BOHRF 2004 Preface

Preface to the British Occupational Health Research Foundation (BOHRF) Occupational asthma guidelines.

Asthma is a condition of chronic inflammation of the airways, characterised by widespread airflow limitation that is reversible, either spontaneously or with treatment over short periods of time. The inflammation results in hyper-responsiveness of the airways to many stimuli e.g. cold air, cigarette smoke, exercise, etc and in the clinical setting to methacholine and histamine. Symptoms include wheeze, cough, shortness of breath and chest tightness and are often worse at night or in the early morning.

Asthma is common, affecting adults and children of all ages. It is especially prevalent in the UK, where 4% of adults report asthma1. Adult asthma may be a continuation of childhood asthma, reactivation of quiescent childhood asthma or new-onset asthma. Between a third and two-thirds of adult asthmatic patients develop asthma for the first time during working years 2,3,4.

Asthma is "work-related" when there is an association between symptoms and work. The different types of work-related asthma should be distinguished, since the implications to the worker and the occupational health management of the disease differ. Work-related asthma includes two distinct categories:

  • work aggravated asthma, i.e. pre-existing or coincidental new onset adult asthma which is made worse by non-specific factors in the workplace, and
  • occupational asthma i.e. adult asthma caused by workplace exposure and not by factors outside of the workplace. Occupational asthma can occur in workers with or without prior asthma.

Occupational asthma can be subdivided into:

  • allergic occupational asthma characterised by a latency period between first exposure to a respiratory sensitiser at work and the development of symptoms, and
  • irritant-induced occupational asthma that occurs typically within a few hours of a high concentration exposure to an irritant gas, fume or vapour at work.

Workplace agents that induce asthma through an allergic mechanism can be broadly divided into those of high and low molecular weight. The former are usually proteins and appear to act through a type I, IgE associated hypersensitivity. Whilst some low molecular weight chemicals are associated with the development of specific IgE antibodies, this is not the case for the majority.

Occupational factors account for 9-15% of cases of asthma in adults of working age 5. Almost 90% of cases of occupational asthma are of the allergic type 2,6,7,8,9,10 and therefore this is the focus of this evidence review. The term occupational asthma is used throughout the guidelines to mean allergic occupational asthma unless specified otherwise.

Occupational asthma is the most frequently reported work-related respiratory disease in many countries, including the UK 8. The Health and Safety Executive (HSE) estimate that 1,500 to 3,000 people develop occupational asthma each year. This rises to 7,000 cases a year if work-aggravated asthma is included. The disease may leave people severely disabled having to take early retirement, while many others have to change jobs to avoid contact with the substance, which caused their asthma. HSE estimates that the costs to society of new cases of occupational asthma are up to £1.1bn over 10 years.

Occupational asthma is unique in that it is the only type of asthma that is readily preventable. Prevention depends on the effective control of exposure to respiratory sensitisers in the workplace. Occupational asthma has important long-term adverse health and economic consequences. Although symptoms may resolve completely with early diagnosis and early removal from exposure, many patients fail to recover even when completely removed from exposure. In rare cases, occupational asthma has been fatal. Thus prevention is the most important factor in reducing the impact of occupational asthma on individual workers and on society at large.

Evidence-based guidelines are becoming the benchmarks for practice in many areas of health care and the process used to prepare such guidelines is well established. This evidence review and the recommendations derived from it concentrate on interventions and outcomes. The aim is to provide a robust approach to the prevention, identification and management of occupational asthma, based on and using the best available medical evidence.

Anthony Newman Taylor and Paul Nicholson
Chairman and Deputy Chairman of the Research Working Group

  1. Asthma Burden. In: Loddenkemper R (ed). The European Lung White Book. The first comprehensive survey on respiratory health in Europe. European Respiratory Society. 2003. pp 16-25.
  2. Milton DK, Solomon GM, Rosiello RA, et al. Risk and incidence of asthma attributable to occupational exposure among HMO members. Am J Ind Med, 1998; 33: 1-10.
  3. Tarlo SM, Leung K, Broder I, et al. Asthmatic subjects symptomatically worse at work. Chest, 2000; 118: 1309-1314.
  4. Blanc PD, Eisner, Israel L et al. The association between occupation and asthma in general medical practice. Chest, 1999; 115: 1259-1264.
  5. Blanc PD & Toren K. How much adult asthma can be attributed to occupational factors? Am J Med, 1999; 107: 580-7.
  6. Ameille J, Pauli G, Calastreng-Crinquand A, et al. Reported incidence of occupational asthma in France, 1996-99. The ONAP programme. Occup Environ Med, 2003; 60: 136-141.
  7. Chatkin JM, Tarlo SM, Liss G, et al. The outcome of asthma related to irritant exposures: a comparison of irritant-induced asthma and irritant aggravation of asthma. Chest, 1999;116: 1780-1785.
  8. Meyer JD, Holt DL, Cherry N, et al. SWORD 98: surveillance of work-related and occupational respiratory disease in the UK. Occup Med (Lond), 1999; 49: 485-9.
  9. Hnizdo E, Esterhuizen TM, Rees D, et al. Occupational asthma as identified by the Surveillance of Work-related and Occupational Respiratory Diseases programme in South Africa. Clin Exp Allergy, 2001; 31: 32-9.
  10. Provencher S, Labreche F, De Guire. Physician based surveillance for occupational respiratory diseases: the experience of PROPULSE, Quebec, Canada. Occup Environ Med, 1997; 54: 272-6.

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