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Diagnostic approach in cases with suspected work-related asthma

by Tor B. Aasen, P. Sherwood Burge, Paul K Henneberger, Vivi Schlünssen and Xaver Baur[on behalf of the ERS Task Force on the Management of Work-related Asthma* ] and EOMSociety

Background: Work-related asthma (WRA) is a major cause of respiratory disease in modern societies. The diagnosis and consequently an opportunity for prevention are often missed in practice.

Methods: Based on recent studies and systematic reviews of the literature methods for detection of WRA and identification of specific causes of allergic WRA are discussed.

Results and Conclusions: All workers should be asked whether symptoms improve on days away from work or on holidays. Positive answers should lead to further investigation. Spirometry and non-specific bronchial responsiveness should be measured, but carefully performed and validly analysed serial peak expiratory flow or forced expiratory volume in one second (FEV1) measurements are more specific and confirm occupational asthma in about 82% of those still exposed to the causative agent. Skin prick testing or specific immunoglobulin E assays are useful to document allergy to high molecular weight allergens. Specific inhalational challenge tests come closest to a gold standard test, but lack standardisation, availability and sensitivity. Supervised workplace challenges can be used when specific challenges are unavailable or the results non-diagnostic, but methodology lacks standardisation. Finally, if the diagnosis remains unclear a follow-up with serial measurements of FEV1 and non-specific bronchial hyperresponsiveness should detect those likely to develop permanent impairment from their occupational exposures.

COPD Causation and Workplace Exposures: An Assessment of Agreement among Expert Clinical Raters

David Fishwick, Anthony Darby, Eva Hnizdo, Chris Barber, Jade Sumner, Richard Barraclough, Charlotte Bolton, Sherwood Burge, Peter Calverley, Nick Hopkinson, Jennifer Hoyle, Rod Lawson, Robert Niven, Tony Pickering, Keith Prowse, Peter Reid, Chris Warburton, and Paul D. Blanc

April 2013, Vol. 10, No. 2 , Pages 172-179 (doi:10.3109/15412555.2012.737072)

Background. Although occupational exposure is a known risk factor for Chronic Obstructive Pulmonary Disease (COPD), it is difficult to identify specific occupational contributors to COPD at the individual level to guide COPD prevention or for compensation. The aim of this study was to gain an understanding of how different expert clinicians attribute likely causation in COPD. Methods. Ten COPD experts and nine occupational lung disease experts assigned occupational contribution ratings to fifteen hypothetical cases of COPD with varying combinations of occupational and smoking exposures. Participants rated the cause of COPD as the percentage contribution to the overall attribution of disease for smoking, occupational exposures and other causes. Results. Increasing pack-years of tobacco smoking was associated with significantly decreased proportional occupational causation ratings. Increasing weighted occupational exposure was associated with increased occupational causation ratings by 0.28% per unit change. Expert background also contributed significantly to the proportion of occupational causation rated, with COPD experts rating on average a 9.4% greater proportion of occupational causation per case. Conclusion. Our findings support the notion that respiratory physicians are able to assign attribution to different sources of causation in COPD, taking into account both smoking and occupational histories. The recommendations on whether to continue to work in the same job also differ, the COPD experts being more likely to recommend change of work rather than change of work practice.

Concise guidance: diagnosis, management and prevention of occupational asthma

Paul J Nicholson, Associate medical director, Paul Cullinan, Professor in occupational and environmental respiratory disease and Sherwood Burge, Professor in occupational lung diseases

doi: 10.7861/clinmedicine.12-2-156 Clin Med April 1, 2012 vol. 12 no. 2 156-159

This concise guidance, prepared for physicians, summarises the British Occupational Health Research Foundation guideline for the prevention, identification and management of occupational asthma. Approximately one in six people of working age who develop asthma have work-related asthma, where work has either caused or aggravated their disease. Physicians who assess working adults with asthma need to ask the patient about their job and the materials they work with, and be aware of those that carry particular risks; they should also ask whether symptoms improve regularly on days away from work. A diagnosis of occupational asthma (ie asthma caused by work) should not be made on the basis of history alone, but be supported by immunological and physiological investigations of proven diagnostic benefit. Following a validated diagnosis of occupational asthma, physicians should recommend early avoidance of further exposure, because this offers the best chance of complete recovery. If appropriate and timely interventions are not taken, the prognosis of occupational asthma is poor, with only approximately one-third of workers achieving full symptomatic recovery.

Lack of effect of nitrogen dioxide exposure on heart rate variability in patients with stable coronary heart disease and impaired left ventricular systolic function

Alison Scaife, Justin Barclay, Graham S Hillis, Janaki Srinivasan, David W Macdonald, John A S Ross, Jon G Ayres

Occup Environ Med 2012;69:587-591 doi:10.1136/oemed-2011-100126

Objectives Epidemiological studies of air pollution on cardiovascular health show associations of cardiac mortality and admissions with exposure to nitrogen dioxide (NO2) at low concentrations. These associations could be causal or NO2 could be acting as a surrogate measure for another air pollutant, most likely ultrafine particles. No studies of cardiac susceptibility to acute exposure to NO2 have been undertaken.

Methods Randomised controlled exposures to NO2 (400?ppb for 1?h) and air in subjects with coronary heart disease and impaired left ventricular systolic function not taking ? adrenoceptor blocking drugs.

Results There were no significant changes in heart rate, blood pressure, leucocyte coping capacity or any heart rate variability measure following NO2 exposure compared with air.

Conclusion These findings suggest that NO2 does not affect heart rate variability at these concentrations (which are high for urban background levels) and in the absence of other pollutants. While a synergistic effect has not been ruled out, these data lend support to the idea that the epidemiological data associating cardiac outcomes with NO2 are more likely due to an associated pollutant rather than NO2 itself.

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