Occupational Asthma

When should someone suspect occupational asthma?

Work-related asthma is not uncommon but may be less well known. There are many explanations for
this. First, the relationship between asthma symptoms and work may not be obvious to patients.
Second, a doctor may not think to ask specifically about any work-related symptoms. Third, a
clinician may not feel confident in assessing work-related asthma. Lastly, there is limited information
regarding occupational asthma and its causes in international asthma guidelines.
There are two main types of work-related asthma. Occupational asthma is caused by exposure to air in
the work environment. Meanwhile, in asthma that is exacerbated by work, various non-specific
factors in the workplace can worsen asthma symptoms, but the asthma is not caused by work. The
characteristics of these two conditions are not easy to distinguish from each other. Work-exacerbated
asthma is common and is estimated to affect one-fifth of working asthma patients.
Recognizing occupational asthma is challenging in many ways. For one thing, the observation that
symptoms may worsen at work (or improve afterwards) may not be possible. In addition, work-related
factors can cause asthma (either de novo or due to asthma) or can worsen pre-existing asthma
symptoms. A clinician should consider the possibility of a diagnosis of occupational asthma in
working-age patients who have new symptoms of asthma, reappearance of asthma in childhood,
worsening of asthma control, or when unexplained airflow obstruction is detected (table 1). Suspicion
will be higher if the patient works in a high-risk job or is exposed to asthma-causing agents at work
(table 2). Based on the underlying mechanisms, there are two types of occupational asthma with
different clinical features which are summarized in the following section and in table 3.

Severe asthma triggered by sensitizers

Occupational asthma triggered by sensitizers is considered the most common type of occupational
asthma and is triggered by high molecular weight or low molecular weight agents . HMW agents are
(glyco)proteins of animal, plant, or microbial origin, which have the ability to cause sensitization
mediated by immunoglobulin (Ig) E. LMW agents are synthetic chemicals, metals, and other natural
agents that are thought to cause immunological reactions , however specific IgE antibodies are often
not detected (table 2). Occupational asthma triggered by sensitizers always requires repeated periods
of exposure to the allergen before the onset of symptoms. It is during this “latent period” that
sensitization and immunological responses develop. The latent period can vary from weeks to years,
but the highest risk of developing asthma is in the first 2 years after exposure.
Asthma symptoms that improve after leaving work also increase the likelihood of a diagnosis of
occupational asthma, but the relationship between symptoms and work is not always clear. Some
occupational asthma patients may report that their symptoms occur at work or while doing certain
jobs, while others may experience more pronounced symptoms in the afternoon or evening, that is,
outside the workplace. In addition, triggers outside of work, such as cigarette smoke, exercise, and
cold air, can worsen existing symptoms. The pattern of overt work-related symptoms generally
decreases with increasing duration of asthma. These features emphasize the importance of considering
the possibility of occupational asthma, even when the patient experiences few symptoms at work and
most symptoms outside the workplace. Occupational asthma caused by HMW agents is more
common in people with atopy and almost always occurs in conjunction with occupational rhinitis and
conjunctivitis. These symptoms may begin before, or at the same time as, asthma symptoms.
Therefore, any patient with work-related upper or lower respiratory symptoms should raise clinical
suspicion. Occupational asthma induced by LMW agents is less common in rhinitis, and usually has a
delayed asthmatic response, especially compared with asthma induced by HMW agents.