Occupational Asthma Dr afshin gheidi Occupational Asthma Defined

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Occupational Asthma Dr afshin gheidi

Occupational Asthma Dr afshin gheidi

Occupational Asthma Defined as a disease characterized by variable airflow obstruction and/or airway hyper

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.

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

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 (immunologically mediated)

Sensitizer-induced OA Causes : • Agents can cause asthma by Ig. E-dependent or Ig.

Sensitizer-induced OA Causes : • Agents can cause asthma by Ig. E-dependent or Ig. Eindependent mechanisms. • Over 300 agents in the workplace have been implicated in causing asthma.

High molecular weight agents • • • Animal derived material ………………………………………………. . Dander Excreta

High molecular weight agents • • • Animal derived material ………………………………………………. . Dander Excreta Secretions Serum Animal, poultry and insect work, veterinary medicine, fishing and fish processing, I aboratory work Plant derived material ………………………………………… Flour Bakery Grain elevator and terminal and feed Grain mill Oil manufacture Food processing Castor bean Sawmill, carpentry, furniture work Printing Coffee bean Healthcare Latex Wood dust Vegetable gum Psyllium Latex Enzymes…………………………………………………………… a-amylase Papain Bakery Food processlnq Pharmaceutical Alcalase industry Detergent enzyme industry Bacillus subti/is derived enzyme

Low molecular weight agents • Spray paints………………………………………… Maufacture of plastic, foam Insulation Toluene diisocyanate

Low molecular weight agents • Spray paints………………………………………… Maufacture of plastic, foam Insulation Toluene diisocyanate Automobile spray paint Dimethyl phenyl diisocyanate Hexamethylene dilsocyanate • Wood dust………………………………………… Western red cedar Sawmill worker, carpenter, furn iture maker • Acid anhydride……………………………………… Users of plastics, epoxy resins • Biocides…………………………………………… Formaldehyde Glutaraldehyde Chloramine T Healtncareworkers • Colophony – fluxes…………………………………… Electronic workers

Sensitizer-induced OA PATHOPHYSIOLOGY • Results from a complex pathogenic cascade involving a number of

Sensitizer-induced OA PATHOPHYSIOLOGY • Results from a complex pathogenic cascade involving a number of different inflammatory cells and mediators • Th 2 like CD 4 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 • High molecular weight compounds (>5 k. Da) include flour, laboratory animal

Sensitizer-induced OA • High molecular weight compounds (>5 k. Da) include flour, laboratory animal proteins, and detergent enzymes. • Are usually proteins or polysaccharides, and induce specific Ig. E antibodies that mediate the asthmatic response • Often affect atopic subjects and Ig. E specific antibodies can be detected in most affected asthmatics.

Sensitizer-induced OA PATHOPHYSIOLOGY… • Low molecular weight agents such as platinum, anhydrides, & isocyanates

Sensitizer-induced OA 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 Ig. E antibodies, similar to large molecular weight agents. • Diisocyanates and plicatic acid (the agent responsible for Western red cedar asthma) may utilize Ig. E independent mechanisms.

Final pathologic features in the airways • • • Subepithelial fibrosis. Hypertrophy of airway

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.

Sensitizer-induced OA EXPOSURE FACTORS • Exposure is the single most important determinant of the

Sensitizer-induced OA 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

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

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

CLINICAL FEATURES AND DIAGNOSIS … • • • Spirometry and non-specific challenge testing Serial

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

Sensitizer-induced OA MANAGEMENT • Removal from further exposure to that agent • Medical treatment

Sensitizer-induced OA 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.

Sensitizer-induced OA OUTCOME worse outcomes : longer duration of symptoms and exposure. Delayed diagnosis. Greater severity.

Sensitizer-induced OA PREVENTION • Primary prevention • Secondary prevention

Sensitizer-induced OA PREVENTION • Primary prevention • Secondary prevention

Irritant-induced OA (non imunologically mediated)

Irritant-induced OA (non imunologically mediated)

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

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 &

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

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

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

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

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

PREVENTION • Good occupational hygiene practices in the workplace • worker education

Aggravation of Asthma

Aggravation of Asthma

CAUSES Irritants (at exposure levels which can be far less than that usually associated

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.

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

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

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

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.

PREVENTION • Largely directed at the individual who has asthma. • Pre employment counseling.

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