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By:Shamsizadeh,Shahrooz 1386.08.23 Slide 2 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. Slide 3 1. Airway inflammation 2. Airway obstruction 3. Airway hyper responsiveness (+/-) Reversible obstruction(+/- treatment). As a consequence of working environment. Not to stimuli of the outside the work. Slide 4 Sensitizer-induced O.A(immunologically) Irritant-induced O.A(non-immunologically) Aggravation of asthma Slide 5 High molecular weight Animal derived Planet derived Enzymes Irritant agents Chlorine Acetic acid Isocyanides Low molecular weight Spray paint Wood dust Acid anhydride biocides Colophony-fluxes Slide 6 H.M.W is protein & polysaccharide >5kd Ig-E dependent or not dependent Mast cell & macrophage Lym CD4+,IL 4,5,13 L.M.W unknown cause Hapten (platinum,isocyanat,anhydrid) Platinum is with Ig-E PMN,Lym CD8+,IL 2,INF Slide 7 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) Slide 8 Rapid Airway Dysfunction Syndrome (RADS) Single high level of exposure to irritant fume, gases and smoke. Short duration between exposure and response. Immunologic and neurological inflammation is the mechanism of RADS. Is RADS come to asthma? Slide 9 With onset of 24h Persistence symptom for at least 12w Objective evidence of asthma: Hyper responsiveness Response to bronchodilator No previously asthma or COPD Calcium oxide, nitrogen oxides, welding fumes, spray paint, Slide 10 Dose-response relationship Duration of sensitization(>1 m up to 2year) and dependent to: Dose Duration Susceptibility Skin contact (isocyanate) such as respiratory contact is important. Environmental agents (smoking,platinum,O3,diesel gases,air allergen.) Slide 11 1. Atopy : HMW such as detergent enzymes. 2. Smoking: 1.platinum worker is the highest risk factor 2.Laboratory animal handler 3.Tetracholorophthalic anhydride. 3. non-allergic bronchial hyper- responsiveness. 4. Genetic(diisocyanate, platinum, red cedar) 5. Upper air way symptom(rhinitis &conjunctivitis). Slide 12 Prior asthma and aggregated with work: 1.Drugs(asprin,beta bloker,tarterazin,sulphit agent) 2.Environment(O3,SO2,NO2). 3.Infections(RSV, influenza, para flu, rhinovirus). 4.Exercise (cold and dry ventilation). 5.Psychological conditions(vogues and endorphin). 6.Non active smokers. Slide 13 Related to: Air way hyper sensitivity Severity of asthma Pharmalogical control of asthma Patient can come back to work if Exposure limited Well treated with drugs How about sensitized O.A? Slide 14 Dyspnea,cough, wheezing. Some or all of persons involved. Latency(month to years or acute) Onset(rapid, late, dual) History of atopy, rhinitis, conjunctivitis Environmental investigation Ventilation, protective devices Proper usage Slide 15 1. Spirometry (base and serial) for work related 10% of FEV1 before and after. 2. Methacholine or histamin challenge test after 10-14 holydays associated with 3time Pc20. 3. P.E.F serial (the best test for O.A). 4. Immunological tests(specific IgEHMW &platinum) 5. FeNO, sputum induced analysis(4-6 h and Eos) 6. C.X.R Slide 16 I. Occupational symptoms. II. Serial P.E.F III. Serial spirometry IV. Challenge test Slide 17 Slide 18 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 Is you sleep ever broken by: Wheeze? Difficulty with breathing? Yes/no Do you ever wake up in the morning with: wheeze? Difficulty with breathing? Yes/no Do you ever wheeze: If you are in a smoky room? If you are in a very dusty place? Yes/no Screening questionnaire 91% sensitivity and 96 % specificity Slide 19 1. Substitution 2. Ventilation 3. Change of procedure 4. Restriction of employment 5. Free from smoke 6. Accidental education 7. Environmental screening 8. Protective devices Slide 20 Loss of exposure Protective devices for RADS and work agg asthma Avoid from smoking,dust,fume (for irritant) Follow up with: a.Serial PFT b.Specific challenge tests Slide 21 StepSymptomNight Symptom Lung function medication STEP 1: Mild intermittent Symptoms two times a week Asymptomatic and normal PEF between exacerbations two times a month FEV1 or PEF 80 percent predicted PEF variablitytwo times a week but < one time a day Exacerbations may affect activity > two times a month FEV1 or PEF 80 percent predicted PEF variablity 20 to 30 percent Lo w-dose inhaled corticosteroids STEP 3: Moderate persistent Daily symptoms Exacerbations two times a week > one time a week FEV1 or PEF >60 but 30 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 FrequentFEV1 or PEF 60 percent predicted PEF variablity >30 percent High-dose inhaled corticosteroids AND Long-acting inhaled beta 2- agonists Slide 22 Associated with: Exposure duration Exposure amount after clinical symptom Severity of symptoms(by PFT, challenge tests) Sensitivity to west red cedar, Isocyanides Corticosteroid inhalation Reduce exacerbation: Proper environmental control Proper education Proper drug treatment