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Occupational and work-aggravated asthma

Occupational and work-aggravated asthma. Dennis Nowak. Institut and Outpatient Clinic for Occupational and Environmental Medicine Ludwig-Maximilians-Universität München dennis.nowak@med.uni-muenchen.de. L M U. Site & intensity of the injury. Physico-chemical properties

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Occupational and work-aggravated asthma

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  1. Occupational and work-aggravated asthma Dennis Nowak Institut and Outpatient Clinic for Occupational and Environmental Medicine Ludwig-Maximilians-Universität München dennis.nowak@med.uni-muenchen.de LMU

  2. Site & intensity of the injury • Physico-chemical properties • Particle size…<5u go deeper • Concentration… • Solubility • Density… lighter (as) go deeper • Reactivity… higher (NH4) more damage • Duration of exposure Signs of alertness • Rate / depth of breathing • Host response variability / susceptibility • Host defense mechanisms

  3. Mechanisms Toxic Inflammatory • Irritant : farm dust, chemicals • Allergic : flour (bakers) • Sensitizers : toluene di-isocyanates • Infectious : brucellosis Carcinogenic uranium

  4. Symptoms • Cough • Expectoration • Hemoptysis • Dyspnea at rest and/or on exertion • Wheezing • Chest tightness / pain • Upper airways symptoms • Fever, chills, other

  5. UPPER ITIS • BRONCHITIS • ASTHMA-LIKE • ASTHMA • BRONCHIOLITIS • BOOP AIRWAYS local • PULM. EDEMA • PNEUMONITIS • FIBROSIS EXPOSURE ALVEOLI systemic • NEUROTOXINS • FEVERS

  6. Airways exposure Acute low Chronic low Acute massive chemical bronchitis Chronic Bronchitis Asthma-like disease RADS Allergic asthma

  7. Definition Occupational asthma A.Asthma B. Onset after entering workplace C. Association of symptoms to workplace D1. Agent known to cause OAor D2. Work-related changes in FEV1 or PEFs +/or D3. “ “ “ “ hyperreactivity +/or D4. Positive specific challenge test +/or D5. Clear sx onset after irritant exposure

  8. OA and BHR: Definition (1) e.g.,“Occupational asthma is a disease characterized by variable airflow limitation and / or airway hyper-responsiveness due to causes and conditions attributable to a particularoccupational environment and not to stimuli encountered outside the workplace.“ Bernstein, I.L., Asthma in the workplace, 1993

  9. OA and BHR: Definition (2) Generally:Inducers: cause airway inflammation and BHR Inciters: trigger airway narrowing in patients with BHR, increase frequency of symptoms in pts. with pre-existing asthmaThus, only inducers should be considered causal agents Bernstein, I.L., Asthma in the workplace, 1993

  10. Work-aggravated asthma Pre-existing or concurrent asthma that isaggravated by irritants or physical stimuli at the workplace Tarlo S. et al., Chest 118 (2000) 1309:16 % of asthmatics Saarinen K. et al., ERJ 22 (2003) 305: 21 % of asthmatics

  11. OA and BHR: Pathogenesis, types of disease Inducers: common aeroallergens  EAR, LARLAR  inflammation , BHR  Even if no obstruction: inflam. , BHR   may require removal from work Inciters: exercise, cold air, etc. no change in inflammation or BHR  may require exposure  or therapy 

  12. Occupational Asthma NO LATENCY IRRITANT-INDUCED LATENCY IgE MEDIATED SPECIFIC NON-IgE

  13. Immunologic IgE mediated High molecular wght Low molecular haptens ? Cell mediated Low molecular Nonimmunologic Irritant-toxic Grain, crab, castor beans Woods, gum acacia Animal dander, urine Epoxy resins Chloramine T Platinum salts di-isocyanates Red Cedar Cobalt Ammonia, chlorine Etiology Mechanism: Inducers

  14. Obstructive pattern • FEV1,FVC,FEV1/FVC • FEF, PEFR • RAW, • RV/TLC • Bronchodilators • Provocation tests • History • Exam • Lung Function • Skin tests • Blood: eosinophils, serology-RAST • Radiology • Therapeutic trial

  15. OA and BHR: Types of disease Occupational asthma - immunological - non-immunological including RADS Work-aggravated asthma Variant syndromes - eosinophilic bronchitis - potroom asthma - asthma-like syndrome (e.g., organic dusts)

  16. OA and BHR: Pathogenesis, types of disease - typical agents • High molecular weight agents flour, latex • Low molecular weight agentsplatinum salts • Irritants (RADS)chlorine, phosgen • Potroom AsthmaHF, SO2, (aluminium chloride? fluoride?) • Asthma-like Syndromeendotoxin, NH3 Atopic asthma

  17. OA and BHR: Diagnostic approach History, questionnaire, SPT, specific IgE (if possible) Non-specific provocation challenge (e.g., MCh) if possible at the end of a working week after at least two weeks with relevant exposure positive negative Lung function monitoring by the patientfor at least 3 wks with / withoutworkplace exposure Specific challenge under laboratory conditions with suspected agent / extract and / or suspicious un-suspicious positive negative Lung function monitoring at the workplace vs. non-exposure Mostly no asthma (exception: e.g., isocyanateasthma) suspicious un-suspicious Probably occupational asthma Probably non-occupational asthma

  18. OA and BHR: Diagnostic approach (1) Questionnaire: good primary tool work-relatedness rhinoconjunctivitis? sensitivity good, spec. +/-Skin prick test: quick, simple, safe limited by lack of available/ standardized extractsSpecific IgE: bit less sensitive, bit more specific same limits as SPT

  19. OA and BHR: Diagnostic approach (2) Spirometry: routine spirometry far less sensitive than questionnaire!Cross-shift spirometry: sensitivity better, but much better on multiple days!MCh challenge: if negative, mostly excludes OAChange in BHR: +++, > 2 doubling concentrations Induced sputum: HMW agents: eosinophils  LMW agents: eos. , neutro.  Exhaled NO: usefulness questionable for OA

  20. Mobile, onsite peak flow monitoring / spirometry mechanic electronic

  21. P.S. Burge, W. Anees

  22. Workplace provocation challenge

  23. OA and BHR: Exposure-response relationship - Exposure intensity (dose?) - Isocyanate asthma: peak levels! - No effect level? Flour dust < 0.5 mg/m3 Alpha-amylase 0.25 ng/m3 Rat urin protein 0.7 µg/m3 Latex allergens 0.6 ng/m3 cow allergen 20-30 µg/g dust - Upper end of dose-response curve flattens - Atopy, atopic rhinitis, atopic asthma - Smoking: only risk factor for platinum salt asthma

  24. IMMEDIATE REACTION LATE REACTION FEV1 O DUAL REACTION PROGRESSIVE-PROLONGED

  25. HOME-------------WORK-----HOME—WORK--HOMEWORK Rx

  26. Reactive Airways DysfunctionSyndrome • Asthma-like syndrome • Abrupt onset within 12-24 hrs • After high irritant exposure • Recurrent and persistant > 3 months • No preexisting respiratory complaints • Airflow obstruction or • Non-specific airways hyperreactivity

  27. Prognosis Can not be predicted by severity, exposure, type,... Progress Persistent Recurrent Resolves Exposure ceases

  28. RADS Odor-triggered Irritant-assoc. Panic attacks Vocal Cord Dysfunction

  29. K.B., *13.03.71 Peak flow protocol

  30. E.P., *15.03.1966 (hairdresser) Peak flow record

  31. U.M., *21.08.48 Peak flow record

  32. OA and BHR: Prognosis (1) Inducer Red cedar Red cedar Colophony Isocyanates Isocyanates Isocyanates Isocyanates Crabs Crabs Varia Varia Subjects (n) 38 75 20 12 50 20 22 31 31 32 28 Duration of follow-up (J) 0,5-4 1-9 1,3-3,8 1-3 >4 0,5-4 1 0,5-2 4,8-6 0,5-4 4-11 Persistence of symptoms (%) 29 49 90 66 82 50 77 61 100 93 100 Persistence of BHR 38/28 (100%) 25/33 (76%) 7/20 (35%) 7/12 (58%) 12/19 (63%) 9/12 (75%) 17/22 (77%) 28/31 (91%) 26/31 (84%) 31/32 (97%) 25/2 (96%)

  33. OA and BHR: Prognosis (2) Cessation of exposure: Persistence of symptoms: 61 % Persistence of BHR: 75 % Reduction of exposure: Persistence of symptoms: 93 % Persistence of BHR: 95 % Vandenplas, O., et al., ERJ 22 (2003) 689-697

  34. OA and BHR: Prevention (1) Cullinan, P., et al., ERJ 22 (2003) 853, from: Cathcart, M., et al., Occup. Med. 47 (1997) 473

  35. OA and BHR: Prevention (2) Cullinan, P., et al., ERJ 22 (2003) 853, from: Allmers, H., et al., JACI 110 (2002) 318

  36. Work-aggravated asthma: Prevention Work environment plays an importantrole in the aggravation of symptomsof established asthma. Tertiary prevention!!!

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