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Occupational / work-related asthma, definitions, epidemiology

Tallinn 17.9.2003. Occupational / work-related asthma, definitions, epidemiology. H. Keskinen MD Finnish Institute of Occupational Health. Historical notes.

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Occupational / work-related asthma, definitions, epidemiology

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  1. Tallinn 17.9.2003 Occupational / work-related asthma, definitions, epidemiology H. Keskinen MD Finnish Institute of Occupational Health

  2. Historical notes • Olaus Magnus 1555: "When sifting the chaff from the wheat, one must carefuly consider the time when a suitable wind is available that sweeps away the harmful dust. …congests in the throat and threatens the life organs.." • Ramazzini 1713: flour dust caused asthmatic symptoms in millers and bakers. • 1911-1936 platinum salts, chromium and phthalic anhydride - the first chemicals causing asthma • Diagnostics: bronchial provocation tests by Prof. Pepys and coworkers began 30 years ago at Brompton Hospital, London UK

  3. Types of bronchial asthma • Extrinsic • common environmental allergies • work-related causes • occupational asthma (due to sensitization) • RADS (due to irritation) • Intrinsic asthma • cause not known • may be partly work-related?

  4. Work-related Asthma • Occupational asthma • induced by sensitization (traditional OA) • due to irritants in high exposure (RADS) • byssinosis • Worsening of pre-existing asthma due to exposure at work • (Asthma caused by long-lasting but not very high exposure to irritants?)

  5. Occupational asthma Variable airways narrowing causally related to exposure in the working environment to airborne dusts, gases, vapours and fumes. Newman Taylor AJ, Thorax 1980;35:241-245

  6. Occupational asthma • Asthma induced by sensitization to an agent inhaled at work • fulfils the classic criteria for an allergic response: • asthma occurs usually in a minority of those exposed • asthma develops only after an initial symptom-free period or exposure • asthmatic responses are provoked by the inhalation of the induce such changes in other similarly exposed persons

  7. Occupational asthma • Causes, > 200 specific caused identified • proteins (animal, vegetable, microbiological) • low-molecular-weight chemicals • Mechanisms • IgE-mediated (proteins, some chemicals) • non-immunological mechanisms (chemicals) • Contributory factors • level of exposure • atopy ?? • smoking ??

  8. Diagnostic criteria • Allergy practice forum: Guidelines for the diagnosis of occupational asthma. Subcommittee on "Occupational Allergy" of the European Academy of Allergology and Clinical Immunology. Clin Exp Allergy 1992;2 • Criteria differ in different countries according to their legislation.

  9. Finland: Act on Occupational Diseases (1343/88) "An occupational disease, entitled to compensation according to the…(Acts 608/48, 102/81, 154/35) is a disease probably principally caused by any physical factor, chemical substance or biological agent encountered in the course of work done under contract of employment, in public service or in public office or as agricultural entrepreneur, as prescribed in those acts."

  10. Finland: Ordinance on Occupational Diseases (1347/88) …the factor…. should be present in a person´s work...to such an extend that its exposure effect is sufficient to cause the disease in question, unless it is stated that the disease has been clearly caused by exposure outside work.(the factors and diseases are listed)

  11. Finland: compensations for occupational disease • Investigations • Medication • Doctor´s fees • Sick leave compensation • When transferred to another more suitable job with a lower salary, the difference is largely compensated • Re-education • The pension for total disability is higher than for non occupational disability

  12. Occupational Asthma in Finland N The Finnish Register of Occupational Diseases

  13. Examples of annual indidence rates per 100 000 employed workers in 1989-95 in Finland (Karjalainen et al. Occupational asthma in Finland, 2000) Occupation Men Women Bakers 444 408 Plywood and fiberboard workers 64 214 Spray painters 223 144 Farmers 120 191 Veterinary surgeons 171 34 Other chemical processing workers 146 143 Welders 76 - Platers and sheet metal workers 33 72 Plastic product workers 68 63 Electrical equipment assemblers 29 65 Floor layers 54 - Packers 21 49 Hairdressers 33 37 All 17 18

  14. INCIDENCE OF OA (incidence/million/year) UK 1992-97 Physician reports 38 McDonald 20 00 France 1997 Physician reports 26 Kopferschmitt 2002 Germany 1995 Compensation 51 Baur 1998 Finland 1989-95 Compensation 174 + physician reports Karjalainen 2000 Sweden 1990-92 Self-reports for compensation 80 Torén et al 1996 Assuming an adult-onset asthma incidence of 2-3/1000/year, the rates correspond to 1-5% of all adult-onset asthma Nordman H. Woreal 2003

  15. Asthma attributable to work-related factors? • Blanc and Thorén, AmJMed 1999;107(43 studies) 9% /15% • Canada 2000 18% Johnson et al. AJRCCM 2000 • Finland 2001 men 29%, women 17%(Karjalainen et al. AJRCCM 2001;164 )agricultural work, manufacturing work and service work

  16. Excess incidence of asthma among Finnish cleaners employed in different industries All female cleaners followed for incidence of asthma (register linkages), in 1986-1998, compared to administrative workers: RR • All cleaners 1.50 • Highest risks: cleaners inmanufacture of basic metals 2.47food production 2.19 (Karjalainen et al. 2002)

  17. The numbers of cases reported as occupational asthma are much lower than the epidemiologically calculated estimates of adult-onset asthma attributable to work. • Why? • there is underreporting/underdiagnosis of cases • caused by well-established causative agents • unknown causative agents • mechanisms other than those covered by the • reporting/compensation schemesNordman H, Woreal 2003

  18. Prevalences of occupational asthma • Snow-crab processors 21% • Laboratory animal workers 7-10% • Latex in hospital workers 2% • Diisocyanates 8-20% • Phthalic anhydride 18% • TCPA 3.2% • Plicatic acid 3.4-7%

  19. Prognosis of occupational asthma • Barker et al. Occupational asthma caused by tetrachlorophthalic anhydride: A 12 years follow-up. J Allergy Clin Immunol 1998;101:717-9Since 1979 TCPA used as epoxy hardener1979-1989 seven cases of occupational asthma1980 the plant was closed • Follow-up: questionaire, PEF-follow-up, spirometry, hyperreactivity, TCPA-HSA-RAST • The symptoms decreased at first, then no more. All had symptoms. Hyperreactivity had persisted. The level of specific IgE-antibodies declined, half-time 1 year.

  20. Prognosis of occupational asthma • Piirilä et al. Lung-term follow up of HDI, MDI and TDI induced asthma. Am J Resp Crit Care Med 2000. • FIOH 1976-1992, 245 new cases of diisocyanate induced asthma, follow-up 10 (3-19) years • questionaire, 121 examined, lung function tests, spes. IgE antibodies • 82 % still with symptoms35% continuous asthma medication • 22% of symptomless persons had impairment in spirometry, 25% were hyperreactive and 18% had increased PEF variation

  21. Work-related Asthma • Occupational asthma • induced by sensitization (traditional OA) • due to irritants in high exposure (RADS) • byssinosis • Worsening of pre-existing asthma due to exposure at work • (Asthma caused by long- lasting but not very high exposure to irritants?)

  22. RADS (Reactive airways dysfunction syndrome) • Brooks et al. Reactive Airways Dysfunction Syndrome (RADS) Persistent Asthma Syndrome after High Level Irritant Exposures, Chest 1985 :88 • high level exposure to an irritant • no latency period before symptoms • asthmatic symptoms

  23. RADS: diagnostic criteria (Brooks 1985, Chang-yeung 1995, Alberts 1996, Gautrin 1999) 1. Single or several exposures to gas, smoke, fume or vapor which was present in very high concentrations and was irritant in nature. 2. Dyspnea, cough, asthmatic symptoms occurring usually within 24 hours after the exposure. 3. No latency time before symptoms. 4. Obstruction in spirometric values or in PEF follow-up or unspecific bronchial hyperreactivity in histamine or metacholine challenge test. 5. Possible earlier obstructive lung diseases clearly distinguished from the accidental incident. 6. Symptoms and functional findings last several months or remain permanentPiirilä et al. Ärsytyksen aiheuttama astma. Duodecim 2002;118

  24. Causes of RADS in 1990-99/FIOH Exposure Exposure time • Nitric and sulphuric oxides, CO, leakage in an exhaust flue (2 cases) 15 min • Ammonium, leakage in refrigeration flue 3 h • Soda lye dust and fume, cleaning of a boiler, breakdown situation 8 h • Nitric acid, leaking tank 5 min • Thermal degradation products of freon, soldering of a leaking freon pipe 2-3 min • Hydrogen chloride, emission from adjacent plant 5 min • Aluminium iodide, hydrogen iodide, chemical demonstration 1 min • Chlorine dioxide, leakage during maintenance work of paper plant 1 h • Sodium metasilicate, sodium dichlorine isocyanurate, dishwasher detergent, cook apprentice < 1 min • Flame-cutting fumes of stainless steel 12 h + 12 hDuration of symptoms 2-7 years • (Piirilä et al. 2002)

  25. RADS in practice • Acute situation: • symptoms, obstruction • treatment: asthma treatment • description of the accident, definition and duration of exposure, • Investigations • chest X-ray • spirometry, histamine test • PEF follow-up ( with bronchodilator) • diffusion capacity • bronchoscopy, BAL ? • Follow-up • follow-up minimum one year, permanent asthma medication when needed

  26. Work-related Asthma • Occupational asthma • induced by sensitization (traditional OA) • due to irritants in high exposure (RADS) • byssinosis • Worsening of pre-existing asthma due to exposure at work • (Asthma caused by long-lasting but not very high exposure to irritants?)

  27. Byssinosis • Symptoms related to exposure to impurities in cotton, flax, hemp dusts, described by Ramazzini already in 1705. • Opening of bales, cleaning, carding. Develops after >10 years of exposure. • Chest tightness, difficulty of breathing on first day of the work week. Also decrease of the second capacity described. • Etiology: endotoxins? • At first no symptoms on the following days. Chronic disease after long-term exposure. • High exposure / high prevalence. • Prevention: dust control • In Finland last case of byssinosis was reported in 1989.

  28. Work-related Asthma • Occupational asthma • induced by sensitization (traditional OA) • due to irritants in high exposure (RADS) • byssinosis • Worsening of pre-existing asthma due to exposure at work • (Asthma caused by long-lasting but not very high exposure to irritants?)

  29. Worsening of pre-existing asthma • Tarlo et al. Chest 2000;118 731 asthmatics, retrospective review. : 16 % of adult onset working asthmatics reported their asthma be worse at work.31% of them had either likely or possible OA and 49% had aggravation of underlying asthma. • Saarinen et al. Eur Respir J 2003;222613 asthmatics, 969 currently employed21% reported work-aggravated symptoms • exposure to dusts • abnormal temperatures • poor indoor air quality • physicaally strenuous work • chemicals

  30. Bronchial asthma developed while working under long-term but not very high exposure to irritants • Not defined as occupational asthma to-day • No diagnostic criteria • Elevated risk of asthma:Solvents Antti-Poika et al 1992, Torén et al 1996, Xu et al 1993Contruction and textile workers Ng et al 1994Cleaners Konevigas et al 1999, Karjalainen et al 2001Moulds Jaakkola et al 2001, Thorn et al 2001Metal plating, electric machinery Arif et al 2002, Karjalainen 2002

  31. Conclusion • Occupational asthma, based on sensitization to agents encountered at work, is the best defined and documented type of work-related asthma but underdiagnosed. • RADS is a special subgroup of occupational asthma induced without a latency period by a high level of exposure to irritants. • Prevention (decreasing exposure) is important, because the prognosis is not very good. • Work-related asthma includes also worsening of pre-existing asthma due to harmful exposure at work, and presumably also asthma developed in long-term but not very high exposure to irritants, not defined as occupational diseases to-day. Prevention of exposure is also important.

  32. Literature • Asthma in the Workplace, editors Bernstein IL, Chang-yeung M, Bernstein DI,1999, Marcel Dekker Inc. New York Basel • Brooks SM, Weiss MA, Bernstein IL. Reactive Airways Dysfunction Syndrome (RADS) Persistent Asthma Syndrome after High Level Irritant Exposures, Chest 1985 ;88:376-384. • Karjalainen A, Kurppa K, Martikainen R, Klaukka T, Karjalainen J. Work is Related to a Substaantial Rortion of Adult-onset Asthma Incidence in the Finnish Polulation. Am. J. Respir. Crit. Care Med. 2001;164:565-568. • Karjalainen A, Kurppa K, Virtanen S, Keskinen H, Nordman H. Incidence of Occupational Asthma by Occupation and Industry in Finland. Am. J. Ind. Med. 2000;37:451-458. • Karjalainen A, Martikainen R, Karjalainen J, Klaukka T, Kurppa K. Excess incidence of asthma among Finnish cleaners employd in different industries. Eur Respir J. 2002;19:90-95. • Newman Taylor AJ, Pickering CAC. Occupational asthma and byssinosis. In RW Parkes, Occupational Lung Disorders, Third edition1994, Butterworth Heineman Ltd, UK, • Nordman H, Hytönen M, Keskinen H. Ammattinuha ja -astma. Allergologia, toim. Haahtela T, Hannuksela M, Terho E.O. Kustannusosakeyhtiö Duodecim, 1999:372-390. • Nordman H, Keskinen H: Keuhkojen ammattitaudit. Kirjassa Keuhkosairaudet, toim. Kinnula V. Laitinen L.A.L, Tukiainen P. Kustannusosakeyhtiö Duodecim, 2000:602-624. • Piirilä P, Espo T, Keskinen H, Grenquist-Norden B, Saalo A, Nordman H. Ärsytyksen aiheuttama astma. Duodecim 2002;118:369-76.

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