Download Managing work-aggravated asthma

WORK-RELATED ASTHMA
Spo Kgalamono
WRA is common
 Most common OLD in high income countries
 Recent evidence - WRA accounts for up to 1 in 4 new cases (25%) of
adult asthma ( a 4-fold increase in 3 decades)
 Now probably the commonest in SA
 Newer agents being identified
 While the number of agents causing OA is increasing, the major
causes remain the same (wheat, isocyanates, wood dusts, etc)
 Under-reporting and under identification still persist

Sherwood Burge. Recent developments in occupational asthma. 2010

Asthma in the Workplace textbook
NIOH Cases 2015 /2016
Rhinitis
9%
Obstructive
Airway
Diseases
Other dieases
33%
OA
32%
58%
COPD
26%
Evolving
Classification of WRA
Latent period
Allergic (sensitizer)
Occupational asthma
Caused

Typically without latent period
RADS and not-so-sudden
(low-dose IIA)
Work-related asthma
Work exacerbated
Pre-existing or coincidental, triggered nonspecifically
These groups are not mutually exclusive. OA can be followed by WEA
Occupational asthma
Definition
“Occupational asthma is a form of work-related
asthma characterized by variable airflow obstruction,
airway hyperresponsiveness, and airway
inflammation attributable to a particular exposure in
the workplace and not due to stimuli encountered
outside the workplace”
Bernstein IL et al. Asthma in the workplace, 2006.
Exposure in the
workplace
Irritants
high levels
allergens/sensitizers
Sensitization
• IgE-dependent
• IgE-independent
OCCUPATIONAL ASTHMA
Immunologic
Occupational asthma
Caused
Irritant-induced
Work-related asthma
Work exacerbated
Pre-existing or coincidental, triggered nonspecifically
Case of immunologic occ asthma
40 year old male
Spray painter for the past 8
years.
No history of childhood asthma
Makeshift Booth – inadequate
ventilation.
Respirator – cartridges not
changed regularly
Now asthma symptoms . Better
away from work. Worse from
Wednesday onwards.
Natural history
Common Sensitizers
(Incomplete List!)
Low MW
 Isocyanates
 Anhydrides
 Metal salts
 Epoxy resins
 Fluxes
 Persulfate
 Aldehydes
High MW
 Pharmaceuticals
 Animal proteins
 Latex
 Cereals
 Seafood
 Proteolytic enzymes
Some newly established causes
 Diesel – irritant. Also acts as an adjuvant for sensitisation to
aeroallergens. Cases of OA wit latency have been described in bus garage
workers where diesel exhaust was the most likely cause
 Cleaning materials – some may be sensitizers
(ammonium compounds, sodium hypochlorite, wax- removing substances ethanolamines )
 Cobalt (diamond polishing, drill bits – hard metal, metal-working fluids)
 Cosmetic products – (Argan powder)
Occupational Asthma – sensitizer induced
 Characterised by work-related asthma appearing after a latency
period
 Caused by most high- and certain low-molecular weight agents
 After sensitization, low levels may cause symptoms /
anaphylaxis
 Sensitization increases with continued exposure
 If IgE mediated, may correlate with immunological tests
 Circular Instruction 176 - COID
Factors modifying risk for sensitizer
induced Occupational Asthma
 Industrial factors
 Nature of occupational agent
 Molecular weight, reactivity
 Level of exposure (spills, etc)
 Duration of exposure

Host factors
 Atopy – atopic ind more likely to develop asthma
 Genetic susceptibility - Limited studies in terms of what genes
exactly are implicated
 Occupational rhinitis and conjunctivitis – upper and lower airways
share a common and possibly interconnected inflammatory
process - united airways
 Cigarette smoking in some
Immunologic
Occupational asthma
Caused
Irritant-induced
Work-related asthma
Work exacerbated
Pre-existing or coincidental, triggered nonspecifically
Irritant-Induced Asthma (IIA)
 RADS – OA without latency
OR non-immunological OA
that occurs after a single high
level exposure to irritants
 ACCP recommends inclusion
of “Not-so-sudden IIA”
(repeated low dose exposure
to irritants) as part of IIA
 Clinical classification of IIA is
proposed
EAACI position paper: irritant‐induced asthma
Allergy. Volume 69, Issue 9, pages 1141-1153, 4 JUL 2014 DOI: 10.1111/all.12448
Reactive Airways Dysfunction Syndrome
(RADS) Circular Instruction 177 - COID
 No previous history of asthma
 Acute, high level exposure to toxic/irritant
 Respiratory symptoms within 24 hrs of exposure
 Pulmonary function showing reversible obstruction or positive
non-specific bronchial hyperactivity (methacholine challenge test)
 Persistent respiratory symptoms and bronchial hyperreactivity for
at least 3 months
Latent period
Allergic
Occupational asthma
Caused by work
Without latent
Irritant-induced RADS
Chronic low exposure
Work-related asthma
Work exacerbated
Pre-existing or coincidental, triggered nonspecifically
Case
32 year old man.
18 months photocopier in
poorly ventilated room.
Fugitive ammonia exposure
from factory floor. No
sensitizers.
Asthma from high school.
Well controlled until a year
ago.
Now triggered by ammonia
and photocopying; in past 6
months two emergency
room treatments, increased
medication and 8 days sick
absence. Better on holiday.
Lung function test
Work-exacerbated asthma
 Very common
 Worsening of pre-existing asthma (not necessarily
occupational) due to causes and conditions
attributable to a particular occupational
environment and not to stimuli encountered
outside the workplace
 Aggravation is typically due to an occupational
irritant but can be due to allergens
Work-aggravated asthma
Instruction 118 - COID
 Medical history indicating pre-existing asthma
 Presence of workplace exposures (cold air, strenuous
work, dust, etc) associated with onset of asthma or
worsening symptoms
 Increase in symptoms or medication requirements or
work-related changes in PEFR
 Pulmonary function showing reversible obstruction or
positive non-specific bronchial hyperactivity
(methacholine challenge test)
Evaluation of work-related asthma
• Diagnosis
• Two basic questions
• First, does the patient have asthma?
• Is the asthma caused or exacerbated by the
work place, or by some other explanation
Diagnosis
 Asthma – objective evidence. History important
 Exposure to an established cause
 Chronological relation with work
 After 1st exposure
 Symptoms/airflow/airway responsiveness worse at
work, better away
 Immediate, late, dual
 Challenge testing before and after work
 Serial peak flow measurements - OASYS
Established cause
Serial Peak flow measurements 2 hourly – at least 4X a day
several weeks on and off work
Challenges:
Literacy level
Fabrication of results
Consistency – days away from work
 The OASYS system developed by Burge is freely
available www.occupationalasthma.com
Supporting evidence
 Tests of sensitization
 Specific IgE
 (Total IgE not useful – waste of money)
 Specific skin prick tests
Tests of sensitization -SPT
 Demonstrates an allergic
response to a specific
allergen. In conjunction
with hx and exam, SPT can
help confirm presence of
allergy
Alternative explanations for asthma
 Upper respiratory infection at onset of symptoms
 COPD – could this explain the sx
 Smoking
 Medications (beta blockers, NSAIDs) – can precipitate
asthma and drug abuse (heroin, cocaine can cause
asthma exacerbations)
 Gastro-0esophageal reflux symptoms
Management of WRA
 Prevent /Reduce / avoid exposure in workplace
 Once asthmatic – Removal from exposure , particularly if
sensitizer still present
 Surveillance measures:
 Periodic monitoring of work place exposures, questionnaires,
spirometry, tests of sensitization
 Medications – ICS mainstay
 Address any non-occupational factors
Workplace considerations

Respirator use
 Does the job require use of a respirator?
 Is the employee comfortable?

Heavy physical work?

Access to care?
(e.g. severe and underground)
ATS Respiratory Protection Guidelines. Am J
Crit Care Med 1996;154:1153-1165
Occupational asthma prognosis
 Prognosis worse if:
 longer duration of exposure,
 greater severity / frequency of symptoms

“Early initiation of inhaled steroids yielded greater improvement than later
initiation”
Nicholson et al. OEM. 2005; 62: 290 -9
 Timely removal should result in improvement – in rare cases resolution
of asthma
 Restriction from exposure or removal from the job often has significant
socioeconomic consequences:
 Loss of income
 Unemployment
 Higher medication costs in those remaining in exposure

Be reasonably sure of the diagnosis and cause of OA before
recommending job change
New entity – Asthma COPD
Overlap Syndrome (ACOS)
 Are asthma and COPD a continuum of the same disease?
 Clinical distinction between severe asthma and COPD is often
difficult
 Although majority of asthmatics will have reversible airway
obstruction, a segment of patients can have severe lung
function compromise that looks like COPD
 In many patients features of both are seen – ‘’overlap
syndrome” is increasingly being recognised
 Up to 50% of older patients with obstructive airway disease can
be classified as having overlap syndrome (cross between
asthma and COPD)
Key messages
 Physiologic confirmation of OA is important but remains
challenging
 Integrated management of allergic rhinitis and asthma highly
recommended
 Early diagnosis, management and removal from exposure
improves prognosis
 Prevention is key
 All types of OA are compensable in SA
 NB: Review literature regularly for updates
Acknowledgment
 Prof D. Rees
 NIOH Clinic patients
Latest updates on OA
www.occupationalasthma.com
Current guidelines and
consensus statements
 Canadian Thoracic Society
 BOHRF
 ACCP
 EAACI
Watch out for the red flags!!!!
Causes of High IgE
 Atopy
 Parasitic infections
 Auto-immune diseases
 Malignancy
 Air pollution(cigarette, diesel) stimulate the
production of IgE without initiating
sensitisation
 Some sensitizers may also be irritants: TDI
Asthma
in the workplace
Occupational Asthma
(caused by
the workplace)
Sensitizer–induced
OA (with latency)
Work exacerbated
Asthma
(pre-existing, coincidental,
triggered non-specifically
Irritant–induced OA
• Acute (RADS)
• Chronic low- dose
EAACI position paper: irritant induced asthma: Allergy 69 (2014) 1141 - 1153