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JOURNAL READING SUBDIVISION ALLERGY IMMUNOLOGY

Occupational
OccupationalAsthma
Asthma

SRI HANDAYANI LUBIS

Introduction
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Asthma common in the general

population, including those in the workforce.


Work exposures can cause or exacerbate
asthma and can also be associated with
asthma variants (e.g., eosinophilic bronchitis
and aluminum potroom asthma).
Asthma can affect the ability to work.
Occupational asthma asthma due to
conditions attributable to work exposures
and not to causes outside the workplace.

Sensitizer-Induced Asthma
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Occupational asthma can be caused by a specific

workplace sensitizer agent that induces asthma


through mechanism associated with a specific
immunologic response.
Occupational sensitizers commonly highmolecular weight agents (>10 kD, usually a protein
or glycopeptide) cause production of specific IgE
antibodies & typical allergic responses.
Low-molecular-weight occupational chemicals can
also cause sensitization and asthma.

Nonsensitizing, Irritant-Induced
Occupational Asthma
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Irritant-induced occupational asthma

occupational asthma occurs from exposure to


agents airway irritants & absence of sensitization.
Low concentrations of airborne irritating
chemicals at work could induce asthma (termed
by some authors not-so-sudden asthma or lowdose reactive airways dysfunction syndrome).
Previous atopic disease or childhood asthma and
the long-term low-level exposure raised the
possibility that symptoms may have resulted from
exacerbation of underlying airway
hyperresponsiveness or coincidental onset of
asthma, rather than occupational asthma itself.

Epidemiology
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Occupational asthma reported in a minority of

workers exposed to most known sensitizing agents


(usually 10% or less in cross-sectional studies).
Analysis of population attributable risk 16.3% of
all cases of adult-onset asthma caused by
occupational exposure.
There is discrepancy between rates asthma
diagnosed by a health professional as being work
related (4.7% of all new asthma cases) and rates
self-reported cases of work-related asthma (18.2%
of all new asthma cases);
Explanation for the difference occupational
asthma is underrecognized in clinical practice.

Pathophysiology
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Pathophysiological occupational asthma similar

to those of nonwork-related asthma, including an


IgE dependent mechanism associated with high
molecular-weight sensitizing agents and some lowmolecular-weight sensitizers.
For asthma induced by other low-molecular-weight
sensitizers, such as diisocyanates, and for irritant
induced asthma, the mechanisms are incompletely
delineated.

Diagnosis Sensitizer-Induced Asthma


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Occupational asthma should be suspected in

every adult with new-onset asthma.


A latency period ranging from weeks to years after
the first exposure to the sensitizer observed
before the initial onset of work-related symptoms.
Sensitizer-induced symptoms begin variably at
the beginning of the work shift, toward its end, or
even in the evening after working hours;
Remission or improvement occurs during
weekends and holidays.

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Diagnosis Irritant-Induced
Asthma
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Relies on a suggestive clinical history along with

the demonstration of airflow limitation or airway


hyperresponsiveness.

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Prevention
Preventionand
andManagement
Management

Sensitizer-Induced14Asthma
Primary prevention aims to prevent

sensitization to work-place agents, by replace


known sensitizing agents with nonsensitizers.
Secondary prevention includes :
early identification of workers with occupational
exposure to asthma-causing agents by medical
surveillance (periodic respiratory questionnaires
with or without spirometry and immunologic tests)
investigations to confirm diagnosis and
then remove the person from further exposure.

To prevention of further exposure when possible,

involves tertiary prevention with pharmacologic


management that follows 15
clinical-practice guidelines.
Complete avoidance of exposure to the causal agent
remains the management of immunologic
occupational asthma and reduced exposure is less
beneficial than exposure cessation
Immunotherapy has been tested for a few sensitizing
agents with IgE-dependent reactions.
Although immunotherapy can reduce cutaneous and
respiratory symptoms, systemic reactions often
occur.
Improvement with the monoclonal anti-IgE antibody
omalizumab reported in a few patients with
occupational asthma who remained exposed to the
causal agent.

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Irritant-Induced Asthma
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The most straight forward cases of irritant-induced

asthma are due to accidental exposure.


Prevention include :
occupational-hygiene measures that
ensure the safety of workers in environments,
containment,
good ventilation,
worker education regarding safety practices, and,
when other measures are not sufficient, use of fittested respiratory protective devices.

Conclusions
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Improved understanding of occupational asthma

may enhance our knowledge about other types of


asthma.
To minimize the risk of long-term impairment
from occupational asthma health care
practitioners should consider this diagnosis early
in their evaluation of adults with symptoms of
asthma.

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THANK YOU

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