Occupational Asthma

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PatientPlus articles are written by UK doctors and are based on research evidence, UK and European Guidelines. They are designed for health professionals to use, so you may find the language more technical than the condition leaflets.

See also: Asthma - Peak Flow Diary written for patients

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:

  • Hypersensitivity-induced occupational asthma (the majority of cases).
  • Irritant-induced asthma - reactive airways dysfunction syndrome (RADS).

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  • Occupational factors account for at least one in six cases of adult asthma.[2] 
  • It is now the most common occupational lung disease and incidence is between 12-300 cases per million workers per year.[2] However, the incidence is probably higher, as many cases of occupational asthma remain unrecognised.[2] 
  • The most common irritants for occupational asthma are isocyanates, flour/grain, adhesives, metals, resins, colophony, fluxes, latex, animals, aldehydes and wood dust.[2][3]

Risk factors[2]

Individuals who may be exposed to occupational asthma include:

  • Cooks, bakers and pastry makers.
  • Healthcare and dental care workers.
  • Laboratory animal workers.
  • Car repairers, spray painters.
  • Electricians.
  • Those working in welding, soldering and metalwork.
  • Woodworkers.
  • Food processing workers.
  • Chemical processing workers.
  • Textile, plastics and rubber manufacturing workers.
  • Farmers.
  • Cleaners.
  • Those working in other jobs exposed to dusts and fumes.
  • Hairdressers.

An occupational cause for asthma should be considered in anyone with adult onset or reappearance of childhood asthma. Adults with airflow obstruction should be asked whether they are better on days away from work or when on holiday.[4] 

  • The diagnosis should be suspected in all adults with airflow limitation, and positively searched for in those with high-risk occupations or exposures.
  • Importantly, ask about any symptoms of rhinitis or conjunctivitis, as these are now recognised as preceding the development of occupational asthma.[2] 
  • 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.

Patients with pre-existing asthma aggravated nonspecifically 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.

Early diagnosis is the key to reducing morbidity.[5] 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.[6] 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:
    • 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. 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.[2] 
  • 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:[7]
      • 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.[8]
  • 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.[8]
  • Markers of inflammation of exposure may also be helpful - eg, exhaled nitrous oxide or sputum eosinophil counts, but these may not be readily available.[2][7]

The optimal management of occupational asthma remains uncertain.[9] 

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, 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.[5] 
  • 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.[2] 

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.

  • Prognosis is improved by early identification and early avoidance of further exposure to the cause of occupational asthma.
  • Screening in the workplace should be promoted - for example, health questionnaires and/or measures of FEV1 and FVC.[2][5] 
  • Staff educational programmes are also important.[2] 
  • 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.[10]

Further reading & 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 Jun;22(2):244-8. doi: 10.4104/pcrj.2013.00038.
  2. Standards of care for occupational asthma; British Thoracic Society (2008)
  3. Occupational Asthma in Great Britain 2013; Health and Safety Executive
  4. British guideline on the management of asthma; Scottish Intercollegiate Guidelines Network - SIGN (Oct 2014)
  5. Guidelines for the management of work-related asthma; European Respiratory Society (2012)
  6. Workers' Health and Safety; Health and Safety Executive
  7. Peden D, Reed CE; Environmental and occupational allergies. J Allergy Clin Immunol. 2010 Feb;125(2 Suppl 2):S150-60.
  8. Beach J, Russell K, Blitz S, et al; A systematic review of the diagnosis of occupational asthma. Chest. 2007 Feb;131(2):569-78.
  9. Vandenplas O, Dressel H, Nowak D, et al; What is the optimal management option for occupational asthma? Eur Respir Rev. 2012 Jun 1;21(124):97-104. doi: 10.1183/09059180.00004911.
  10. Peden DB, Bush RK; Advances in environmental and occupational respiratory diseases in 2009. J Allergy Clin Immunol. 2010 Mar;125(3):559-62.

Disclaimer: This article is for information only and should not be used for the diagnosis or treatment of medical conditions. EMIS has used all reasonable care in compiling the information but make no warranty as to its accuracy. Consult a doctor or other health care professional for diagnosis and treatment of medical conditions. For details see our conditions.

Original Author:
Dr Colin Tidy
Current Version:
Peer Reviewer:
Prof Cathy Jackson
Document ID:
2534 (v25)
Last Checked:
Next Review:

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