Less than five years of exposure or a single exposure to a high-concentration agent can result in symptoms. Coughing, wheezing, nasal irritation, shortness of breath, and chest tightness are the most common symptoms, all of which worsen after work and improve during time away from work. Pre-existing asthma can be exacerbated by similar agents.

Asthma is characterized by recurrent episodes of wheezing, shortness of breath, chest tightness, and coughing. Sputum may be produced from the lung by coughing but is often hard to bring up. During recovery from an attack, it may appear pus-like due to high levels of white blood cells called eosinophils. Symptoms are usually worse at night and in the early morning or in response to exercise or cold air. Some people with asthma rarely experience symptoms, usually in response to triggers, whereas others may have marked and persistent symptoms.

Occupational asthma is an occupational lung disease and a type of asthma. Like other types of asthma, it is characterized by airway inflammation, reversible airways obstruction, and bronchospasm, but it is caused by something in the workplace environment.

Symptoms include shortness of breath, tightness of the chest, nasal irritation, coughing and wheezing. The first person to use it in reference to a medical condition was Hippocrates, and he believed that tailors, anglers and metalworkers were more likely to be affected by the disease. Although much research has been done since, the inflammatory component of asthma was recognized only in the 1960s.

Hypersensitivity pneumonitis is a related condition, with many occupational examples (e.g. flock worker's lung, farmer's lung, and indium lung). However, although overlapping in many cases, hypersensitivity pneumonitis may be distinguished from occupational asthma in that it isn't restricted to only occupational exposure, and involves type III hypersensitivity and type IV hypersensitivity rather than the type I hypersensitivity of asthma. Also, unlike asthma, hypersensitivity pneumonitis targets lung alveoli rather than bronchi.

Exercise can trigger bronchoconstriction both in people with or without asthma. It occurs in most people with asthma and up to 20% of people without asthma. Exercise-induced bronchoconstriction is common in professional athletes. The highest rates are among cyclists (up to 45%), swimmers, and cross-country skiers. While it may occur with any weather conditions, it is more common when it is dry and cold. Inhaled beta2-agonists do not appear to improve athletic performance among those without asthma, however, oral doses may improve endurance and strength.

Feline asthma occurs with the inflammation of the small passageways of a cat’s lungs, during the attack the lungs will thicken and constrict making it difficult to breathe. Mucus may be released by the lungs into the airway resulting in fits of coughing and wheezing. Some cats experience a less severe version of an asthma attack and only endure some slight coughing. The obvious signs that a cat is having a respiratory attack are: coughing, wheezing, blue lips and gums, squatting with shoulders hunched and neck extended, rapid open mouth breathing or gasping for air, gagging up foamy mucus and overall weakness.

In the acute form of HP, symptoms may develop 4–6 hours following heavy exposure to the provoking antigen. Symptoms include fever, chills, malaise, cough, chest tightness, dyspnea, rash, swelling and headache. Symptoms resolve within 12 hours to several days upon cessation of exposure.

Acute HP is characterized by poorly formed noncaseating interstitial granulomas and mononuclear cell infiltration in a peribronchial distribution with prominent giant cells.

On chest radiographs, a diffuse micronodular interstitial pattern (at times with ground-glass density in the lower and middle lung zones) may be observed. Findings are normal in approximately 10% of patients." In high-resolution CT scans, ground-glass opacities or diffusely increased radiodensities are present. Pulmonary function tests show reduced diffusion capacity of lungs for carbon monoxide (DLCO). Many patients have hypoxemia at rest, and all patients desaturate with exercise. Extrinsic allergic alveolitis may eventually lead to Interstitial lung disease.

Patients with subacute HP gradually develop a productive cough, dyspnea, fatigue, anorexia, weight loss, and pleurisy. Symptoms are similar to the acute form of the disease, but are less severe and last longer. On chest radiographs, micronodular or reticular opacities are most prominent in mid-to-lower lung zones. Findings may be present in patients who have experienced repeated acute attacks.

The subacute, or intermittent, form produces more well-formed noncaseating granulomas, bronchiolitis with or without organizing pneumonia, and interstitial fibrosis.

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.

An exacerbation (attack) of asthma is experienced as a worsening of asthma symptoms with breathlessness and cough (often worse at night). In acute severe asthma, breathlessness may be so severe that it is impossible to speak more than a few words (inability to complete sentences).

On examination, the respiratory rate may be elevated (more than 25 breaths per minute), and the heart rate may be rapid (110 beats per minute or faster). Reduced oxygen saturation levels (but above 92%) are often encountered. Examination of the lungs with a stethoscope may reveal reduced air entry and/or widespread wheeze. The peak expiratory flow can be measured at the bedside; in acute severe asthma the flow is less than 50% a person's normal or predicted flow.

Very severe acute asthma (termed "near-fatal" as there is an immediate risk to life) is characterised by a peak flow of less than 33% predicted, oxygen saturations below 92% or cyanosis (blue discoloration, usually of the lips), absence of audible breath sounds over the chest ("silent chest"), reduced respiratory effort and visible exhaustion or drowsiness. Irregularities in the heart beat and abnormal lowering of the blood pressure may be observed.

The various non-allergic NSAID hypersensitivity syndromes affect 0.5–1.9% of the general population, with AERD affecting about 7% of all asthmatics and about 14% of patients with severe asthma. AERD, which is more prevalent in women, usually begins in young adulthood (twenties and thirties are the most common onset times although children are afflicted with it and present a diagnostic problem in pediatrics) and may not include any other allergies. Most commonly the first symptom is rhinitis (inflammation or irritation of the nasal mucosa), which can manifest as sneezing, runny nose, or congestion. The disorder typically progresses to asthma, then nasal polyposis, with aspirin sensitivity coming last. Anosmia (lack of smell) is also common, as inflammation within the nose and sinuses likely reaches the olfactory receptors.

The respiratory reactions to aspirin vary in severity, ranging from mild nasal congestion and eye watering to lower respiratory symptoms including wheezing, coughing, an asthma attack, and in rare cases, anaphylaxis. In addition to the typical respiratory reactions, about 10% of patients with AERD manifest skin symptoms like urticaria and/or gastrointestinal symptoms such as abdominal pain or vomiting during their reactions to aspirin.

In addition to aspirin, patients usually also react to other NSAIDs such as ibuprofen, and to any medication that inhibits the cyclooxygenase-1 (COX-1) enzyme, although paracetamol (acetaminophen) in low doses is generally considered safe. NSAID that are highly selective in blocking COX-2 and do not block its closely related paralog, COX-1, such as the COX-2 inhibitors celecoxib and rofecoxib, are also regarded as safe. Nonetheless, recent studies do find that these types of drugs, e.g. acetaminophen and celecoxib, may trigger adverse reactions in these patients; caution is recommended in using any COX inhibitors. In addition to aspirin and NSAIDs, consumption of even small amounts of alcohol also produces uncomfortable respiratory reactions in many patients.

Almost all patients have clinically diagnosed asthma, and present with wheezing (usually episodic in nature), coughing, shortness of breath and exercise intolerance (especially in patients with cystic fibrosis). Moderate and severe cases have symptoms suggestive of bronchiectasis, in particular thick sputum production (often containing brown mucus plugs), as well as symptoms mirroring recurrent infection such as pleuritic chest pain and fever. Patients with asthma and symptoms of ongoing infection, who do not respond to antibiotic treatment, should be suspected of ABPA.

With single or prolonged exposure by inhalation the lungs may become sensitized to beryllium. Berylliosis has an insidious onset and runs an indolent course. Some people who are sensitized to beryllium may not have symptoms. Continued exposure causes the development of small inflammatory nodules, called granulomas. Of note, the authors of a 2006 study suggested that beryllium inhalation was not the only form of exposure and perhaps skin exposure was also a cause, as they found that a reduction in beryllium inhalation did not result in a reduction in CBD or beryllium sensitization.

Granulomas are seen in other chronic diseases, such as tuberculosis and sarcoidosis, and it can occasionally be hard to distinguish berylliosis from these disorders. However, granulomas of CBD will typically be non-caseating, i.e. not characterized by necrosis and therefore not exhibiting a cheese-like appearance grossly.

Ultimately, this process leads to restrictive lung disease (a decrease in diffusion capacity).

The earliest symptoms are typically cough and shortness of breath. Other symptoms include chest pain, joint aches, weight loss, and fever.

Rarely, one can get granulomas in other organs including the liver.

The onset of symptoms can range from weeks up to tens of years from the initial exposure. In some individuals, a single exposure to beryllium can cause berylliosis.

This disease is an inflammation of the alveoli in the lungs. Initial symptoms are breathlessness especially after sudden exertion or when exposed to temperature change and can be very similar to asthma, hyperventilation syndrome or pulmonary embolism. One of the defining characteristics of "bird fanciers lung" is that many medical tests will show a normal range of results and it will be identified by X-ray or CT scans showing physical changes to the lung structure (a ground glass appearance). If someone with BFL has been exposed to avian proteins they will see symptoms within 4–6 hours. Symptoms include chills, fever, breathlessness, non-productive cough and chest discomfort. In the chronic form there is usually anorexia, weight loss, extreme tiredness and progressive interstitial fibrosis which is the most disabling feature of the disease as this causes scarring on the lungs which reduces the lungs ability to move air in and out, and as a result sufferers have repeated chest infections and ultimately struggle to breathe. This condition is occasionally fatal.

Acute severe asthma is an acute exacerbation of asthma that does not respond to standard treatments of bronchodilators (inhalers) and corticosteroids. Symptoms include chest tightness, rapidly progressive dyspnea (shortness of breath), dry cough, use of accessory respiratory muscles, fast and/or labored breathing, and extreme wheezing. It is a life-threatening episode of airway obstruction and is considered a medical emergency. Complications include cardiac and/or respiratory arrest.

It is characterized histologically by smooth muscle hypertrophy and basement membrane thickening.

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 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.

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.

It might be expected that people with E.I.B. would present with shortness of breath, and/or an elevated respiratory rate and wheezing, consistent with an asthma attack. However, many will present with decreased stamina, or difficulty in recovering from exertion compared to team members, or paroxysmal coughing from an irritable airway. Similarly, examination may reveal wheezing and prolonged expiratory phase, or may be quite normal. Consequently, a potential for under-diagnosis exists. Measurement of airflow, such as peak expiratory flow rates, which can be done inexpensively on the track or sideline, may prove helpful.

Berylliosis, or chronic beryllium disease (CBD), is a chronic allergic-type lung response and chronic lung disease caused by exposure to beryllium and its compounds, a form of beryllium poisoning. It is distinct from acute beryllium poisoning, which became rare following occupational exposure limits established around 1950. Berylliosis is an occupational lung disease.

The condition is incurable, but symptoms can be treated.

Bronchiolitis obliterans is a lung disease characterized by fixed airway obstruction. Inflammation and scarring occur in the airways of the lung, resulting in severe shortness of breath and dry cough.

FEV1 (forced expiratory volume in 1 second) should be above 80% of predicted values to be considered normal. Bronchiolitis obliterans reduces this to between 16% and 21%.

Symptoms include dry cough, shortness of breath and wheezing.

The symptoms can start gradually, or severe symptoms can occur suddenly.

The exact criteria for the diagnosis of ABPA are not yet universally agreed upon, though working groups have proposed specific guidelines.

ABPA should be suspected in patients with a predisposing lung disease—most commonly asthma or cystic fibrosis— and is often associated with chronic airway limitation (CAL). Patients generally present with symptoms of recurrent infection such as fever, but do not respond to conventional antibiotic therapy. Poorly-controlled asthma is a common finding, with a case series only finding 19% of ABPA patients with well-controlled asthma. Wheezing and hemoptysis (coughing up blood) are common features, and mucus plugging is seen in 31–69% of patients.

Bird fancier's lung is a type of hypersensitivity pneumonitis caused by bird droppings. The lungs become inflamed with granuloma formation.

Bird fancier's lung (BFL), also called "bird-breeder's lung" and "pigeon-breeder's lung", is a subset of hypersensitivity pneumonitis (HP). This disease is caused by the exposure to avian proteins present in the dry dust of the droppings and sometimes in the feathers of a variety of birds. Birds such as pigeons, parakeets, cockatiels, shell parakeets (budgerigars), parrots, turtle doves, turkeys and chickens have been implicated.

People who work with birds or own many birds are at risk. Bird hobbyists and pet store workers may also be at risk.

Signs and symptoms of flock worker's lung include rales (crackling noises caused by fluid in the lungs), dyspnea (shortness of breath), and coughing. Abnormalities seen on a computed tomography (CT) scan of the lungs can include ground glass opacity and reticular opacity. The typical histopathology in flock worker's lung is bronchiolocentric interstitial pneumonitis and lymphocytic bronchiolitis with lymphocytic hyperplasia. Occasionally, desquamative interstitial pneumonia and bronchiolitis obliterans organizing pneumonia can be seen.

Other symptoms described in flock workers include pleuritic chest pain and atypical chest pain. Most cases described have been chronic and progressive. Lung function in individuals with flock worker's lung is generally diminished, with both restrictive and obstructive defects found.

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.

The signs and symptoms of allergies in a child are:

- Chronic symptoms resembling the cold that last more than a week or two.

- Cold-like symptoms that appear during the same time each year

- Repeated difficulty breathing, wheezing and breathing

- Cold-like symptoms that happen at night

- Cold-like symptoms that happen during exercise

- Chronic rashes or patches of skin that are dry, itchy, look like scales

- Cold-like symptoms that appear after eating a certain food

- Hives

- Swelling of face, arms or legs

- Gagging, coughing or wheezing, vomiting or significant abdominal pain

- Itching or tingling sensations in the mouth, throat or ears