Abstract

WORKSHOP EXECUTIVE SUMMARY AND BOTTOM-LINE ISSUES
The strengths of this Workshop include representatives from multiple disciplines, from basic science, environmental science, epidemiology, occupational hygiene, and clinician researchers.

The international participation reflects WRA as a worldwide concern, although still understudied in many developing countries. It is a potentially preventable and curable problem, important for public and occupational health, and the outcome of research has potential for policy changes.

WEA and OA represent important clinical problems, and patients need as accurate a diagnosis as feasible with support for best management and future occupation; misdiagnosis can be as harmful as missing the diagnosis, leading to inappropriate advice to change a job with potentially adverse financial and social consequences.

WEA is common, but further consensus is needed as to clinical and research definitions and diagnostic criteria.

OA is a valuable model for non-OA, having a clearly defined single specific causative agent.

definitions need to be clearer to allow valid comparisons between studies. The concept of work-reactivated asthma seems useful. For the phenotype of eosinophilic bronchitis, it remains unclear whether this is a different disease or a different stage of asthma.

None of the current diagnostic tests for OA is perfect in isolation. If new tests are added, such as induced sputum eosinophils, it is important to have studies to determine the diagnostic gain from these before adding or substituting them for other tests.

Patients studied from tertiary centers may not represent the full spectrum of disease, and can have more psychiatric/psychological co-morbidity than in primary care settings. There is a need to balance the medical and socio-economic impacts of job changes for workers with OA.

The potential of markedly reduced exposure, as has been successful for OA from natural rubber latex in allowing sensitized healthcare workers to continue to work, should be investigated.

Physicians need to consider, and influence, compensation systems to provide appropriate support and retraining for workers with OA.

A major advance in recent years has been the understanding that the OA incidence due to sensitizers largely relates to the exposure levels. Workplace controls should focus on reduction of exposure rather than worker susceptibility in the prevention of OA. In that light, we now need well performed intervention studies to demonstrate effects of preventive measures and means to implement them widely and to enable change. There is a need also to increase employer and government commitments to prevention and appropriate compensation, and a need to be able to ensure preventive measures.

Genetic studies may provide helpful data, insofar as gene–environmental interactions may be relevant to mechanisms of disease. Relative to idiopathic disease, the population with OA due to high-molecular-weight antigens has a well defined phenotype, set of exposures, and sensitizer-based mechanism of disease. The disadvantage of relatively small sample size could be overcome by collaborative studies using hypothesis-generating and hypothesis-testing analytic strategies.

Mechanisms of sensitization remain less clear for many low molecular weight sensitizers, such as diisocyanates. Further understanding may lead to better immunologic testing that could be relevant to exposure assessment, diagnosis, and disease management. The role of irritants in asthma causation and exacerbation, acting alone or as adjuvants or
co-factors, also requires more research.

Large knowledge gaps exist in work-related rhinitis and in global aspects of WRA and related disability.

Finally, the need for research addressing work-related asthma was particularly glaring, not only to advance knowledge in this area but also to attract the best young researchers for the future.

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