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.¹

Irritant-induced asthma (reactive airways dysfunction syndrome - RADS) accounts for about 10% of all cases of occupational asthma. The remaining 90% are attributable to hypersensitivity induced occupational asthma. 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 non-specific responsiveness and a compatible history. The prognosis varies, but there is a good likelihood of improvement.

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.² The Material Safety Data Sheets (MSDS) may provide information on hazardous substances in the work environment and should be available from the employer.

• Occupational factors accounts for at least 10% of adult new or recurrent asthma.^3,4
• It is now the commonest 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.⁵

Risk factors³

• 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

• 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.³
• 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.⁶

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.

A thorough history and serial PEFR's, 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 day³), 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 peak expiratory flow rate 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 non-specific hyper-responsiveness after days at and away from work:
  • If unable to measure peak flow, or if there are questions of record validity, non-specific 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 non-specific responsiveness outside the normal range.
• Measure of specific 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.
  • 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
    • 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 non-specific bronchial provocation test with a specific skin-prick test or specific IgE test may be an appropriate alternative.¹⁰
  • Although positive results of single non-specific 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.¹⁰

The British Occupational Health Research Foundation (BOHRF) Algorithm

(Used with kind permission)

• Patients who may have work-related asthma should be referred quickly to a chest physician or occupational health physician.³
• 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.

Effects on employment and reduced income.

• Improvement in FEV₁ can be maintained for a year after last exposure, and improvement in non-specific responsiveness for more than two years.¹¹
• Prognosis is improved by early identification and early avoidance of further exposure to the cause of occupational asthma.³
• 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.¹²
• Delay assessment of long-term impairment for at least two years following relocation away from exposure.