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.

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.

A number of other health conditions occur more frequently in those with asthma, including gastro-esophageal reflux disease (GERD), rhinosinusitis, and obstructive sleep apnea. Psychological disorders are also more common, with anxiety disorders occurring in between 16–52% and mood disorders in 14–41%. However, it is not known whether asthma causes psychological problems or psychological problems lead to asthma. Those with asthma, especially if it is poorly controlled, are at high risk for radiocontrast reactions.

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.

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.

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.

, one of the Four Big Pollution Diseases of Japan, occurred in the city of Yokkaichi in Mie Prefecture, Japan, between 1960 and 1972. The burning of petroleum and crude oil released large quantities of sulfur oxide that caused severe smog, resulting in severe cases of chronic obstructive pulmonary disease, chronic bronchitis, pulmonary emphysema, and bronchial asthma among the local inhabitants. The generally accepted sources of the sulfur oxide pollution were petrochemical processing facilities and refineries that were built in the area between 1957 and 1973.

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.

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.

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.

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.

In 1973, Breslin et al. tested the effects of alcoholic beverage consumption on the respiratory symptoms of 11 asthmatic subjects who gave a history of asthma attacks following certain alcoholic beverages. In response to ingesting the type of beverage that the subjects reported to provoke their symptoms, six developed the asthmatic symptom of chest tightness, two developed a symptom often associated with asthma, rhinitis, and one subject developed both chest tightness and rhinitis. Symptoms developed almost immediately after ingestion, inhalation of fumes from the beverages did not precipitate symptoms, and bronchoconstriction in response to the ingestion was confirmed in the three patients evaluated by pulmonary function tests. The study suggested that these reactions were induced by non-alcoholic allergens that were contained in or contaminated the beverages. In 1978 a non-asthmatic female of Japanese descent with a history of moderately severe bronchoconstriction responses to various alcoholic beverages and in 1981 an asthmatic Japanese male with a similar history beer or 95% pure ethanol were studied and found to develop bronchoconstriction after drinking apple juice but not after drinking apple juice per se; intravenous infusion or inhalation of ethanol also caused bronchospasm responses in the male subject. These studies suggested that alcohol itself caused the asthmatic symptoms triggered by alcoholic beverages. A subsequent study in 1986 found that 9 of 18 patients with a history of red wine-induced asthma symptoms showed bronchoconstriction in response to ingesting red wine; the response correlated positively with the amount of sulfur dioxide contained in the provocative wine. The study suggested that the reaction was not allergen-induced but rather triggered by sulfur dioxide, a sulfur dioxide-related agent, or an agent whose levels in alcohol beverages correlated positively with those of sulfur dioxide. Finally, a questionnaire survey of 366 asthmatic patients conducted in 2000 found that 33% reported asthma symptoms in response to alcoholic beverages; there was a significant association between wine-induced asthma and asthma triggered by sulfite-containing foods, by aspirin, and by nonsteroidal anti-inflammatory drugs (NSAID) other than aspirin. The study suggested the salicylate-"contaminates" in wine may contribute to these responses. In other studies, D.P. Agarwal and colleagues associated race-based variations in the activity alcohol-metabolizing enzymes with the occurrence of alcohol flush reactions to alcohol and alcoholic beverages in certain Asian populations. This early work is the basis for further studies that have defined not only many alcohol-induced flush reactions but also many alcohol-induced respiratory reactions as due to racially associated genetic differences in alcohol-metabolizing enzymes.

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.

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.

In 1955, the Ministry of International Trade and Industry began its policy to transition Japan's primary fossil fuel source from coal to petroleum. To accomplish that goal, construction of the Daichi Petrochemical Complex was begun in 1956. The complex contained an oil refinery, a petrochemical plant, and a power station. This was the first petrochemical complex constructed in Japan.

In 1960, the government of Prime Minister Hayato Ikeda accelerated the growth of petrochemical production as part of its goal to double individual incomes of Japanese citizens over a 10-year period. Also in 1960, MITI announced that a second complex was to be constructed on reclaimed land in northern Yokkaichi. The second complex went online in 1963. As demand for ethylene and other petrochemicals rose, a third complex was constructed which began production in 1972. Yokkaichi transferred its energy production from coal to oil more quickly than the rest of the nation. The oil used in Yokkaichi was primarily imported from the Middle East, which contained 2% sulfur in sulfur containing compounds, resulting in a white-colored smog developing over the city.

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

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.

Samter's triad goes by several other names:

A sufferer who has not yet experienced asthma or aspirin sensitivity might be diagnosed as having:

- Non-allergic rhinitis

- Non-allergic rhinitis with eosinophilia syndrome (NARES)

Acute bronchitis, also known as a chest cold, is short term inflammation of the bronchi of the lungs. The most common symptom is a cough. Other symptoms include coughing up mucus, wheezing, shortness of breath, fever, and chest discomfort. The infection may last from a few to ten days. The cough may persist for several weeks afterwards with the total duration of symptoms usually around three weeks. Some have symptoms for up to six weeks.

Exercise-induced bronchoconstriction can be difficult to diagnose clinically given the lack of specific symptoms and frequent misinterpretation as manifestations of vigorous exercise. There are many mimics that present with similar symptoms, such as vocal cord dysfunction, cardiac arrhythmias, cardiomyopathies, and gastroesophageal reflux disease. It is also important to distinguish those who have asthma with exercise worsening, and who consequently will have abnormal testing at rest, from true exercise-induced bronchoconstriction, where there will be normal baseline results. Because of the wide differential diagnosis of exertional respiratory complaints, the diagnosis of exercise-induced bronchoconstriction based on history and self-reported symptoms alone has been shown to be inaccurate and will result in an incorrect diagnosis more than 50% of the time.. An important an often over-looked differential diagnosis is exercise-induced laryngeal obstruction EILO. The latter can co-exist with EIB and is best differentiated using objective testing and continuous laryngoscopy during exercise (CLE) testing.

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.

Chronic bronchitis is defined as a productive cough that lasts for three months or more per year for at least two years. Most people with chronic bronchitis have chronic obstructive pulmonary disease (COPD). Protracted bacterial bronchitis is defined as a chronic productive cough with a positive bronchoalveolar lavage that resolves with antibiotics. Symptoms of chronic bronchitis may include wheezing and shortness of breath, especially upon exertion and low oxygen saturations. The cough is often worse soon after awakening and the sputum produced may have a yellow or green color and may be streaked with specks of blood.

Alcohol-induced respiratory reactions, also termed alcohol-induced asthma and alcohol-induced respiratory symptoms, are increasingly recognized as a pathological bronchoconstriction response to the consumption of alcohol that afflicts many people with a "classical" form of asthma, the airway constriction disease evoked by the inhalation of allergens. Alcohol-induced respiratory reactions reflect the operation of different and often racially related mechanisms that differ from those of classical, allergen-induced asthma.