Occupational Asthma By ziba Loukzadeh M D Occupational
Occupational Asthma By : ziba Loukzadeh, M. D Occupational Medicine department Yazd University of Medical Sciences
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.
Definition 1. Airway obstruction Ø 2. 3. Ø Ø Reversible obstruction(+/- treatment) Airway inflammation Airway hyper responsiveness As a consequence of working environment Not to stimuli of the outside the work
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
Relationship between asthma and workplace exposure may fit any of the following patterns: 1. 2. 3. 4. 5. 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
Work-related O-A work induced O-A sensitizer induced work aggravated O-A irritant induced
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
Sensitizer O. A H. M. W ØIg-E dependent ØMast cell & macrophage L. M. W ØIg-E dependent Ø Hapten (platinum, isocyanat) ØUnknown mechanism
Pathophysiology of Sensitizer O. A Air way inflammation paramount feature of asthma. Air way inflammation cause: ◦ Obstruction ◦ Hypersensitivity Air way response include: ◦ Rapid(1 -2 h) ◦ Late (4 -8 h) ◦ Dual (1 -2 & 4 -8 h)
Exposure factors Dose-response relationship Latency period (>1 month up to 2 year) and dependent to: ◦ Dose ◦ Duration ◦ Susceptibility Skin contact (isocyanate) such as respiratory contact is important. Environmental agents (smoking, O 3, diesel gases, air allergen. )
Host factors 1. Atopy : HMW such as detergent enzymes 2. Smoking: ◦ platinum worker is the highest risk factor 3. non-allergic bronchial hyper-responsiveness 4. Genetic: isocyanate, platinum, red cedar, TMA 5. Upper air way symptom (rhinitis & conjunctivitis)
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
Diagnosis 1. Spirometry across work shift: ↓ 10% of FEV 1 2. Serial monitoring of MCT: 3 time ↑Pc 20 3. Serial monitoring of PEF 4. Immunological tests: Ø specific Ig. E →HMW & platinum Ø Skin test 5. Specific challenge test: gold standard 6. NO, sputum induced analysis (Eos)
mechanical
electronic
Sample chart
Serial monitoring of MCT/ Serial monitoring of PEF
Management 1. 2. Removal from further exposure to that agent Medical treatment like non-occupational asthma If exposure is occasionally → wear protective respirator & fallow up
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
Prevention 1. 2. 3. 4. 5. 6. Engineering control 1. Substitution 2. Change of procedure 3. isolation Ventilation Protective devices Restriction of employment Free from smoke Environmental screening
Sudden adult-onset asthma (RADS) ◦ After acute, massive, single exposure Not-so-sudden, adult-onset asthma ◦ After repeated, moderate-level exposure
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
RADS Criteria Onset of symptom within 24 h Persistence symptom for at least 12 w Objective evidence of asthma: ◦ Hyper responsiveness ◦ Response to bronchodilator No previously asthma, COPD, …
Exposure factors Single high level exposure to irritant
Host factors Atopy → no Smoking → no
diagnosis Criteria No investigation can prove the association with workplace
Management Ø Proper environmental control Ø Proper education Ø Proper drug treatment Ø Protective devices for RADS Ø Avoid from smoking , dust , fume Ø Control further high level exposure
Prognosis Symptoms persist for a few months – several years
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 24 h) May be airflow obstruction Positive MCT Exposure is intermittent or continuous Exposure persists for a few days to a few wks 1. 2. 3. 4. 5. 6. Exposure lasts longer than 16 wks before onset of asthma → Dx is highly suspect Evaluate susceptibility factors (90% of individual) 7. Atopy Asthma in remission
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
Work related asthma Prior asthma and aggregated with work: 1. 2. 3. 4. 5. 6. Drugs (aspirin, beta blocker, tarterazin) Environment (O 3, SO 2, NO 2) Infections (RSV, influenza, para flu, rhinovirus). Exercise (cold and dry ventilation) Psychological Non active smokers
Common triggers to work-related aggravation of asthma Cigarette smoke Fumes from cleaning agents Dusts Paint Cold air Exercise Any irritants
Airway hyper responsiveness → low level irritant (O 3, respiratory infection, smoking) → bronchoconstriction If asthma is well treated & avoid allergens → able to work with low level irritant (unlike S-OA)
Diagnosis 1. Symptoms worsen at work & improve at home + exposure at work to irritants 2. Objective evidence of asthma 3. Objective evidence of worsening at work Change in symptoms Medication PEF
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
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
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 longterm worsening of asthma and clinically usually resolve within a few weeks after cessation
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
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 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 91% sensitivity & 96 % specificity
Step Symptom Night Symptom Lung function medication STEP 1: Mild intermittent Symptoms two times a week Asymptomatic and normal PEF between exacerbations <two times a month FEV 1 or PEF >80 percent predicted PEF variability <20 percent Exacerbations may occur, A course of systemic corticosteroids is recommended. STEP 2: Mild persistent Symptoms > two times a week but < one time a day Exacerbations may affect activity > two times a month FEV 1 or PEF >80 percent predicted PEF variability 20 to 30 percent Lo w-dose inhaled corticosteroids STEP 3: Moderate persistent Daily symptoms Exacerbations two times a week > one time a week FEV 1 or PEF >60 but <80 percent predicted PEF variability >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 Frequent FEV 1 or PEF 60 percent predicted PEF variability >30 percent High-dose inhaled corticosteroids AND Long-acting inhaled beta 2 -agonists
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