In my opinion occupational asthma commonly complicates pre-existing asthma. I think the literature is confused, and often uses the term work agravated asthma. I think this means different things to different people. I take it to mean pre-existing asthma whose control is more difficult in a particular job; this might be due to earlier waking, cycling to work, or a non-specific irritant at work.
Others take it to include asthma due to sensitisation to an occupational allergen in a worker with pre-existing asthma. I call this occupational asthma provided that the work exposure regularly causes a deterioration in lung function, and this is not due to circadian rhythms.
Occupational asthma is due wholly or partly to agents met with at work. Once occupational asthma has developed, asthma is nearly always provoked in addition by non-specific factors such as exercise, cold air and respiratory infections, so that occupational exposure is rarely the only provoking factor in a worker with occupational asthma. Occupational asthma may also develop in workers with pre-existing asthma, where the consequences of a diagnosis may be equally great as those with no pre-existing asthma. Those with pre-existing asthma are probably at increased risk of developing occupational sensitisation to most occupational agents.
In the UK, compensation by the DSS (under the Department of Health and Social Security Act of 1975) states that occupational asthma is asthma whose primary cause is a sensitising agent inhaled at work. It is qualified by saying there is usually a preliminary period ranging from days to years before the onset of symptoms, which occur during the working week and often remit during absence from work. Removal from exposure to the sensitising agent may lead to remission of asthma, although sensitisation can be permanent.
Some like to place qualifications on the diagnosis of occupational asthma; the following classification is suggested. The first three or four come within the traditional classification of occupational asthma.
1. Occupational asthma occurring for the first time after exposure to an occupational sensitiser, with specific IgE to the relevant occupational allergen. A latent period of exposure without symptoms would be present, and symptoms with trivial exposure common after sensitisation has occurred. Laboratory animal allergy would be a classical example.
2. Occupational asthma without specific IgE to a relevant occupational allergen, but with the other features of sensitisation, such as a latent interval and subsequent symptoms with levels of exposure which do not affect non-sensitised asthmatics. Most isocyanate-induced asthma would come into this group, which is clinically and histologically indistinguishable from the first group.
3. Occupational asthma as above in an individual with previous non-occupational asthma. In this situation the occupational exposure would not be the cause of the underlying asthma, but the additional sensitisation would necessitate a change of work practice or employment. A good example would be a doctor or nurse who has controlled asthma not interfering with work, who develops latex sensitisation. There is enough latex allergen in the air of many hospital wards to provoke asthma in a highly sensitised individual and preclude work in health-care premises.
4. Occupational asthma induced by a single large exposure. Asthma induced by a single large exposure to an occupational agent with subsequent asthma induced by low level exposure. This is similar to occupational asthma with sensitisation, but no latent interval is necessary. Several cases have followed isocyanate spills.
5. Irritant induced occupational asthma. Asthma is work-related but occurs on first exposure to a recognised respiratory irritant, with persisting asthma and regular improvement away from exposure. Regular exposure to sulphur dioxide in a smelter would be an example. The consequences for the affected individual’s work are the same as for a sensitiser, but exposure to very low levels should not cause problems.
6. Irritant induced asthma. Asthma starting within 24 hours of a single large exposure, and persisting afterwards, usually accompanied by increased non-specific bronchial responsiveness. Subsequent usual level exposure to the same agent does not provoke the asthma (and so continuing employment is not jeopardised). Large exposures to chlorine are the commonest cause. Some call this reactive airways dysfunction syndrome.
7. Occupational bronchial hyper-responsiveness. There are some workers with respiratory symptoms who do not have airflow obstruction or changes in peak expiratory flow, who have increased levels of non-specific responsiveness after work exposure, with improvement when away from exposure. These changes can also be reproduced with specific provocation testing. They do not fulfil even a broad definition of asthma, but never the less have work-related symptoms and abnormal physiology. It might represent the earliest evidence of disease in an individual who will later develop true occupational asthma, but this awaits confirmation.
I have had a look at some of my challenge studies. The first colophony challenge paper (Clinical Allergy 1978;8:1-14) showed that 5/21 challenge positive workers had pre-existing asthma.
The Shield data regularly shows cases with pre-existing asthma reported with occupational asthma. It was 19% of the reports in 2003 (see the Shield section in this website)
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