The diagnosis is based upon a history of symptoms after exposure to the allergen and clinical tests. A physician may take blood tests, seeking signs of inflammation, a chest X-ray and lung function tests. The sufferer shows a restrictive loss of lung function.

Precipitating IgG antibodies against fungal or avian antigens can be detected in the laboratory using the traditional Ouchterlony immunodiffusion method wherein 'precipitin' lines form on agar plate. The ImmunoCAP technology has replaced this time consuming, labor-intensive method with their automated CAP assays and FEIA (Fluorescence enzyme immunoassay) that can detect IgG antibodies against Aspergillus fumigatus (Farmer's lung or for ABPA) or avian antigens (Bird Fancier's Lung).

Although overlapping in many cases, hypersensitivity pneumonitis may be distinguished from occupational asthma in that it is not restricted to only occupational exposure, and that asthma generally is classified as a type I hypersensitivity. Unlike asthma, hypersensitivity pneumonitis targets lung alveoli rather than bronchi.

Lung biopsies can be diagnostic in cases of chronic hypersensitivity pneumonitis, or may help to suggest the diagnosis and trigger or intensify the search for an allergen. The main feature of chronic hypersensitivity pneumonitis on lung biopsies is expansion of the interstitium by lymphocytes accompanied by an occasional multinucleated giant cell or loose granuloma.

When fibrosis develops in chronic hypersensitivity pneumonitis, the differential diagnosis in lung biopsies includes the idiopathic interstitial pneumonias. This group of diseases includes usual interstitial pneumonia, non-specific interstitial pneumonia and cryptogenic organizing pneumonia, among others.

The prognosis of some idiopathic interstitial pneumonias, e.g. idiopathic usual interstitial pneumonia (i.e. idiopathic pulmonary fibrosis), are very poor and the treatments of little help. This contrasts the prognosis (and treatment) for hypersensitivity pneumonitis, which is generally fairly good if the allergen is identified and exposures to it significantly reduced or eliminated. Thus, a lung biopsy, in some cases, may make a decisive difference.

Diagnosis of occupational asthma uses several techniques.

A non-specific bronchial hyperreactivity test can be used to help diagnose occupational asthma. It involves testing with methacholine, after which the forced expiratory volume in 1 second (FEV) of the patient is measured. This test is often used for measuring the intensity of a person's asthma and to confirm that the person needs to be treated for asthma.

Other non specific tests could require the patient to run for a few minutes at a continuous pace. In this case, the individual’s peak expiratory flow rate (PEFR) is measured, showing how fast a person can exhale. PEFR can also be measured at work to see if there is a difference from the PEFR in a controlled environment. Measuring PEFR at work is a highly reliable test for occupational asthma.

A skin prick test is usually performed on the inner forearm where a grid is marked and a drop of the allergens to be tested are placed on the arm in the grid. Once this has been done, the skin is pricked through the drop using a lancet. Reactions, if any, occur within 10 to 15 minutes and these results can then be analyzed.

Immunoglobulin E is an antibody found in human blood and is effective against toxins. Since it can also trigger allergic reactions to specific allergens like pollen, the IgE test is performed to evaluate whether the subject is allergic to these substances.

A spirometer is a device used to measure timed expired and inspired volumes, and can be used to help diagnose occupational asthma.

Specific inhalation challenges test for reactions to substances found in the workplace. One method is a whole body sealed chamber where the patient is exposed to articles that are present in their workplace. This method has the advantage of being able to assess, albeit highly subjectively, ocular and nasal symptoms as well as a reduction in FEV. Another test requires the patient to breathe aerosols of the suspected asthmagens through an oro-facial mask. These asthmagens are aerosolized using closed circuit chambers, and the quantities and concentrations administered are minute and extremely stable, to minimize the risk of exaggerated responses.

Prevention of occupational asthma can be accomplished through better education of workers, management, unions and medical professionals. This will enable them to identify the risk factors and put in place preventive measures, including respiratory protection and exposure limits.

The differential diagnosis for berylliosis includes:

- Sarcoidosis

- Granulomatous lung diseases

- Tuberculosis

- Fungal infections

- Granulomatosis with polyangiitis

- Idiopathic pulmonary fibrosis

- Hypersensitivity pneumonitis

- Asthma

Of these possibilities, berylliosis presents most similarly to sarcoidosis. Some studies suggest that up to 6% of all cases of sarcoidosis are actually berylliosis.

Definitive diagnosis of berylliosis is based on history of beryllium exposures, documented beryllium sensitivity and granulomatous inflammation on lung biopsy. Given the invasive nature of a lung biopsy diagnosis can also be based on clinical history consistent with berylliosis, abnormal chest x-ray or CT scan findings, an abnormalities in pulmonary function tests.

Establishing beryllium sensitivity is the first step in diagnosis. The beryllium lymphocyte proliferation test (BeLPT) is the standard way of determining sensitivity to beryllium. The test is performed by acquiring either, peripheral blood or fluid from a bronchial alveolar lavage, and lymphocytes are cultured with beryllium sulfate. Cells are then counted and those with elevated number of cells are considered abnormal. Those exposed persons with two abnormal BeLPT tested with peripheral blood, or one abnormal and one borderline result, are considered beryllium sensitized. Also, those with one abnormal BeLPT tested with fluid from a bronchial alveolar lavage are considered sensitized.

Chest radiography findings of berylliosis are non-specific. Early in the disease radiography findings are usually normal. In later stages interstitial fibrosis, pleural irregularities, hilar lymphadenopathy and ground-glass opacities have been reported. Findings on CT are also not specific to berylliosis. Findings that are common in CT scans of people with berylliosis include parenchymal nodules in early stages. One study found that ground-glass opacities were more commonly seen on CT scan in berylliosis than in sarcoidosis. In later stages hilar lymphadenopathy, intersitial pulmonary fibrosis and pleural thickening.

Berylliosis is an occupational disease. Relevant occupations are those where beryllium is mined, processed or converted into metal alloys, or where machining of metals containing beryllium and recycling of scrap alloys occurs. It is associated with aerospace manufacturing, microwave semiconductor electronics, beryllium mining or manufacturing of fluorescent light bulbs (which once contained beryllium compounds in their internal phosphor coating). Beryllia was used in lamp manufacture because of ceramic's obvious virtues for insulation and heat resistance, and also because beryllia could be made transparent. Certain welding anodes along with other electrical contacts and even non-sparking tools are made of beryllium copper alloy and the subsequent machining of such materials would cause the disease as well.

The only prevention for FLD is ventilating the work areas putting workers at risk and using face masks to filter out the antigens attempting to enter the lungs through the air.

Depending on the severity of the symptoms, FLD can last from one to to weeks, or they can last for the rest of one’s life. Acute FLD has the ability to be treated because hypersensitivity to the antigens has not yet developed. The main treatment is rest and reducing the exposure to the antigens through masks and increased airflow in confined spaces where the antigens are present. Another treatment for acute FLD is pure oxygen therapy. For chronic FLD, there is no true treatment because the patient has developed hypersensitivity meaning their FLD could last the rest of their life. Any exposure to the antigens once hypersensitivity can set off another chronic reaction.

Exogenous lipid pneumonia is rare in the general population, but occupational accidents may not be uncommon in fire performers. Diagnosis is usually made on the basis of history of exposure to hydrocarbon fuels, symptoms, and radiological findings. The radiological findings are nonspecific, and the disease presents with variable patterns and distribution. For this reason, lipoid pneumonia may mimic many other diseases, and the diagnosis is often delayed.

Chest X-rays taken shortly after the accident may or may not be abnormal, but typically over time show infiltrates in the lower lobes of the lungs. High-resolution CT will frequently demonstrate abnormalities, including opacities, pleural effusion, consolidation, or pulmonary nodules. Histopathology of lung biopsy or bronchoalveolar lavage may indicate lipid-laden macrophages. Laboratory results may show highly elevated inflammatory markers.

BFL symptoms improve in the absence of the bird proteins which caused the disease. Therefore, it is advisable to remove all birds, bedding and pillows containing feathers from the house as well as washing all soft furnishings, walls, ceilings and furniture. Certain small mammals kept as pets have the same or similar proteins in their fur and feces and so should be removed. Peak flow measurements will indicate a lung condition however a spirometric test on lung capacity and patients ability to move air in and out of the lungs plus in more advanced cases an X-ray test or CT scan is available to confirm whether someone has the disease or not. Steroid inhalers similar to those used for asthma are effective or in cases where the patient finds inhaling difficult high dosages of steroids combined with bone density protecting drugs are used to treat a person with BFL, reducing the inflammation and hopefully preventing scarring. Recovery varies from patient to patient depending on what stage the condition was at when the patient consulted the doctor, the speed of diagnosis and application of the appropriate treatment to prevent residual damage to the lungs and many make a full recovery. However, BFL may reoccur when in contact with birds or other allergens.

Chest radiography is usually the first test to detect interstitial lung diseases, but the chest radiograph can be normal in up to 10% of patients, especially early on the disease process.

High resolution CT of the chest is the preferred modality, and differs from routine CT of the chest. Conventional (regular) CT chest examines 7–10 mm slices obtained

at 10 mm intervals; high resolution CT examines 1-1.5 mm slices at 10 mm

intervals using a high spatial frequency reconstruction algorithm. The HRCT therefore provides approximately 10 times more resolution than the conventional CT chest, allowing the HRCT to elicit details that cannot otherwise be visualized.

Radiologic appearance alone however is not adequate and should be interpreted in the clinical context, keeping in mind the temporal profile of the disease process.

Interstitial lung diseases can be classified according to radiologic patterns.

The following are precautionary measures that can be taken to avoid the spread of bagassosis:

1. Dust control-prevention /suppression of dust such as wet process, enclosed apparatus, exhaust ventilation etc. should be used

2. Personal protection- masks/ respirators

3. Medical control- initial medical examination & periodical checkups of workers

4. Bagasse control- keep moisture content above 20% and spray bagasse with 2% propionic acid

Investigation is tailored towards the symptoms and signs. A proper and detailed history looking for the occupational exposures, and for signs of conditions listed above is the first and probably the most important part of the workup in patients with interstitial lung disease. Pulmonary function tests usually show a restrictive defect with decreased diffusion capacity (DLCO).

A lung biopsy is required if the clinical history and imaging are not clearly suggestive of a specific diagnosis or malignancy cannot otherwise be ruled out. In cases where a lung biopsy is indicated, a trans-bronchial biopsy is usually unhelpful, and a surgical lung biopsy is often required.

General treatment principles are removal from exposure, protection of the airway (i.e., preemptive intubation), and treatment of hypoxemia. Concomitant airway injury with acute bronchospasm often warrants treatment with bronchodilators because of the airway obstruction.

A beneficial role for corticosteroids has not been established by controlled trials in humans. Despite the lack of controlled evidence of efficacy, anecdotal reports of benefits from systemic corticosteroid use continue to appear.

Prophylactic antibiotic drugs have not proved to be efficacious in toxic lung injury. Antibiotics should be reserved for those patients with clinical evidence of infection.

The course of treatment of fire breather's pneumonia remains controversial. Administration of bronchodilators, corticosteroids, and prophylactic antibiotics to prevent secondary infection, is a common course of treatment. Some studies suggest that steroids may improve outcomes in severely affected individuals, yet these data are only based on a limited number of patients. The use of gastric decontamination to prevent subsequent pulmonary injury from hydrocarbon ingestion is controversial. It may have potential benefit in large (> 30 cc), intentional ingestion of compounds with systemic toxicity.

Prognosis after peak symptoms is typically good, with most patients making a full recovery in weeks to months.

UIP may be diagnosed by a radiologist using computed tomography (CT) scan of the chest, or by a pathologist using tissue obtained by a lung biopsy. Radiologically, the main feature required for a confident diagnosis of UIP is honeycomb change in the periphery and the lower portions (bases) of the lungs. The histologic hallmarks of UIP, as seen in lung tissue under a microscope by a pathologist, are interstitial fibrosis in a "patchwork pattern", honeycomb change and fibroblast foci (see images below).

It can be classified into acute interstitial pneumonitis, blood pneumonitis, lymphocytic interstitial pneumonitis, radiation pneumonitis, and uremic pneumonitis.

Endogenous lipoid pneumonia and non-specific interstitial pneumonitis has been seen prior to the development of pulmonary alveolar proteinosis in a child.

The diagnosis can be confirmed by lung biopsy. A videoscopic assisted thoracoscopic wedge biopsy (VATS) under general anesthesia may be necessary to obtain enough tissue to make an accurate diagnosis. This kind of biopsy involves placement of several tubes through the chest wall, one of which is used to cut off a piece of lung to send for evaluation. The removed tissue is examined histopathologically by microscopy to confirm the presence and pattern of fibrosis as well as presence of other features that may indicate a specific cause e.g. specific types of mineral dust or possible response to therapy e.g. a pattern of so-called non-specific interstitial fibrosis.

Misdiagnosis is common because, while overall pulmonary fibrosis is not rare, each individual type of pulmonary fibrosis is uncommon and the evaluation of patients with these diseases is complex and requires a multidisciplinary approach. Terminology has been standardized but difficulties still exist in their application. Even experts may disagree with the classification of some cases.

On spirometry, as a restrictive lung disease, both the FEV1 (forced expiratory volume in 1 second) and FVC (forced vital capacity) are reduced so the FEV1/FVC ratio is normal or even increased in contrast to obstructive lung disease where this ratio is reduced. The values for residual volume and total lung capacity are generally decreased in restrictive lung disease.

Rapid progression from initial symptoms to respiratory failure is a key feature. An x-ray that shows ARDS is necessary for diagnosis (fluid in the small air sacs (alveoli) in both lungs). In addition, a biopsy of the lung that shows organizing diffuse alveolar damage is required for diagnosis. Other diagnostic tests are useful in excluding other similar conditions, but history, x-ray, and biopsy are essential. These other tests may include basic blood work, blood cultures, and bronchoalveolar lavage.

The clinical picture is similar to ARDS, but AIP differs from ARDS in that the cause for AIP is not known.

Treatment is with corticosteroids and possibly intravenous immunoglobulins.

The differential diagnosis includes other types of lung disease that cause similar symptoms and show similar abnormalities on chest radiographs. Some of these diseases cause fibrosis, scarring or honeycomb change. The most common considerations include:

- chronic hypersensitivity pneumonitis

- non-specific interstitial pneumonia

- sarcoidosis

- pulmonary Langerhans cell histiocytosis

- asbestosis

Chemical pneumonitis is inflammation of the lung caused by aspirating or inhaling irritants. It is sometimes called a "chemical pneumonia", though it is not infectious. There are two general types of chemical pneumonitis: acute and chronic.

Irritants capable of causing chemical pneumonitis include vomitus, barium used in gastro-intestinal imaging, chlorine gas (among other pulmonary agents), ingested gasoline or other petroleum distillates, ingested or skin absorbed pesticides, gases from electroplating, smoke and others. It may also be caused by the use of inhalants.

Mendelson's syndrome is a type of chemical pneumonitis.

Mineral oil should not be given internally to young children, pets, or anyone with a cough, hiatus hernia, or nocturnal reflux, because it can cause complications such as lipoid pneumonia. Due to its low density, it is easily aspirated into the lungs, where it cannot be removed by the body. In children, if aspirated, the oil can work to prevent normal breathing, resulting in death of brain cells and permanent paralysis and/or retardation

Arterial blood gases may reveal hypoxemia when tested in a lab. Respiratory alkalosis may also be present. Peripheral lymphocytosis can be observed. A lung biopsy may also be indicated.

Pneumonitis or pulmonitis is an inflammation of lung tissue due to factors other than microorganisms. Those can be radiation therapy of the chest , exposure to medications used during chemo-therapy, the inhalation of debris (ie animal dander), of food particles during vomiting, herbicides or fluorocarbons and some systemic diseases.

It is distinguished from pneumonia on the basis of causation as well as its manifestation since pneumonia can be described as pneumonitis combined with consolidation and exudation of lung tissue due to infection with microorganism.