A description of Work related asthma, Occupational Asthma and Work exacerbated asthma References: Murray and Nadel's Textbook of Respiratory Medicine American College of Chest Physicians 2008 Consensus Statement Hope you find it useful.

1. Occupational Asthma
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4. Does history of childhood
asthma exclude Oa?

5. ACCP
 “De novo asthma or the recurrence of
previously quiescent asthma (i.e., asthma as a
child or in the distant past that has been in
remission) induced by either sensitization to a
specific substance or a chemical, at work,
which is termed sensitizer-induced OA, or by
exposure to an inhaled irritant at work, which
is termed irritant- induced OA”
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6. Overview
 Up to 25% of all adult asthma cases
maybe work-related asthma
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7.  Work-exacerbated asthma:Work-exacerbated asthma:
– Exacerbation of preexisting asthma due toExacerbation of preexisting asthma due to
non-specific irritants encountered at worknon-specific irritants encountered at work
 Occupational asthma:Occupational asthma:
– New-onset asthma’ from workplaceNew-onset asthma’ from workplace
exposure to sensitizers and/or irritantsexposure to sensitizers and/or irritants
Types of WRA
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8. Types of Occupational Asthma
 Sensitizer-induced OA
 HMW sensitizers
 LMW sensitizers
 Irritant-induced OA (non-immunologic)
 Reactive airways dysfunction syndrome (RADS)
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9.  Asthma like disordersAsthma like disorders ( OTDs)( OTDs)
– vegetable dust ,animal confinementvegetable dust ,animal confinement
buildingbuilding
– associated with systemic symptomsassociated with systemic symptoms
– no latency periodsno latency periods
– neutrophilic airway inflammationneutrophilic airway inflammation
 Eosinophillic bronchitisEosinophillic bronchitis
– develop chronic airway obstructiondevelop chronic airway obstruction
ORGANIC TOXIC DUST SYNDROME
Asthma like disorders
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11. Things that may initiate an asthma attackThings that may initiate an asthma attack
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12. Airway
Remodeling
Symptoms
Smooth Muscle
Dysfunction
Airway
Inflammation
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13. INFLAMMATIONINFLAMMATION
Airflow Limitation
SYMPTOMS
Cough Wheeze
Dyspnoea
TRIGGERS
Allergens, Exercise,
Cold Air, SO2 Particulates
Airway
Hyperresponsiveness
INDUCERS
Allergens, Chemical sensitizers,
Air pollutants,
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15. Sensitizer Occupational
Asthma
 sensitization to a specific chemical agent in the
workplace over a period of time
 (>80%) of cases of occupational asthma
 latency period
 specific antigen
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17. Common Sensitizers
High MW
 Animals
 Latex
 Flour
 Enzymes
 HMW Agents
 Organic proteins/
polysaccharides
 Type-I Hypersensitivity
 Atopy
 IgE antibodies
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20. Low MWLow MW
• IsocyanatesIsocyanates
• PersulfatePersulfate
• AldehydesAldehydes
• MetalsMetals
• Wood dustsWood dusts
Common Sensitizers
 LMW Agents(< 5Kd)
 Too small to be complete
allergens
 Immunologic mechanism-
Cell Mediated reactions
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24.  What is the most important environmental risk
factor for the development of OA?
 Intensity of exposure
 Cigarette smoking
 Genetic susceptibility
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25. Risk Factors
 Environmental Factors
 Host related factors
 Occupational Rhinitis
 Atopy
 Pre exposure sensitisation
 Genetic
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26. Irritant induced
OCCUPATIONAl asthma

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28.  Single, very high exposureSingle, very high exposure
 Not related to the immune system.Not related to the immune system.
 Airways hyperactivity + irritant exposureAirways hyperactivity + irritant exposure
 May be induced by any irritating exposureMay be induced by any irritating exposure
 Provoke epithelial cell damage and persistentProvoke epithelial cell damage and persistent
inflammatory response and airway remodelinginflammatory response and airway remodeling
Irritant Induced OccupationalIrritant Induced Occupational
AsthmaAsthma
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29.  History of intolerance to second-handHistory of intolerance to second-hand
tobacco smoketobacco smoke
 Some irritant exposures may also beSome irritant exposures may also be
sensitizingsensitizing
 “Gassings”
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30. Pathophysiology
 Intensity of exposure
 Physical properties
 Chemical reactivity
 Water soluble , > 5um
 Water insoluble , 0.5 to 5 um
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32. Examples
 Spills of volatile compounds
 Accidental release of Irritants under pressure
 Accidental fire with release of thermal
degradation products
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33. Reactive airways dysfunction
syndrome
 No latency period
 They do not develop symptoms after
reexposure to low concentrations of the irritant
that initiated the symptoms
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35. Sensitizer-inducedSensitizer-induced
 Specific antigenSpecific antigen
 Minimal exposureMinimal exposure
 PPE oftenPPE often
insufficient toinsufficient to
control symptomscontrol symptoms
 Medical removalMedical removal
usually necessaryusually necessary
Irritant-inducedIrritant-induced
 Any irritantAny irritant
 Moderate to heavyModerate to heavy
exposureexposure
 PPE often effectivePPE often effective
in preventingin preventing
episodesepisodes
 Medical removalMedical removal
the last resortthe last resort
Occupational Asthma
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37. Work Exacerbated Asthma
 There is preexisting or concurrent asthma. The onset of
asthma may have predated current employment or
happened first while at the worksite of interest but was
not caused by specific exposures within that workplace.
 An increased frequency of asthma symptoms,
medication use, or health care utilization is temporally
associated with work. Medical test results may
document more frequent abnormalities.
 Workplace exposures or conditions that can exacerbate
asthma exist.
 Occupational asthma (asthma caused by a specific,
identified workplace exposure) is unlikely.
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38. Work Exacerbated Asthma
 Preexisting or concurrent asthma
 Increased frequency of asthma symptoms
 Workplace conditions
 Occupational asthma is unlikely.
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39. Agents
 Chemicals
 Dust
 Smoke
 Paints
 Cleaning products
 Exercise
 Emotional Stress
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40. Suspected when
 Asthma is difficult to control
 Worsening of symptoms
 Increase in medication at work
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41. Diagnosis of Occupational Asthma
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42. OA should be suspected
in every adult with new
onset asthma

43. Can the diagnosis of OA be made only on
the basis of a compatible history ?
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44. History
 Wheezing and nasal itching at work
 Associated allergic rhinitis and conjunctivitis
 Dysphonia at work has negative predictive
value
 Industy , exposure, co workers, MSDS,
temporal relationship with work hours
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45. Latency period is 2 years
for sensitiser induced oa

46. – SpirometrySpirometry
– Tests of NSBHTests of NSBH
-- Specific inhalation-- Specific inhalation
challengechallenge
-- PEFR monitoring-- PEFR monitoring
-- Immunologic testing-- Immunologic testing
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47. Identify
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49. PEF
 Electronic
 4 readings daily
 Medication should remain unchanged
 2 weeks at work, 2 weeks off work
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50.  PEF vs Time over several weeks, including work andPEF vs Time over several weeks, including work and
free daysfree days
 Diurnal variation ofDiurnal variation of >> 20% on work days20% on work days
 Sensitivity 75% / Specificity 100%Sensitivity 75% / Specificity 100%
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51.  Medication allowed:
 keep constant & at
minimum dose...
 beta-2 agonist on
demand only
 continue inhaled
steroids/theophylline
 avoid, if possible, long-
acting beta-2-agonist
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53.  Computer generatedComputer generated
diagnostic aiddiagnostic aid
 Provides a probabilityProvides a probability
score based on thescore based on the
plotted dataplotted data
 More sensitive thanMore sensitive than
experienced visualexperienced visual
analysisanalysis
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54. Limitations
 Falsification
 Not able to leave work
 Does not identify agent
 Variable interpretationVariable interpretation
 Subject not exposed during monitoringSubject not exposed during monitoring
 Poor compliancePoor compliance
 Change in medicationChange in medication
 BronchitisBronchitis
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55. at and away from work
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56.  Impractical for screening workerImpractical for screening worker
populationspopulations
 No evidence that pre-screening canNo evidence that pre-screening can
predict development of OApredict development of OA
 For workers with high risk, use toFor workers with high risk, use to
evaluate for OA while still activelyevaluate for OA while still actively
exposed at workexposed at work
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57.  Bronchoprovocation Study: methacholine or histamineBronchoprovocation Study: methacholine or histamine
induced fall in FEV1induced fall in FEV1 >> 20%20%
 PC20 (provocative concentration ) < 8 mg/ml (normalPC20 (provocative concentration ) < 8 mg/ml (normal
>16 mg/ml)>16 mg/ml)
 Correlates with asthma severityCorrelates with asthma severity
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58.  ““Gold-standard”Gold-standard”
 SIC tests consist of exposing the subjects to the
suspected occupational agent in the laboratory and/or
at the workplace
• Decrease in FEV1 ofDecrease in FEV1 of >> 20% in response to specific20% in response to specific
agentagent
 Performed at specialized centers; limited by precisePerformed at specialized centers; limited by precise
knowledge of the agentknowledge of the agent
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59. SIC
 IndicationsIndications
– Diagnosis in doubtDiagnosis in doubt
– Finding exact agent in complex workplaceFinding exact agent in complex workplace
– Medical-legal purposesMedical-legal purposes
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60. SIC
 reference tests
 time consuming
 Sensitiser induced OA
 False negatives- inadequate concentration,
patient on treatment
 WORK PLACE CHALLENGE TESTING
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62.  Exhaled nitric oxide (eNO) correlates withExhaled nitric oxide (eNO) correlates with
measures of airway inflammationmeasures of airway inflammation
 Sputum analysisSputum analysis
– Cell counts change before spirometry or BHRCell counts change before spirometry or BHR
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63.  Skin Test: (Skin Test: (IgE )IgE )
 Valid for HMW allergensValid for HMW allergens
 Requires good allergen extractsRequires good allergen extracts
 Frequently not available commerciallyFrequently not available commercially
 When positive, means presence of sensitizationWhen positive, means presence of sensitization
 Lack of standardised reagentsLack of standardised reagents
 RASTRAST

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66. Significant social and financial
consequences
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68.  Complete avoidance
 Medication not better than
avoidance
 Protective devices?
 Lower exposure?
 Allergen immunotherapy?
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70.  OA is not always reversible after
cessation of exposure to the
sensitizing agent.
 Asthma symptoms and airway
hyperresponsiveness (AHR) persist in
approximately 70%
 Treatment according to guidelines
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71. Immunotherapy
 Sensitiser induced OA
 Allergen should be established
 Route –
 NRL, wheat, cat allergen, venom from bees
 Duration of treatment
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72. Permanently and
completely disabled
For jobs involving exposure to the sensitizing
agent

73. 1.Pre-placement Assessment
2. Exposure control
3. PPE & Awareness
MSDS
Early detection
- periodic respiratory questionnaire
- spirometry
- skin testing
1.Employee Accommodations
2.Job Retraining
3.Upgrading standards of care
primary
prevention
Tertiary
prevention
Secondary
prevention
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74. Socio economic impact
More severe asthma
Higher healthcare utilization
Higher indirect costs
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77.  Occupational asthma, based on sensitization to agentsOccupational asthma, based on sensitization to agents
encountered at work, is the best defined and documentedencountered at work, is the best defined and documented
type of work-related asthma but under diagnosed.type of work-related asthma but under diagnosed.
 RADSRADS
 Prevention (decreasing exposure) is important, because thePrevention (decreasing exposure) is important, because the
prognosis is not very good.prognosis is not very good.
 Work-related asthma includes also worsening of pre-existingWork-related asthma includes also worsening of pre-existing
asthma due to harmful exposure at workasthma due to harmful exposure at work
Conclusion
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78. a.LMW agents
b.HMW agents
c.Irritant substancesc
Chemicals, metals and wood
dust are

79. a.1
b.4
c.8
d.16
What is the normal value of pc
20 for methacholine challenge

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81. Immunotherapy is used for
• A. HMW agents
• B. LMW agents
• C. Both
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82. What is SLIT?

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