Section 1: Difficulties pre-employment
Asthma patients are just as likely as others to choose jobs which potentially entail exposure to irritating or sensitising agents in the workplace,1 but this is not necessarily unwise.
However, patients may be concerned that employers will make employment decisions on the basis of an applicant's history of current, or even past, asthma.
The breadth of job sectors in which those with asthma are disadvantaged is remarkable. Among many others, fire and rescue services, bakeries, the police and military, many chemical industries and even the construction sector may enquire of job applicants whether they have or have had asthma and make employment or placement decisions in the light of any such declaration.
A good employer, of course, will recognise that such decisions must, if they are not to contravene disability legislation, be made on a case-by-case basis and that all reasonable adjustments to a job must be made to accommodate the employee with asthma. There is anecdotal evidence that such good practice is not universal.
Range of disease
It is well recognised in medicine that asthma encompasses a range of disease that extends from that which is mild enough to permit Premier League football to that which renders some patients housebound.
Most cases of asthma are mild and current treatments are almost always effective enough to allow a normal lifestyle.
In terms of management there are two issues which GPs should keep in mind:
First, most patients with asthma need not be dissuaded from pursuing whichever career they choose.
Reasonable exceptions will include those few who have particularly unstable or unpredictable symptoms. They may be advised that to work in irritant atmospheres might prove troublesome, at least until their disease has achieved some degree of stability, either through better treatment, improved adherence or simply with the passage of time.
Interestingly, there is no firm evidence that having asthma per se confers any greater risk of developing respiratory sensitisation from an airborne workplace allergen (see below).
This belies the less reassuring fact that atopy does increase individual risk, at least in relation to many workplace allergens.
Most patients with asthma, especially whose disease began in childhood, are of course atopic.
Secondly, any doctor making a diagnosis of asthma, whether they are working in primary or secondary care, should be aware that the label may have important implications for the patient's career, current or future.
Section 2: Work-exacerbated asthma: 'My job makes my asthma worse'
Around a fifth of employees who have asthma report that their symptoms are worse when they are at work.2
Some validity to this figure is provided by the observation that the proportion is higher among those who work in jobs where such a direct relationship is plausible; that is, in jobs where there is a likelihood of exposure to irritant dusts or fumes.
At face value this figure is worryingly high. Research in this area, however, is deficient in several important respects.
First, it provides no information on how much worse any symptoms are, nor whether there is any relationship with asthma severity.
Second, and critically, the findings are not accompanied by any estimate of how many people without asthma, indeed how many without any chronic disease at all, would report feeling 'worse' when they are at work.
General experience, and what evidence there is on sickness absence, suggests that far less than a third of employees with asthma experience significant difficulties at work.
Asthma which is causally unrelated to, but provoked by work is termed work-exacerbated asthma (WEA). It needs to be distinguished, conceptually and as far as possible practically, from true occupational asthma (OA), which arises directly from exposure encountered in the workplace.
The management, implications and legal consequences of WEA and OA are very different and confusion of the two may be disastrous.
Dozens of factors at work may exacerbate pre-existing asthma. Commonly they include non-specific dusty or irritant atmospheres, cold temperatures, dry air, heavy physical demands and even early morning shift work.
Making the diagnosis
Every practitioner will consider their patient's occupation in the context of their illness. It is often valuable to make enquiries of patients who have asthma into whether they are struggling in their work. Where there are such difficulties, the distinction between WEA and OA needs to be considered.
Managing the condition
If the problem is one of work-exacerbated asthma then it is helpful to establish a relationship with the patient's occupational health service if possible (barely 20 per cent of employees have access to such a service).
Most cases of WEA can be effectively managed with enhanced pharmaceutical control and expert attention to troublesome exposures. It should be rare for all but very few patients with WEA to require a change in occupation.
Patients with WEA are not eligible to claim statutory industrial disease benefit.
|Agents that commonly cause occupational asthma|
|High molecular mass*||Low molecular mass|
|Animal proteins||Any work with animals||Diisocyanates
Other chemical processing
|Tropical wood dusts||Wood work|
|Pollens||Any work with plants||Persulfate salts (hair bleach)
|Seafood and fish processing
|Reactive dyes||Textile workers|
|* these agents induce a specific IgE response|
Section 3: Occupational asthma: 'My job gave me asthma'
OA is asthma that arises directly and causally from an exposure encountered in the workplace. In some industries it is common. Within any general practice it will be present in around 5 per cent of the asthma list.3
OA is certainly under-recognised and has far more profound implications than WEA.
Two implications are especially important.
First, it is generally accepted that the prognosis of OA is worse if after the disease has developed, there is continuing exposure to the causative agent. Thus the advice to most patients with OA, and their employers, is that further exposure should cease.
Since most cases of OA reflect a hypersensitive immune response, achieving sufficient exposure control is generally very difficult without 'relocating' the affected worker.
Relocation in a large firm may be easy. In a smaller workplace or one where the relevant exposure is unavoidable, internal relocation may be impossible in which cases the patients may not be able to continue in that job.4 Second, an employer who learns that a worker has developed OA is legally bound under the Reporting of Injuries, Diseases and Dangerous Occurrences Regulations 1995 to report the matter to the Health and Safety Executive.
This triggers an inspection of the workplace and often a demand for improvements which may be extensive and expensive. At this point any anonymity that patient may have had is lost. It may be uncomfortable for the employee to experience this. Hence an accurate diagnosis is critically important.
Making the diagnosis
An occupational aetiology should be considered in any employed adult who has:
- new onset asthma
- childhood asthma which has deteriorated, or
- childhood asthma which is proving difficult to treat.
Particular attention should be paid to those working in high-risk occupations. While several hundred workplace agents have been reported to cause OA, most cases of the disease arise from a far smaller number (see box, section 2).
Nonetheless, any working adult with asthma should be asked regularly whether their disease improves when they are away from work. Similar enquiry into nasal symptoms (blockage, discharge, sneezing) is important since these are a frequent accompaniment of OA. Most cases of OA reflect an immune response to a workplace allergen, hence the disease exhibits a latency. It does not generally manifest until a period of at least several months after first exposure.
Once suspicion is raised, the diagnosis requires confirmation. In most cases this is achieved through the careful use of available techniques, immunology testing and function testing. At this point, many will seek the assistance of a respiratory physician with a special interest in occupational lung diseases,5 of whom there are perhaps a dozen in the UK.
For occupational agents that are of high molecular mass - mostly proteins - skin prick or serum-specific IgE assay will determine whether there is evidence of sensitisation.
Skin prick tests can help diagnosis (Photograph: SPL)
Specific serum assays for many agents are available through most hospital laboratories, but not all are well standardised, and it is important to request the correct test. A negative test result is helpful in excluding the diagnosis of respiratory allergy to a workplace protein; a positive test confirms sensitisation but does not confirm the presence of asthma.
The picture is far more complex for the many respiratory sensitising agents that are of low molecular mass (chemical agents).
Some of these produce detectable IgE responses but many do not. The few commercially available assays are poorly standardised.
A diagnosis of OA should rarely be made in the absence of functional evidence. The simplest technique is serial measurement of peak flow. Critically this needs to be done in a very different manner than that usually employed in the monitoring of asthma.
First, measurements need to be taken at work and at home at least four times a day for a period of at least four weeks; anything less is too insensitive.
Second, the measurements are best interpreted if they are plotted with daily means and both maximum and minimum values, rather than by each value separately as is the norm.
A characteristic history, positive immunology (if available) and a clear peak flow record of deterioration at work is usually sufficient evidence for OA.
Occasionally further testing is required; this usually takes the form of specific provocation testing as an inpatient - a procedure available in only a few UK hospitals.
Section 4: Managing occupational asthma
An employee who has developed a respiratory sensitisation to an agent they encounter at work will find that their asthma only improves when any further exposure is controlled and, in general, avoided altogether.
Some temporary relief may be afforded through standard asthma treatments, perhaps with the addition of an antihistamine, but the aim in each case should remain exposure avoidance.
This entails some difficult decisions. It is a kindness, on the part of both the patient's employer and health carers, to allow a limited period of time to make the necessary adjustments. There is no evidence those who have OA caused by one agent are at enhanced risk of developing the same disease from another.
In many cases the functional prognosis of OA is good. An accurate diagnosis and careful management affords one of the few instances when asthma is curable. Not all cases are so fortunate and a proportion of patients with the disease will find only partial improvement, even when they are no longer exposed.
There is limited evidence that the prognosis is worse if there has been a long period (several years) of symptomatic exposure, hence the advice to avoid exposure once a diagnosis is reached.
There is some evidence that any incomplete improvement reaches a plateau two years after the avoidance of exposure.
Patients whose symptoms persist should be treated according to standard guidance.
In other words, patients with OA often fare less well. Many who have lost their jobs will find re-employment difficult. Anger, anxiety and depression are not uncommon.
Any employed patient who has developed OA is eligible to make a claim for industrial injuries disablement benefit, under a statutory no-fault scheme which will award compensation for those judged to be at least 14 per cent disabled by their disease.
1. Radon K, Huemmer S, Dressel H, et al. Do respiratory symptoms predict job choices in teenagers? Eur Respir J 2006; 27(4): 774-8.
2. Henneberger PK, Derk SJ, Sama SR, et al. The frequency of workplace exacerbation among health maintenance organisation members with asthma. Occup Environ Med 2006; 63(8): 551-7.
3. de Bono J, Hudsmith L. Occupational asthma: a community based study. Occup Med (Lond). 1999; 49(4): 217-9.
4. Cannon J, Cullinan P, Newman Taylor A. Consequences of occupational asthma. BMJ 1995; 311(7005): 602-3.
5. Fishwick D, Barber CM, Bradshaw LM, et al. Standards of care for occupational asthma. Thorax 2008; 63: 240-50.