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.

Farmer’s lung reactions can be categorized as acute and chronic reactions. Acute and chronic reactions have the same symptoms but for chronic reactions, the symptoms are much more severe. Farmer’s lung symptoms include:

- Chills

- Fever

- Irritating/harassing cough

- Runny nose

- Sputum streaked with blood

- Tightness of the chest

- Difficult and laboured breathing

- Crackling of breath

- Muscular pain

- Depression

These symptoms develop between four and eight hours after exposure to the antigens. In acute attacks, the symptoms mimic pneumonia or flu. In chronic attacks, there is a possibility of the victim going into shock and dying from the attack.

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.

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.

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.

Some symptoms and signs of Bagassosis include breathlessness, cough, haemoptysis, slight fever. Acute diffuse bronchiolitis may also occur. An xray may show mottling of lungs or a shadow.

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.

The only cause of Farmer’s lung is repeated exposure to tiny microorganisms which inhabit moldy hay. They are inhaled and often provoke the creation of IgE antibodies that circulate in the bloodstream, these types of immune response are most often initiated by exposure to thermophilic actinomycetes (most commonly "Saccharopolyspora rectivirgula"), which generates IgG-type antibodies. Following a subsequent exposure, IgG antibodies combine with the inhaled allergen to form immune complexes in the walls of the alveoli in the lungs. This causes fluid, protein, and cells to accumulate in the alveolar wall which slows blood-gas interchange and compromises the function of the lung. After multiple exposures, it takes less and less of the antigens to set off the reaction in the lung. The most prominent antigens are thermophilic actinomycetes and fungi.

Allergic bronchopulmonary aspergillosis (ABPA) is a condition characterised by an exaggerated response of the immune system (a hypersensitivity response) to the fungus "Aspergillus" (most commonly "Aspergillus fumigatus"). It occurs most often in patients with asthma or cystic fibrosis. "Aspergillus" spores are ubiquitous in soil and are commonly found in the sputum of healthy individuals. "A. fumigatus" is responsible for a spectrum of lung diseases known as aspergilloses.

ABPA causes airway inflammation, leading to bronchiectasis—a condition marked by abnormal dilation of the airways. Left untreated, the immune system and fungal spores can damage sensitive lung tissues and lead to scarring.

The exact criteria for the diagnosis of ABPA are not agreed upon. Chest X-rays and CT scans, raised blood levels of IgE and eosinophils, immunological tests for "Aspergillus" together with sputum staining and sputum cultures can be useful. Treatment consists of corticosteroids and antifungal medications.

Bagassosis has been shown to be due to a thermophilic actinomycetes for which the name thermoactinomycetes sacchari was suggested.

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.

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.

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 typical symptoms of UIP are progressive shortness of breath and cough for a period of months. In some patients, UIP is diagnosed only when a more acute disease supervenes and brings the patient to medical attention.

The cause of the scarring in UIP may be known (less commonly) or unknown (more commonly). Since the medical term for conditions of unknown cause is "idiopathic", the clinical term for UIP of unknown cause is idiopathic pulmonary fibrosis (IPF). Examples of known causes of UIP include systemic sclerosis/scleroderma, rheumatoid arthritis, asbestosis, and prolonged use of medications such as nitrofurantoin or amiodarone.

Feeding problems are common in infants with BPD, often due to prolonged intubation. Such infants often display oral-tactile hypersensitivity (also known as oral aversion).

Physical findings:

- hypoxemia;

- hypercapnia;

- crackles, wheezing, & decreased breath sounds;

- increased bronchial secretions;

- hyperinflation;

- frequent lower respiratory infections;

- delayed growth & development;

- cor pulmonale;

- CXR shows with hyperinflation, low diaphragm, atelectasis, cystic changes.

Lycoperdonosis is a respiratory disease caused by the inhalation of large amounts of spores from mature puffballs. It is classified as a hypersensitivity pneumonitis (also called extrinsic allergic alveolitis)—an inflammation of the alveoli within the lung caused by hypersensitivity to inhaled natural dusts. It is one of several types of hypersensitivity pneumonitis caused by different agents that have similar clinical features. Typical progression of the disease includes symptoms of a cold hours after spore inhalation, followed by nausea, rapid pulse, crepitant rales (a sound like that made by rubbing hairs between the fingers, heard at the end of inhalation), and dyspnea. Chest radiographs reveal the presence of nodules in the lungs. The early symptoms presented in combination with pulmonary abnormalities apparent on chest radiographs may lead to misdiagnosis of the disease as tuberculosis, histiocytosis, or pneumonia caused by "Pneumocystis carinii". Lycoperdonosis is generally treated with corticosteroids, which decrease the inflammatory response; these are sometimes given in conjunction with antimicrobials.

The disease was first described in the medical literature in 1967 by R.D. Strand and colleagues in the "New England Journal of Medicine". In 1976, a 4-year-old was reported developing the disease in Norway after purposely inhaling a large quantity of "Lycoperdon" spores to stop a nosebleed. "Lycoperdon" species are sometimes used in folk medicine in the belief that their spores have haemostatic properties. A 1997 case report discussed several instances of teenagers inhaling the spores. In one severe case, the individual inhaled enough spores so as to be able to blow them out of his mouth. He underwent bronchoscopy and then had to be on life support before recovering in about four weeks. In another instance, a teenager spent 18 days in a coma, had portions of his lung removed, and suffered severe liver damage. In Wisconsin, eight teenagers who inhaled spores at a party presented clinical symptoms such as cough, fever, shortness of breath, myalgia, and fatigue within a week. Five of the eight required hospitalization; of these, two required intubation to assist in breathing. The disease is rare, possibly because of the large quantity of spores that need to be inhaled for clinical effects to occur. Lycoperdonosis also occurs in dogs; in the few reported cases, the animals had been playing or digging in areas known to contain puffballs. Known species of puffballs implicated in the etiology of the published cases include the widespread "Lycoperdon perlatum" (the "devil's snuff-box", "L. gemmatum") and "Calvatia gigantea", both of the Lycoperdaceae family.

Pulmonary Langerhans cell histiocytosis, silicosis, coal workers pneumoconiosis, carmustine related pulmonary fibrosis, respiratory broncholitis associated with interstitial lung disease.

- Lower lung predominance

Idiopathic pulmonary fibrosis, pulmonary fibrosis associated with connective tissue diseases, asbestosis, chronic aspiration

- Central predominance (perihilar)

Sarcoidosis, berylliosis

- Peripheral predominance

Idiopathic pulmonary fibrosis, chronic eosinophilic pneumonia, cryptogenic organizing pneumonia

Prolonged high oxygen delivery in premature infants causes necrotizing bronchiolitis and alveolar septal injury, with inflammation and scarring. This results in hypoxemia. Today, with the advent of surfactant therapy and high frequency ventilation and oxygen supplementation, infants with BPD experience much milder injury without necrotizing bronchiolitis or alveolar septal fibrosis. Instead, there are usually uniformly dilated acini with thin alveolar septa and little or no interstitial fibrosis. It develops most commonly in the first 4 weeks after birth.

Symptoms of pulmonary fibrosis are mainly:

- Shortness of breath, particularly with exertion

- Chronic dry, hacking coughing

- Fatigue and weakness

- Chest discomfort including chest pain

- Loss of appetite and rapid weight loss

Pulmonary fibrosis is suggested by a history of progressive shortness of breath (dyspnea) with exertion. Sometimes fine inspiratory crackles can be heard at the lung bases on auscultation. A chest x-ray may or may not be abnormal, but high-resolution CT will frequently demonstrate abnormalities.

Treatment usually involves adrenaline (epinephrine), antihistamines, and corticosteroids.

If the entire body is involved, then anaphylaxis can take place, which is an acute, systemic reaction that can prove fatal.

Pulmonary edema, connective tissue diseases, asbestosis, lymphangitic carcinomatosis, lymphoma, lymphangioleiomyomatosis, drug-induced lung diseases

- Lymphadenopathy

Sarcoidosis, silicosis, berylliosis, lymphangitic carcinomatosis, lymphoma, lymphocytic interstitial pneumonia

In many patients, symptoms are present for a considerable time before diagnosis. The most common clinical features of IPF include the following:

- Age over 50 years

- Dry, non-productive cough on exertion

- Progressive exertional dyspnea (shortness of breath with exercise)

- Dry, inspiratory bibasilar "velcro-like" crackles on auscultation (a crackling sound in the lungs during inhalation similar to Velcro being torn apart slowly, heard with a stethoscope).

- Clubbing of the digits, a disfigurement of the finger tips or toes (see image)

- Abnormal pulmonary function test results, with evidence of restriction and impaired gas exchange.

Some of these features are due to chronic hypoxemia (oxygen deficiency in the blood), are not specific for IPF, and can occur in other pulmonary disorders. IPF should be considered in all patients with unexplained chronic exertional dyspnea who present with cough, inspiratory bibasilar crackles, or finger clubbing.

Assessment of "velcro" crackles on lung auscultation is a practical way to improve the earlier diagnosis of IPF. Fine crackles are easily recognized by clinicians and are characteristic of IPF.

If bilateral fine crackles are present throughout the inspiratory time and are persisting after several deep breaths, and if remaining present on several occasions several weeks apart in a subject aged ≥60 years, this should raise the suspicion of IPF and lead to consideration of an HRCT scan of the chest which is more sensitive than a chest X-ray. As crackles are not specific for IPF, they must prompt a thorough diagnostic process.

Some examples:

- Allergic asthma

- Allergic conjunctivitis

- Allergic rhinitis ("hay fever")

- Anaphylaxis

- Angioedema

- Urticaria (hives)

- Eosinophilia

- Penicillin allergy

- Cephalosporin allergy

- Food allergy

- Sweet itch