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BackgroundEstablishing whether patients are exposed to a ‘known cause’ is a key element in both the diagnostic assessment and the subsequent management of hypersensitivity pneumonitis (HP).ObjectiveThis study surveyed British interstitial lung disease (ILD) specialists to document current practice and opinion in relation to establishing causation in HP.MethodsBritish ILD consultants (pulmonologists) were invited by email to take part in a structured questionnaire survey, to provide estimates of demographic data relating to their service and to rate their level of agreement with a series of statements. A priori ‘consensus agreement’ was defined as at least 70% of participants replying that they ‘Strongly agree’ or ‘Tend to agree’.Results54 consultants took part in the survey from 27 ILD multidisciplinary teams. Participants estimated that 20% of the patients in their ILD service have HP, and of these, a cause is identifiable in 32% of cases. For patients with confirmed HP, an estimated 40% have had a bronchoalveolar lavage for differential cell counts, and 10% a surgical biopsy. Consensus agreement was reached for 25 of 33 statements relating to causation and either the assessment of unexplained ILD or management of confirmed HP.ConclusionsThis survey has demonstrated that although there is a degree of variation in the diagnostic approach for patients with suspected HP in Britain, there is consensus opinion for some key areas of practice. There are several factors in clinical practice that currently act as potential barriers to identifying the cause for British HP patients.

The second Jack Pepys Workshop on Occupational Asthma was held in Toronto, Canada, in May 2004. The present report summarises key questions and research needs as identified by the international participants. The audiotapes from the workshop discussions were summarised by the organising chairs of the Symposium and the resulting document was circulated for input from all invited workshop participants. In total, 100 key questions and research needs were identified. Identified needs included: provision of different definitions depending on the use of data; explanations for differences in frequency studies; and better characterisation of genetic and environmental determinants of occupational asthma. The role of irritants and the pathogenesis of various forms of work-related asthma need further research, and there are also questions and research needs for diagnosis, prevention and understanding of persistence and airway remodelling. In conclusion, although advances have been made in the understanding of occupational asthma and other work-related asthma, further key issues remain that need addressing.

Interstitial lung diseases (ILD), including those related to connective tissue disease (CTD), and idiopathic pulmonary fibrosis (IPF) carry high morbidity and mortality. Great efforts are under way to develop and investigate meaningful treatments in the context of clinical trials. However, efforts have been challenged by a lack of validated outcome measures and by inconsistent use of measures in clinical trials. Lack of consensus has fragmented effective use of strategies in CTD-ILD and IPF, with a history of resultant difficulties in obtaining agency approval of treatment interventions. Until recently, the patient perspective to determine domains and outcome measures in CTD-ILD and IPF had never been applied. Efforts described here demonstrate unequivocally the value and influence of patient involvement on core set development. Regarding CTD-ILD, this is the first OMERACT working group to directly address a manifestation/comorbidity of a rheumatic disease (ILD) as well as a disease not considered rheumatic (IPF). The OMERACT 11 proceedings of the CTD-ILD Working Group describe the forward and lateral process to include both the medical and patient perspectives in the urgently needed identification of a core set of preliminary domains and outcome measures in CTD-ILD and IPF.

Rationale: Clinical trial design in interstitial lung diseases (ILDs) has been hampered by lack of consensus on appropriate outcome measures for reliably assessing treatment response. In the setting of connective tissue diseases (CTDs), some measures of ILD disease activity and severity may be confounded by non-pulmonary comorbidities. Methods: The Connective Tissue Disease associated Interstitial Lung Disease (CTD-ILD) working group of Outcome Measures in Rheumatology-a non-profit international organisation dedicated to consensus methodology in identification of outcome measures-conducted a series of investigations which included a Delphi process including >248 ILD medical experts as well as patient focus groups culminating in a nominal group panel of ILD experts and patients. The goal was to define and develop a consensus on the status of outcome measure candidates for use in randomised controlled trials in CTD-ILD and idiopathic pulmonary fibrosis (IPF). Results: A core set comprising specific measures in the domains of lung physiology, lung imaging, survival, dyspnoea, cough and health-related quality of life is proposed as appropriate for consideration for use in a hypothetical 1-year multicentre clinical trial for either CTD-ILD or IPF. As many widely used instruments were found to lack full validation, an agenda for future research is proposed. Conclusion: Identification of consensus preliminary domains and instruments to measure them was attained and is a major advance anticipated to facilitate multicentre RCTs in the field.

The aim of the European Respiratory Society work-related asthma guidelines is to present the management and prevention options of work-related asthma and their effectiveness. Work-related asthma accounts for 5-25% of all adult asthma cases and is responsible for a significant socioeconomic burden. Several hundred occupational agents, mainly allergens but also irritants and substances with unknown pathological mechanisms, have been identified as causing work-related asthma. The essential message of these guidelines is that the management of work-related asthma can be considerably optimised based on the present knowledge of causes, risk factors, pathomechanisms, and realistic and effective interventions. To reach this goal we urgently require greatly intensified primary preventive measures and improved case management. There is now a substantial body of evidence supporting the implementation of comprehensive medical surveillance programmes for workers at risk. Those workers who fail surveillance programmes need to be referred to a clinician who can confirm or exclude an occupational cause. Once work-related asthma is confirmed, a revised risk assessment in the workplace is needed to prevent further cases. These new guidelines confirm and extend already existing statements and recommendations. We hope that these guidelines will initiate the much-needed research that is required to fill the gaps in our knowledge and to initiate substantial improvements in preventative measures.

The American Thoracic Society/European Respiratory Society jointly created a Task Force on "Outcomes for COPD pharmacological trials: from lung function to biomarkers" to inform the chronic obstructive pulmonary disease research community about the possible use and limitations of current outcomes and markers when evaluating the impact of a pharmacological therapy. Based on their review of the published literature, the following document has been prepared with individual sections that address specific outcomes and markers, and a final section that summarises their recommendations.

Biomechanical lumbo-spinal strain and intense physical work are the characteristic hallmarks of mining work.To determine the prevalence and predisposing factors for Low Back Pain (LBP) among male underground gold miners at the Obuasi gold mine in Ghana.This is a cross sectional study on 280 male underground gold miners from June to October 2001 with a structured questionnaire administered through interviews.The twelve months prevalence of low back pain among miners was 67%. The mean age of the workers was 40 years (+/- 5.6, ranging from 27 to 53 years). Increasing age was significantly associated with low back pain, (P=0.05) OR 2.07 (95% CI 0.99 to 4.34) after adjustment for smoking and occupation. Prevalence of LBP was highest among workers performing engineering (82%) duties. Heavy physical work (77%), was identified as a major cause of LBP, which could be prevented by the use of lifting aids (16%).The prevalence of low back pain in this group is comparable with that obtained from other studies in Africa and Europe. Training and education as a means of reducing LBP was suggested by just a few of the respondents.

Background: At present there is no internationally agreed definition of occupational asthma and there is a lack of guidance regarding the resources that should be readily available to physicians running specialist occupational asthma services. Aims: To agree a working definition of occupational asthma and to develop a framework of resources necessary to run a specialist occupational asthma clinic. Method: A modified RAND appropriateness method was used to gain a consensus of opinion from an expert panel of clinicians running specialist occupational asthma clinics in the UK. Results: Consensus was reached over 10 terms defining occupational asthma including: occupational asthma is defined as asthma induced by exposure in the working environment to airborne dusts vapours or fumes, with or without pre-existing asthma; occupational asthma encompasses the terms “sensitiser-induced asthma” and “acute irritant-induced asthma” (reactive airways dysfunction syndrome (RADS)); acute irritant-induced asthma is a type of occupational asthma where there is no latency and no immunological sensitisation and should only be used when a single high exposure has occurred; and the term “work-related asthma” can be used to include occupational asthma, acute irritant-induced asthma (RADS) and aggravation of pre-existing asthma. Disagreement arose on whether low dose irritant-induced asthma existed, but the panel agreed that if it did exist they would include it in the definition of “work-related asthma”. The panel agreed on a set of 18 resources which should be available to a specialist occupational asthma service. These included pre-bronchodilator FEV1 and FVC (% predicted); peak flow monitoring (and plotting of results, OASYS II analysis); non-specific provocation challenge in the laboratory and specific IgE to a wide variety of occupational agents. Conclusion: It is hoped that the outcome of this process will improve uniformity of definition and investigation of occupational asthma across the UK.

Symptoms of obstructive lung disease in domestic cleaners have been related to the use of bleach and other irritant cleaning products. The short-term effects of cleaning exposures on respiratory symptoms and peak expiratory flow (PEF) were investigated in domestic cleaners with respiratory disorders. In a panel study, 43 female domestic cleaners with a recent history of asthma and/or chronic bronchitis completed a 2-week diary, collecting information on respiratory symptoms, PEF and cleaning exposures. Mixed regression models were used to assess daily changes in symptoms and PEF associated with specific cleaning exposures. The probability of having work-related asthma was individually assessed by a computerised diagnostic system and an occupational asthma expert. Lower respiratory tract symptoms were more common on working days and were predominantly associated with exposure to diluted bleach, degreasing sprays/atomisers and air fresheners. Associations with upper respiratory tract symptoms and PEF were less apparent. Eleven (30%) subjects scored positively for work-related asthma. It is concluded that exposure to certain irritant cleaning products aggravates lower respiratory tract symptoms in female domestic cleaners with asthma or chronic bronchitis.

Recent developments in occupational asthma are reviewed. There are now three independent estimates of the incidence of occupational asthma in the general working population, which all identify the same high risk occupational groups (particularly those exposed to isocyanates and flour or wheat). The incidence of occupational asthma principally depends on the agent and level of exposure. The property of a small molecular weight chemical to bind to and alter the structure of body proteins seems important. Smoking both increases the number of workers developing specific IgE to occupational agents, and the number developing occupational asthma. The relation between increased non-specific bronchial responsiveness and occupational asthma is reviewed. Occupational sensitisation may be the cause of hyperresponsiveness, or develop in those with pre-existing hyperresponsiveness. Around 20% of workers with occupational asthma have measurements within the normal range. Once occupational asthma develops, removal from exposure, particularly if delayed, often results in continuing asthma. Finally the prevention of occupational asthma is discussed.

In some countries inhaled corticosteroids are widely prescribed for patients with chronic obstructive pulmonary disease (COPD), despite the lack of good studies to support their use. In the last 12 months these three important large, parallel group, placebo controlled studies have reported at scientific meetings but, at the time of going to press with this article, they have not been published. This review will give an individual view of what has been presented, and provide a basis for the assessment of the trials when they are published. All three studies used similar definitions of COPD and excluded patients with a clinical diagnosis of asthma or significant bronchodilator responsiveness. The Copenhagen study also excluded those with a prednisolone response, which was found in only 5% of their otherwise unselected population. The Copenhagen study started with a random population survey which identified all those with an FEV1/VC ratio of

The use of methyl xanthine derivatives for the treatment of bronchospasm is limited by unwanted side-effects which are frequently dose related. Potentiation of the bronchodilating effects of these derivatives would therefore have obvious clinical advantages. This paper reports the results of a trial designed to elucidate whether potentiation occurs between aminophylline and ketotifen.

In order to examine a possible mechanism of action of ketotifen in asthma, a double-blind study was undertaken to determine whether ketotifen showed any effects on the beta-adrenergic system in asthmatic patients. The effects of ketotifen 1 mg b.i.d. for one month on the changes in spirometry, plasma potassium and serum glucose levels induced by sequential doses of inhaled, nebulized salbutamol was compared with placebo. In addition the degree of inhibition caused by local salbutamol on the wheal volume due to intradermal prostaglandin E and bradykinin, was compared following ketotifen and placebo. Nebulized salbutamol produced consistent improvements in spirometry and changes in potassium and glucose levels. Local salbutamol significantly decreased the wheal volume induced by intradermal prostaglandin E and bradykinin. However, none of these salbutamol-induced effects were altered following ketotifen or placebo. Ketotifen, in the doses used, has no demonstrable effect on the beta-adrenergic system in asthmatic patients.