Occupational Asthma

1. Occupational Asthma By : zibaLoukzadeh, 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 asthmaand 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 • High molecular weight • Animal derived • Plant derived • Enzymes • Irritant agents • Chlorine • Acetic acid • Isocyanides • Low molecular weight • Spray paint • Wood dust (western red cedar) • Acid anhydride • biocides • Colophony-fluxes

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)

11. Exposure factors • Dose-response relationship • Latency period (>1 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

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 • Engineering control • Substitution • Change of procedure • isolation • Ventilation • Protective devices • Restriction of employment • Free from smoke • 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 91% sensitivity & 96 % specificity