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.

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.

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.

New criteria by the ABPA Complicated Asthma ISHAM Working Group suggests a 6-stage criteria for the diagnosis of ABPA, though this is yet to be formalised into official guidelines. This would replace the current gold standard staging protocol devised by Patterson and colleagues. Stage 0 would represent an asymptomatic form of ABPA, with controlled asthma but still fulfilling the fundamental diagnostic requirements of a positive skin test with elevated total IgE (>1000 IU/mL). Stage 6 is an advanced ABPA, with the presence of type II respiratory failure or pulmonary heart disease, with radiological evidence of severe fibrosis consistent with ABPA on a high-resolution CT scan. It must be diagnosed after excluding the other, reversible causes of acute respiratory failure.

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.

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 prognosis for asthma is generally good, especially for children with mild disease. Mortality has decreased over the last few decades due to better recognition and improvement in care. In 2010 the death rate was 170 per million for males and 90 per million for females. Rates vary between countries by 100 fold.

Globally it causes moderate or severe disability in 19.4 million people as of 2004 (16 million of which are in low and middle income countries). Of asthma diagnosed during childhood, half of cases will no longer carry the diagnosis after a decade. Airway remodeling is observed, but it is unknown whether these represent harmful or beneficial changes. Early treatment with corticosteroids seems to prevent or ameliorates a decline in lung function. Asthma in children also has negative effects on quality of life of their parents.

COPD may need to be differentiated from other causes of shortness of breath such as congestive heart failure, pulmonary embolism, pneumonia, or pneumothorax. Many people with COPD mistakenly think they have asthma. The distinction between asthma and COPD is made on the basis of the symptoms, smoking history, and whether airflow limitation is reversible with bronchodilators at spirometry. Tuberculosis may also present with a chronic cough and should be considered in locations where it is common. Less common conditions that may present similarly include bronchopulmonary dysplasia and obliterative bronchiolitis. Chronic bronchitis may occur with normal airflow and in this situation it is not classified as COPD.

A chest X-ray and complete blood count may be useful to exclude other conditions at the time of diagnosis. Characteristic signs on X-ray are overexpanded lungs, a flattened diaphragm, increased retrosternal airspace, and bullae, while it can help exclude other lung diseases, such as pneumonia, pulmonary edema, or a pneumothorax. A high-resolution computed tomography scan of the chest may show the distribution of emphysema throughout the lungs and can also be useful to exclude other lung diseases. Unless surgery is planned, however, this rarely affects management. An analysis of arterial blood is used to determine the need for oxygen; this is recommended in those with an FEV less than 35% predicted, those with a peripheral oxygen saturation less than 92%, and those with symptoms of congestive heart failure. In areas of the world where alpha-1 antitrypsin deficiency is common, people with COPD (particularly those below the age of 45 and with emphysema affecting the lower parts of the lungs) should be considered for testing.

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.

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.

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.

Reactive airways dysfunction syndrome (RADS) is a term proposed by Stuart M. Brooks and colleagues in 1985

It can also manifest in adults with exposure to high levels of chlorine, ammonia, acetic acid or sulphur dioxide, creating symptoms like asthma. These symptoms can vary from mild to fatal, and can even create long-term airway damage depending on the amount of exposure and the concentration of chlorine. Some experts classify RADS as occupational asthma. Those with exposure to highly irritating substances should receive treatment to mitigate harmful effects.

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.

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.

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.

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.)

All divers should be free of conditions and illnesses that would negatively impact their safety and well-being underwater. The diving medical physician should be able to identify, treat and advise divers about illnesses and conditions that would cause them to be at increased risk for a diving accident.

Some reasons why a person should not be allowed to dive are as follows:

- Disorders that lead to altered consciousness: conditions that produce reduced awareness or sedation from medication, drugs, marijuana or alcohol; fainting, heart problems and seizure activity.

- Disorders that substantially increase the risk of barotrauma injury conditions or diseases that are associated with air trapping in closed spaces, such as sinuses, middle ear, lungs and gastrointestinal tract. Severe asthma is an example.

- Disorders that may lead to erratic and irresponsible behavior: included here would be immaturity, psychiatric disorders, diving while under the influence of medications, drugs and alcohol or any medical disorder that results in cognitive defects.

Conditions that may increase risk of diving disorders:

- Patent foramen ovale

- Diabetes mellitus — No serious problems should be expected during dives due to hypoglycaemia in divers with well-controlled diabetes. Long-term complications of diabetes should be considered and may be a contrindication.

- Asthma

Conditions considered temporary reasons to suspend diving activities:

- Pregnancy—It is unlikely that literature research can establish the effect of scuba diving on the unborn human fetus as there is insufficient data, and women tend to comply with the diving industry recommendation not to dive while pregnant.

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 symptoms of VCD are often inaccurately attributed to asthma, which in turn results in the unnecessary and futile intake of corticosteroids, bronchodilators and leukotriene modifiers, although there are instances of comorbidity of asthma and VCD.

The differential diagnosis for vocal cord dysfunction includes vocal fold swelling from allergy, asthma, or some obstruction of the vocal folds or throat. Anyone suspected of this condition should be evaluated and the vocal folds (voice box) visualized. In individuals who experience a persistent difficulty with inhaling, consideration should be given to a neurological cause such as brain stem compression, cerebral palsy, etc.

The main difference between VCD and asthma is the audible stridor or wheezing that occurs at different stages of the breath cycle: VCD usually causes stridor on the inhalation, while asthma results in wheezing during exhalation. Patients with asthma usually respond to the usual medication and see their symptoms resolve. Clinical measures that can be done to differentiate VCD from asthma include:

- rhinolaryngoscopy: A patient with asthma will have normal vocal cord movement, while one with VCD will display vocal cord abduction during inhalation

- spirometry: A change in the measure following the administration of a bronchodilator is suggestive of asthma rather than VCD

- chest radiography: The presence of hyperinflation and peribronchial thickening are indicative of asthma, as patients with VCD will show normal results.

Recompression treatment in a hyperbaric chamber was initially used as a life-saving tool to treat decompression sickness in caisson workers and divers who stayed too long at depth and developed decompression sickness. Now, it is a highly specialized treatment modality that has been found to be effective in the treatment of many conditions where the administration of oxygen under pressure has been found to be beneficial. Studies have shown it to be quite effective in some 13 indications approved by the Undersea and Hyperbaric Medical Society.

Hyperbaric oxygen treatment is generally preferred when effective, as it is usually a more efficient and lower risk method of reducing symptoms of decompression illness, However, in some cases recompression to pressures where oxygen toxicity is unacceptable may be required to eliminate the bubbles in the tissues that cause the symptoms.

The most effective diagnostic strategy is to perform laryngoscopy during an episode, at which time abnormal movement of the cords, if present, can be observed. If the endoscopy is not performed during an episode, it is likely that the vocal folds will be moving normally, a 'false negative' finding.

Spirometry may also be useful to establish the diagnosis of VCD when performed during a crisis or after a nasal provocation test. With spirometry, just as the expiratory loop may show flattening or concavity when expiration is affected in asthma, so may the Inspiratory loop show truncation or flattening in VCD. Of course, testing may well be negative when symptoms are absent.

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.