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 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.

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 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 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.)

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.

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.

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.

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.

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.

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.

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.

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.

Beginning shortly after the opening of the first complex in 1956, severe cases of chronic obstructive pulmonary disease, chronic bronchitis, pulmonary emphysema, and bronchial asthma rose quickly among the local inhabitants. Taller smokestacks were implemented, but these simply spread the pollution over a wider area and did not help alleviate the reported health issues.

Fish caught in Ise Bay developed a bad taste, causing local fishermen to petition the government for compensation for their unsaleable fish in 1960.

A class action court case was brought against Showa Yokkaichi Oil and initially adjudicated in September 1970. The class was ruled to contain 544 individuals, but that number has increased over the ensuing years.

A 2008 study by researchers from the Mie University Graduate School of Medicine and the Hiroshima University Natural Science Center for Basic Research and Development indicated a 10 to 20-fold higher mortality rates as a result of COPD and asthma in the affected populations of Yokkaichi versus the general population of Mie Prefecture.

Initial attempts to alleviate the problem by raising the height of smokestacks to disperse the pollutants over a larger area proved ineffective. Eventually flue-gas desulfurization was implemented on a large scale, leading to an improvement in the health of local populace.

Yokkaichi asthma has been identified in rapidly industrializing areas in the rest of the world, including Mexico City and mainland China.

Thunderstorm asthma is the triggering of an asthma attack by environmental conditions directly caused by a local thunderstorm. It has been proposed that during a thunderstorm, pollen grains can absorb moisture and then burst into much smaller fragments with these fragments being easily dispersed by wind. However, there is no experimental evidence confirming this theory. While larger pollen grains are usually filtered by hairs in the nose, the smaller pollen fragments are able to pass through and enter the lungs, triggering the asthma attack.

There have been events where thunderstorms have caused asthma attacks across cities such that emergency services and hospitals have been overwhelmed. The phenomenon was first recognised and studied after three recorded events in the 1980s; in Birmingham, England, in 1983 and in Melbourne, Australia in 1987 and 1989. Since then there have been further reports of widespread thunderstorm asthma in Wagga Wagga, Australia; London, England; Naples, Italy; Atlanta, United States; and Ahvaz, Iran. A further outbreak in Melbourne, in November 2016, that overwhelmed the ambulance system and some local hospitals, resulted in at least nine deaths. There was a similar incident in Kuwait in early December, 2016 with at least 5 deaths and many admissions to the ICU.

Many of those affected during a thunderstorm asthma outbreak may have never experienced an asthma attack before.

It has been found 95% of those that were affected by thunderstorm asthma had a history of hayfever, and 96% of those people had tested positive to grass pollen allergies, particularly rye grass. A rye grass pollen grain can hold up to 700 tiny starch granules, measuring 0.6 to 2.5 μm, small enough to reach the lower airways in the lung.

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.

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.

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.

Health care professionals are at risk of occupational influenza exposure; during a pandemic influenza, anyone in a close environment is at risk, including those in an office environment.

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.

Individuals with an obstructive pulmonary disorder such as bronchitis may present with a decreased FEV1 and FEV1/FVC ratio on pulmonary function tests. Unlike other common obstructive disorders such as asthma or emphysema, bronchitis rarely causes a high residual volume (the volume of air remaining in the lungs after a maximal exhalation effort).