Asthma Management Handbook

Investigating suspected work-related asthma

Recommendations

For all workers with asthma, ask whether asthma symptoms improve on days away from work or during holidays. If so, investigate further.

How this recommendation was developed

Consensus

Based on clinical experience and expert opinion (informed by evidence, where available), with particular reference to the following source(s):

  • Aasen et al. 20131

When new-onset asthma or worsening of asthma control appears to be caused by workplace factors, consider offering referral to a specialist (e.g. respiratory physician, occupational physician or allergist) with experience in investigating and managing work-related asthma.

How this recommendation was developed

Consensus

Based on clinical experience and expert opinion (informed by evidence, where available).

Take a detailed history asking about exposure to airborne substances, and the pattern and timing of symptoms.

Table. Examples of common sensitising agents and occupations associated with exposure

Agent

Occupations

Low molecular weight agents

Wood dust (e.g. western red cedar, redwood, oak)

  • Carpenters
  • Builders
  • Model builders
  • Sawmill workers
  • Sanders

Isocyanates

  • Automotive industry workers
  • Adhesive workers
  • Chemical industry
  • Mechanics
  • Painters
  • Polyurethane foam production workers

Formaldehyde

  • Cosmetics industry
  • Embalmers
  • Foundry workers
  • Hairdressers
  • Healthcare workers
  • Laboratory workers
  • Tanners
  • Paper, plastics and rubber industry workers

Platinum salts

  • Chemists
  • Dentists
  • Electronics industry workers
  • Metallurgists
  • Photographers

High molecular weight agents

Latex

  • Food handlers
  • Healthcare workers
  • Textile industry workers
  • Toy manufacturers

Flour and grain dust

  • Bakers
  • Combine harvester drivers
  • Cooks
  • Farmers
  • Grocers
  • Pizza makers

Animal allergens (e.g. urine, dander)

  • Animal breeders
  • Animal care workers
  • Jockeys
  • Laboratory workers
  • Pet shop workers
  • Veterinary surgery workers

Source: Adapted from Hoy R, Abramson MJ, Sim MR. Work related asthma. Aust Fam Physician 2010; 39: 39-42. Available from: http://www.racgp.org.au/afp/201001/35841

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Table. Questions to consider for patients with suspected work-related asthma

Was there any unusual exposure to any substance at work within the 24 hours before symptoms began?

Did the person’s co-workers experience respiratory symptoms?

Does the person’s asthma symptoms improve when away from work (e.g. weekends, holidays)?

Are symptoms of rhinitis or conjunctivitis worse at work?

Source: Adapted from Tarlo SM, Balmes J, Balkissoon R et al. Diagnosis and management of work-related asthma: American College Of Chest Physicians Consensus Statement. Chest 2008; 134(3 Suppl): 1S-41S. Available from: http://journal.publications.chestnet.org/article.aspx?articleid=1044851

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Table. Features of history in work-related asthma

 

Work-exacerbated asthma

Occupational asthma

Sensitiser-induced occupational asthma Irritant-induced occupational asthma

Onset of asthma symptoms

Before or during working life

Typically weeks to months after first exposure to sensitiser

Typically within 24 hours of major exposure to respiratory irritant

Pattern of asthma symptoms

Worse on workdays

Worse during or after work shift and improve when away from work

Persist for at least 12 weeks with no previous chronic lung disease

Other factors

Exposure to dust, smoke, fumes, cold

Exposure to known sensitiser

Exposure to large amount of respiratory irritant

Adapted from:

Hoy R, Abramson MJ, Sim MR. Work related asthma. Aust Fam Physician 2010; 39: 39-42. Available from: http://www.racgp.org.au/afp/201001/35841

Tarlo SM, Liss GM. Occupational asthma: an approach to diagnosis and management. Can Med Assoc J 2003; 168: 867-71. Available from: http://www.cmaj.ca/content/168/7/867.full

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How this recommendation was developed

Adapted from existing guidance

Based on reliable clinical practice guideline(s) or position statement(s):

  • Hoy et al. 20102
  • Tarlo et al. 20083

Advise patients to ask their employer to provide information about substances used in the workplace, including a safety data sheet.

How this recommendation was developed

Adapted from existing guidance

Based on reliable clinical practice guideline(s) or position statement(s):

  • Hoy et al. 20102
  • Tarlo et al. 20083

More information

Definition and prevalence of work-related asthma

Work-related asthma includes work-exacerbated asthma (worsening of asthma control due to workplace factors) and occupational asthma (new-onset asthma).

An estimated 25% of adults with asthma have work-related asthma.3

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Work-exacerbated asthma

Work-exacerbated asthma refers to worsening of asthma control due to workplace factors (e.g. inhalation of airborne substances, physical exertion or exposure to cold air). It occurs in an estimated 22% of adults with asthma.4

People with work-exacerbated asthma experience symptoms on more days, use more healthcare resources and have lower quality of life than people with asthma that is unrelated to work.4 Persistent exposure to workplace factors that worsen asthma control might result in greater loss of lung function than would occur if the person were not exposed to these factors, but this has not been clearly demonstrated.4

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Occupational asthma

Occupational asthma refers to new-onset asthma caused by exposure to an airborne substance in the workplace (sensitiser or irritant).

An estimated 16–20% of adult-onset asthma is caused by workplace exposure to sensitisers or irritants.5, 6 Hundreds of substances are known to cause occupational asthma and more are identified each year.2 Many of these are found in Australian workplaces.7

Occupational asthma is preventable if exposure to sensitisers and irritants is identified and controlled.

Undiagnosed occupational asthma results in ongoing poor asthma control, increasing dose requirements for asthma medicines, and possibly irreversible decline in lung function.2, 8 Deaths from occupational asthma have been reported.2, 9

There are two forms of occupational asthma:

  • sensitiser-induced occupational asthma (allergic mechanism)
  • irritant-induced occupational asthma (non-allergic mechanism).

Sensitiser-induced occupational asthma

Sensitiser-induced occupational asthma develops after a period of exposure (a few days to several years) to a specific substance (e.g. inhaled protein or other chemical) in the workplace.2

People with a history of atopy have higher risk of developing sensitiser-induced occupational asthma when exposed to some antigens (e.g. animal proteins, flour). Symptoms of rhinitis (e.g. sneezing, nasal congestion) often occur at work before occupational asthma develops.3

Employers should be aware of the risk associated with the use of sensitising agents and should control workers’ exposure, as far as is practical.7 Comprehensive lists of identified sensitising agents are available from the OASYS research group, Midland Thoracic Society, UK and the UK government Health and Safety Executive.

Table. Examples of common sensitising agents and occupations associated with exposure

Agent

Occupations

Low molecular weight agents

Wood dust (e.g. western red cedar, redwood, oak)

  • Carpenters
  • Builders
  • Model builders
  • Sawmill workers
  • Sanders

Isocyanates

  • Automotive industry workers
  • Adhesive workers
  • Chemical industry
  • Mechanics
  • Painters
  • Polyurethane foam production workers

Formaldehyde

  • Cosmetics industry
  • Embalmers
  • Foundry workers
  • Hairdressers
  • Healthcare workers
  • Laboratory workers
  • Tanners
  • Paper, plastics and rubber industry workers

Platinum salts

  • Chemists
  • Dentists
  • Electronics industry workers
  • Metallurgists
  • Photographers

High molecular weight agents

Latex

  • Food handlers
  • Healthcare workers
  • Textile industry workers
  • Toy manufacturers

Flour and grain dust

  • Bakers
  • Combine harvester drivers
  • Cooks
  • Farmers
  • Grocers
  • Pizza makers

Animal allergens (e.g. urine, dander)

  • Animal breeders
  • Animal care workers
  • Jockeys
  • Laboratory workers
  • Pet shop workers
  • Veterinary surgery workers

Source: Adapted from Hoy R, Abramson MJ, Sim MR. Work related asthma. Aust Fam Physician 2010; 39: 39-42. Available from: http://www.racgp.org.au/afp/201001/35841

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Irritant-induced occupational asthma

Irritant-induced occupational asthma is due to an inflammatory (non-immunological) response of the lower respiratory tract to exposure to an irritant in the workplace. Respiratory symptoms typically occur within minutes to hours of exposure.2 Reactive airways dysfunction syndrome (a type of irritant-induced occupational asthma) occurs after a single massive exposure to an irritant.2

Recurrent low-level exposure might also result in irritant-induced occupational asthma, but this has not been clearly demonstrated.2

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Investigation of work-related asthma symptoms

Asking all workers with asthma whether their asthma symptoms improve when away from work is a useful screening tool. Those who answer 'yes' need investigation for work-related asthma.1

Investigation of suspected work-related asthma is complex. It involves confirming the diagnosis of asthma, identifying the workplace as the cause of asthma symptoms, and identifying the specific causal agents. This involves taking a detailed history, further investigations (e.g. serial peak expiratory flow measurement, skin prick tests, bronchial provocation [challenge] testing) and sometimes worksite visits.23

People with suspected work-related asthma should ask their employer to provide a safety data sheet containing information about the constituents and properties of substances used at the workplace. Information about safety data sheets (previously called Material Safety Data Sheets) is available from Safe Work Australia.

Accurate diagnosis and documentation are essential to support a potential Workers Compensation claim. This normally requires a report from a specialist with experience investigating work-related asthma.

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Definition of variable expiratory airflow limitation

Most of the tests for variable expiratory airflow limitation are based on showing variability in FEV1. While reduced FEV1 may be seen with many other lung diseases (or due to poor spirometric technique), a reduced ratio of FEV1 to FVC indicates airflow limitation.10 Normal FEV1/FVC values derived from population studies vary,1112 but are usually greater than:11

  • 0.85 in people aged up to 19 years
  • 0.80 in people aged 20–39 years
  • 0.75 in people aged 40–59 years
  • 0.70 in people aged 60–80 years.

In children, it is less useful to define expiratory airflow limitation according to a specific cut-off for FEV1/FVC ratio, because normal values in children change considerably with age.12

Some spirometers provide predicted normal values specific to age group. If these are available, a FEV1/FVC ratio less than the lower limit of normal (i.e. less than the 5th percentile of normal population) indicates airflow limitation.

Variable expiratory airflow limitation (beyond the range seen in healthy populations) can be documented if any of the following are recorded:

  • a clinically important increase in FEV1 (change in FEV1 of at least 200 mL and 12% from baseline for adults, or at least 12% from baseline for children) 10–15 minutes after administration of bronchodilator
  • clinically important variation in lung function (at least 20% change in FEV1) when measured repeatedly over time (e.g. spirometry on separate visits)
  • a clinically important reduction in lung function (decrease in FEV1 of at least 200 mL and 12% from baseline on spirometry, or decrease in peak expiratory flow rate by at least 20%) after exercise (formal laboratory-based exercise challenge testing uses different criteria for exercise-induced bronchoconstriction)
  • a clinically important increase in lung function (at least 200 mL and 12% from baseline) after a trial of 4 or more weeks of treatment with an inhaled corticosteroid
  • clinically important variation in peak expiratory flow (diurnal variability of more than 10%)
  • a clinically important reduction in lung function (15–20%, depending on the test) during a test for airway hyperresponsiveness (exercise challenge test or bronchial provocation test) measured by a respiratory function laboratory.

Notes

Patients referred to a respiratory function laboratory may be asked not to take certain medicines within a few hours to days before a spirometry visit.

A clinically important increase or decrease in lung function is defined as a change in FEV1 of at least 200 mL and 12% from baseline for adults, or at least 12% from baseline for children, or a change in peak expiratory flow rate of at least 20% on the same meter.1310 A clinically important increase in FVC after administering bronchodilator may also indicate reversible airflow limitation, but FVC is a less reliable measure in primary care because FVC may vary due to factors such as variation in inspiratory volume or expiratory time.

The finding of ‘normal’ lung function during symptoms reduces the probability that a patient has asthma, but a clinically important improvement in response to bronchodilator or inhaled corticosteroid can occur in patients whose baseline value is within the predicted normal range.

The greater the variation in lung function, the more certain is the diagnosis of asthma. However, people with longstanding asthma may develop fixed airflow limitation.

Reversibility in airflow limitation may not be detected if the person is already taking a long-acting beta2 agonist or inhaled corticosteroid.

Airflow limitation can be transient and does not necessarily mean that the person has asthma (e.g. when recorded during a severe acute infection of the respiratory tract). Ideally, airflow limitation should be confirmed when the patient does not have a respiratory tract infection. Reduction in lung function during a respiratory tract infection with improvement in lung function after its resolution, commonly occurs in people with asthma, but can also be seen in patients with COPD or in healthy people without either asthma or COPD.14,15

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Referral options for investigation of work-related asthma

To identify a specialist with experience investigating work-related asthma, consult the Thoracic Society of Australia and New Zealand or the Australasian Faculty of Occupational and Environmental Medicine.

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References

  1. Aasen TB, Burge PS, Henneberger PK, et al. Diagnostic approach in cases with suspected work-related asthma. J Occup Med Toxicol. 2013; 8: 17. Available from: http://www.occup-med.com/content/8/1/17
  2. Hoy RF, Abramson MJ, Sim MR. Work related asthma - diagnosis and management. Aust Fam Physician. 2010; 39: 39-42. Available from: http://www.racgp.org.au/afp/201001/35841
  3. Tarlo SM, Balmes J, Balkissoon R, et al. Diagnosis and management of work-related asthma: American College Of Chest Physicians Consensus Statement. Chest. 2008; 134(3 Suppl): 1S-41S. Available from: http://journal.publications.chestnet.org/article.aspx?articleid=1044851
  4. Henneberger PK, Redlich CA, Callahan DB, et al. An official american thoracic society statement: work-exacerbated asthma. Am J Respir Crit Care Med. 2011; 184: 368-78. Available from: http://ajrccm.atsjournals.org/content/184/3/368.long
  5. Torén K, Blanc PD. Asthma caused by occupational exposures is common – a systematic analysis of estimates of the population-attributable fraction. BMC Pulm Med. 2009; 9: . Available from: http://www.biomedcentral.com/1471-2466/9/7
  6. Dykewics MS. Occupational asthma: Current concepts in pathogenesis, diagnosis, and management. J Allergy Clin Immunol. 2009; 123: 519-528. Available from: http://www.jacionline.org/article/S0091-6749(09)00214-0/fulltext
  7. Sim M, Abramson MJ, LaMontagne T, et al. Occupational asthma – detection, surveillance and prevention of the disease burden. Final report. Monash University Department of Epidemiology and Preventive Medicine, Melbourne, 2005.
  8. Anees W, Moore VC, Burge PS. FEV1 decline in occupational asthma. Thorax. 2006; 61: 751-5. Available from: http://thorax.bmj.com/content/61/9/751.long
  9. Ortega HG, Kreiss K, Schill DP, Weissman DN. Fatal asthma from powdering shark cartilage and review of fatal occupational asthma literature. Am J Ind Med. 2002; 42: 50-4. Available from: http://www.ncbi.nlm.nih.gov/pubmed/12111690
  10. Pellegrino R, Viegi G, Brusasco V, et al. Interpretative strategies for lung function tests. Eur Respir J. 2005; 26: 948-968. Available from: http://erj.ersjournals.com/content/26/5/948
  11. National Heart Lung and Blood Institute (NHLBI) National Asthma Education and Prevention Program. Expert Panel Report 3: guidelines for the diagnosis and management of asthma. Full report 2007. US Department of Health and Human Services National Institutes of Health, Bethesda, 2007. Available from: http://www.nhlbi.nih.gov/health-pro/guidelines/current/asthma-guidelines/full-report
  12. Quanjer PH, Stanojevic S, Cole TJ, et al. Multi-ethnic reference values for spirometry for the 3-95-yr age range: the global lung function 2012 equations. Eur Respir J. 2012; 40: 1324-43. Available from: http://www.ncbi.nlm.nih.gov/pubmed/22743675
  13. Levy ML, Quanjer PH, Booker R, et al. Diagnostic Spirometry in Primary Care: Proposed standards for general practice compliant with American Thoracic Society and European Respiratory Society recommendations. Prim Care Respir J. 2009; 18: 130-147. Available from: http://www.ncbi.nlm.nih.gov/pubmed/19684995
  14. Collier AM, Pimmel RL, Hasselblad V, et al. Spirometric changes in normal children with upper respiratory infections. Am Rev Respir Dis. 1978; 117: 47-53. Available from: http://www.ncbi.nlm.nih.gov/pubmed/619724
  15. Melbye H, Kongerud J, Vorland L. Reversible airflow limitation in adults with respiratory infection. Eur Respir J. 1994; 7: 1239-1245. Available from: http://www.ncbi.nlm.nih.gov/pubmed/7925901