Differentials

Work-exacerbated asthma

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Non-specific worsening of pre-existing or coincidental asthma due to workplace irritants such as dust and fumes, or common allergens that may be present in the workplace.​​[71]

Usually a history of preceding asthma before current employment, which is associated with worsening asthma symptoms.

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Negative specific inhalation challenge (when the correct agent is identified) and lack of change in serial non-specific bronchial hyper-responsiveness (NSBHR) testing are suggestive of work-exacerbated asthma.

However, lack of change in airway responsiveness away from the suspected work agent does not exclude occupational asthma (OA). Advanced or long-standing sensitiser-induced OA may be associated with less temporal variability in symptoms and lung function with workplace exposure.

Occupational eosinophilic bronchitis

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Bronchitis (chronic cough) worse at work may be present but without other manifestations of asthma (e.g., wheezing).[43]

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Sputum eosinophilia (worse at work) in the absence of demonstrable variable airflow limitation or non-specific airway hyper-responsiveness.[84]

Coincidental non-occupational asthma

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Asthma is a common condition that frequently will present initially, or recur in adult life.

The clinician should take a history of the home environment to identify other potential allergens such as cats or dust. Unrelated asthma should be considered if no features of irritant-induced occupational asthma (OA), a workplace sensitiser, or objective evidence of worsening at the workplace to suggest sensitiser-induced OA are identified.[36][85]

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Clinical diagnosis: lack of features to suggest irritant-induced OA, or lack of changes in symptoms, medication needs, pulmonary function, or bronchial hyper-responsiveness associated with workplace exposures that suggest sensitiser-induced OA make the presence of non-occupational asthma more likely.

Hypersensitivity pneumonitis

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Many substances that cause occupational asthma may also cause hypersensitivity pneumonitis (HP), including diisocyanate exposure.

In HP, wheezing does not tend to be a prominent feature, and patients with the acute form may experience fevers and chills.

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Absence of (or mild) non-specific bronchial hyper-responsiveness (NSBHR).

Other pulmonary function abnormalities associated with HP include a restrictive ventilatory defect and impairment in gas transfer.

Chest x-ray shows patchy, nodular infiltrates in acute and subacute HP; fibrosis in chronic HP.

High-resolution CT chest in chronic HP shows ground-glass shadowing/attenuation and poorly defined micronodules. There is extensive honeycombing in late stages.

Chronic bronchitis/COPD

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Dyspnoea may occur with or without wheezing, cough, or sputum. Examination may show barrel chest, hyper-resonance to percussion, and distant breath sounds.

It is estimated that approximately 15% of COPD may be work-related from exposure to factors such as mineral and organic dusts.[86] COPD should especially be considered if there is a history of tobacco use and less day-to-day variability in symptoms.

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Lack of significant variability in airflow obstruction and an absence of, or only mild, non-specific bronchial hyper-responsiveness (NSBHR; although COPD and asthma may co-exist).

Vocal cord dysfunction

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Upper airway disorders commonly mimic asthma.[87]

Asthma may be present in addition to vocal cord dysfunction.

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Pulmonary function testing may suggest extrathoracic airflow limitation caused by paradoxical vocal cord movement by the presence of a flattened inspiratory flow volume loop.[88]

Lack of objective airflow obstruction or non-specific bronchial hyper-responsiveness (NSBHR) is supportive of the diagnosis; however, assessment by an otolaryngologist and speech therapist experienced in the field is recommended.[87]

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