Spirometry is recommended to aid in diagnosis and management. It is the single best test for asthma. If the FEV1 measured by this technique improves more than 12% and increases by at least 200 milliliters following administration of a bronchodilator such as salbutamol, this is supportive of the diagnosis. It however may be normal in those with a history of mild asthma, not currently acting up. As caffeine is a bronchodilator in people with asthma, the use of caffeine before a lung function test may interfere with the results. Single-breath diffusing capacity can help differentiate asthma from COPD. It is reasonable to perform spirometry every one or two years to follow how well a person's asthma is controlled.

The methacholine challenge involves the inhalation of increasing concentrations of a substance that causes airway narrowing in those predisposed. If negative it means that a person does not have asthma; if positive, however, it is not specific for the disease.

Other supportive evidence includes: a ≥20% difference in peak expiratory flow rate on at least three days in a week for at least two weeks, a ≥20% improvement of peak flow following treatment with either salbutamol, inhaled corticosteroids or prednisone, or a ≥20% decrease in peak flow following exposure to a trigger. Testing peak expiratory flow is more variable than spirometry, however, and thus not recommended for routine diagnosis. It may be useful for daily self-monitoring in those with moderate to severe disease and for checking the effectiveness of new medications. It may also be helpful in guiding treatment in those with acute exacerbations.

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.

Urinary cystyl-leukotriene or urinary LTE4 can be used after a supervised challenge with aspirin. In aspirin sensitivity, no change in N-methylhistamine is observed; while LTE4 levels are increased. This test however lacks sensitivity and has a 25 percent false negative rate among affected persons.

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.

The first stage involves exposing the skin to Aspergillus fumigatus antigens; an immediate reaction is hallmark of ABPA. The test should be performed first by skin prick testing, and if negative followed with an intradermal injection. Overall sensitivity of the procedure is around 90%, though up to 40% of asthmatic patients without ABPA can still show some sensitivity to Aspergillus antigens (a phenomenon likely linked to a less severe form of ABPA termed severe asthma with fungal sensitization (SAFS)).

Serum blood tests are an important marker of disease severity, and are also useful for the primary diagnosis of ABPA. When serum IgE is normal (and patients are not being treated by glucocorticoid medications), ABPA is excluded as the cause of symptoms. A raised IgE increases suspicion, though there is no universally accepted cut-off value. Values can be stated in international units (IU/mL) or ng/mL, where 1 IU is equal to 2.4 ng/mL. Since studies began documenting IgE levels in ABPA during the 1970s, various cut-offs between 833–1000 IU/mL have been employed to both exclude ABPA and to warrant further serological testing. Current consensus is that a cut-off of 1000 IU/mL should be employed, as lower values are encountered in SAFS and asthmatic sensitization.

IgG antibody precipitin testing from serum is useful, as positive results are found in between 69–90% of patients, though also in 10% of asthmatics with and without SAFS. Therefore, it must be used in conjunction with other tests. Various forms exist, including enzyme-linked immunosorbent assay (ELISA) and fluorescent enzyme immunoassay (FEIA). Both are more sensitive than conventional counterimmunoelectrophoresis. IgG may not be entirely specific for ABPA, as high levels are also found in chronic pulmonary aspergillosis (CPA) alongside more severe radiological findings.

Until recently, peripheral eosinophilia (high eosinophil counts) was considered partly indicative of ABPA. More recent studies show that only 40% of ABPA sufferers present with eosinophilia, and hence a low eosinophil count does not necessary exclude ABPA; for example patients undergoing steroid therapy have lower eosinophil counts.

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.

Culturing fungi from sputum is a supportive test in the diagnosis of ABPA, but is not 100% specific for ABPA as "A. fumigatus" is ubiquitous and commonly isolated from lung expectorant in other diseases. Nevertheless, between 40–60% of patients do have positive cultures depending on the number of samples taken.

The International Olympic Committee recommends the eucapnic voluntary hyperventilation (EVH) challenge as the test to document exercise-induced asthma in Olympic athletes. In the EVH challenge, the patient voluntarily, without exercising, rapidly breathes dry air enriched with 5% for six minutes. The presence of the enriched compensates for the losses in the expired air, not matched by metabolic production, that occurs during hyperventilation, and so maintains levels at normal.

Diagnosis is typically based on a person's signs and symptoms. The color of the sputum does not indicate if the infection is viral or bacterial. Determining the underlying organism is typically not needed. Other causes of similar symptoms include asthma, pneumonia, bronchiolitis, bronchiectasis, and COPD. A chest X-ray may be useful to detect pneumonia.

Another common sign of bronchitis is a cough which lasts ten days to three weeks. If the cough lasts a month or a year it may be chronic bronchitis. In addition to having a cough a fever may be present. Acute bronchitis is normally caused by a viral infection. Typically these infections are rhinovirus, para influenza, or influenza. No specific testing is normally needed to diagnose acute bronchitis.

In addition to any issues of treatment compliance, and maximised corticosteroids (inhaled or oral) and beta agonist, brittle asthma treatment also involves for type 1 additional subcutaneous injections of beta2 agonist and inhalation of long acting beta-adrenoceptor agonist, whilst type 2 needs allergen avoidance and self-management approaches. Since catastrophic attacks are unpredictable in type 2, patients may display identification of the issue, such as a MedicAlert bracelet, and carry an epinephrine autoinjector.

Some people have reported relief of symptoms by following a low-salicylate diet such as the Feingold diet. Aspirin is quickly converted in the body to salicylic acid, also known as 2-Hydroxybenzoic acid. Sommer "et al." reported a multi-center prospective randomized cross-over trial with 30 patients following a low-salicylate diet for 6 weeks. This study demonstrated a clinically significant decrease in both subjective and objective scoring of severity of disease, but made note of the challenge for patients in following what is a fairly stringent diet.

A diet low in omega-6 oils (precursors of arachidonic acid), and high in omega-3 oils, may also help. In a small study, aspirin-sensitive asthma patients taking 10 grams of fish oil daily reported relief of most symptoms after six weeks, however symptoms returned if the supplement was stopped.

Owners often notice their cat coughing several times per day. Cat coughing sounds different from human coughing, usually sounding more like the cat is passing a hairball. Veterinarians will classify the severity of feline asthma based on the medical signs. There are a number of diseases that are very closely related to feline asthma which must be ruled out before asthma can be diagnosed. Lungworms, heartworms, upper and lower respiratory infections, lung cancer, cardiomyopathy and lymphocytic plasmacytic stomatitis all mimic asthmatic symptoms. Medical signs, pulmonary radiographs, and a positive response to steroids help confirm the diagnosis.

While radiographs can be helpful for diagnosis, airway sampling through transtracheal wash or bronchoalveolar lavage is often necessary. More recently, computed tomography has been found to be more readily available and accurate in distinguishing feline tracheobronchitis from bronchopneumonia.

Feline asthma and other respiratory diseases may be prevented by cat owners by eliminating as many allergens as possible. Allergens that can be found in a cat’s habitual environment include: pollen, molds, dust from cat litter, perfumes, room fresheners, carpet deodorizers, hairspray, aerosol cleaners, cigarette smoke, and some foods. Avoid using cat litters that create lots of dust, scented cat litters or litter additives. Of course eliminating all of these can be very difficult and unnecessary, especially since a cat is only affected by one or two. It can be very challenging to find the allergen that is creating asthmatic symptoms in a particular cat and requires a lot of work on both the owner’s and the veterinarian's part. But just like any disease, the severity of an asthma attack can be propelled by more than just the allergens, common factors include: obesity, stress, parasites and pre-existing heart conditions. Dry air encourages asthma attacks so keep a good humidifier going especially during winter months.

Prevention is by not smoking and avoiding other lung irritants. Frequent hand washing may also be protective. Treatment of acute bronchitis typically involves rest, paracetamol (acetaminophen), and NSAIDs to help with the fever. Cough medicine has little support for its use and is not recommended in children less than six years of age. There is tentative evidence that salbutamol may be useful in those with wheezing; however, it may result in nervousness and tremors. Antibiotics should generally not be used. An exception is when acute bronchitis is due to pertussis. Tentative evidence supports honey and pelargonium to help with symptoms. Getting plenty of rest and fluids is also often recommended.

Field-exercise challenge tests that involve the athlete performing the sport in which they are normally involved and assessing FEV after exercise are helpful if abnormal but have been shown to be less sensitive than eucapnic voluntary hyperventilation.

Status asthmaticus is slightly more common in males and is more common among people of African and Hispanic origin. The gene locus glutathione dependent S-nitrosoglutathione (GSNOR) has been suggested as one possible correlation to development of status asthmaticus.

Interventions include intravenous (IV) medications (e.g. magnesium sulfate), aerosolized medications to dilate the airways (bronchodilation) (e.g., albuterol or ipratropium bromide/salbutamol), and positive-pressure therapy, including mechanical ventilation. Multiple therapies may be used simultaneously to rapidly reverse the effects of status asthmaticus and reduce permanent damage of the airways. Intravenous corticosteroids and methylxanthines are often given. If the person with a severe asthma exacerbation is on a mechanical ventilator, certain sedating medications such as ketamine or propofol, have bronchodilating properties. According to a new randomized control trial ketamine and aminophylline are also effective in children with acute asthma who responds poorly to standard therapy.

Diagnosis of alcohol-induced respiratory symptoms can be strongly suggested on the bases of survey questionnaires. Questionnaires can be devised to determine the specific types of alcoholic beverages eliciting reactions; reactions evoked by one or only a few but not other types of alcoholic beverage, particularly when the offending beverage(s) is wine and/or beer, suggest that the reactions are due to classical allergic reaction to allergens in the beverage; reactions to all or most types of alcoholic beverages favors a genetic (i.e. acetaldehyde-induce) basis. Further differentiation between these two causes can be tested under medical supervision be determining if ingestion of a water-diluted pure ethanol solution elicits reactions or if an offending alcoholic beverage but not the same beverage without ethanol elicits reactions. Either result would favor an acetaldehyde-induced genetic basis for the reaction.

Diagnosis of alcohol sensitivity due to the accumulation of acetaldehyde in individuals bearing the glu487lys ALDH2 allele can be made by measuring the diameter of the erythema (i.e. red) area developing under a 15 millimeter skin patch plaster soaked in 70% ethanol and applied for 48 hours (ethanol patch test); erythema of 15 millimeters is considered positive with a false positive ratio ([100 x {number of individuals with a positive patch test}]/{number of individuals with a normal ALDH2 genotype}) of 5.9% and a false negative ratio ([100 x {number of individuals with a negative patch test}]/{number of individuals with a glu487lys ALDH2 allele}) of 0%. To resolve ambiguities in or replace the ethanol patch test for other reasons, a polymerase chain reaction using special primers and conditions can be used to directly detect the glu487lys ALDH2 genes. For other causes of acetaldehyde-induced alcohol sensitivities, the ethanol patch test will need to be tested for verification of its acetaldehyde basis and appropriate polymerase chain reactions will likewise be needed to verify a genetic basis for symptoms.

Diagnosis of alcohol sensitivity due to allergic reactivity to the allergens in alcoholic beverages can be confirmed by standard skin prick tests, skin patch tests, blood tests, challenge tests, and challenge/elimination tests as conducted for determining the allergen causing other classical allergic reactions (see allergy and Skin allergy tests.)

Eosinophilic pneumonia is diagnosed in one of three circumstances: when a complete blood count reveals increased eosinophils and a chest x-ray or computed tomography (CT) identifies abnormalities in the lung, when a biopsy identifies increased eosinophils in lung tissue, or when increased eosinophils are found in fluid obtained by a bronchoscopy (bronchoalveolar lavage [BAL] fluid). Association with medication or cancer is usually apparent after review of a person's medical history. Specific parasitic infections are diagnosed after examining a person's exposure to common parasites and performing laboratory tests to look for likely causes. If no underlying cause is found, a diagnosis of AEP or CEP is made based upon the following criteria. AEP is most likely with respiratory failure after an acute febrile illness of usually less than one week, changes in multiple areas and fluid in the area surrounding the lungs on a chest x-ray, and greater than 25% eosinophils on a BAL. Other typical laboratory abnormalities include an elevated white blood cell count, erythrocyte sedimentation rate, and immunoglobulin G level. Pulmonary function testing usually reveals a restrictive process with reduced diffusion capacity for carbon monoxide. CEP is most likely when the symptoms have been present for more than a month. Laboratory tests typical of CEP include increased blood eosinophils, a high erythrocyte sedimentation rate, iron deficiency anemia, and increased platelets. A chest x-ray can show abnormalities anywhere, but the most specific finding is increased shadow in the periphery of the lung, away from the heart.

This includes:

- Asthma

- Environmental allergic reaction

- Granulomatosis with polyangiitis (Wegner's syndrome)

- Allergic bronchopulmonary aspergillosis

- Churg-Strauss syndrome

- Loeffler's syndrome

- Acute eosinophilic pneumonia

- Chronic eosinophilic pneumonia (Carrington's disease)

- Polyarteritis nodosa

- Parasitic infections

- Tropical pulmonary eosinophilia

- Tuberculosis

- Fungal infection

- Sarcoidosis

- Drug reaction with eosinophilia and systemic symptoms

- Mastocytosis

- Lymphoproliferative hypereosinophilic syndrome

- Myeloproliferative hypereosinophilic syndrome

Avoidance of ethanol is the safest, surest, and cheapest treatment. Indeed, surveys find a positive correlation between high incidences of glu487lys ALDH2 allele-related alcohol-induced respiratory reactions as well as other causes of these reactions and low levels of alcohol consumption, alcoholism, and alcohol-related diseases. Evidently, people suffering these reaction self-impose avoidance behavior. There is a proviso here: ethanol, at surprisingly high concentrations, is used as a solvent to dissolve many types of medicines and other ingredients. This pertains particularly to liquid cold medicines and mouthwashes. Ethanol avoidance includes avoiding the ingestion of and, depending on an individual's history, mouth washing with, such agents.

Type H1 antagonists in the histamine antagonist family of drugs were tested in Japanese volunteers with alcohol-induced asthma (who presumably have glu487lys ALDH2 allele-associated asthma) and found to be completely effective in blocking bronchoconstriction responses to alcoholic beverages; these blockers, it is suggested, may be taken 1–2 hours before consumption of alcohol beverages as a preventative of alcohol-induced respiratory reactions. In the absence of specific studies on the prevention of classical alcohol induced rhinitis and asthma due to allergens in alcoholic beverages, see asthma section on Prevention and rhinitis section on Prevention of allergen-induced reactions.

In the absence of specific studies on the treatment of acute alcohol-induced bronchoconstriction and rhinitis, treatment guidelines should probably follow those of their comparable allergen-induced classical allergic reactions (see asthma section on Treatment and rhinitis section on Treatment) but possibly favoring the testing of H1 antagonist anti-histamines as part of the initial protocol.

The 2005 "Oxford Textbook of Medicine" distinguishes type 1 brittle asthma by "persistent daily chaotic variability in peak flow (usually greater than 40 per cent diurnal variation in PEFR more than 50 per cent of the time)", while type 2 is identified by "sporadic sudden falls in PEFR against a background of usually well-controlled asthma with normal or near normal lung function". In both types, patients are subject to recurrent, severe attacks. The cardinal symptoms of an asthma attack are shortness of breath (dyspnea), wheezing, and chest tightness. Individuals with type 1 suffer chronic attacks in spite of ongoing medical therapy, while those with type 2 experience sudden, acute and even potentially life-threatening attacks even though otherwise their asthma seems well managed.

When first defined by Margaret Turner-Warwick in 1977, the term brittle asthma was used specifically to describe type 1, but as studies into the phenotype were conducted the second type was also distinguished. The condition is rare. 1999's "Difficult Asthma" estimates a prevalence of approximately .05% brittle asthma sufferers among the asthmatic population. Though found in all ages, it is most commonly found in individuals between the ages of 18 and 55; it is present in both sexes, though type 1 has been diagnosed in three times as many women as men. Hospitalization is more frequent for type 1 than type 2.

Testing is available to help identify any environmental or food allergies. Caregivers and clinicians can assess the child for the development of an allergy by noting the presence of signs and symptoms and history of exposure.