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Occupational asthma

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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What is occupational asthma?

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


Occupational asthma can be categorised into:2

  • Sensitiser-induced asthma: (asthma induced by an agent that causes a specific immunologic response.

  • Irritant-induced asthma: asthma induced by exposure to airway irritants, in the absence of sensitisation. This was originally described as "reactive airways dysfunction syndrome (RADS)", a severe form of irritant-induced asthma; subsequent definitions broadened the criteria.

Occupational asthma describes asthma that occurs de novo due to exposure to an agent at work. Work-exacerbated asthma is a different concept; it describes pre-existing asthma that is worsened by exposure to agents encountered at work, but is not caused by it.

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How common is occupational asthma? (Epidemiology)

  • 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.

  • The most common irritants for occupational asthma are isocyanates, flour/grain, wood dusts, cleaning products, hair products, enzymes, and epoxy and other resins.

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.3

Individuals who may be exposed to occupational asthma include:4

  • 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.

Occupational asthma symptoms (presentation)

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-exacerbated asthma) should be distinguished from those with pre-existing asthma who become additionally sensitised to an occupational agent.5

  • The BTS/SIGN guidelines recommend screening for occupational asthma with the following questions. A positive answer should trigger further investigation for occupational asthma:

    • Are you the same, better, or worse on days away from work?

    • Are you the same, better, or worse on holiday?

  • 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.

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Differential diagnosis

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.6

Diagnosing occupational asthma

Early diagnosis is the key to reducing morbidity.7 The decision to label a case of asthma as being occupationally induced remains a matter of clinical judgement, and can be complex.7 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.8 The Material Safety Data Sheets (MSDS) may provide information on hazardous substances in the work environment and should be available from the employer.

Individuals with suspected occupational asthma should be referred early for specialist assessment; ideally in an occupational lung disease service, if available, or secondary care asthma service, if not.7 9


A diagnosis of occupational asthma cannot be made on history alone, even if highly suggestive. Standard objective criteria should be used to confirm the diagnosis of asthma. Diagnostic tests for occupational asthma tend to become less sensitive over time if exposure to the cause has stopped, or reduced significantly, so should be carried out as early as possible.

Investigations include:

  • Serial peak expiratory flow (PEF) recordings. These are only helpful if the individual is still exposed to the suspected causative agent(s), and need to be measured on work days and rest days away from work. Specialist occupational asthma services often use computerised quantitative analytic methods for these. Minimum requirements for sufficient-quality PEF recordings include:

    • At least four readings a day, prebronchodilator where possible. Aiming for 2 hourly recordings during waking hours is helpful.

    • Carried out for at least 3 weeks, ideally with at least 3 days at work for each work period, and three series of consecutive days at work with three periods away.

    • A contemporaneous recording of work times, exposures, tasks, and medication use.

    • Ideally, maintenance asthma medication doses should be kept constant during the recording period.

  • Spirometry should be undertaken in all people with suspected occupational asthma, with measurements of forced expiratory volume in one second (FEV1) and forced vital capacity (FVC) made.

  • 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 confirm immunological sensitisation to a workplace allergen, but not occupational asthma (or the risk of it developing).

  • Fractional exhaled nitric oxide (FeNO) and sputum eosinophils. These have an established role in assessing people with suspected asthma, but there is limited evidence of their utility in diagnosing occupational asthma.

  • Specific bronchial provocation testingis the gold standard for making a diagnosis of occupational asthma. However, this is a specialised diagnostic technique, and not widely available in the UK; most patients are diagnosed using other investigations.7

    • Specific bronchial provocation tests are potentially hazardous and should only be used in centres with sufficient expertise and experience. Indications for specific bronchial provocation tests include:

      • Confirming a new cause of occupational asthma.

      • Identifying the exact cause of occupational asthma, to allow suitable workplace modifications.

      • Confirming the diagnosis of occupational asthma if other tests are inconclusive or unfeasible.

  • 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.10

  • 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.11

Occupational asthma treatment and management

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. Total removal from exposure probably improves symptoms and lung function more than reduction of exposure, but total removal from exposure increases the risk of unemployment.12 Individuals who remain at work with reduced exposures (eg, in a lower-exposure role, or using respiratory protective equipment) are around 14 times more likely to remain in employment than workers who have completely ceased exposure.12

Employers are obliged by the Equality Act 2010 to make reasonable adjustments for any employees with disability due to occupational asthma. In addition, following written notification of a diagnosis of occupational asthma amongst their employees, British employers are legally obliged to report the case to the Health and Safety Executive, to review their existing control measures, and to survey the health of other exposed workers.7

In the UK, people with occupational asthma are eligible to make a claim for the Industrial Injuries Disablement Benefit. Some also make civil claims against their employer for personal injury.

The pharmacological management of occupational asthma is assumed to be the same as for any other cause of asthma, following national guidelines.7 However, the evidence base for pharmacological treatment in occupation asthma specifically is limited.13


  • Anxiety, depression, and poor quality of life are more common amongst people with occupational asthma.14 15

  • Effects on employment and income can be substantial (and contribute to mental health and psychosocial difficulties). Over half of individuals who cease occupational exposures entirely are out of work at 3-5 years post-diagnosis.12 It may be extremely difficult to find alternative employment.

  • Individuals who remain in work may experience high rates of sickness absence.

  • Amongst individuals who continue in the same job, without adaptations, symptoms usually persist or worsen, despite treatment. They are at increased risk of a rapid decline in lung function, which can lead to fixed airflow obstruction.16


  • Prognosis in occupational asthma is largely determined by two factors:7

    • Duration of exposure to the causative agent.

    • Level of exposure to the causative agent.

  • The prognosis of individuals with occupational asthma is better if they are removed from exposure quickly, particularly within a year of first symptoms.17

  • When complete cessation of exposure is possible, about 25-30% of people experience a full symptom recovery over 3-5 years, and another 30-35% experience improved asthma symptoms with treatment.12

  • Screening in the workplace should be promoted - for example, health questionnaires and/or measures of FEV1 and FVC.18

  • 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.

Irritant induced asthma7

Irritant induced asthma (IIA) is distinct from sensitiser-induced asthma. IIA describes asthma that develops due to a direct irritant effect of inhaled agents, without immunological sensitisation. IIA was previously known as reactive airways dysfunction syndrome.19

In IIA, asthma symptoms occur rapidly within 24 hours of an exposure to very high levels of irritant gases, fumes, vapour, or smoke. In the original description of IIA, symptoms persisted for at least three months, but other reports suggest that symptoms can resolve over a few weeks.

IIA is diagnosed by the presence of nonspecific bronchial hyper-reactivity, or significant bronchodilator reversibility of obstructive-pattern spirometry, and a compatible history.

Standard asthma therapy is used to treat IIA. There are limited data on the long-term prognosis of IIA, but at least some people experience complete resolution, so asthma medication should be reviewed regularly, and stopped if possible. Some people, however, have permanent respiratory disability.20

Because IIA is inflammatory, and not allergic, individuals can return to their usual work environment, as long as measures are in place to prevent further high-level exposures.

Further reading and references

  • Global Initiative for Asthma (GINA)
  • Asthma; Health and Safety Executive
  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. Tarlo SM, Lemiere C; Occupational asthma. N Engl J Med. 2014 Feb 13;370(7):640-9. doi: 10.1056/NEJMra1301758.
  3. Baur X, Aasen TB, Burge PS, et al; The management of work-related asthma guidelines: a broader perspective. Eur Respir Rev. 2012 Jun 1;21(124):125-39. doi: 10.1183/09059180.00004711.
  4. Lemiere C; When to suspect occupational asthma. Can Respir J. 2013 Nov-Dec;20(6):442-4.
  5. Tiotiu AI, Novakova S, Labor M, et al; Progress in Occupational Asthma. Int J Environ Res Public Health. 2020 Jun 24;17(12):4553. doi: 10.3390/ijerph17124553.
  6. Tarlo SM; Update on work-exacerbated asthma. Int J Occup Med Environ Health. 2016;29(3):369-74. doi: 10.13075/ijomeh.1896.00676.
  7. Barber CM, Cullinan P, Feary J, et al; British Thoracic Society Clinical Statement on occupational asthma. Thorax. 2022 May;77(5):433-442. doi: 10.1136/thoraxjnl-2021-218597. Epub 2022 Mar 21.
  8. The Control of Substances Hazardous to Health Regulations 2002, 2002 No. 2677.
  9. Asthma: diagnosis, monitoring and chronic asthma management; NICE Guideline (November 2017 - last updated April 2021)
  10. British guideline on the management of asthma; Scottish Intercollegiate Guidelines Network (SIGN), British Thoracic Society (BTS), NHS Scotland (2003 - revised July 2019)
  11. Beach J, Russell K, Blitz S, et al; A systematic review of the diagnosis of occupational asthma. Chest. 2007 Feb;131(2):569-78.
  12. Henneberger PK, Patel JR, de Groene GJ, et al; Workplace interventions for treatment of occupational asthma. Cochrane Database Syst Rev. 2019 Oct 8;10(10):CD006308. doi: 10.1002/14651858.CD006308.pub4.
  13. 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.
  14. Moullec G, Lavoie KL, Malo JL, et al; Long-term socioprofessional and psychological status in workers investigated for occupational asthma in quebec. J Occup Environ Med. 2013 Sep;55(9):1052-64. doi: 10.1097/JOM.0b013e31829904ab.
  15. Lipszyc JC, Silverman F, Holness DL, et al; Comparison of Psychological, Quality of Life, Work-Limitation, and Socioeconomic Status Between Patients With Occupational Asthma and Work-Exacerbated Asthma. J Occup Environ Med. 2017 Jul;59(7):697-702. doi: 10.1097/JOM.0000000000001066.
  16. Anees W, Moore VC, Burge PS; FEV1 decline in occupational asthma. Thorax. 2006 Sep;61(9):751-5. doi: 10.1136/thx.2005.054080. Epub 2006 May 2.
  17. Fishwick D, Barber CM, Bradshaw LM, et al; Standards of care for occupational asthma: an update. Thorax. 2012 Mar;67(3):278-80. doi: 10.1136/thoraxjnl-2011-200755. Epub 2011 Dec 9.
  18. Guidelines for the management of work-related asthma; European Respiratory Society (2012)
  19. Brooks SM, Weiss MA, Bernstein IL; Reactive airways dysfunction syndrome (RADS). Persistent asthma syndrome after high level irritant exposures. Chest. 1985 Sep;88(3):376-84. doi: 10.1378/chest.88.3.376.
  20. Walters GI, Huntley CC; Updated review of reported cases of reactive airways dysfunction syndrome. Occup Med (Lond). 2020 Oct 27;70(7):490-495. doi: 10.1093/occmed/kqaa133.

Article history

The information on this page is written and peer reviewed by qualified clinicians.

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