Has the greatest prevalence of any work-related pulmonary disease in industrialised countries (25 to 28%).
It accounts for a significant proportion of asthma in general adult population
(5 to 15%).
Variable airway limitation and/or bronchial hyper responsiveness caused by exposure to agents in a particular workplace separate from those outside the work environment.
Airway hyper-responsiveness – increased responsiveness of the airways to non-specific provocative stimuli. Smaller than normal doses of stimuli (exercise, cold or dry air) provoke acute transient airway narrowing. Pre-existing or concurrent asthma can also be exacerbated by workplace stimuli (work-aggravated asthma).
1. Irritant-induced asthma - toxic damage to the airway epithelium
- chlorine, ammonia, sulphur dioxide, nitrogen oxides
2. Hypersensitivity-induced asthma - acquired specific hypersensitivity
- proteins (animal excreta, flour, enzymes, latex)
- synthetic chemicals (isocyanates, acid anhydrides)
- complex molecules (penicillins, colophony)
- microbial (harvest moulds, bacterial enzymes)
— avoiding exposure can reduce the severity of asthma, airway inflammation and airway responsiveness.
– cause acute transient airway narrowing in pre-existing asthma, effects on the airways can be additive.
1. Physical (exercise, cold air)
2. Chemical (sulphur dioxide inhaled in subtoxic doses)
3. Pharmacological (histamine, methacholine)
— avoiding exposure will reduce the frequency of provoked attacks but
not the magnitude of airway responsiveness.
(Click here for figure) (Click here for .pdf version)
1. Differentiation of asthma from other causes of respiratory symptoms, such
as chronic airflow limitation.
2. Differentiation of occupational cause from non-occupational.
3. Differentiation of initiated asthma from exacerbation of pre-existing asthma.
- General questioning to identify respiratory symptoms, including rhinitis/erythema,
identifying possible prodromal symptoms
- Smoking and atopy are related to development
- Exposure to a recognised or identified agent
- Initial symptom-free period
- Knowledge of current and previous work environments
- Symptoms that develop at work and increase as the week progresses
- Symptoms that improve during absence from work such as weekends or holidays
- There may be a number of other people similarly effected
- Symptoms may occur after a single exposure incident to an agent (irritant-induced)
- Outside influences may point a cause of symptoms (hobbies/pets/other businesses)
The pattern of symptoms may not identify an occupational cause, such as late
reactions often occurring at night, which may mimic constitutional asthma.
- Identification of airway hyperactivity and reversibility
- Serial peak expiratory flow measurements taken two hourly during work and
holiday (for a minimum of 1 to 2 weeks)
- Immunological investigations using skin prick testing with identified sensitisers
or estimation of specific serum IgE using RAST/ELISA
- Respiratory challenges with methacholine or histamine to determine hyperresponsiveness
- Inhalation challenge tests with occupational agents (early, late and dual
responses)
The risk of long-term/persistent asthma is directly related to the severity
and duration of symptoms at the time of diagnosis, and to the duration of exposure
to the initiating cause after the onset of respiratory symptoms.
(positive relationship between exposure intensity and sensitisation)
- avoidance of exposure
- identification of agents
- Changes in processes such as the use of granules instead of powders
- Measurement of agent concentrations in the work environment
- The important role of occupational hygiene
- ventilation/air filtration/humidity
- respiratory protection (mask/breathing apparatus)
- respiratory surveillance
- Regulation and legislation
- Reporting to SWORD (surveillance of work related and occupational respiratory
disease)
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