologic data, temporal trends, and case reports (which were excluded from the original evidence-based review) must be relied on to supplement traditional RCT evidence. Indeed, several of the suggestions ultimately reached in the Consensus Document are based on the strength and consistency of observational studies.

Throughout the process of development of the Consensus Document, expert consensus was reached whereby all panel members came to agreement, as follows: by panel discussions, including e-mail communications, conference calls, and two face-to-face meetings, which allowed any differing views to be expressed and modifications of wording to be made in order to achieve consensus. The writing groups and the executive committee of the panel extensively reviewed each section during the writing process, and the entire panel received each full draft for comments and discussion. A final conference provided an opportunity for the entire panel to review and discuss the document. Following final revisions and one final review by the executive committee and the full panel, the Consensus Document was reviewed and approved by the ACCP Health and Science Policy Committee, the ACCP Occupational Disease Network, and the ACCP Board of Regents. These reviews were performed prior to endorsement by the Canadian Thoracic Society and the Canadian Society of Allergy and Clinical Immunology. The document has not been field tested. Institutional research ethics board approval was not sought for this project, which consisted of the review of published data and achievement of expert consensus.