Guidelines for the
management of
work-related
asthma
ERS TASK FORCE REPORT
Eur Respir J 2012;39:529-545
OCCUPATIONAL EXPOSURE
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Pneumoconiosis
Work-related asthma
Work-related COPD
Work-related infections
Work-related rhinitis
Mr AD: 32 years
platinum mine worker
Working underground since 2011
Jan 2012: Chest tightness
Rx: Asthavent and TB treatment for 7
months
Smoker for 3 years; quit Jan 2012
Always using dust mask and ‘respirator’
since Aug 2012
3 Jan 2013: serious ‘asthma attack’ and
referred to specialist but no asthma
found
No known allergies or asthma symptoms
before / no family history of asthma
Pre: Post %Chng
FEV1: 78%
90%
15%
RV: 147 %
Raw: 206 %
Skintest: House dust mite 4+
IgE: 504 (N= 0-22)
MELISA platinum LPT : 1 (neg)
Dx: Work-related asthma
ERS TASK FORCE REPORT
Guidelines for the management of work-related asthma
Work-aggravated asthma
Worsening of pre-existing
asthma due to causes and
conditions attributable to a
particular occupational
environment and not to
stimuli encountered outside
the workplace
Worker has a concurrent
history of asthma that was
not induced by an exposure
in the workplace
Aggravation is typically due
to an occupational irritant
Some workers may, after a
latent period, experience
worsening of asthma with
regular daily exposure to
agents that can cause IgEmediated allergies in others
Mr TN: 27 years
chrome mine worker
Underground 2006 until 2012
May 2012: Dyspnoea/wheezing
Rx: LABA/ICS
Dyspnoea improve but still severe
dyspnoea during running (+/- 200 m)
No allergies or asthma symptoms
before/ No family history of asthma
Pre
Post %change
FEV1: 65%
80%
22%
RV: 206%
Raw: 286%
Skin test: grass 4+ maize 3+ feathers 2+
IgE: 1189 (N= 0-22)
Rx: Prednisone, LABA/ICS, Venteze,
Loratadine
Dx: Work-related asthma
Occupational asthma
Occupational asthma is a
disease characterised by
variable airflow limitation
and/or hyperresponsiveness
associated with
inflammation due to causes
and conditions attributable
to a particular occupational
environment and not to
stimuli encountered outside
the workplace
• IgE-mediated asthma
after a latency period
• Irritant asthma with or
without a latency period,
including reactive
airways dysfunction
syndrome (RADS) which
results from high
exposure
• Asthma due to a specific
occupational agent with
unknown pathomechanism
Mr JJ: 49 years
Vanadium mine worker
Non smoker
Work in production unit / very dusty
No dyspnoea at rest / mild cough
Dyspnoea with moderate exercise
Allergies: trees 3+ wheat 3+ maize 2+
Pre Post
%change
FEV1: 35% 41%
18%
RV:
334%
Raw: 126%
Diffusion: 75%
Dx: 1. Work-related asthma
2. Work-related COPD
Work-related COPD
Welding fumes
Isocyanates
Potroom
Aluminium
Cadmium
Metals
Ammonia
Tobacco smoke
Wood dust
Cotton
Endotoxin
Vanadium
Coal dust
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Potential causes of OA
Can also cause COPD without any
acute symptoms to suggest asthma
Some workers with symptoms
suggestive of OA develop
predominantly fixed airway
obstruction more suggestive of COPD
Some of these may improve over
long periods away from exposure,
but some do not
The pathology of these workers
developing predominantly fixed
airway obstruction is unknown
Symptoms in asthmatics that do not
improve during weekends or holidays
may indicate a progressive course
typical of COPD
Some overlap between OA and COPD
Key questions of the guidelines for the
management of work-related asthma
• Key question1: How are work-related asthma cases
diagnosed and how should they be diagnosed ?
• Key question 2: What are the risk factors (host and
exposure) for a bad outcome ?
• Key question 3: What is the outcome of different
management options in subjects who are already
affected ?
Key question 1:
Diagnosing work-related
asthma
1. Tests that separate asthma from normality or
other lung diseases
2. Tests that identify the workplace as the
cause of respiratory symptoms
3. Tests that identify the agent causing workrelated asthma
Tests that separate asthma from
normality or other lung diseases
• Spirometry and tests for
reversibility
• Increased diurnal variation
in PEF
• Sputum eosinophilia
• Exhaled nitric oxide
Tests may all be normal in
individuals with
occupational asthma
confirmed with specific
challenge tests
No measure of lung
function or inflammatory
marker is sufficiently
sensitive to be used to
exclude occupational
asthma suggested by
history
Tests that identify the workplace as
the cause of respiratory symptoms
• Screening questionnaires for
respiratory symptoms
• Serial peak flow measurements
• Pre- to post-shift changes in
lung function
• Changes in NSBHR at and away
from work
PEF: minimum criteria
are >3 weeks of usual
work exposure with
measurement at least
4x/day; or 8 work
days and 3 rest days
with 2-hourly
measurements
Pre- and post-shift
measurements of
FEV1 and changes in
NSBHR after a twoweek removal from
work are less sensitive
and less specific
Tests that identify the agent causing workrelated asthma
• Specific IgE
• Skin-prick
measurements
• Specific inhalation
challenge (SIC)
Both skin-prick and specific IgE are
highly sensitive for detecting type 1
sensitisation and occupational
asthma caused by most high
molecular weight agents but are not
specific for diagnosing occupational
asthma
Carefully controlled SIC tests come
closest to a gold standard test for
many agents causing occupational
asthma
A negative SIC test in a worker with
otherwise good evidence of
occupational asthma is not to
exclude the diagnosis
Specific inhalation challenge
Platinum salts:
-specific
-safe but late reactions possible
-performed in a clinical setting
where emergencies can be
treated adequately
-sensitivity higher than that of
skin prick tests
-workers with a systemic reaction
in skin tests and with obstructive
airway disease should not be
tested
Bronchial hyper reactivity to
metacholine is of little value
for a prediction of the
reaction in bronchial
provocation tests
Does not correlate with skin
and bronchial reactivity to
platinum salts
Consequences of occupational asthma
development for the individual worker
Degree of proof
required depends
on the
consequences of
OA development
for the individual
worker
• If the worker is likely to lose
his job OA should be
confirmed physiologically and
the specific agent causing the
OA should be identified
• If it is possible to relocate the
worker away from exposure
without loss of income, a
precise diagnosis is less
important
• Criteria for legal compensation
vary between different
administrations and different
countries
Key question 2:
What are the risk factors
(host and exposure) for a
bad outcome
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Lungfunction
Duration of exposure
Atopic status
Smoking status
Gender
Age
Agent
SIC pattern
• Lower lung volumes, higher NSBHR,
or a stronger asthmatic response to
SIC at diagnosis are risk factors for a
bad OA outcome
• Longer symptomatic exposure
relates to a worse OA outcome
• No relationship between atopy and
OA outcome
• Smoking at time of diagnosis not
related to OA outcome
• Data consider gender in OA
outcome is contradictory
• Older age is associated with poorer
OA prognosis
• HMW agents seem to cause longer
duration of BHR compared with
LMW
Key question 3:
Outcome of different
management options in
subjects who are already
affected
• Persistent exposure
• Pharmacological
treatment
• Complete avoidance
of exposure
• Relocation
• Personal protective
equipment
• Persistent exposure to the causal
agent is more likely to be associated
with asthma and NSBHR persistence,
as well as an accelerated decline in
FEV1, compared with complete
avoidance of exposure
• Insufficient evidence that Rx with
ICS/LABA is able to prevent the longterm deterioration of asthma in
subjects who remain exposed to the
agent causing OA
• Substantial long-term morbidity as
complete avoidance of exposure to
the causal agent results in symptom
recovery and resolution of NSBHR in
less than 33% of affected people
Key question 3:
Outcome of different
management options in
subjects who are already
affected
• Persistent exposure
• Pharmacological
treatment
• Complete avoidance of
exposure
• Relocation
• Personal protective
equipment
• Reduction of exposure to
the causal agent can lead to
improvement or resolution
of symptoms and NSBHR
but is less beneficial than
cessation of exposure
• Personal respiratory
equipment can result in an
improvement but not a
complete suppression of
respiratory symptoms and
airway obstruction in the
short-term
Recommendations (1)
1. Occupational asthma should be confirmed by objective
physiological tests and in cases of allergic pathogenesis by
immunological tests (S/H)
2. All adults with new, recurrent or deteriorating symptoms of
asthma, COPD or rhinitis should be asked about their job,
materials with which they work and whether they improve when
away from work (S/H)
3. Health practitioners should consider that early recognition and
diagnosis of work-related asthma is recommended as a shorter
symptomatic period after diagnosis is associated with a better
outcome (S/H)
4. Smoking habit and atopy should not be taken into account when
assessing the prognosis for medical legal purposes (S/M)
Recommendations (2)
1. Patients, physicians and employers should be informed that
persistence of exposure to the causal agent is likely to result in a
deterioration of asthma symptoms and airway obstruction (S/M)
2. Patients and their attending physicians should be aware that
complete avoidance of exposure is associated with the highest
probability of improvement but may not lead to a complete
recovery from asthma (S/M)
3. The use of respiratory protective equipment should not be
regarded as a save approach, especially in the long-term and in
patients with severe asthma (S/L)
4. Anti-asthma medications should not be regarded as a reasonable
alternative to environmental interventions (S/VL)