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.¹

Classification

Patients can fall into two categories:

1. Hypersensitivity-induced occupational asthma - 90% of cases.
2. Irritant-induced asthma - reactive airways dysfunction syndrome (RADS), which accounts for about 10% of all cases.

Epidemiology

• Occupational factors account for at least 10% of adult new or recurrent asthma.^2,3
• It is now the most common occupational lung disease in the developed world with over 400 reported causes.
• Isocyanates and flour/grain are responsible for the highest proportion of new cases of occupational asthma.⁴

Risk factors²

• Baking, pastry making.
• Healthcare and dental care workers.
• Laboratory animal work.
• Car repairers, spray painting.
• Electricians.
• Welding, soldering, metalwork.
• Woodwork.
• Food processing.
• Chemical processing.
• Textile, plastics and rubber manufacture.
• Farmers.
• Cleaners.
• Other jobs exposed to dusts and fumes.

Presentation

• The diagnosis should be suspected in all adults with airflow limitation, and positively searched for in those with high-risk occupations or exposures.
• Work-related asthma is suggested if asthma symptoms improve when away from work or deteriorate when at work.²
• 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.⁵

Differential diagnosis

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.

Diagnosis

The decision to label a case of asthma as being occupationally-induced remains a matter of clinical judgment. 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.

Investigations

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,²) dynamic lung function and reversibility testing.
  • 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.⁷ 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 a criterion-based expert system.⁷
• Measurements of nonspecific hyper-responsiveness after days at and away from work:
  • If unable to measure peak flow, or if there are questions of record validity, nonspecific responsiveness with methacholine or histamine can be measured after a period at and away from work exposure.⁸
  • The diagnostic sensitivity is only about 40%, substantially worse than serial peak flow measurements.
  • Not all workers with occupational asthma have measures of nonspecific responsiveness outside the normal range.
• 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.
• Specific bronchial provocation testing:
  • Specific inhalation challenge with controlled exposures to workplace agents and suitable controls is the gold standard for diagnosis. Tests are difficult to do, are not widely available, and are not available for some types of workplace exposures.⁹
  • Specific bronchial provocation tests are potentially hazardous and in most cases they are inappropriate. Specific inhalation tests should only be used in a limited number of circumstances:^9,10
    • 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.
  • When specific inhalation challenge testing is not available, the combination of a nonspecific bronchial provocation test with a specific skin-prick test or specific IgE test may be an appropriate alternative.¹¹
  • 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
• Markers of inflammation of exposure may also be helpful, e.g. exhaled nitrous oxide or sputum eosinophil counts, but these may not be readily available.⁹

Management

The British Occupational Health Research Foundation (BOHRF) Algorithm

Guidelines for the Identification, Management and Prevention of Occupational Asthma - www.bohrf.org.uk/content/asthma.html © British Occupational Health Research Foundation, 6 St Andrew's Place, Regent's Park, London, NW1 4LB. Used with permission.

• Patients who may have work-related asthma should be referred quickly to a chest physician or occupational health physician.²
• 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.
• 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.

Complications

Effects on employment and reduced income - data highlight the following impact of occupational asthma:¹²

• 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 effect personal household income but also company performance.

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

Prognosis

• Improvement in forced expiratory volume in one second (FEV1) can be maintained for a year after last exposure, and improvement in nonspecific responsiveness for more than two years.¹³
• Prognosis is improved by early identification and early avoidance of further exposure to the cause of occupational asthma.²
• 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.¹⁴
• Delay assessment of long-term impairment for at least two years following relocation away from exposure.

Reactive airways dysfunction syndrome

In patients with reactive airways dysfunction syndrome (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

Document references

1. Bernstein IL, Chan-Yeung M, Malo JL et al. Asthma in the Workplace 2nd ed. 1999 (Marcel Dekker, New York)
2. British Occupational Health Research Foundation; Work-related asthma and rhinitis: case finding and management in primary care
3. Malo JL, Chan-Yeung M; Occupational asthma. J Allergy Clin Immunol. 2001 Sep;108(3):317-28. [abstract]
4. Health and Safety Executive; Occupational Asthma; Causal agents for occupational asthma
5. Malo JL, Ghezzo H, L'Archeveque J, et al; Is the clinical history a satisfactory means of diagnosing occupational asthma? Am Rev Respir Dis. 1991 Mar;143(3):528-32. [abstract]
6. Health and Safety Executive; Control of Substances Hazardous to Health (COSHH)
7. Burge PS, Pantin CF, Newton DT, et al; Development of an expert system for the interpretation of serial peak expiratory flow measurements in the diagnosis of occupational asthma. Midlands Thoracic Society Research Group. Occup Environ Med. 1999 Nov;56(11):758-64. [abstract]
8. Moscato G, Malo JL, Bernstein D; Diagnosing occupational asthma: how, how much, how far? Eur Respir J. 2003 May;21(5):879-85. [abstract]
9. Peden D, Reed CE; Environmental and occupational allergies. J Allergy Clin Immunol. 2010 Feb;125(2 Suppl 2):S150-60. [abstract]
10. Health and Safety Executive; Guidance MS25 Medical Aspects of Occupational Asthma. 2nd edition, HMSO, 1998
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. [abstract]
12. Health and Safety Executive; Draft Approved Code of Practice on Occupational Asthma: Regulatory Impact Assessment (Post Consultation); Jan 2003
13. Perfetti L, Cartier A, Ghezzo H, et al; Follow-up of occupational asthma after removal from or diminution of exposure to the responsible agent: relevance of the length of the interval from cessation of exposure. Chest. 1998 Aug;114(2):398-403. [abstract]
14. Gannon PF, Weir DC, Robertson AS, et al; Health, employment, and financial outcomes in workers with occupational asthma. Br J Ind Med. 1993 Jun;50(6):491-6. [abstract]
15. Peden DB, Bush RK; Advances in environmental and occupational respiratory diseases in 2009. J Allergy Clin Immunol. 2010 Mar;125(3):559-62. [abstract]

Internet and further reading

• British Occupational Health Research Foundation; Occupational Asthma: Identification, Management and Prevention: Evidence Based Review and Guidelines

Acknowledgements