1. F. Lortie-Monette, MD, MSc, CSPQ, MBA
THE UNIVERSITY OF WESTERN ONTARIO Department of Epidemiology & Biostatistics
2003
F. Lortie-Monette, MD, MSc, CSPQ, MBA

2. OCCUPATIONAL ASTHMA

3. OCCUPATIONAL ASTHMA
The 1999 Canadian Asthma Consensus Report was the result of a May 1998 meeting of 61 Canadian physicians -- respirologists, pediatricians, allergists and emergency and family physicians -- under the leadership of the Asthma Committee of the Canadian Thoracic Society.

4. Occupational Asthma:. the most prevalent occupational lung disease
Occupational Asthma: the most prevalent occupational lung disease in industrial countries
 new onset asthma (occupational asthma) OR
 work-aggravation of pre-existing asthma (specially if general asthma control had been suboptimal or if asthma was relatively severe).
Causes:
Irritants, allergens, viral infections.

5. DIAGNOSIS OF OCCUPATIONAL ASTHMA:
Asthma starting at work is not always work-related asthma
But 
work-related asthma should be considered in
all working asthmatics

6. Most commonly,. occupational asthma with latency
Most commonly, occupational asthma with latency (immunologic mechanism) :
1.1 sensitization to a high-molecular weight agent
(   )
1.2 sensitization to a low-molecular weight agent
(these include highly reactive chemicals like isocyanates, and may act as haptens, combining with body proteins; mostly IgE independent mechanisms;
_________
Sensitization accounts for over ninety percent of OA cases reported to the Ontario’s Workplace and Safety Insurance Board.

7. Less commonly,. occupational asthma without a latency
Less commonly, occupational asthma without a latency period (RADS/Irritant-Induced Asthma):
high level, acute exposure to an irritant
(eg chlorine, ammonia)  
resulting in airway injury.

8. Reactive Airways Dysfunction Syndrome (RADS):
no prior lung disease; onset within 24 hours of work exposure;
objective evidence of asthma;
symptoms for at least 3 months (can persist for months or years)
re-exposure to low levels unlikely to trigger asthma ...moderate or high levels of exposure to respiratory irritants could aggravate symptoms.

9. Irritant-Induced Asthma (IIA):
 one or more high level,
acute exposure to an irritant;
 symptoms occurring up to 7 days post exposure

10. LOW MOLECULAR WEIGHT AGENTS CAUSING OCCUPATIONAL ASTHMA
Occupations at Risk
Isocyanates
(prevalence of isocyanate-induced asthma in exposed workers is close to 10%).
spray painters, insulation installers, manufacturers of plastics, rubbers, foam and coating;
manufacturers of cars, planes and trains
wood dusts (cedar, oak)
sawmills workers, carpenters
acid anhydrides
users of plastics, epoxy resins
aliphatic amines (e.g., ethylenediamine)
shellac and lacquer handlers, solderers
metals, fluxes, (platinum salts, cobalt, colophony)
platinum refineries, hard metal grinding, electronic (soldering)
chloramine-T
janitorial work, cleaners
dyes
textile and dye manufacturing
persulphate
hairdresser
formaldehyde, glutaraldehyde
embalming, hospital workers
acrylates
adhesives handlers
drugs (e.g., antibiotics, psyllium)
pharmaceutical
manufacturing/packaging, health workers

11. Most Common Causes of Asthma

12. Number of Allowed Claims
Number of allowed claims for OA induced by diisocyanates and OA induced by other causes by year of onset. A significant change occurred in the proportion of OA induced by diisocyanates and OA induced by other causes in the years 1987–93 (p=0.001).

13. Ontario Legislation
In Ontario, legislation introduced in 1983:
Requiring monitoring of diisocyanate concentrations to maintain 8 hour average concentrations below 5 ppb,
short term exposure concentrations below 20 ppb.

14. Medical Surveillance Measures
A pre-employment respiratory questionnaire, and spirometry;
Repeated respiratory questionnaires every 6 months and spirometry at least on an annual basis.
Workers with lower respiratory symptoms on questionnaire, or changes is spirometry required to have a medical assessment:
ability to continue work with diisocyanates.

15. Changes in Rates and Severity of Compensation Claims for Asthma due to Diisocyanates
In Ontario:
Numbers of claims for OA induced by diisocyanates:
9-15 claims/year in
55-58 claims/year in
19-20 claims/year by

16. COMMON HIGH MOLECULAR WEIGHT AGENTS CAUSING OCCUPATIONAL ASTHMA
Occupations at Risk
Plant-derived substances:
flour and grain dusts
latex
enzymes
gums
bakers, millers
health workers
detergent making, detergent users,
pharmaceutical workers,
food processing,
meat tenderizer producer
carpet makers,
pharmaceutical workers

17. COMMON HIGH MOLECULAR WEIGHT AGENTS CAUSING OCCUPATIONAL ASTHMA - continued
Occupations at Risk
Animal-derived allergens:
laboratory animals
crab/seafood
egg protein
grain mites, insects
animal handlers, laboratory workers
seafood processing
egg production
silk workers

18. CAUSES OF OCCUPATIONAL SENSITIZATION (examples)
Bakeries
wheat,
other cereals,
enzymes (e.g., fungal amylase)
Health care workers
natural rubber latex in gloves,
psyllium in laxatives,
penicillin-derived antibiotics, glutaraldehyde
Laboratories
animal proteins,
enzymes,
antibiotics,
other pharmaceutical products
Companies using or making polyurethane foam or spray paints
Diisocyanates
Electronic workers
colophony, amines, acrylic glues

19. Diagnosing Occupational Asthma:
Stepwise procedure:
(i) Does the patient have asthma (variable airflow limitation/bronchial hyperresponsiveness)?
(ii) Is the asthma work-related?
(iii) What are the causative and/or triggering substance or work environments?
What workplace modifications would make it safe for the patient to continue working or return to work and/or would protect coworkers?

20. Diagnosing Occupational Asthma
Pulmonary function tests pre- and post-bronchodilator

21. Diagnosis
The physical examination of an asthma patient is often deceptively normal and is a poor indicator of the degree of airflow obstruction. Objective measurements of airflow obstruction are needed to confirm the diagnosis of asthma and assess its severity. Spirometry and PEF should be repeated regularly to assess asthma control and evaluate the efficacy of therapy. When age or lack of cooperation prevent the performance of the necessary objective measurements, the diagnosis and evaluation is necessarily based on the history and physical examination.

22. Diagnosing Occupational Asthma: History
Review the exposure history (MSDS);
duration of exposure varies…
40% develop symptoms within 2 years
20%…after 10 years of exposure

23. Diagnosing Occupational Asthma:History
Improvement during weekends or vacations?
Patterns: if worse
less than 1 hour after starting workimmediate asthmatic response
4-6 hours after work start, sometimes in eveningdelayed/late response
May have dual/biphasic response

24. Diagnosing Occupational Asthma: Immunological Tests
Skin prick tests: available for allergens such as animal or plant extracts
Serum radio-immunosorbent (RAST) or enzyme-linked allergosorbent (ELISA) tests to identify specific IgE antibodies: miss common sensitizers such as isocyanates.

25. ADVANTAGES and DISADVANTAGES OF DIAGNOSTIC METHODS for OCCUPATIONAL ASTHMA
Questionnaire
Simple,
Sensitive
Low specificity
Immunologic testing
Only for high-molecular- weight and some low-molecular- weight agents;
identifies sensitization,
not work disease;
many allergens not available commercially
Bronchial responsiveness to methacholine or histamine
Not specific for occupational asthma;
occupational asthma not ruled out by a negative test
Measurement of FEV before or after work
Inexpensive
Low sensitivity and specificity
FEV1 post bronchodilator: 12% or more (ideally 15%); 20% with repeated measurements or after steroids.
PEF: 20% or more post-bronchodilator or after repeated measurements

26. Diagnosing Occupational Asthma
tests positive for asthma
exposure to allergen(s) at work
history consistent with work-related asthma
Note: specific challenge tests with suspected allergens not always possible (need specialized facilities)

27. Additional Tests for Occupational Asthma
Serial recording of PEF values, along with diary of symptoms:
qid X 2-4 weeks
time consuming/subject to inaccuracies
diurnal variability of at least 20% is suggestive of asthma

28. Diagnosing Occupational Asthma
Serial histamine or methacholine challenges within 24 hours of typical work exposure, and after 2-4 weeks off:
normal methacholine response virtually rules out work-related asthma

29. Management: Treat the asthma: control of nonoccupational triggers;
asthma medications;
patient education;
Work exposure for sensitizers-induced occupational asthma:
avoid any further exposure by workplace modifications or moving patient:
early removal from exposure best outcome.
eg pets, house dust mites, tobacco

30. Consider co-workers (are they at risk?)
Monitor patient’s course.
The majority of patients with occupational asthma
with latency do not recover, even after several
years away from exposure. There is bronchial
hyperresponsiveness, with chronic airway
inflammation.

31. EXAMPLES OF OCCUPATIONAL DISEASES
chronic obstructive lung
cadmium
Infections:
human-to-human
animal to human
soil to human
tuberculosis
hantavirus
coccidiomycoses
granulomatous lung disease
beryllium
hypersensitivity pneumonitis
(allergic alveolitis)
organic dusts
pulmonary fibrosis
asbestos, silica
bronchogenic carcinoma
asbestos

32. Hypersensitivity Pneumonitis (allergic alveolitis)
Condition localized to the alveoli
Produces mainly restrictive lung disease
Cause: inhalation of tiny antigens such as spores of microorganisms or avian proteins

33. Hypersensitivity Pneumonitis
The most common: farmer’s hypersensitivity pneumonitis (FHP) or farmer’s lung:
Symptoms most prevalent in cold wet climates that favour fungal overgrowth, and in the winter months when stored crops are used for animal feed.

34. Hypersensitivity Pneumonitis (examples)
Farmer’s Lung
Bird Fancier’s Lung
Humidifier Lung
Wood Worker’s Lung
Mouldy hay & straw
Bird droppings & feathers
Water from humidifiers & air conditioners
Bark stripping; wood pulp & chips

35. Hypersensitivity Pneumonitis: Acute Presentation
Acute immunologic reaction to antigenic challenge from organic dusts:
Symptoms of dry cough, dyspnea, fever, chills, and fatigue.
Symptoms arise 4-6 hours after exposure, persist up to 12 hours, followed by spontaneous recovery

36. Hypersensitivity Pneumonitis: Chronic
Exposure to the sensitizing agent on a recurrent basis can result in irreversible lung damage (pulmonary fibrosis, reduced lung function and impaired gas exchange)
Symptoms:
Cough with sputum
Dyspnea, chills and fever
Fatigue & weight loss
Fine basilar inspiratory crackles

37. Hypersensitivity Pneumonitis Treatment
Stop exposure to the causative antigen
Steroids

38. The End

39. EXAMPLES OF OCCUPATIONAL DISEASES - continued
Wood work
wood dusts (e.g., plicatic acid in red cedar),
fungal spores,
phenol-formaldehyde resins,
formaldehyde in particle board
Metal work
complex platinum salts,
nickel,
cobalt,
chromium compounds
Working with plants, fish, animals or insects
almost any plant, fish,
animal or insect protein with airborne or skin exposure