Occupational asthma

Overview 
Theory 
Diagnosis 
Management 
Follow up 
Resources 

Occupational asthma (OA) should be considered in all adults with asthma.[59]

Following the clinical and exposure history, the diagnosis of OA requires the clinician to:

objectively establish the diagnosis of asthma, and then
confirm a relationship between asthma and work.

For a valid assessment, the investigation of OA should be undertaken before the worker leaves the workplace, as avoidance of exposure may influence the reliability of the test procedures. This is particularly true for patients with sensitiser-induced OA. Assessment of suspected sensitiser-induced OA should ideally occur when the patient has recently been exposed to the suspected sensitiser and has recently experienced asthma symptoms.[23]

Prompt diagnosis is important, as prolonged exposure to a sensitising agent may result in poorer clinical outcomes. However, an accurate diagnosis of sensitiser-induced OA is also of extreme importance, as this diagnosis may incur very significant work limitations that may impair a patient's ability to maintain employment.[59] If possible, diagnosis is best made by referral to a specialist with expertise in occupational asthma.[60][61]

Irritant-induced OA also requires a careful objective diagnosis to ensure correct management and compensation decisions.

Establishment of the diagnosis of asthma

Diagnosis of asthma is based on:

Compatible clinical history (typically recurrent episodes of dyspnoea, chest tightness, wheezing, or coughing).
Investigations that demonstrate variable airflow limitation (significant bronchodilator response on spirometry, non-specific bronchial hyper-responsiveness [NSBHR] to histamine or methacholine). These should be assessed using recommended protocols and definitions for positive responses.[62][63]
Exclusion of other respiratory pathology (chest imaging such as with a chest x-ray should be considered).[64]

For patients with irritant-induced OA, exclusion of previous respiratory disease is helpful in the diagnosis.

With consent, information should be obtained from the patient's primary care physician to establish whether the patient has received asthma treatment in the past. Where available, any previous pulmonary function tests carried out before the exposure incident should be obtained.

Establishment of work-relatedness of asthma

A full medical history should be taken including details of any recognised risk factors for OA (e.g., high-level exposure to sensitiser, atopy, and cigarette smoking).

A comprehensive occupational history should include questions about the patient's current and previous employment, with a focus on identifying exposure to a known sensitiser or any history of respiratory exposure to a high-level irritant.[24][65][66][67] Haz-Map: information on hazardous agents and occupational diseases Opens in new window A lack of recognised risk factors or exposure to a known sensitiser does not exclude a diagnosis of sensitiser-induced OA. If available, the patient should provide material safety data sheets of the substances used at the workplace.

A workplace visit may be required to measure exposure to any potentially sensitising agent.[23] The visit represents an opportunity to identify other workers affected by respiratory symptoms.[37] This assessment may be performed by an occupational hygienist.

The patient should be systematically questioned regarding the temporal relationship between symptoms and work exposure. Specifically, they should be asked about whether symptoms are worse, the same, or better on days away from work, while on holiday, during longer breaks, between shifts, or on weekends.[60][61] It should be noted, however, that advanced sensitiser-induced OA may be associated with less temporal variability in symptoms with workplace exposure. In some patients, asthma symptoms may be worse after finishing their shift than when at work.

For suspected sensitiser-induced OA, investigations should seek to objectively demonstrate a relationship between asthma and exposures.[37][68][69]

In the case of irritant-induced asthma, any documentation (timing and exposure details) of the acute work exposure event would be helpful in the diagnosis.

Investigations

A combination of investigations may be required to establish the diagnosis. This is often best achieved by early referral to a specialist with expertise in this area (pulmonary, allergy, or occupational).[59][60][61]

Supportive investigations include:[23][37][54][70]

Spirometry
Serial peak expiratory flow
Serial assessment of NSBHR
Immunological tests to identify sensitisation, such as skin prick testing (SPT) and immunoglobulin E (IgE) assays[Figure caption and citation for the preceding image starts]: Skin prick test results with natural rubber latex in a nurse with occupational asthmaFrom Tarlo SM, Wong L, Roos J, et al. Occupational asthma caused by latex in a surgical glove manufacturing plant. J Allergy Clin Immunol. 1990:85:626-631. Used with permission [Citation ends].

Initial tests

Spirometry should be performed in all patients with suspected occupational asthma.[23][70] If spirometry is not available, peak expiratory flow (PEF) may be used.[59] PEF is less objective than spirometry. Excessive variability in expiratory lung function is suggestive of a diagnosis of asthma.[59] A bronchodilator reversibility test should be performed in patients presenting with work-related respiratory symptoms. Serial PEF recordings are useful when the patient is still exposed to the potential causal agent and is able to record measurements during and away from work.[23][70]

An NSBHR challenge that significantly improves when the patient is away from work supports the diagnosis of sensitiser-induced OA, unless confounding factors such as a respiratory tract infection are present.[23][37][70] Serial tests (at work and off work) should be performed within 8 weeks. The off-work test should be performed after at least 10 days away from work.[37] Diagnosis of irritant-induced OA is supported by progressive improvement in methacholine or histamine responsiveness after an initial positive response following the exposure incident. However, absence of improvement does not exclude the diagnosis.[37]

NSBHR has a high negative predictive value when assessed while the patient is working, exposed to the suspected agent, and symptomatic.[71] In patients whose history suggests sensitiser-induced OA, the combination of single-measurement NSBHR with specific skin prick tests or IgE in prescreened patients seems to have high specificity.[68]

SPT should be used in combination with a clinical history and supportive pulmonary function tests.[23][37][70] There are few commercially available or standardised skin reagents for occupational agents.

Chest x-ray is not diagnostic of asthma, but is indicated in the assessment of respiratory symptoms to exclude other pathologies.[64]

Other tests

Specific serum IgE testing is performed only in specialised laboratories and used primarily for research purposes.[37] Specific serum IgE antibodies to high molecular weight allergens may be demonstrated.[23] IgE antibodies to sensitisers may, however, be demonstrated in a proportion of asymptomatic exposed workers.[40]

Specific serum IgE to low molecular weight sensitisers such as diisocyanates, trimellitic anhydride, and platinum salts may be demonstrated in some patients with sensitiser-induced occupational asthma.[23][37][55][72]

For many occupational allergens, serum IgE antibodies are less sensitive but more specific for the diagnosis than SPT.[37][73]

Additional testing for sensitiser-induced OA

The specific inhalation challenge (SIC; exposure to the specific agent) is considered the reference standard diagnostic investigation for sensitiser-induced OA.[23][37][54][69][70] However, it may only be available in a few specialised centres.

Workplace challenges can be performed. They may be especially useful if there are several potential sensitisers, but are time-consuming and difficult to organise.[23][37][69][70]

Assessment of eosinophil count via induced sputum cytology and fractional exhaled nitric oxide (FeNO) measurement may improve the sensitivity of SIC; their role in routine diagnosis of OA has not been established.[23]

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