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This article is for Medical Professionals

Professional Reference articles are designed for health professionals to use. They are written by UK doctors and based on research evidence, UK and European Guidelines. You may find one of our health articles more useful.

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Occupational asthma is a disease characterised by variable airflow limitation and/or airway hyper-responsiveness due to causes and conditions attributable to a particular occupational environment and not to stimuli encountered outside the workplace. The relationship between asthma and the workplace is important to consider in all cases of adult asthma[1].

Patients can fall into two categories[2]:

  • Hypersensitivity-induced occupational asthma (the majority of cases).
  • Irritant-induced asthma - reactive airways dysfunction syndrome (RADS).
  • The true frequency of occupational asthma is not known but under-reporting is likely. It is estimated that occupational asthma may account for about
    9-15% of adult-onset asthma[3].
  • The most common irritants for occupational asthma are isocyanates, flour/grain, adhesives, metals, resins, colophony (rosin), fluxes, latex, animals, aldehydes and wood dust[4].

Risk factors

Several hundred occupational agents, mainly allergens but also irritants and substances with unknown pathological mechanisms, have been identified as causing work-related asthma[5].

Individuals who may be exposed to occupational asthma include[6]:

  • Flour mill workers, bakers, pastry makers.
  • Healthcare workers, laboratory technicians.
  • Laboratory animal workers, farmers, food industry, sea food processing.
  • Detergent production, pharmaceutical industry.
  • Polyurethane production, plastic industry, insulation, molding, spray painting.
  • Metal refinery, metal alloy production, electroplating, welding.
  • Cleaners.
  • Adhesives, dental and orthopaedic materials, sculptured fingernails, printing inks, paints and coatings.
  • Hairdressers.
  • Epoxy resin workers.
  • Textile workers, food industry workers.
  • Sawmill workers, carpenters, cabinet and furniture makers.

The diagnosis of occupational asthma should be suspected in all adults with symptoms of airflow limitation and it should be positively searched for in those with high-risk occupations or exposures. Patients with pre-existing asthma aggravated non-specifically by dust and fumes at work (work-aggravated asthma) should be distinguished from those with pre-existing asthma who become additionally sensitised to an occupational agent[3].

  • Ask about any symptoms of rhinitis or conjunctivitis, as these may precede the development of occupational asthma[7].
  • Work-related asthma is suggested if asthma symptoms improve when away from work or deteriorate when at work (see algorithm, below).
  • Symptoms of airflow limitation are improved on days away from work and on holiday. However, this is not specific for occupational asthma and may also include those with asthma due to agents at home (who may improve on holidays) and those who do much less physical exertion away from work.
  • In general, the history is more useful in excluding occupational asthma rather than in confirming it. A significant proportion of workers with symptoms that improve on days away from work or on holiday have been shown by objective tests not to have occupational asthma.

Work-exacerbated asthma is the term used to describe the worsening of asthma related to work but not the causation of asthma by work. It is common and has been reported to occur for about 20% of adults with asthma when at work[8].

Early diagnosis is the key to reducing morbidity[9]. The decision to label a case of asthma as being occupationally induced remains a matter of clinical judgement. Identifying the specific cause of occupational asthma is often much more difficult than identifying an asthma-work relationship. The Control of Substances Hazardous to Health Regulations require an employer to identify all exposures at work, to assess and prevent or control risks and to give workers information about any risks and the methods for controlling them[10]. The Material Safety Data Sheets (MSDS) may provide information on hazardous substances in the work environment and should be available from the employer.

A thorough history and serial peak expiratory flow rates (PEFRs), with or without immmunological tests, allow an experienced physician to make an accurate diagnosis in the majority of cases.

  • Confirm that the patient has asthma and does not have other forms of obstructive lung disease or non-respiratory causes of breathlessness[11]:
    • Standard measures including serial peak flow measurements (recorded at least four times a day), dynamic lung function and reversibility testing (see algorithm, below).
    • All patients should have measures of forced vital capacity (FVC) and forced expiratory volume in one second (FEV1).
  • In patients with a history of heavy cigarette consumption, measurement of transfer factor may be useful in excluding emphysema.
  • Confirming a relationship between asthma and work exposure:
    • Serial measurements of PEFR at home and at work: this is often the most appropriate first step[1]. Measurements should be made every two hours from waking to sleeping for four weeks, keeping treatment constant and documenting times at work. There should be:
      • At least three days in each consecutive work period.
      • At least three series of consecutive days at work with three periods away from work (usually about three weeks).
      • At least four evenly spaced readings per day.
    • The analysis is best done with the aid of computerised systems.
  • Measure of specific immunoglobulin E (IgE) to an occupational agent:
    • IgE measurements are possible for most biological agents and a few low molecular weight chemicals.
    • Common agents where IgE measurements help include latex in healthcare workers, flour and enzymes in bakers, rodent urine extracts and animal epithelia in laboratory animal workers and veterinary surgeons, and acid anhydrides in exposed workers.
    • These tests detect specific IgE from certain allergens but are not sensitive for making the diagnosis of asthma or occupational asthma[7].
  • Specific bronchial provocation testing:
    • Specific bronchial provocation tests are potentially hazardous and in most cases they are inappropriate. They should only be used in tertiary centres. Specific inhalation tests should only be used in a limited number of circumstances[12]:
      • To identify previously unknown causative agents.
      • To distinguish the causative agent from others if this otherwise proves difficult in complex environments.
      • Where there are persisting doubts about the diagnosis and definite advice is needed on future employment at a particular workplace.
      • For research into the underlying mechanisms of occupational asthma (for which appropriate ethical approval and written informed consent by the subject are required).
  • Specific bronchial challenges should only be conducted in specialised units familiar with the performance and interpretation of such tests. Exposure needs to be the same as that which is likely to be encountered in the workplace.
  • The combination of a nonspecific bronchial provocation test with a specific skin-prick test or specific IgE test may be adequate to make a diagnosis of occupational asthma[13].
  • Skin-prick testing or tests for specific IgE should be used in the investigation of occupational asthma caused by high molecular weight agents but should not be used in the investigation of occupational asthma caused by low molecular weight agents[3].
  • Although positive results of single nonspecific bronchial provocation tests, specific skin prick tests, or serum-specific IgE testing increase the likelihood of occupational asthma, a negative result does not exclude occupational asthma[13].
  • Markers of inflammation of exposure may also be helpful - eg, exhaled nitrous oxide or sputum eosinophil counts, but these may not be readily available[7, 12].

Relocation away from exposure should occur as soon as diagnosis is confirmed and ideally within 12 months of the first work-related symptoms of asthma[3].

The optimal management of occupational asthma otherwise remains uncertain[14].

The British Occupational Health Research Foundation (BOHRF) Algorithm

BOHRF Algorithm
  • Patients who may have work-related asthma should be referred quickly to a chest physician or occupational health physician (see algorithm, above).
  • The aim of management is to identify the cause, to remove the worker from exposure and for the worker to have worthwhile employment.
  • Options also include removing the cause from the workplace, or redeploying the worker to alternative jobs[9].
  • Premature advice to leave the occupation is inadvisable.
  • Relocation away from exposure should occur within 12 months of the first work-related symptoms of asthma.
  • Occupational asthma may persist despite removal from the causal agent and it may become a chronic condition with a long-term effect on morbidity[7].

Effects on employment and reduced income - data highlight the following impact of occupational asthma:

  • Almost half of those affected will have to change their job as a result of loss of income.
  • Of those who do not change jobs, there is a high incidence of time taken off work, estimated at 14 days per year.
  • Both of the aforementioned points not only affect personal household income but also company performance.

Although not hugely documented, it is also important to be vigilant about the effects that occupational asthma can have on mental health and well-being.

  • The prognosis of individuals with occupational asthma is better if they are removed from exposure quickly, particularly within a year of first symptoms[11].
  • Screening in the workplace should be promoted - for example, health questionnaires and/or measures of FEV1 and FVC[9].
  • Staff educational programmes are also important[7].
  • Improvement in FEV1 can be maintained for a year after last exposure, and improvement in nonspecific responsiveness for more than two years.
  • Several studies have shown that the prognosis for workers with occupational asthma is worse for those who remain exposed for more than one year after symptoms develop, compared with those removed earlier.
  • Delay assessment of long-term impairment for at least two years following relocation away from exposure.

In patients with RADS, wheezing starts within 24 hours (usually less) of a single large exposure to an irritant. The condition is inflammatory and does not involve immunological recognition of the irritant; therefore, continued low-level exposure to the causative agent can be tolerated without problems. RADS is diagnosed by the presence of nonspecific responsiveness and a compatible history. The prognosis varies but there is a good likelihood of improvement. More recently, research suggests that initial exposure can have long-term effects, including airway eosinophilia and remodelling[15].

Further reading and references

  1. Fishwick D, Barber C, Walker S, et al; Asthma in the workplace: a case-based discussion and review of current evidence. Prim Care Respir J. 2013 Jun22(2):244-8. doi: 10.4104/pcrj.2013.00038.

  2. Friedman-Jimenez G, Harrison D, Luo H; Occupational asthma and work-exacerbated asthma. Semin Respir Crit Care Med. 2015 Jun36(3):388-407. doi: 10.1055/s-0035-1550157. Epub 2015 May 29.

  3. British Guideline on the management of asthma; Scottish Intercollegiate Guidelines Network - SIGN (2016)

  4. Occupational Asthma in Great Britain 2014; Health and Safety Executive

  5. Baur X, Aasen TB, Burge PS, et al; The management of work-related asthma guidelines: a broader perspective. Eur Respir Rev. 2012 Jun 121(124):125-39. doi: 10.1183/09059180.00004711.

  6. Lemiere C; When to suspect occupational asthma. Can Respir J. 2013 Nov-Dec20(6):442-4.

  7. Standards of care for occupational asthma; British Thoracic Society (2008)

  8. Tarlo SM; Update on work-exacerbated asthma. Int J Occup Med Environ Health. 201629(3):369-74. doi: 10.13075/ijomeh.1896.00676.

  9. Guidelines for the management of work-related asthma; European Respiratory Society (2012)

  10. Workers' Health and Safety; Health and Safety Executive

  11. Fishwick D, Barber CM, Bradshaw LM, et al; Standards of care for occupational asthma: an update. Thorax. 2012 Mar67(3):278-80. doi: 10.1136/thoraxjnl-2011-200755. Epub 2011 Dec 9.

  12. Peden D, Reed CE; Environmental and occupational allergies. J Allergy Clin Immunol. 2010 Feb125(2 Suppl 2):S150-60.

  13. Beach J, Russell K, Blitz S, et al; A systematic review of the diagnosis of occupational asthma. Chest. 2007 Feb131(2):569-78.

  14. Vandenplas O, Dressel H, Nowak D, et al; What is the optimal management option for occupational asthma? Eur Respir Rev. 2012 Jun 121(124):97-104. doi: 10.1183/09059180.00004911.

  15. Peden DB, Bush RK; Advances in environmental and occupational respiratory diseases in 2009. J Allergy Clin Immunol. 2010 Mar125(3):559-62.