Occupational AsthmaOccupational Asthma

Dr afshin Dr afshin gheidigheidi

Occupational Asthma

Defined as a disease characterized by

variable airflow obstruction and/or airway hyper responsiveness due to causes & conditions attributable to a particular working environment & not to stimuli encountered outside the workplace.

Epidemiology

◙ OA has become the most common occupational lung disease in developed countries .

◙ Asthma affects 5-10% of the population worldwide and in developed countries.

◙ About 13% of all new onset asthma can be related to occ

OCCUPATIONAL ASTHMA

Sensitizer-induced OA (immunologically mediated)

Irritant-induced OA (non Imunologically mediated)

Work-related aggravation of asthma

Sensitizer-induced OA (immunologically mediated)

Sensitizer-induced OA

Causes :

• Agents can cause asthma by IgE-dependent or IgE-independent mechanisms.

• Over 300 agents in the workplace have been implicated in causing asthma.

High molecular weight agents

• Animal-derived material ……………………………………………………………………………………………..

Dander Excreta Secretions Serum• Plant-derived material

…………………………………………………………………………………… Flour Grain Castor bean Coffee bean Wood dust Vegetable gum Psyllium Latex•

Enzymes………………………………………………………………………………………………………………………

a-amylase Papain Alcalase Bacillus subti/is derived enzyme

Animal, poultry and insect work, veterinary medicine, fishing and fish processing, I aboratory work

Bakery Grain elevator and terminal and feed mill Oil manufacture Food processing Sawmill, carpentry, furniture work Printing Healthcare Latex

Bakery Food processlnq Pharmaceutical industry Detergent enzyme industry

Low molecular weight agents

• Spray paints……………………………………………………………………………………

Toluene diisocyanate Dimethyl phenyl diisocyanateHexamethylene dilsocyanate • Wood

dust……………………………………………………………………………………. Western red cedar• Acid

anhydride………………………………………………………………………………

• Biocides……………………………………………………………………………………….

Formaldehyde Glutaraldehyde Chloramine T • Colophony –

fluxes……………………………………………………………………………

Maufacture of plastic, foam Insulation Automobile spray paint

Sawmill worker, carpenter, furn iture maker

Users of plastics, epoxy resins

Healtncareworkers

Electronic workers

PATHOPHYSIOLOGY

• Results from a complex pathogenic cascade involving a number of different inflammatory cells and mediators

• Th2-like CD4 T cells (secrete IL-4, IL-5, and IL-B) play a key role in recognizing antigens and co ordinating the complex acute and chronic asthmatic responses.

Sensitizer-induced OA

Sensitizer-induced OA

• High molecular weight compounds (>5 kDa) include flour, laboratory animal proteins, and detergent enzymes.

• Are usually proteins or polysaccharides, and induce specific IgE antibodies that mediate the asthmatic response

• Often affect atopic subjects and IgE specific antibodies can be

detected in most affected asthmatics .

PATHOPHYSIOLOGY…

• Low molecular weight agents such as platinum, anhydrides, & isocyanates likely act as haptens, combining with amino groups on proteins to form an antigen

• Platinum induce specific IgE antibodies, similar to large molecular weight agents.

• Diisocyanates and plicatic acid (the agent responsible for Western

red cedar asthma) may utilize IgE independent mechanisms.

Sensitizer-induced OA

Final pathologic features in the airways

• Subepithelial fibrosis.• Hypertrophy of airway smooth muscle.• Edema of the airway wall.• Accumulation of inflammatory cells .• Obstruction of the airway lumen by exudate and/or mucus.

EXPOSURE FACTORS

• Exposure is the single most important determinant of the

incidence of OA .

• A dose-response relationship .

• Concomitant environmental exposures

Sensitizer-induced OA

HOST DETERMINANTS

• Atopy

• Smoking

• Non-allergic bronchial hyper-responsiveness

• Genetic markers

• Upper airway symptoms

Sensitizer-induced OA

CLINICAL FEATURES AND DIAGNOSIS

• History

• Affects only a portion of exposed workers and develops after a variable latent period of exposure.

• Symptoms typically develop from several months to years after the onset of exposure.

• Delayed symptoms after work in the evening

Sensitizer-induced OA

CLINICAL FEATURES AND DIAGNOSIS …

• Spirometry and non-specific challenge testing• Serial monitoring of bronchial hyper -responsiveness • Serial monitoring of PEF • Immunologic tests• Specific challenge tests• New techniques

MANAGEMENT

• Removal from further exposure to that agent

• Medical treatment

• Protective equipment

Sensitizer-induced OA

OUTCOME

worse outcomes :

longer duration of symptoms and exposure .

Delayed diagnosis .

Greater severity.

Sensitizer-induced OA

PREVENTIONPREVENTION

• Primary prevention

• Secondary prevention

Sensitizer-induced OA

Irritant-induced OA (non imunologically mediated)

CAUSES

• The best example is reactive airways dysfunction syndrome (RADS).

• Non immunological mechanisms

• Exposure to a single, high level of irritant gases, fumes, and smoke

EXPOSURE FACTORS

Exposure conditions are central to the

diagnosis of irritant induced asthma & RADS.

CLINICAL FEATURES AND DIAGNOSIS

History may be of the acute onset of asthma symptoms within 24 hours of a high exposure to a respiratory irritant .

Criteria for diagnosis of irritant-induced asthma

Onset of asthma symptoms, usually within 24 hours following exposure to a high level of a respiratory irritant agent.

Persistence of symptoms for at least 12 weeks.

Objective evidence of asthma: airway hyper-responsiveness on histamine or methacholine challenge, or airflow limitation with significant bronchodilator responsiveness (at least 12% increase in FEVl).

No previously documented evidence of asthma or other chronic lung disease.

MANAGEMENT

Workers should be managed in the same way as those with aggravation of underlying asthma

OUTCOME

Much less information available

some had persistence Of asthma for several years while other had clearing within a few months

PREVENTION

• Good occupational hygiene practices in the workplace

• worker education

Aggravation of Asthma

CAUSES

Irritants (at exposure levels which can be far less

than that usually associated with RADS )

EXPOSURE FACTORS

• Even low concentrations of respiratory irritants can aggravate pre-existing asthma.

• Second-hand cigarette smoke, cleaning agents, paints, fumes, dust .

• Viral upper respiratory infections .

• A relevant allergen exposure .

CLINICAL FEATURES AND DIAGNOSIS

• History of asthma symptoms which worsen at work and improve to some extent after the work shift

• Objective evidence of asthma

• Objective demonstration of worsening of asthma at work

MANAGEMENT

• Optimize the medical management of their asthma.

• Limiting exposure to relevant environmental allergens and non-occupational irritants

• Education

OUTCOME

• Little published documentation as to the outcome of work-related aggravation of asthma

• Often there is a temporary aggravation of asthma at work ( if there have been unusually high exposures to irritants ) .

PREVENTION

• Largely directed at the individual who has asthma .

• Pre-employment counseling .

THE END