Titlebook: Occupational Asthma; Torben Sigsgaard,Dick Heederik Book 2010 Birkh?user Basel 2010 Occupational disease.Pulmonary disease.Respiratory Inf

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Prevention of work-related asthma seen from the workplace and the public health perspective, tools for prevention of WRA, divided into primary and secondary prevention. For each tool, the available evidence for the effectiveness of the tool is summarized, and examples are provided. Primary prevention addresses healthy workers or persons with asthma due to causes unrelated to work. The prin

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Design, conduct and analysis of surveys on work-related asthma,onstrations of effectiveness of interventions. Hypotheses dictate survey design, which include cross-sectional, case-control, cohort, and intervention studies. Tools for characterizing medical risk factors and outcomes include questionnaires, spirometry, tests of bronchial hyperreactivity, exhaled i

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,The history of research on asthma in the workplace — Development, victories and perspectives,accurate, and scales for assessing impairment/disability are now available. Estimates of the proportion of asthma cases that can be ascertained as OA are now proposed. In a more general way, OA has been proposed as a model of the onset and persistence of asthma in humans.

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Population-attributable fraction for occupation and asthma,few years later a task force of the American Thoracic Society (ATS) summarized the general population-based studies in this field, ending up with a median value of 15%. We have summarized data from publications that have appeared since 2000 and the median value from these publications is 14.4% (rang

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Definition and diagnosis of occupational asthma,f the questionnaire of any adult with new onset asthma. Monitoring of peak expiratory flows at and off work is a useful tool but may not be sufficiently sensitive or specific; combining it with monitoring of the provocative concentration of methacoline inducing a 20% fall in FEV1 and possibly sputum

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Work-exacerbated asthma,n in non-industrial workplaces such as schools and offices are commonly implicated. WEA can lead to substantial adverse outcomes, similar to OA. Management of WEA should focus on reducing work exposures and optimizing standard medical management.

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Mechanisms of occupational asthma caused by low-molecular-weight chemicals,ces in T cell subpopulations, cytokine balances and effector cells involved chemical-induced OA may well depend on processes that might differ substantially from those of atopic asthma. Furthermore, the involvement of the transient receptor potential channels in chemical-induced OA and irritant-indu