Occupational Asthma

Definition, and Frequency

"Occupational asthma is a disease characterised by variable air flow 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" (Bernstein et al 1993). Within this definition two types of occupational asthma can be distinguished: 

In the first instance, there is agreement, that the syndrome of chest tightness, wheezing, shortness of breath, dry cough etc, which appears after a latent period of occupational exposure constitutes occupational asthma. 

The second category of occupational asthma is that developing without a period of latency and often associated with exposure to high concentrations of irritants. Its symptoms may be somewhat different from that of asthma that follows a latent period. This is often referred to as Reactive Airways Dysfunction Syndrome (RADS). 

laboratory mice It should be borne in mind that the airways that are afflicted by asthma are a continuation of the airways starting in the nose. It is therefore not surprising that many asthma cases also have rhinitis, (often preceding the asthma). Rhinitis literally means inflammation of the nose. Its symptoms are commonly those which the lay person associates with "hay fever" - an itchy, blocked or runny nose, often red and accompanied by sneezes. There may also be eye symptoms (itchy, glazed or runny). Thus sensitisation to certain animals (see photo) tends to manifest as rhinitis and conjunctivitis, together with asthma. Occupational asthma may also be associated with urticaria

Approximately 70,000 people in the UK according to the results of a sample questionnaire in the 1990 Labour Force Survey, believed that during a one year period they had symptoms of asthma caused, or made worse by substances breathed at work (Hodgson et al - Health and Safety Executive (HSE) Report - 1993). It is therefore an important cause of work-related ill-health, and is probably the commonest cause of new cases of occupational lung disease in general. Throughout the UK information about the newly diagnosed cases, and their causes is continuously collected through the SWORD scheme (Meredith and McDonald 1994). 

Workers may be unaware of the possible relationship between their symptoms and their work. Even if they do suspect a link, they may still be reluctant to present their concerns to any doctor, fearing adverse consequences for their employment.Since GPs see patients as individuals they may be at a disadvantage when compared to say, occupational physicians, in making the connection between work and symptoms.Employers often have inadequate surveillance procedures to measure the frequency of occupational asthma. Even when cases are brought to their attention, they do not always fulfil their legal obligation of reporting. Occupational physicians and chest physicians are usually well placed to diagnose cases. 

In the UK, di-isocyanate exposures, notably toluene di-isocyanate from exposures in occupations such as spray painting, and other work involving urethane varnishes or foams, certain waterproofing agents etc. clearly feature as the highest of the reported categories of causative agents (Meredith and MacDonald 1994). 

Another important causal agent is colophony fume, from soldering especially in the electronics industry. Colophony arises from pine resin and contains abietic acid, and other resin acids which are used as fluxes in soldering. 

However, a very wide range of chemicals, and of agents of biological origin, have been described as causes of occupational asthma. 

Prevalence and incidence data for occupational rhinitis are limited but a Finnish study suggests that high molecular weight substances of biological origin - such as flour, wood dust, and animal dander - feature highest in the frequency of cases referred for investigation (Kanerva et al 1993). 

However, for the health care professional dealing with individual workers, or with groups of workers in a workplace, it is not the national incidence of the disease that matters. Rather, it is essential to get a grasp of the likely risk - i.e. the incidence in relation to defined jobs and tasks, and hence occupational exposures to specific agents. 

A Basis for Primary Prevention

Can chemical structure be a useful tool in determining whether a substance may present an occupational asthma hazard? There are features of molecular structure of substances hazardous to health which appear more likely to be associated with a substance being a potential cause of occupational asthma (Agius et al 1991). An abstract of earlier work is available, and it is hoped to make more recent developments known in due course.
Assessing exposure entails a scrutiny of who does what, where, and how. It requires a familiarity with the methods and circumstances of the work which, in combination with measurements, will produce a clear picture of the intensities and patterns of exposure. One of the difficulties in assessing exposures quantitatively is that the identity of the agent directly responsible for, or most closely associated with, the risk of asthma or rhinitis may be unclear, as is the case with baker's asthma. 

The photograph (right) was taken in a bakery, where flour dust was liberally scattered. The baker suffered from occupational asthma, and it was difficult for the employer to appreciate that something as apparently innocuous as flour could cause asthma, especially in conditions of high exposure.


There may be difficulties which relate to the time weighting of the monitoring: should eight-hour average exposure be the focus or should it be peak exposures? 

What about people who are infrequently exposed? 

When exposures carry the risk of occupational asthma and rhinitis, the assessment should proceed as follows: 

  • identify the tasks giving higher exposure, often by inspection;
  • take measurements of personal exposures sufficient to gain an estimate of the mean and range of concentrations; and
  • take additional samples at relevant background locations and of lower exposure and of lower exposure tasks.

The HSE's guidance, Preventing Asthma at Work (HSE 1994) may be helpful in setting up exposure assessments. 

Estimating the magnitude of health risk has to be tailored carefully to the actual circumstances under scrutiny. The conclusions should be based on two main factors: 


  • the severity of the possible consequences of excessive exposure; and
  • the likelihood of these adverse outcomes in the light of what is known about the intensities and patterns of exposure.

As regards reasonably practicable precautions,the fundamental question is: What, in a given situation, are the control measures which would reduce the risk to an acceptably low level? 

To answer this question one needs to determine what knowledge exists of the harmful properties of the substance and how well founded that knowledge is. A thorough familiarity with the circumstances and patterns of exposure is required, and account must be taken of any special characteristics of the exposed population. 

For specific exposures, there is good evidence that the risk of sensitisation is related to the exposure level. In other words - the higher the concentration of inhaled agent, the greater the likelihood of becoming sensitised and of experiencing symptoms of rhinitis and/or asthma. However it is difficult to set exposure limits below which exposures can be regarded as 'safe' in an absolute sense - although the risk might be very low. Moreover it is possible that once sensitised, the airborne concentrations at which symptoms could be provoked might be even lower than the concentrations responsible for sensitisation in the first place. 

Airborne exposure to respiratory sensitisers may carry a risk of asthma. Since this may be a potentially life-threatening condition, one must be confident that the risk of contracting it is very low before concluding that all reasonably practicable measures have been applied in implementing control through containment and ventilation.

The most effective means of control is to prevent exposure altogether, either by not doing the task in question or by substituting the sensitiser for a less harmful material, although this is not always feasible. For example if a di-isocyanate based paint or varnish is being used, one should question whether a much less hazardous paint which simply dries out without curing can be applied instead. This might entail the need for re-painting at more frequent intervals, depending on the circumstances. 

The photograph (right), depicting control measures, shows a pharmaceutical process worker tipping dust from a tray into a hopper.It illustrates a combination of control measures used when handling a substance, in the pharmaceutical industry, that may cause occupational asthma. The hopper is provided with local exhaust ventilation; the tray is covered by polythene, and the operator is wearing personal protection including an airhood, which includes a personal supply of breathing air.


Similar principles of protection may be applied in a wide variety of industrial circumstances, involving exposure to man-made chemicals, or to natural products. Man-made exposures range from car spray painting with di-isocyanates, to soldering with colophony flux or the manufacture or use of acid anhydrides to make resins. Naturally occurring biological agents which may cause sensitisation range from mammalian urinary proteins, to locusts used in laboratories, to the processing of foods such as salmon, crabs, prawns or shrimps, and to rubber latex.
The second photograph (right), illustrating control measures, shows a radiographer in a general hospital. The processing of X-ray films may be associated with the release of various respiratory irritants, such as sulphur dioxide, glutaraldehyde, and acetic acid. Some of these may cause asthma. 

By using sealed bottles of photographic reagents and introducing them into the processor using a closed system, as shown in the image, exposure can be considerably reduced. Inadequately controlled glutaraldehyde exposure in the health service, notably in the cleaning of endoscopes, such as in bronchoscopy and gastroscopy, has been responsible for serious ill-health in some nurses, and other health care workers. Formaldehyde is another aldehyde implicated in the causation of occupational asthma.



This is the chemical formula of glutaraldehyde: 


Other methods of control might need to be considered. For example,it might be possible to change the formulation of enzymes from fine dust into granules - which are less likely to generate aerosols - or to increase the relative humidity of environments where cyanoacrylates are handled (since water vapour will cause cyanoacrylate monomer to polymerise and become practically harmless by comparison). 

Personal protection, albeit the last line of defence, may play an important role in situations where control at source is clearly impracticable. Thus, for example, in paint-spraying with di-isocyanates, full-face respiratory protection is the bare minimum level of acceptable protection. In animal handling laboratories, powered filtering facepiece respirators may be a useful adjunct to other forms of control. Similarly, personal protective equipment would clearly be appropriate if a process plant was undergoing maintenance or being upgraded.

Health Surveillance and Secondary Prevention

For some categories of respiratory sensitisers, there is good evidence that factors such as smoking and atopy may increase the likelihood of sensitisation. Atopy is a characteristic of a large proportion of the population - perhaps even as many as 1 in 3 - depending on the exact criteria used. Atopics tend to be sensitive to common allergens such as those of house dust mites and grass pollens. Occupational sensitisation to some very important asthmagens, notably di-isocyanates, does not seem to bear any relationship at all to atopy. However, the likelihood of sensitisation to some other agents such as laboratory animal allergens or other large molecules of biological origin, is increased in atopics. Thus it is important to consider whether the extra risk associated with atopy should justify using tests or questionnaires for atopy as a discriminant to keep people out of employment. 

The law requires that exposure should be controlled such that almost all the population can work without an increased risk to their health. A strategy that relies on excluding about one-third of the potential workforce would implicitly be an admission that the work is not deemed safe for a large proportion of the community and would arguably fall foul of the law on that account. 

Published research indicates that exclusion of atopics might still allow into employment more people who would become sensitised than the number of those whose sensitisation had been averted. Evidence of atopy per se is not, therefore, adequate justification for refusing employment where there is exposure to respiratory sensitisers.(Newill et al 1986; Seaton et al 1994). 

Some studies have shown that smoking is a bigger and more significant prior determinant of the risk of sensitisation, whereas the risk associated with atopy is insignificant (Venables et al 1989). 

It must be stressed that prevention of work-related disease should rest primarily on making the workplace safer for workers rather than by using poorly validated criteria for excluding individuals from employment.Health surveillance is an important aspect of secondary prevention (HSE 1990; HSE 1991): 


  • It enables the early identification of adverse health effects in individuals. 
  • It may supplement environmental monitoring in assessing control.
  • Health surveillance may itself contribute to the process of hazard and risk assessment.
  • Health surveillance should be accompanied by information regarding hazardous substances to which the employees are exposed, the respiratory symptoms which may result, the potential long-term risks and therefore, the need to report these symptoms to the occupational health service.

Health surveillance records collected for statutory purposes need to be securely and confidentially stored for at least 40 years from the date of the last entry (HSC 1995). 

Trends of symptom prevalence, suggesting sensitisation in relation to different categories of employees, workplaces, and tasks should be investigated. 

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