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

OCCUPATIONAL ASTHMA

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.

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.

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

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.

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.

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.

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

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

Most Common Causes of Asthma

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).

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.

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.

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 1980-83 55-58 claims/year in 1988-90 19-20 claims/year by 1992-93

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

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

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

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?

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

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.

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

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

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.

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

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)

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

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

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

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.

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

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

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.

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

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

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

Hypersensitivity Pneumonitis Treatment Stop exposure to the causative antigen Steroids

The End

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