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The Fifth Jack Pepys Workshop on Asthma in the Workplace Comparisons Between Asthma in the Workplace and Non–Work-Related Asthma Jean-Luc Malo, Susan M

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The Fifth Jack Pepys Workshop on Asthma in the Workplace Comparisons Between Asthma in the Workplace and Non–Work-Related Asthma Jean-Luc Malo, Susan M AMERICAN THORACIC SOCIETY DOCUMENTS An Official American Thoracic Society Workshop Report: Presentations and Discussion of the Fifth Jack Pepys Workshop on Asthma in the Workplace Comparisons between Asthma in the Workplace and Non–Work-related Asthma Jean-Luc Malo, Susan M. Tarlo, Joaquin Sastre, James Martin, Mohamed F. Jeebhay, Nicole Le Moual, Dick Heederik, Thomas Platts-Mills, Paul D. Blanc, Olivier Vandenplas, Gianna Moscato, Fred ´ eric ´ de Blay, and Andre ´ Cartier; on behalf of the ATS ad hoc committee on Asthma in the Workplace THIS OFFICIAL WORKSHOP REPORT OF THE AMERICAN THORACIC SOCIETY (ATS) WAS APPROVED BY THE ATS BOARD OF DIRECTORS,MARCH 2015 Abstract WEA is important among workers with preexisting asthma and may overlap with irritant-induced asthma, a type of OA. The fifth Jack Pepys Workshop on Asthma in the Workplace Induced sputum cytology can confirm airway inflammation, focused on the similarities and differences of work-related but specific inhalation challenge is the reference standard asthma (WRA) and non–work-related asthma (non-WRA). diagnostic test. Inhalation challenges are relatively safe, with the WRA includes occupational asthma (OA) and work-exacerbated most severe reactions occurring with low-molecular-weight asthma (WEA). There are few biological differences in the agents. Indirect health care costs account for about 50% of total mechanisms of sensitization to environmental and occupational asthma costs. Workers with poor asthma control (WRA or non- allergens. Non-WRA and OA, when due to high-molecular-weight WRA) are less likely to be employed. Income loss is a major agents, are both IgE mediated; it is uncertain whether OA due to contributor to the indirect costs of WRA. Overall, asthma outcomes low-molecular-weight agents is also IgE mediated. Risk factors probably are worse for adult-onset than for childhood-onset asthma for OA include female sex, a history of upper airway symptoms, but better for OA than adult-onset non-WRA. Important aspects of and a history of bronchial hyperresponsiveness. Atopy is a risk management of OA are rapid and proper confirmation of the factor for OA due to high-molecular-weight agents, and exposure diagnosis and reduction of exposure to sensitizers or irritants at work to cleaning agents is a risk factor for both OA and non-WRA. and home. Correspondence and requests for reprints should be addressed to Susan M. Tarlo, M.B. B.S., Toronto Western Hospital, EW7-449, 399 Bathurst St, Toronto, ON, M5T 2S8, Canada. E-mail: [email protected] Ann Am Thorac Soc Vol 12, No 7, pp S99–S110, Jul 2015 Copyright © 2015 by the American Thoracic Society DOI: 10.1513/AnnalsATS.201505-281ST Internet address: www.atsjournals.org Overview Outcomes that is worsened by an occupational Introduction Management exposure but not caused by an occupational Methods Pharmacologic and Other Treatment exposure) (1) (Figure 1). Mechanisms and Pathophysiology Conclusions The Jack Pepys Workshop is held every Epidemiology and Risk Factors 3 years to discuss WRA (2). The fifth Allergens and Irritants workshop was held in Montreal in 2013 Allergens Overview and focused on the similarities and Irritants differences of WRA and non-WRA. Key Diagnosis and Clinical Aspects Work-related asthma (WRA) is a term conclusions were: Nosological Aspects that includes occupational asthma d Occupational asthma (OA) is a useful Methods of Diagnosis (i.e., asthma that is caused by an model for studying non-WRA because the Psychosocial and Economic Impacts occupational exposure) and work- exposure that causes OA is often easily Outcomes and Management exacerbated asthma (WEA) (i.e., asthma identified and workplace interventions American Thoracic Society Documents S99 AMERICAN THORACIC SOCIETY DOCUMENTS presentation was followed by extensive Work-related asthma (WRA) Non work-related asthma (non-WRA) discussion. The content of each presentation is available online (www.asthma-workplace. com). After the workshop, each presenter Occupational Work-exacerbated asthma (OA) submitted a summary of his or her asthma (WEA) – caused by work presentation and the accompanying discussion. The summaries were collated by the co-chairs (J.L.M. and S.M.T.) into a single workshop report. The presenters Sensitizer-induced Irritant-induced and co-chairs composed the writing occupational asthma (OA) occupational asthma (OA) committee. The full writing committee reviewed and approved the final Figure 1. Entities discussed in the Workshop. workshop report. facilitate studies of both the disease course a series of short presentations, each followed and the impact of treatment. by extensive discussion. The fifth Jack Pepys d The mechanisms and pathophysiology of Workshop was held in Montreal in 2013 Mechanisms WRA and non-WRA are similar. Both can and focused on the similarities and and Pathophysiology be initiated by immunological responses or differences of WRA and non–work-related irritant exposures, and both can have asthma (non-WRA). Occupational asthma (OA) and non-WRA predominantly eosinophilic or neutrophilic are the result of interactions between airway inflammatory responses. environmental factors and host factors d There are important differences in Methods (Tables 1 and 2). Environmental factors the success of preventing WRA relevant to OA include the route of exposure compared with non-WRA. These Forty-five international experts from (skin or respiratory), the type of causative differences are likely related to the various disciplines were invited to the agent, and the causative agent’s airborne timing and feasibility of preventative workshop. In addition, there was a small characteristics (particle size, structure, interventions. Preventative measures number of self-registered participants. volatility), level (concentration, duration of for WRA that require work changes Invitees were selected on the basis of exposure), and mode (gas or particle). Host are often associated with negative publications in the area of WRA or general factors relevant to OA include sex, atopy, socio-economic impacts; this is asthma. Represented specialties included nonspecific bronchial hyperresponsiveness, a deterrent to the implementation of occupational medicine, pulmonary rhinitis, and genetic susceptibility (3). preventative measures, especially if medicine, and basic science research. Potential genetic factors include glutathione they lead to cessation of employment. Participants disclosed any potential conflicts S-transferase (GSTP1 and GSTM1) and d In both WRA and non-WRA, of interest to the ATS and were managed in N-acetyltransferase (4), antioxidant genes exacerbations can be due to multiple accordance with the policies and procedures (5), catenins (6), and the Th2 response (7). triggers. The severity of the exacerbation of the ATS. Both OA and non-WRA due to depends upon the exposure and the Topics for discussion at the high-molecular-weight agents (i.e., agents severity of the underlying asthma. workshop were selected by an that generally contain proteins) have an International Advisory Committee (J.L. IgE-mediated mechanism of sensitization. M., S.M.T., G.M., D.B., O.V., and P.C.). OA due to high-molecular-weight agents is Introduction They included comparisons of WRA and an IgE-mediated response to an non-WRA in each of the following occupational allergen, whereas non-WRA Work-related asthma (WRA) is a term that domains: mechanisms and can be an IgE-mediated response to an includes occupational asthma (i.e., asthma pathophysiology (J.S. and J.G.M.), environmental allergen. It is uncertain that is caused by work) and work- epidemiology and risk factors (M.J. and whether OA due to low-molecular-weight exacerbated asthma (WEA) (i.e., asthma N.L.M.), allergens and irritants (T.P.M. agents (i.e., agents that are usually that is worsened by work but not initially and D.H.), diagnosis and clinical aspects chemical products) is also IgE mediated (8). caused by work) (1) (Figure 1). It has been (F.D.B. and G.S.), psychosocial and Arguing for an IgE-mediated mechanism estimated that at least 15% of adult asthma economic aspects (P.D.B. and O.V.), and are its clinical features, pattern of Th2 is work related. Some studies have reported outcomes and management (J.L.M. and cytokines, and pathological features and the that more than 25% of working adults with A.C.). The program was approved by the finding that treatment with anti-IgE asthma have exacerbations of asthma at ATS’s Environmental and Occupational humanized antibody was effective in some work. Health Assembly Planning Committee. patients with OA due to low-molecular- A Jack Pepys Workshop on WRA After a tribute to Professor Jack Pepys, weight agents (9). Arguing against an has been held every 3 years since 2000, short presentations were given by IgE-mediated mechanism are the failure to alternating between Toronto, Ontario and internationally acknowledged experts, who detect specific IgE antibodies against most Montreal, Quebec, Canada. The format is briefly reviewed the evidence. Each of the low-molecular-weight agents and the S100 AnnalsATS Volume 12 Number 7| July 2015 AMERICAN THORACIC SOCIETY DOCUMENTS Table 1. Aspects of mechanisms and pathophysiology Nonoccupational Asthma Occupational Asthma Immunological OA Irritant-induced OA For some agents/some patients an IgE- IgE-dependent response for high- Acute phase: “toxic reaction”; chronic phase: dependent response, for others unknown molecular-weight agents; variable or inflammation and remodeling. initiating mechanisms. unknown for
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