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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
Other dieases33%
Rhinitis9%
OA32%
COPD26%
Obstructive Airway
Diseases
58%
NIOH Cases 2015 /2016
Evolving
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 non-
specifically
Classification of WRA
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.
OCCUPATIONAL ASTHMA
Sensitization
• IgE-dependent
• IgE-independent
Exposure in the
workplace
allergens/sensitizers
Irritants high levels
Immunologic
Occupational asthma
Caused
Irritant-induced
Work-related asthma
Work exacerbated
Pre-existing or coincidental, triggered non-
specifically
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 latencyperiod
▪ 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 non-
specifically
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 non-
specifically
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
Case
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 asthmaInstruction 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
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
Asthmain the workplace
Occupational Asthma(caused by
the workplace)
Work exacerbated Asthma
(pre-existing, coincidental, triggered non-specifically
Sensitizer–inducedOA (with latency)
Irritant–induced OA • Acute (RADS)
• Chronic low- dose
EAACI position paper: irritant induced asthma: Allergy 69 (2014) 1141 - 1153
