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Asbestos-related
lung conditions
Other
occupational
lung diseases
Assessment
Investigations
Management
The authors
Dr Subash Srikantha
respiratory and sleep specialist
in private practice, St Leonards,
Liverpool and the Woolcock Clinic,
Glebe, NSW; and conjoint lecturer,
school of medicine, University of
NSW.
Occupational lung diseases
Background
IN this industrialised era, workers
are exposed to hundreds of potentially hazardous materials, with
the associated risk of developing
occupational-related health conditions. Increasingly, environmental
exposures are being recognised as an
important cause of pulmonary disease. Occupational lung disease is one
of the leading causes of work-related
death and disability in Australia.
Causal factors include the inhalation of irritant chemical vapours and
gases, organic and inorganic dusts,
sensitising agents and toxic fumes,
which adversely affect both the upper
and lower respiratory tracts.
Australia was the world’s largest
Table 1: Anatomical location of occupational diseases
Anatomical location Examples of occupational diseases
Upper airways
Rhinitis, laryngitis, nasal ulceration, cancer of the
nasopharynx
Conducting airways
Occupational asthma, bronchitis, bronchiolitis, COPD,
bronchial cancer
Lung parenchyma
Pneumoconiosis (silicosis, asbestosis), lung cancer
Pleura
Pleural plaques, diffuse pleural thickening, pleural
effusions, mesothelioma
asbestos user per capita in the world
during the 20th century. This resulted
in a significant health burden to the
workers who were mining, processing or using asbestos products. Due
to the long latency from exposure
to disease, the number of cases of
asbestos-related mesothelioma is
increasing despite the fact that asbestos production ended in 1987 and the
importation of asbestos products was
completely banned in 2003.
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Recent decades have seen a
marked increase in awareness about
the adverse health effects of hazardous exposures in the workplace.
This has resulted in tighter workplace regulations and industrial
legislation to safeguard the health
of workers. Each state government
now has a WorkCover Authority
focused on workplace safety. Among
other things, these authorities assist
with compensation of workers with
occupational lung diseases.
Occupational lung diseases can
be categorised into groups according to:
• Anatomical location (table 1).
cont’d next page
Dr Michael Hibbert
senior respiratory and sleep
specialist, department of
respiratory and sleep medicine,
Royal North Shore Hospital, St
Leonards; and lecturer, Northern
Clinical School , University of
Sydney, NSW.
Copyright © 2013
Australian Doctor
All rights reserved. No part of
this publication may be
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8 March 2013 | Australian Doctor |
23
How To TREAT Occupational lung diseases
from previous page
• Inhaled substances (table 2).
• Reaction type.
• Pathophysiological responses.
Occupational
lung
disease
needs to be considered in any current or retired worker, particularly
when the worker is involved in an
industry with exposure to a known
hazardous material. It is important
to be aware of the latency between
exposure and onset of symptoms,
especially in the case of asbestos and
silica exposure, where there may be
a delay of decades before the onset
of symptoms. Similarly in occupational asthma, the onset of symptoms may be delayed for months
to years after the initial exposure
to the allergen. On the other hand,
we should not assume the origins of
respiratory symptoms are caused by
an occupational exposure without a
clear causal relationship.
Early cessation of exposure to a
toxic agent is of paramount importance. Because respiratory symptoms caused by toxic exposures are
nonspecific, recognising their potential relationship to a toxic agent or
agents is essential to proper diagnosis. Continued exposure may result
in irreversible functional decline
and even fatal respiratory disease.
Knowledge about and familiarity with these diseases is critically
important for the primary care physician, who is often the first healthcare provider to see the affected
individuals.
Table 2: Agents responsible for occupational lung diseases
Agent
Industry/occupations
Lung condition
Asbestos
Mining and milling, building and construction,
transport equipment manufacturing
(shipbuilding, railway locomotive building and
maintenance), asbestos product manufacture,
power generation, carpenters and joiners,
metal fitters, boilermakers
Pleural plaques, pleural thickening,
pulmonary fibrosis (asbestosis),
mesothelioma
Beryllium
Aerospace, nuclear power, computer,
automotive electronics
Pulmonary fibrosis (berylliosis),
emphysema, lung cancer
Barium
Petroleum industry
Pulmonary fibrosis
Coal
Coal mining
Pulmonary fibrosis
Centrilobular emphysema
Cadmium
Electronics, metal plating and batteries
Emphysema, lung cancer
Cotton dust
Cotton, flax and hemp workers
Bronchitis, byssinosis, hypersensitivity
pneumonitis
Isocyanates
Spray painting
Asthma, hypersensitivity pneumonitis
Irritant gases (ammonia,
sulphur dioxide, chlorine)
Chemical industry, agriculture, fertilisers
Bronchitis, asthma
Ionising radiation
Radiology, nuclear industry
Pneumonitis, pulmonary fibrosis, lung
cancer
Mouldy hay (thermophilic
actinomycetes)
Agriculture (farmers)
Bronchitis, hypersensitivity pneumonitis
Silica
Sandblasters, miners, tunnelers, millers,
potters, glassmakers, foundry and quarry
workers
Simple silicosis, silicoproteinosis,
progressive massive fibrosis, COPD
Talc
Paint, ceramics, leather, paper
Pulmonary fibrosis
Wood dust
Milling, construction
Hypersensitivity pneumonitis, asthma
Asbestos-related lung conditions
ASBESTOS is a naturally occurring
mineral used since ancient times for
its strength and fire-resistant properties. Due to these properties, asbestos has been widely used in building
materials, fire resistant products and
insulation (lagging).
The most common types of
asbestos fibres are serpentine fibres
(chrysotile or ‘white asbestos’) and
amphiboles (amosite ‘brown asbestos’ and crocidolite ‘blue asbestos’).
Asbestos exposure can result in a
number of lung conditions particularly in the occupational setting
(see the box below). Exposure to
amphibole fibres (crocidolite) confers a greater risk of developing lung
disease than the serpentine fibres of
chrysotile. This relates to the persistence of amphiboles in the lung for
many years after the exposure has
stopped, in comparison with chrysotile fibres, which generally disappear within 10 years.
Asbestos was mined and processed in Australia for more than
100 years. Until 2003, there was
extensive local use and subsequent
exposure in many industries. The
occupations with high incidence of
asbestos exposure are summarised
in table 2. As in other industrialised
countries, the ill-effects from past
exposure are expected to peak later
this decade in Australia, due to the
long lag time between exposure and
disease presentation, particularly in
the case of mesothelioma.
Exposure to asbestos is quantified in terms of the concentration of
inhaled fibres (fibres/mL) with the
highest exposure seen in people who
worked in asbestos mining (up to
100 f/mL) and background community exposure generally measured
at less than 0.01f/mL. The recommended exposure standards for asbestos in air in Australia are 0.1f/mL.
Cumulative exposure is expressed in
fibre/mL/years, similar to the packyear measurement for smoking.
Asbestiform fibres also occur naturally in areas where other minerals,
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| Australian Doctor | 8 March 2013
Figure 1: Pleural plaques as seen on chest X-ray.
Pleural
plaques
Figure 2: Rounded atelectasis.
Benign pleural plaques
All radiology images courtesy of
Dr Greg Briggs and Dr Anne Miller.
Lung conditions related to
asbestos exposure
• Pleural plaques
• Benign pleural effusion
• Rounded atelectasis
• Diffuse pleural thickening
• Asbestosis
• Mesothelioma
• Lung cancer
such as gold and iron ore, have been
exploited, with a consequent risk
of significant lung disease to miners. Currently, the main sources of
exposure to asbestos fibres are old
buildings undergoing renovation or
demolition where building maintenance and demolition workers are
employed. Home owners renovating their own homes are also at risk
of exposure to asbestos fibres.
Plaques are deposits of hyalinised
collagen fibres on the parietal pleura.
They are usually found on the parietal pleura adjacent to the 6th-9th
ribs and along the diaphragm.
Plaques are rarely seen in the lung
apices or costophrenic angles. It
usually takes about 20 years after
exposure to asbestos for plaques to
be evident, and they are often calcified. Up to half of those exposed
to asbestos develop plaques. They
rarely occur bilaterally without
asbestos exposure (figure 1).
Benign pleural plaques are merely
the markers of asbestos exposure
and in isolation do not cause any
symptoms. They have no effect on
lung volumes and do not impair
exercise tolerance or gas exchange.
Regular follow-up of pleural plaques
with imaging is not required due to
their lack of disease potential and
such follow-up has not been shown
to impact on the survival from mesothelioma or lung cancer.
Benign pleural disease
Benign asbestos-related pleural
effusion (BAPE)
Exposure to asbestos can cause
benign pleural plaques, benign
pleural effusions, diffuse pleural
thickening or rounded atelectasis in
the sub-pleural lung parenchyma.
Benign asbestos-related pleural
effusion (BAPE) is usually an exudative unilateral effusion with occasionally eosinophilic predominance
on cell counts. The interval between
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the exposure and the presentation
of effusion may vary from 5-30
years and early onset is correlated
with higher exposures. It usually
resolves spontaneously or may be
followed by diffuse pleural thickening (see below).
Rounded atelectasis
Pleural adhesions caused by asbestos-related pleural inflammation
result in atelectasis of a part of the
sub-pleural lung parenchyma and
appear as a rounded lung mass
on imaging (figure 2). In many
instances when they are large or not
classical in radiological appearance,
biopsy is required to exclude malignancy.
Diffuse pleural thickening
This generally begins as fibrosis of
the visceral pleura with secondary
thickening of the parietal pleura.
Both visceral and parietal pleura
become inseparable, leading to
obliteration of the costophrenic
sulci (figures 3 and 4).
Although commonly a precursor
to diffuse plural thickening, pleural effusion is not a prerequisite for
diffuse thickening. Diffuse plural
thickening may result in dyspnoea
as a result of a reduction in lung
volumes and diffusion capacity.
Asbestosis
Diffuse interstitial pulmonary fibrosis caused by asbestos exposure is
called asbestosis. It is indistinguishable from idiopathic pulmonary
fibrosis except for the presence
of other radiological features of
asbestos exposure such as calcified
pleural plaques or identification
of asbestos fibres or ferruginous
bodies (asbestos fibres coated by
iron) in the lung tissue. Although
the term ‘asbestosis’ is often used
to describe any asbestos-related
disease affecting the lung and the
pleura, it should be confined to pulmonary fibrosis caused by asbestos
exposure.
The development of asbestosis
follows high-level asbestos exposure usually seen only in those
with occupational exposure. Many
patients who develop asbestosis are
asymptomatic for at least 20-30
years after the initial exposure and
a high level of exposure results in a
shorter latency period.
Patients present with an insidious
onset of exertional dyspnoea. Productive cough and wheeze are rare
and, if present, are usually caused
by concomitant smoking-related
lung disease.
Bilateral fine-end inspiratory
crackles and clubbing are seen in
about 40-60% cases. Pulmonary
function
testing
demonstrates
restricted lung volumes with
reduced gas transfer. Laboratory
tests such as sputum and basic
blood tests are unhelpful. High-resolution CT scanning is much more
sensitive than X-ray for assessment,
with interstitial changes seen in the
lower zones early in the course and
progression to honeycombing and
upper lobe involvement as the disease advances. Concurrent smoking
accelerates the progression of fibrosis. Asbestosis is in general a slowly
progressive disease but occasionally
follows a more accelerated course,
leading to respiratory failure.
Malignant mesothelioma
Malignant mesothelioma is an
insidious, aggressive and fatal cancer of the parietal pleura with a
median survival of 12 months from
diagnosis. Occasionally it may
involve the mesothelial surfaces of
the peritoneal cavity, pericardium
and tunica vaginalis. Eighty-five per
cent of cases are caused by asbestos
exposure in an occupational setting.
It may also occur with very lowlevel asbestos exposure occasioned
by activities such as washing the
clothes of someone working in an
asbestos-related work environment.
The lifetime risk of mesothelioma in
a population exposed to asbestos is
in the range of 5-10%.
Crocidolite fibre exposure causes
the greatest risk for the development of malignant mesothelioma.
The latency between first exposure
and the development of malignant
mesothelioma varies from 15-60
years, with patients most commonly presenting in their 50s, 60s or
70s. The most frequent presenting
symptoms of pleural mesothelioma
are dyspnoea, often related to a
pleural effusion, and non-pleuritic
chest pain.
Occasionally it may present as
an asymptomatic unilateral pleural
effusion on routine imaging.
The initial chest X-ray findings
often show the presence of a pleural effusion or pleural thickening.
Figure 3: Chest X-ray of the thorax demonstrating asbestos-related diffuse
pleural thickening. Note the overall reduction in right lung volume.
Figure 5: Imaging findings in pleural mesothelioma. A: Chest X-ray
demonstrating the four classic findings: pleural thickening, pleural effusion,
decreased thoracic volume, and no shift of the mediastinum to the affected
side. B and C: CT scans demonstrating pleural thickening, loculated pleural
effusion, and pleural nodularity.
Pleural
thickening
othelioma. Soluble mesothelinThe most common CT findings
Figure 4: CT thorax of the same patient, demonstrating encasement of the
right hemithorax by the diffuse pleural thickening with overall reduction in
lung volume.
Pleural
thickening
A
are pleural thickening (92%), pleural effusion (74%) (figure 5) and
contraction of a hemithorax. Only
one-fifth of patients will have radiological evidence of asbestosis. It is
also rare for there to be bilateral
involvement with malignancy. A
PET scan may help to differentiate
malignant mesothelioma from diffuse pleural thickening.
A definitive histological diagnosis is essential, given the medicolegal consequences of the diagnosis
and prognostic implications of
particular histological subtypes.
Epithelioid and mixed-type malignant mesothelioma denote a better
prognosis than sarcomatoid mesothelioma.
Closed pleural biopsy or thoracocentesis may produce false-negative results. Surgical intervention
in the form of open thoracotomy
or video-assisted thoracoscopic
surgery has a higher diagnostic
yield and is recommended for the
tissue sampling. After the pleural
biopsy via thoracoscopy or thoracotomy, the surgeons may, if
indicated, perform a pleurodesis
procedure by mechanically irritating the parietal pleura to cause
adhesion of parietal and visceral
pleura to prevent any recurrent
pleural effusions
Although no clear diagnostic
role has been established for serum
tumour markers, both mesothelin
and osteopontin have been used
in the research setting to aid in the
non-invasive diagnosis of mesothelioma.
Mesothelin is a glycoprotein
that is expressed on the surface of
the normal mesothelial cells and is
over-expressed in malignant mes-
related peptides are measured in
serum and pleural fluid and their
sensitivity in detecting malignancy
varies from 16-68% and is limited
to epithelioid types. Osteopontin
is overexpressed in mesothelioma
but has a lower diagnostic yield
than mesothelin. Currently, there
is no serum, pleural fluid or urine
marker that can be used in isolation to diagnose or exclude mesothelioma.
Asbestos-related lung cancer
Lung cancer can occur as a result
of asbestos exposure even in the
absence of pulmonary fibrosis. The
risk is related to the degree of exposure and the presence of asbestosis.
However, it is worth noting that
not everyone who develops lung
cancer in the asbestos exposure setting has asbestosis.
While smoking remains the most
important causative agent for lung
cancer, the combined effect of
asbestos and smoking appears to be
more than additive and approaches
a multiplicative effect. The relative
risk of cancer is increased by up to
60-fold in smokers with asbestos
exposure. There is a dose–response
relationship between asbestos exposure and risk of lung cancer.
The quantitative risk of lung cancer varies according to fibre type
and cumulative exposure. Crocidolite fibres are three times more likely
than chrysolite fibres to cause lung
cancer with the same level of exposure.
Estimates for excess deaths from
lung cancer (ie, compared with the
background rate of deaths from
lung cancer) at very heavy exposures
of 100 f/mL years are of the order
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B
Pleural effusions
Pleural
thickening
with
nodularity
C
of 5-100 per 100,000 for chrysotile
and 150-350 for crocidolite. Overall, it appears that asbestos-related
lung cancer is under-diagnosed and
under-compensated mainly because
of doctors attributing lung cancer
to smoking without considering the
contribution of asbestos in patients,
most of whom are heavy smokers.
cont’d page 26
8 March 2013 | Australian Doctor |
25
How To TREAT Occupational lung diseases
Other occupational lung diseases
Silicosis
SILICOSIS is a fibrotic lung disease caused by inhalation of free
crystalline silica. Given that silica
is the most abundant mineral in
the world, occupational exposure
to respirable crystalline silica dust
particles occurs in a vast number of
industries including mining, quarrying, stone cutting, polishing and
sandblasting.
Phagocytosis of crystalline silica
in the lung triggers an inflammatory cascade with subsequent fibrosis. Impairment of lung function
increases with disease progression,
even after the patient is no longer
being exposed. The cumulative dose
of silica is the most important factor that predicts the development of
silicosis.
On X-ray in simple silicosis,
there are small round opacities,
often symmetrically distributed
with upper-zone predominance and
associated calcification of lymph
nodes. Lung function abnormalities
are uncommon in early disease. In
progressive massive fibrosis (figure 6), opacities larger than 1cm
develop due to coalescing of small
nodules with development of fibrosis and worsening lung function.
Mycobacterial diseases, COPD,
Kaplan’s syndrome (silica nodules
with fibrosis in rheumatoid arthritis patients) and lung cancer are
associated with silica dust exposure. Meta-analyses of cancer risk
in silicosis sufferers show a significant increase, but the effect of silica
exposure on lung cancer is weak
and variable in workers who do
not have silicosis. Silicosis is becoming less common in industrialised
nations through aggressive measures to control airborne dust in the
workplace, but is still a major problem in many developing nations.
Coal workers’ pneumoconiosis
An occupational lung disease
caused by exposure to coal dust,
coal workers’ pneumoconiosis is
also known as ‘black lung disease’
with deposition of coal in the lung
parenchyma.
Simple coal workers’ pneumoconiosis is characterised by the
presence of upper lobe nodular
opacities that can develop into
progressive massive fibrosis with
restrictive impairment of lung func-
Figure 6: Progressive massive fibrosis in silicosis. High-resolution CT showing
bilateral upper lobe predominant large irregular rounded opacities, interlobular
septal thickening with fibrous parenchymal bands and ground glass pattern. It
also shows mediastinal and hilar lymphadenopathy with associated ‘eggshell’
calcification.
tion. The onset of disease is related
to the length and severity of exposure. Silica contamination increases
the pneumoconiosis risk and consequently in some coalminers, pneumoconiosis may represent a mixed
picture of coal pneumoconiosis and
silicosis. Coal workers’ pneumoconiosis can also result in airway
obstruction with focal emphysema
due to small airway inflammation.
The prevalence and mortality rates
from coal workers’ pneumoconiosis
are declining in most industrialised
countries including Australia as a
result of tightened industrial regulations.
Hypersensitivity pneumonitis
Hypersensitivity
pneumonitis
(extrinsic allergic alveolitis) is
a granulomatous disease of the
lungs caused by an immunological response to chronic inhalation
of organic dusts or chemicals, with
more than 300 aetiological agents
reported to date. Only a small proportion of those exposed develop
clinically significant hypersensitivity pneumonitis, although it may
progress to disabling or even fatal
end-stage lung disease. While oral
corticosteroids can improve the
symptoms and radiological appearance in the short term, the definitive
treatment is early recognition and
control of exposure.
Farmer’s lung is one of the most
common forms of hypersensitivity
pneumonitis. Cattle farming, bird
and poultry handling (bird fancier’s
lung), grain and flour processing
and lumber milling are some of the
occupations that are associated with
a risk of developing hypersensitivity
pneumonitis. While many causative agents have been recognised in
occupational dusts, most current
new cases arise from residential
exposure to pet birds (pigeons and
parakeets), contaminated humidifiers, and indoor moulds.
Occupational lung cancer
At least 12 substances found in the
workplace are classified as human
lung carcinogens. These include
asbestos, radon, diesel exhaust
fumes and certain metals such
as arsenic, cadmium, chromium,
beryllium and nickel (table 2, page
24). Occupational exposure is estimated to account for about 5% of
lung cancer in Australia, with most
of them being caused by asbestos.
Occupations and industries
that tend to be associated with an
increased risk of lung cancer include
mining and quarrying, asbestos production, metal industries,
shipbuilding, railroad equipment
manufacturing, gas production and
Assessment
History
A THOROUGH occupational and environmental history is the key in the assessment of potential occupational lung disease. The occupational history should be
documented in detail in chronological order for every
job the patient has ever held, irrespective of duration.
The history for each job should include
• Job title.
• Tasks undertaken/job processes.
• Exposures — type (chemical, gas, fumes, dust) and
level (mild, moderate, high), duration of exposure
(per day, per year).
• Availability and use of respiratory protection and
ventilation methods used.
Any environmental and domestic exposures associated with demolition or renovation should also be
inquired about along with the smoking history. A
thorough history is not only essential for an accurate
diagnosis but also plays an important role in the possible subsequent litigation process. Occupational hygienists can help with accurate assessment of the degree
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| Australian Doctor | 8 March 2013
of exposure (see Online resources, page 28).
A history of progressive shortness of breath, chronic
cough and other constitutional symptoms usually
accompanies the clinical presentation of occupational
lung disease. The transient presence of symptoms in
relation to the work environment is typical in occupational asthma.
Examination
The physical signs related to occupational disease
are minimal and generally unrevealing about specific
causes. The clinical findings include clubbing, inspiratory crackles and wheeze at times. Occasionally pleural effusion is detected clinically. A comprehensive
general physical examination, particularly involving
the cardiac system, remains important, looking for
evidence of advanced signs such as pulmonary hypertension and related cor pulmonale as well as evidence
of alternative differential diagnoses and assessment of
impairment (see Investigations, page 28).
cont’d page 28
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some areas of construction.
Occupational asthma
Occupational asthma is defined
as asthma caused by exposure to
agents encountered in the working environment in those without
pre-existing asthma. In developed
countries, occupational asthma is
the leading form of occupational
lung disease, having supplanted
lung disease related to dust. An
estimated 15% of newly diagnosed cases of asthma in working adults are the consequence of
occupational exposures.
Occupational asthma can occur
as a new onset of asthma caused
by repeated low-level sensitising
exposure (asthma with latency, sensitiser-induced asthma) or asthma
that results from a single heavy
exposure to a potent respiratory
irritant such as chlorine or ammonia (asthma without latency, irritant asthma, or the reactive airways
dysfunction syndrome).
Spray painters (diisocyanatebased paints), bakers (flour), lumber industry workers (red cedar
dust) and cleaners work in some
of the highest risk occupations for
developing occupational asthma.
Most occupational asthma is associated with a latency period of hours
to months. Occupational asthma
should be considered in every case
of adult-onset asthma. Occupational asthma symptoms are identical to patients with asthma without
an occupational exposure.
Another type of work-related
asthma is aggravation of pre-existing asthma by the work environment (work-aggravated asthma).
In this situation, an individual with
pre-existing asthma who is exposed
to factors in the workplace such as
non-specific gases or fumes, smoke
or cold dry air may have an asthmatic attack precipitated by these
factors.
The detailed work history should
include all types of prior occupations and the specific duties that
were performed, the relationship
between the symptoms and the
workplace and any improvement in
symptoms when away from work,
particularly for extended periods
of time. The confirmation of occupational asthma should begin with
spirometry and peak expiratory
flow recordings to assess airflow
obstruction, its reversibility and
variability.
Reversible airflow obstruction
is a key feature in establishing the
diagnosis of asthma, but many asthmatic patients may have normal or
near-normal pulmonary function,
especially during non-exacerbation
periods or due to treatment. In this
instance, a methacholine challenge
test or comparable measure of nonspecific airway hyper-responsiveness (such as a Mannitol challenge
test) during a period of work exposure may help to establish the diagnosis of asthma.
The relationship of exposure
to work is usually confirmed by
serial peak flow measurements
performed at least four times a
day for a period of at least three
weeks at work and three weeks
away from work. Other tests that
can be performed in the assessment of sensitiser-induced occupational asthma include allergen
skin-prick testing and serum-specific IgE testing. Specific challenge
testing with the suspected agent is
not usually performed in Australia
but remains the gold standard of
diagnosis. The patients should not
be asked to leave work or change
their work practices until assessed
by a specialist respiratory physician and the diagnosis of occupational asthma is confirmed, as the
outcome has important medical,
public health, legal and financial
implications.
Workers with occupational
asthma should avoid all future
exposure to the sensitising agent.
This usually requires a change of
job, ideally within the same organisation to minimise hardship to the
worker. While occupational asthma
can resolve after these measures in
about 50% of cases, this is more
likely with earlier diagnosis and
removal from exposure.
Workers with irritant-induced
asthma caused by a single heavy
exposure, who are not sensitised,
can continue working with the
agent at low-level exposure. Treatment of occupational asthma is similar to that for usual asthma with
inhaled steroids and bronchodilators but significant improvement
can result with mere avoidance of
the respiratory irritant.
Investigations
Serum
TAKING an FBC and biochemistry
to exclude non-respiratory causes of
presenting symptoms should form an
early part of the investigative process.
Allergen-specific IgE can be useful in some forms of occupational
asthma (eg, animal house workers).
Precipitants to avian proteins, fungus and thermophilic actinomycetes
may be present in patients exposed to
organic dusts (eg, mouldy hay exposure leading to hypersensitivity pneumonitis) and should be requested in
the pathology.
The diagnostic value of soluble
mesothelin-related peptide is debatable. Currently it is more useful as a
marker for monitoring disease progression in mesothelioma at specialised clinical centres.
Radiology
Chest X-ray is a good screening test,
but provides insufficient detail for
Online resources
complete assessment. High-resolution CT scan of the chest provides
excellent identification of fibrosis,
nodules and ground glass opacities
associated with various occupational lung diseases. Images taken in
the prone position are important to
exclude innocent dependent changes
at the lung bases, which may masquerade as pulmonary fibrosis. A CT
scan of the chest is also important in
identifying pleural plaques — one of
the markers of asbestos exposure,
even when they are not calcified.
Pulmonary function tests
Spirometry is useful as a screening
test, particularly for the diagnosis of
early airway obstruction when FEV1/
forced vital capacity (FVC) is less
than 70%. Serial measurements may
be a simple method for monitoring
progression in fibrotic lung disease
generally with normal or increased
FEV1/FVC ratio.
Reduced lung volume measurements, both residual volume and
total lung capacity, in association
with a lowered carbon monoxide
diffusing capacity (DLCO) strongly
suggest a restrictive defect such as the
pulmonary fibrosis seen in asbestosis.
Serial peak flow measurements
provide evidence for variability in
airflow measurements as seen in
occupational asthma, particularly
when performed at home and at
work. Bronchial provocation testing with mannitol or methacholine
may be helpful in diagnosing occupational asthma. It is important that
this is performed while the patient is
exposed to the irritant.
Other tests
TB screening with Mantoux skin
testing in patients with silicosis is
recommended as there is strong evidence for an association between
silicosis and mycobacterial infection.
Cardiopulmonary exercise testing provides an objective measure
of the overall degree of functional
impairment. An assessment of cardiac function including pulmonary
pressures with an echocardiogram
may be useful in advanced interstitial lung diseases (asbestosis or
silicosis).
Bronchoscopy with bronchioalveloar lavage is rarely useful in
occupational lung diseases other
than in situations where an alternative diagnosis such as infection
needs to be excluded. Histopathological confirmation of the clinical diagnosis may occasionally be
necessary in some cases of occupational interstitial lung disease.
In general, fine-needle aspiration
biopsy or transbronchial lung
biopsy is insufficient for definitive
diagnosis and a larger tissue sample, which can be achieved thoracoscopically, is required.
Management
THERE is no specific management
currently available for most of the
occupational lung diseases.
Steroid therapy for occupational
asthma and hypersensitivity pneumonitis; and surgical intervention
in early occupational lung cancer
are some of the specific therapies
available. Supportive care with the
emphasis on primary and secondary prevention is the current treatment goal. Informing the patient of
the likely work-related nature of the
illness and the options for compensation will form part of the initial
management with formal assessment of functional impairment. For
current workers, further avoidance
of the exposure is paramount.
Patients with benign asbestosrelated conditions such as pleural
plaques can be reassured that no
regular follow-up required. The
management of patients with
asbestosis and other pneumoco-
nioses should focus on secondary
preventive measures including:
• Smoking cessation.
• Withdrawal from further exposure.
• Immunisation with pneumococcal and influenza vaccines.
• Optimal management of concurrent respiratory and other diseases.
• Supplemental oxygen when
resting hypoxaemia or exerciseinduced oxygen desaturations
occurs.
Regular monitoring with respiratory function tests and imaging
every 2-3 years or earlier is recommended with development of a
patient-specific management plan
for symptomatic patients.
Management of malignant mesothelioma is controversial, with no
standard approach currently available. The treatment may vary from
symptom control with pleurodesis
for recurrent malignant pleural
effusion and pain relief to radical
surgery or combined approaches.
No randomised control trials have
demonstrated a survival benefit
with surgical resection. A recent
pilot study in the UK (the MARS
trial), showed no survival benefits
but increased morbidity with surgery compared with non-surgical
approach.1 A palliative approach
with drainage of pleural effusions and systemic chemotherapy
with
a
cisplatin–pemetrexate
combination could be considered.
Molecularly targeted agents have
been trialled in mesothelioma
although additional clinical trials
are required to establish whether
these approaches will have a role
in patient management. Management of lung cancer and asthma
related to occupational exposure
is identical to the management in
general population.
Medicolegal aspects of
occupational lung disease
The medicolegal aspects of occupational lung diseases are complex. Workers compensation is
available through the state-based
WorkCover authorities, as in all
occupational diseases. Diagnosis is usually based on physician
assessment, and income support and retraining are usually
available to patients. NSW has a
specific scheme for asbestos- and
silica-related diseases administered by the Workers’ Compensation Dust Diseases Board.
Common law claims can also
be pursued, especially with
asbestos-related conditions, and
require referral to an appropriate legal representative. The fact
that an employer may no longer
exist does not preclude compensation, as insurers can usually be
located.
Author’s case studies
Case study 1: Mesothelioma
Mr MH was an 89-year-old retired
man, living with his wife. He presented with a three-month history of
increasing shortness of breath, rightsided pleuritic chest pain and a 10kg
weight loss. A CT chest showed a
small right-sided pleural effusion
with pleural plaques. He was a lifelong non-smoker.
Mr MH had had a variety of
occupations in the past but spent
over 30 years working in a power
station and had at least moderate asbestos exposure. Given the
clinical symptoms and the latency
of asbestos exposure, his presentation was very suspicious for a
malignant mesothelioma. Pleural
aspiration revealed an exudate
with no evidence of infection or
malignant cells. While other diagnoses such as primary lung cancer,
metastatic malignancy, infective
or an inflammatory effusion were
possibilities, the most likely diagnosis remained mesothelioma due
to the clinical presentation and
radiology. The possibility of a tho-
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| Australian Doctor | 8 March 2013
racoscopic procedure (eg, videoassisted thoracoscopic surgery)
with a pleural biopsy to obtain
tissue for definitive diagnosis and
to perform a pleurodesis to prevent recurrent pleural effusions
was discussed at length with the
patient. Given the small amount of
the fluid and the marked frailty of
the patient, it was decided that he
should be managed conservatively,
with symptom control, with a presumptive diagnosis of malignant
mesothelioma.
He was started on regular paracetamol and an opiate for pain relief
and was also started on a small dose
of prednisolone to improve his appetite and wellbeing. He was referred
to community palliative care services
for pain management and regular
follow-up. Mr MH’s family also
sought legal representation with the
view to seeking compensation.
He continued to deteriorate with
weight loss and generalised weakness accompanied by increasing
right-sided chest pain and worsening short of breath. A few months
later, he was admitted to hospital
because of significant clinical deterioration. He was managed palliatively and died five days later. A
post-mortem, requested by his family and performed for the purposes
of compensation, confirmed the
diagnosis of mesothelioma.
Discussion points
• A unilateral pleural effusion with
pleuritic pain and constitutional
symptoms in a patient with previous asbestos exposure is highly suspicious of mesothelioma, even with
negative cytology.
• Since surgical and other multimodality therapy in mesothelioma
has no clear survival advantage
with an overall median survival
of only 12 months, the pros and
cons of aggressive therapy vs
comfort care should be discussed
with the patient and next of kin
at diagnosis.
• Adequate analgesia with good
symptom control, early palliative
care referral and a claim for compensation are some of the key facwww.australiandoctor.com.au
US National Institute of
Occupational Safety and Health
Occupational Respiratory Disease
and Surveillance (information
on various occupational lung
diseases, its spread and its impact)
www.cdc.gov/niosh/topics/
surveillance/ords/
Workers’ Compensation Dust
Diseases Board of NSW
Provides a system of no-fault
compensation to people (and their
dependants) who have developed
a dust disease from occupational
exposure to dust as a worker in
NSW
www.ddb.nsw.gov.au
Asbestos Diseases Research
Institute
Aims to improve the prevention,
the diagnosis and treatment of
asbestos-related diseases
www.adri.org.au
Asbestos Diseases Society of SA
Provides counselling, support and
information to asbestos disease
victims in SA
www.adssa-inc.com.au
Australian Mesothelioma
Registry
Monitors all new cases of
mesothelioma diagnosed from
1 July 2010 in Australia
www.mesothelioma-australia.com
Asbestos Awareness
Describes why asbestos is
dangerous, where it can be found
in the home, how to remove it
safely, how to deal with it and how
to dispose of it
www.asbestosawareness.com.au
Safework Australia
Provides national codes of
practice and guidance notes and
reports by the Australian Safety
and Compensation Council on
mesothelioma
www.safeworkaustralia.gov.au
Australian Institute of
Occupational Hygienists
Information about occupational
hygiene and the profession of
occupational hygienist
www.aioh.org.au
tors in mesothelioma management.
Case study 2: Occupational
asthma
A 30-year-old male with no past
history of asthma began working
several years ago as a glazier in a
firm manufacturing windows and
doors. His work took place in a single shared open-plan factory. Wood
machining, wood joinery and glazing
were carried out in adjoining areas.
His job involved cutting glass and
placing glass in windows and doors.
Almost all the wood used in the factory was Western red cedar.
Within 12 months of starting
work he developed rhinitis and dermatitis. Eight years later, he noticed
the gradual onset of cough and chest
tightness. His GP diagnosed asthma
and started him on beclomethasone
and salbutamol. He left his job as he
felt his asthma was work-related and
worked as a courier for a few years.
During this time, he was able to stop
all asthma medications owing to a
lack of asthma symptoms.
cont’d page 30
Reference
1. Treasure T, et al. Extra-pleural
pneumonectomy versus no
extra-pleural pneumonectomy for
patients with malignant pleural
mesothelioma: clinical outcomes
of the Mesothelioma and Radical Surgery (MARS) randomised
feasibility study. Lancet Oncology
2011; 12:763-72.
Further reading
Available on request from
[email protected]
How To TREAT Occupational lung diseases
Figure 7: Serial peak flow readings of 30-year-old male working in a window
and door factory.
SERIAL PEFR
700.0
Maximum
Mean
Minimum
Working
650.0
600.0
550.0
PEFR
from page 28
Some years later, he recommenced
work as a glazier in the same factory as before. Within one month
it became necessary for him to start
taking his asthma medications again
because of symptom recurrence. His
asthma has persisted since and has
become worse in the past year. He
has had two exacerbations of asthma
in the past 12 months requiring
courses of prednisolone. There have
been no spills or accidents at work to
suggest irritant asthma. He is an exsmoker with five pack-year history.
His examination was unremarkable and his baseline spirometry was
normal. He had evidence of nonspecific bronchial hyper-responsiveness with a positive methacholine
challenge. He monitored his serial
peak flows and the results are shown
in figure 7. There was a significant
deterioration in his peak flows at the
start of the working week, with an
improvement on weekends.
A diagnosis of occupational
asthma due to Western red cedar
was made. He was moved to another
500.0
450.0
400.0
350.0
08
08
08
08
08
08
08
08
08
/20
/20
/20
/20
/20
/20
/20
/20
/20
/01
/01
/01
/02
/01
/02
/02
/03
/02
4
7
1
1
8
4
8
1
5
1
0
2
1
2
1
2
Date
part of the factory with no exposure
to Western red cedar and now has no
asthma symptoms, is on no medications and has a normal methacholine
challenge.
Discussion points
• New asthma in a working person
requires documentation of a careful occupational history.
• Occupational exposure to a known
How to Treat Quiz
Occupational lung diseases
— 8 March 2013
1. Which THREE statements are correct
regarding occupational lung disease?
a) It is important to consider occupational lung
disease in any current or retired worker with
respiratory symptoms
b) The upper airways are never affected by
occupational exposure to inhaled irritants
c) Awareness of the latency between exposure
and onset of symptoms is extremely important
in consideration of occupational lung disease
d) A clear causal relationship needs to be
established before attributing the cause
of a patient’s respiratory symptoms to
occupational exposure
2. Which TWO statements are correct
regarding asbestos fibres?
a) Asbestos is a man-made fibre that has been
in use only since the early 1950s
b) Asbestos production ended in Australia
in 1987 and the importation of asbestos
products was completely banned in 2003
c) Serpentine fibres are known as chrysotile
or ‘white asbestos’, while amosite (‘brown
asbestos’) and crocidolite (‘blue asbestos’),
are both amphiboles
d) Blue asbestos, or crocidolite, is a benign
form of asbestos fibre, in contrast to white
asbestos, or chrysotile
3. Which THREE statements regarding
asbestos exposure are correct?
a) Occupational exposure to asbestos is
limited to those involved in asbestos product
manufacture
b) Exposure to asbestos is quantified in terms of
the concentration of inhaled fibres (fibres/mL).
Cumulative exposure is expressed in fibre/mL/
years, similar to the pack-year measurement
for smoking
c) Asbestiform fibres also occur naturally in
cause of occupational asthma, such
as Western red cedar, increases the
likelihood of the diagnosis of occupational asthma.
• Work-related symptoms including rhinitis and dermatitis followed by asthma symptoms are
suggestive of occupational sensitisation. It may take months to
several years before the onset of
asthma symptoms.
•E
vidence of a relationship
between lung function and
attendance at work, with documentation of peak flow measurements, confirms the diagnosis of
occupational asthma and should
be performed before advising a
worker to stop exposure.
•E
vidence of reversible airway
obstruction on spirometry is
very specific for a diagnosis of
occupational asthma while nonspecific bronchial hyper-responsiveness may be helpful when
spirometry is normal with high
clinical suspicion.
•F
urther exposure to the sensitising agent needs to be avoided.
Summary
Occupation-related lung diseases
are common despite workplace
regulations and increased
awareness
A thorough occupational history
is crucial in identifying any workrelated lung conditions
Finding a clear temporal relationship
between symptoms and exposure
is useful, but be aware that current
exposures do not always lead to
immediate symptoms
An occupational agent is a common
culprit in adult-onset asthma and is
under-diagnosed as a result of the
failure to associate symptoms and
work.
Early referral to a respiratory
physician is recommended if there
are ongoing respiratory symptoms
in a patient with occupational
exposure.
Avoidance of exposure to the
causative agent is the main
management strategy to reduce
further lung impairment.
Instructions
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areas where other minerals, such as gold
and iron ore, have been exploited, with a
consequent risk of significant lung disease to
miners
d) Currently, the main sources of exposure to
asbestos fibres are old buildings undergoing
renovation or demolition
4. Which THREE statements regarding benign
pleural disease are correct?
a) Benign plural plaques are deposits of
hyalinised collagen fibres on the parietal
pleura
b) Benign pleural plaques require regular followup with imaging
c) Pleural adhesions due to asbestos-related
pleural inflammation appear as a rounded lung
mass on imaging and often require a biopsy to
exclude malignancy
d) Diffuse pleural thickening generally begins as
fibrosis of the visceral pleura with secondary
thickening of the parietal pleura
5. Which TWO statements regarding
asbestosis are correct?
a) Asbestosis is the correct term to describe all
asbestos-related disease affecting the lung
and pleura
b) Many patients who develop asbestosis are
asymptomatic for at least 20-30 years after
the initial exposure
c) Productive cough and wheeze are rare in
patients suffering from asbestosis
d) Chest X-ray is the gold standard for detection
of asbestosis
6. Which TWO statements are correct
regarding mesothelioma?
a) Malignant mesothelioma has a median
survival of three years from diagnosis
b) Mesothelioma may occur with very-low-
level asbestos exposure occasioned by
activities such as washing the clothes of
someone working in an asbestos-related work
environment
c) The most common CT findings are pleural
thickening (92%), pleural effusion (74%) and
contraction of a hemithorax
d) Diagnosis of mesothelioma can be definitively
established using the serum tumour markers
mesothelin and osteopontin
7. Which THREE statements regarding
silicosis and hypersensitivity pneumonitis
are correct?
a) The mechanism causing silicosis from
inhalation of free crystalline silica is
phagocytosis of the crystalline silica in the
lung, which triggers an inflammatory cascade,
with subsequent fibrosis
b) Short-term occupational exposure to silica
can cause silicosis
c) Hypersensitivity pneumonitis (extrinsic allergic
alveoli) is a granulomatous disease of the
lungs caused by an immunological response
to chronic inhalation of organic dusts or
chemicals
d) Cattle farming, bird and poultry handling (bird
fancier’s lung), grain and flour processing and
lumber milling are some of the occupations
that are associated with a risk of developing
hypersensitivity pneumonitis
8. Which TWO statements are correct
regarding occupational asthma?
a) Occupational asthma is defined as asthma
caused by exposure to agents encountered in
the working environment in workers without
pre-existing asthma
b) An estimated 2% of newly diagnosed
cases of asthma in working adults are the
consequence of occupational exposures
c) The relationship of exposure at work is usually
confirmed by serial peak flow measurements
performed at least four times a day for a
period of at least three weeks at work and
three weeks away from work
d) Frequent doses of oral corticosteroids is the
standard treatment for occupational asthma
9. Which TWO statements regarding
assessment of patients with occupational
lung disease are correct?
a) Identification of the multitude of clinical signs
that develop as a result of occupational lung
disease is essential to diagnosis
b) Industrial hygienists can help with accurate
assessment of the degree of exposure
c) Soluble mesothelin-related peptide is currently
useful as a marker for monitoring disease
progression in mesothelioma at specialised
clinical centres
d) Bronchoscopy with bronchioalveloar lavage is
an important investigation in the diagnosis of
occupational lung disease
10. Which TWO statements regarding
treatment and compensation of
occupational lung disease are correct?
a) Secondary preventive measures for patients
with asbestosis and pneumoconiosis include
smoking cessation, withdrawal from exposure,
and immunisation with pneumococcal and
influenza vaccines
b) Surgical treatment of mesothelioma has
demonstrated survival benefits
c) NSW has a specific compensation scheme
for asbestos- and silica-related diseases
administered by the Workers’ Compensation
Dust Diseases Board
d) Compensation for occupational lung disease
is impossible to obtain if the employer no
longer exists
CPD QUIZ UPDATE
The RACGP requires that a brief GP evaluation form be completed with every quiz to obtain category 2 CPD or PDP points for the 2011-13 triennium. You can
complete this online along with the quiz at www.australiandoctor.com.au. Because this is a requirement, we are no longer able to accept the quiz by post or
fax. However, we have included the quiz questions here for those who like to prepare the answers before completing the quiz online.
how to treat Editor: Dr Barbara Tink
Email: [email protected]
Next week Non-alcoholic fatty liver disease is emerging as the most common cause of liver disease worldwide, despite its being hard to diagnose and having only an estimated true incidence. It is
physiologically linked to insulin resistance and is the hepatic manifestation of the metabolic syndrome. The next How to Treat aims to build awareness of this condition, focusing on its pathogenesis,
diagnosis and management. The author is Dr Leah Gellert, consultant gastroenterologist and hepatologist, Bondi Junction, NSW.
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| Australian Doctor | 8 March 2013
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