By : ziba Loukzadeh, M.DBy : ziba Loukzadeh, M.DOccupational Medicine departmentOccupational Medicine department

Yazd University of Medical SciencesYazd University of Medical Sciences

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.

1. Airway obstruction Reversible obstruction(+/- treatment)

2. Airway inflammation3. Airway hyper responsiveness

As a consequence of working environment Not to stimuli of the outside the work

Definition

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. symptoms occur only at work2. symptoms improve on weekends or vacations3. symptoms occur regularly after the work shift4. symptoms progressively increase over the

course of the work week5. symptoms improve after a change in the work

environment

Work-related O-A

work induced O-A work aggravated O-A

sensitizer induced irritant induced

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

H.M.WIg-E dependentMast cell & macrophage

L.M.WIg-E dependent

Hapten (platinum, isocyanat)Unknown mechanism

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)

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.)

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)

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

1. Spirometry across work shift:↓10% of FEV1

2. Serial monitoring of MCT: 3time ↑Pc20

3. Serial monitoring of PEF

4. Immunological tests: specific IgE →HMW & platinum Skin test

5. Specific challenge test: gold standard

6. NO, sputum induced analysis (Eos)

1. Removal from further exposure to that agent

2. Medical treatment like non-occupational asthma

If exposure is occasionally → wear protective respirator & fallow up

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

1. Engineering control1.Substitution 2.Change of procedure3.isolation

2. Ventilation 3. Protective devices4. Restriction of employment5. Free from smoke6. Environmental screening

Sudden adult-onset asthma (RADS)◦ After acute, massive, single exposure

Not-so-sudden, adult-onset asthma◦ After repeated, moderate-level exposure

Volatile diisocyanates (TDI) Chlorine spills Acid spills, e.g., acetic acid Hypochlorite fumes Chemical fires Welding fumes Spray paint Metam sodium

Onset of symptom within 24h Persistence symptom for at least 12w Objective evidence of asthma:

◦ Hyper responsiveness◦ Response to bronchodilator

No previously asthma, COPD, …

RADS Criteria

Single high level exposure to irritant

Atopy → no

Smoking → no

Criteria

No investigation can prove the association with workplace

Proper environmental control

Proper education

Proper drug treatment

Protective devices for RADS

Avoid from smoking ,dust ,fume

Control further high level exposure

Symptoms persist for a few months – several years

1. Asthma symptoms develop during the time an irritant exposure is occurring

2. No delay between the end of exposure & asthma onset (less than 24h)

3. May be airflow obstruction4. Positive MCT5. Exposure is intermittent or continuous6. Exposure persists for a few days to a few wks

Exposure lasts longer than 16 wks before onset of asthma → Dx is highly suspect

7. Evaluate susceptibility factors (90% of individual) Atopy Asthma in remission

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

Prior asthma and aggregated with work:1. Drugs (aspirin, beta blocker, tarterazin)2. Environment (O3, SO2, NO2)3. Infections (RSV, influenza, para flu, rhinovirus).4. Exercise (cold and dry ventilation)5. Psychological6. Non active smokers

Cigarette smoke

Fumes from cleaning agents

Dusts Paint Cold air Exercise Any irritants

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)

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

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

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

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

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

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/noYes/noYes/no

Is you sleep ever broken by:•Wheeze?•Difficulty with breathing?

Yes/noYes/no

Do you ever wake up in the morning with:•wheeze?•Difficulty with breathing?

Yes/noYes/no

Do you ever wheeze:•If you are in a smoky room?•If you are in a very dusty place?

Yes/noYes/no

91% sensitivity & 96 % specificity

Step Symptom Night Symptom

Lungfunction

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 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

FEV1 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

FEV1 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 FEV1 or PEF 60 percent predicted PEF variability >30 percent

High-dose inhaled corticosteroids AND Long-acting inhaled beta 2-agonists