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Occupational Asthma

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By : ziba Loukzadeh, M.D Occupational Medicine department Yazd University of Medical Sciences Cigarette smoke Fumes from cleaning agents Dusts Paint Cold air Exercise ... – PowerPoint PPT presentation

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Date added: 4 September 2019
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Title: Occupational Asthma


1
Occupational Asthma
  • By ziba Loukzadeh, M.D
  • Occupational Medicine department
  • Yazd University of Medical Sciences

2
Asthma (Introduction)
  • Respiratory diseases cause loss of 5-38 million
    days per year.
  • Asthma is the most common occupational
    respiratory disease In under development
    countries.
  • 5-10 of U.S member.
  • 15-20 of asthma cause from work.

3
Definition
  • Airway obstruction
  • Reversible obstruction(/- treatment)
  • Airway inflammation
  • Airway hyper responsiveness
  • As a consequence of working environment
  • Not to stimuli of the outside the work

4
Diagnosis of occupational asthma
  • diagnosis of asthma and by establishing a
  • relationship between asthma and the work
    environment
  • diagnosis of asthma should only be made
  • when both intermittent respiratory symptoms and
    physiologic evidence of reversible or variable
    airways obstruction are present

5
  • Relationship between asthma and workplace
    exposure may fit any of the following patterns
  • symptoms occur only at work
  • symptoms improve on weekends or vacations
  • symptoms occur regularly after the work shift
  • symptoms progressively increase over the course
    of the work week
  • symptoms improve after a change in the work
    environment

6
  • Work-related O-A
  • work induced O-A work aggravated O-A
  • sensitizer induced irritant induced

7
Sensitizer O.A
  • Low molecular weight
  • Spray paint
  • Wood dust (western red cedar)
  • Acid anhydride
  • biocides
  • Colophony-fluxes
  • High molecular weight
  • Animal derived
  • Plant derived
  • Enzymes
  • Irritant agents
  • Chlorine
  • Acetic acid
  • Isocyanides

8
Sensitizer O.A
  • H.M.W
  • Ig-E dependent
  • Mast cell macrophage
  • L.M.W
  • Ig-E dependent
  • Hapten (platinum, isocyanat)
  • Unknown mechanism

9
Pathophysiology of Sensitizer O.A
  • Air way inflammation paramount feature of asthma.
  • Air way inflammation cause
  • Obstruction
  • Hypersensitivity
  • Air way response include
  • Rapid(1-2h)
  • Late (4-8 h)
  • Dual (1-2 4-8 h)

10
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11
Exposure factors
  • Dose-response relationship
  • Latency period (gt1 month up to 2year) and
    dependent to
  • Dose
  • Duration
  • Susceptibility
  • Skin contact (isocyanate) such as respiratory
    contact is important.
  • Environmental agents (smoking, O3, diesel gases,
    air allergen.)

12
Host factors
  • Atopy HMW such as detergent enzymes
  • Smoking
  • platinum worker is the highest risk factor
  • non-allergic bronchial hyper-responsiveness
  • Genetic isocyanate, platinum,red cedar,TMA
  • Upper air way symptom (rhinitis conjunctivitis)

13
Clinical features
  • cough , wheezing, dyspnea
  • Some of persons involved
  • Latency (month to years)
  • Onset (rapid, late, dual)
  • History of atopy, rhinitis, conjunctivitis
  • Environmental investigation
  • Ventilation , protective devices
  • Proper usage

14
Diagnosis
  • Spirometry across work shift?10 of FEV1
  • Serial monitoring of MCT 3time ?Pc20
  • Serial monitoring of PEF
  • Immunological tests
  • specific IgE ?HMW platinum
  • Skin test
  • Specific challenge test gold standard
  • NO, sputum induced analysis (Eos)

15
mechanical
16
electronic
17
Sample chart
18
Serial monitoring of MCT/ Serial monitoring of
PEF
19
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20
Management
  • Removal from further exposure to that agent
  • Medical treatment like non-occupational asthma
  • If exposure is occasionally ? wear protective
    respirator fallow up

21
Prognoses
  • Majority of patient fail to recover after removal
  • Associated with
  • Exposure duration
  • Exposure amount after clinical symptom
  • Severity of symptoms (by PFT , challenge tests)
  • Delayed diagnosis
  • Inhalational corticosteroids
  • Early recognition of S-OA removal

22
Prevention
  1. Engineering control
  2. Substitution
  3. Change of procedure
  4. isolation
  5. Ventilation
  6. Protective devices
  7. Restriction of employment
  8. Free from smoke
  9. Environmental screening

23
  • Sudden adult-onset asthma (RADS)
  • After acute, massive, single exposure
  • Not-so-sudden, adult-onset asthma
  • After repeated, moderate-level exposure

24
Selected causes of irritant-induced OA
  • Volatile diisocyanates (TDI)
  • Chlorine spills
  • Acid spills, e.g., acetic acid
  • Hypochlorite fumes
  • Chemical fires
  • Welding fumes
  • Spray paint
  • Metam sodium

25
RADS Criteria
  • Onset of symptom within 24h
  • Persistence symptom for at least 12w
  • Objective evidence of asthma
  • Hyper responsiveness
  • Response to bronchodilator
  • No previously asthma, COPD,

26
Exposure factors
  • Single high level exposure to irritant

27
Host factors
  • Atopy ? no
  • Smoking ? no

28
diagnosis
  • Criteria
  • No investigation can prove the association with
    workplace

29
Management
  • Proper environmental control
  • Proper education
  • Proper drug treatment
  • Protective devices for RADS
  • Avoid from smoking ,dust ,fume
  • Control further high level exposure

30
Prognosis
  • Symptoms persist for a few months several years

31
Criteria for not-so-sudden IIA
  • Asthma symptoms develop during the time an
    irritant exposure is occurring
  • No delay between the end of exposure asthma
    onset (less than 24h)
  • May be airflow obstruction
  • Positive MCT
  • Exposure is intermittent or continuous
  • Exposure persists for a few days to a few wks
  • Exposure lasts longer than 16 wks before onset of
    asthma ? Dx is highly suspect
  • Evaluate susceptibility factors (90 of
    individual)
  • Atopy
  • Asthma in remission

32
Pseudoirritant induced asthma
  • Chemical sensitivity
  • 15-30 of general population
  • Asthmalike symptoms after smelling chemical odor
  • Perfume, pesticide, fresh paint, cigarette smoke,
    new carpet, automobile exhaust, marker pens

33
Work related asthma
  • Prior asthma and aggregated with work
  • Drugs (aspirin, beta blocker, tarterazin)
  • Environment (O3, SO2, NO2)
  • Infections (RSV, influenza, para flu,
    rhinovirus).
  • Exercise (cold and dry ventilation)
  • Psychological
  • Non active smokers

34
Common triggers to work-related aggravation of
asthma
  • Cigarette smoke
  • Fumes from cleaning agents
  • Dusts
  • Paint
  • Cold air
  • Exercise
  • Any irritants

35
  • Airway hyper responsiveness ? low level irritant
    (O3, respiratory infection, smoking) ?
    bronchoconstriction
  • If asthma is well treated avoid allergens ?
    able to work with low level irritant (unlike
    S-OA)

36
Diagnosis
  • Symptoms worsen at work improve at home
    exposure at work to irritants
  • Objective evidence of asthma
  • Objective evidence of worsening at work
  • Change in symptoms
  • Medication
  • PEF

37
Management
  • Optimize the medical management of asthma
  • limiting exposure to non-occupational irritants
    Such as tobacco smoke
  • Reduced exposure to non-specific exacerbating
    triggers in the workplace

38
Management
  • Depending on the exacerbating triggers
  • Move to a different work area
  • Changes in ventilation or process
  • Asthma education
  • Appropriate respirator for short-term exposures
    to respiratory irritants
  • Work modification to avoid extreme cold /exercise

39
Prognosis
  • Temporary aggravation of asthma at work if there
    have been unusually high exposures to irritants
    such as when the workplace is being repainted, or
    is under construction
  • Such exposures are not known to cause long-term
    worsening of asthma and clinically usually
    resolve within a few weeks after cessation

40
prevention of work-related aggravation of asthma
  • Optimum non-occupational environmental control
    measure
  • Asthma education
  • Pharmacologic control of underlying asthma
  • Pre-employment counseling
  • Work in a relatively clean environment with
    limited expected exposure to dusts, smoke, fumes,
    and sprays, with moderate workplace temperatures
    and exertional requirements

41
Screening questionnaire
Current health (during the last 4 weeks)
If you run or climb stairs fast do you ever Cough? Wheeze? Get tight in the chest? Yes/no Yes/no Yes/no
Is you sleep ever broken by Wheeze? Difficulty with breathing? Yes/no Yes/no
Do you ever wake up in the morning with wheeze? Difficulty with breathing? Yes/no Yes/no
Do you ever wheeze If you are in a smoky room? If you are in a very dusty place? Yes/no Yes/no
91 sensitivity 96 specificity
42
Step Symptom Night Symptom Lung function medication
STEP 1 Mild intermittent Symptoms two times a week Asymptomatic and normal PEF between exacerbations lttwo times a month FEV1 or PEF gt80 percent predicted PEF variability lt20 percent Exacerbations may occur, A course of systemic corticosteroids is recommended.
STEP 2 Mild persistent Symptoms gt two times a week but lt one time a day Exacerbations may affect activity gt two times a month FEV1 or PEF gt80 percent predicted PEF variability 20 to 30 percent Lo w-dose inhaled corticosteroids
STEP 3 Moderate persistent Daily symptoms Exacerbations two times a week gt one time a week FEV1 or PEF gt60 but lt80 percent predicted PEF variability gt30 percent Low-to-medium dose inhaled corticosteroids and long-acting inhaled beta 2-agonists.
STEP 4 Severe persistent Continual symptoms Limited physical activity Frequent exacerbations Frequent FEV1 or PEF 60 percent predicted PEF variability gt30 percent High-dose inhaled corticosteroids AND Long-acting inhaled beta 2-agonists
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