Download OCCUPATIONAL ASTHMA Sensitizer

Occupational Asthma
Dr afshin gheidi
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 IgEindependent mechanisms.
• Over 300 agents in the workplace have been
implicated in causing asthma.
High molecular weight agents
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Animal-derived material ……………………………………………………………………………………………..
Dander
Excreta Secretions
Serum
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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
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 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 coordinating the complex
acute and chronic asthmatic responses.
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 .
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 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.
Final pathologic features in the airways
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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
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
CLINICAL FEATURES AND DIAGNOSIS …
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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
• Protective equipment
Sensitizer-induced OA
OUTCOME
worse outcomes :
longer duration of symptoms and exposure .
Delayed diagnosis .
Greater severity.
Sensitizer-induced OA
PREVENTION
• Primary prevention
• Secondary prevention
Irritant-induced OA
(nonimunologically mediated)
CAUSES
• The best example is reactive airways dysfunction
syndrome (RADS).
• Nonimmunological 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