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
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
certain animals (see photo) tends to manifest as rhinitis and
conjunctivitis, together with asthma. Occupational asthma may also be
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
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,
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
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
earlier work is available, and it is hoped to make more recent
developments known in due course.
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
When exposures carry the
risk of occupational asthma and rhinitis, the assessment should proceed
- 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
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
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.
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
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
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
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
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).
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
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
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
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.
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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