Occupational Asthma

Dimas Trend Pinaka Baladika

Mahasiswa Program Pendidikan Dokter Spesialis, Fakultas Kedokteran, Universitas Lampung
Departemen Pulmonologi dan Kedokteran Respirasi, Fakultas Kedokteran, Universitas
Lampung

Abstract

Asthma is a respiratory disease commonly found in general medical practice and in various fields of study.
Twenty five percent of adult onset asthma is occupational asthma. Occupational asthma has become the most prevalent
occupational lung disease in developed countries. Allergens that cause occupational asthma are commonly found in work
place such as animal proteins, plant proteins, metal transition, chemical substances, etc. Pathogenesis of disease are based
on immunologically mediated with participation of specific IgE, immunologically mediated without evidence of
participation of IgE and non immunologic. The diagnosis of occupational asthma does not differ from the diagnosis of
general asthma. The difference is that the diagnosis of occupational asthma must be reassured that the exposure to
allergens involves a contact to irritating substance within workplace. The best treatment would be to avoid allergens in the
workplace.1,2

Key words : Occupational asthma (OA), allergens,

Introduction previously quiescent asthma (ie, asthma

as a child or in the distant past that has
Asthma is a disease with many been in remission) induced by either
variations (phenotype), usually sensitization to a specific substance,
characterized by chronic airway which is termed sensitizer-induced OA, or
inflammation. Asthma has two key by exposure to an inhaled irritant at work,
defining features: a history of respiratory which is termed irritant-induced OA.2
symptoms such as wheeze, shortness of Some literature called it work related
breath, chest tightness and cough that asthma instead of OA.
vary over time and in intensity, and
variable expiratory airflow limitation.3 By
definition of occupational asthma (OA) Diagnosis
and asthma are the same, the difference
is due to causes and conditions which are Workers with respiratory symptoms
attributable to a particular occupational may not be aware that work may be a trigger,
or they may suspect a relationship but may
environment. The definition issued by the
not raise this possibility due to fear of job-loss
American College of Chest Physicians
or reduction in income if changes need to be
further stipulates that OA refers to de made at work. Potentially greater education
novo asthmas or the recurrence of of workers abo
by web educational tools, borchures, and exposure at the onset or worseningof asthma
other means and standardized inclusion of symptoms. Changes in the work process that
questions in primary care regarding coincide with the onset of symptoms may
worsening of asthma symptoms with work help identify a culprit agent. Obtaining
and improvement off work (on weekend or material safety data sheets can be helpful in
holidays) may lead to greater recognition of identifying exposure in the work place and
OA. Other aspects of history include details of should be made available to the worker on
request. The history should also include Step1 : Establishing Asthma Diagnosis
questions about high exposure to an irritant The first step in the diagnostic workup
agent at work coinciding with the initial onset is to obtain a clinical and occupational history
of asthma symptoms that would suggest as described earlier. If a worker reports work
irritant-induced asthma. Work exacerbated related lower respiratory symptoms
asthma causes symptoms worse at work, consistent with possible work related asthma,
which may occur on a single occasion with an the next step is to objectively confirm asthma
unusual exposure at work or may occur more by showing reversibility in forced expiratory
regularly with exposure to irritants or volume in 1 second (FEV1) after inhaled
common allergens at work differentiating bronchodilator. Simple spirometry testing
asthma that has coincidentially started while should be performed before and after 2 to 4
working from occupational asthma can be inhalations of albuterol delivered by a
challenging. metered-dose inhaler. An increase in FEV 1 of
at least 12% after bronchodilator treatment
Table 1. Occupational Respiratory History for confirms asthma but alone is not sufficient to
Suspected Occupational Asthma establish a diagnosis of OA.
1. While at your current job, have you If reversibility in FEV1 cannot be
had wheezing, cough, chest tightness, demonstrated, methacholine challenge
or shortness of breath? testing is recommended. The methecoline
2. If you answered yes, do these test is performed by having the patient inhale
symptoms occur immediately after nebulized saline, which is followed by
coming to work?
inhalation of incremental doses of
3. If you answered yes, do these
symptoms begin hours after coming to
methacholine (0.125-25 mg/ml) every 5 to 10
work? If so, how many hours? minutes until a 20% decrease from the post
4. If you answered yes, do these saline FEV1 is observed or until all challenge
symptoms continue after coming home doses have been delivered without any
from work? If so, within how many decrease in FEV1. The provocative
hours and how long do these last? concentration eliciting an FEV1 decrease of
5. If you answered yes, do the symptoms 20% is referred to as the methacholine PC 20
decrease on weekends or vacations? with a positive test reaction defined as PC 20 no
6. How long were you working at your higher than 16 mg/ml.
current job before you first noticed
respiratory symptoms?
7. Are you a current smoker, former
Step 2: Determinng Workplace Connection
smoker? If yes, record pack-years. Once asthma is confirmed, a decrease in lung
8. Have you ever been diagnosed with function during the work shift concomitant
asthma, allergic rhinitis, chronic with exposure to a suspect causative agent is
bronchitis, or chronic obstructive required for confirming OA. The preferred
pulmonary disease? If yes, provide approach is to perform a specific inhalation
details. challenge (SIC) in a specialized laboratory. The
9. Have you experienced nasal or eye SIC is considered the diagnostic gold standard
symptoms (sneezing, itching of the for OA. Serial measurement of peak
nose or eyes) that begin or worsen at
expiratory flow rate (PEFR) during work and
work? If yes, provide details.
10. If the patient does have asthma, list away from work exposure is the alternative
the required controller and rescue approach for confirming OA from an
medication, frequency of occupational sensitizer. OA is confirmed by
exacerbations, and relation of these to consistent decreases in PEFR on days at work
work exposure. while exposed to a suspect causative agent
that increases on days away from work.
Stepwise Evaluation of OA Due to a Workplace monitoring of PEFR has a
Workplace Sensitizer sensitivity of 81% and a specificity of 74% for
correctly identifying OA.
Utility of Allergy Testing for OA
Whenever appropriated, specific IgE testing
with high molecular weight (HMW)
occupational allergens should be conducted
with skin prick testing and or serum specific
IgE. It should be emphasized that specific IgE
determines sensitization status, but alone
does not establish or exclude an OA diagnosis.
A positive skin test or serum specific IgE assay
reaction can assist in establishing causation of
OA especially if allergen exposure to that
substances is associated with work related
decreases in PEFR.
 Asthma Diagnosis
Confirmed

No Yes

Specific Inhalation Serial Peak Expiratory Flow

Challenge Rate (2 weeks at work and
away from work)

Positive

No Occupational
Occupational Asthma
Negative
Asthma

Figure 1. Stepwise approach to evaluating the worker with work related lower respiratory symptoms. Asthma is confirmed
by reversibility in forced expiratory volume in 1 second (FEV 1) or with methacholine testing. If asthma is present, then
occupational asthma (OA) is confirmed by a positive specific inhalation challenge (if available) or serial monitoring of peak
expiratory flow rate for 2 weeks at work and 2 weeks away from work.
 OA is the most common occupational lung disease encountered in clinical practice. In
finlad 2% among new asthma cases are OA. 5 % cases if exposure to isocyanate or wood
dust, 50% cases if exposure to proteolytic enzymes. In adult asthmatic, OA can account for
15%-33% of cases, but delays in diagnosis remain common and lead to worse outcomes. 4
Occupational asthma may encompass both immunological and non-immunological
causes. Immunological OA occurs upon exposure to an agent after a latent period of
immune sensitization, while non immunological asthma may or may not occur after a
latency period of exposure to an agent(s) which does not induce immune sensitization as
determined by currently available technology. 5 respiratory sensitization to an occupational
agent is one of very few well established causes of adult asthma. It is thus potentially
preventable and furthermore offers a rare opportunity to cure an asthmatic patient of their
disease. Moreover, it seems to be a costly disease. In the UK, the total lifetime costs of cases
of occupational asthma reported are estimated to be up £100 million each year. 4,6 In
Indonesia, the author did not find the particular data enough. For these reasons, the disease
has a high profile in industrial legislation in most of the developed world. Therefore
especially faculty of medicine, University of Lampung provides a special place for the field of
agromedicine to provide understanding about work related asthma to governments,
companies, and communities working in the industry.

Spesific causative agents of OA

Although there are hundreds of agents used in the workplace that can cause OA, 50% to
90% of reported cases have been associated with exposure to flour, diisocyanates, latex,
persulfate salts, aldehydes, animals, wood dusts, metals, and enzymes.
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