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.

Classification of silicosis is made according to the disease's severity (including radiographic pattern), onset, and rapidity of progression. These include:

- Chronic simple silicosis: Usually resulting from long-term exposure (10 years or more) to relatively low concentrations of silica dust and usually appearing 10–30 years after first exposure. This is the most common type of silicosis. Patients with this type of silicosis, especially early on, may not have obvious signs or symptoms of disease, but abnormalities may be detected by x-ray. Chronic cough and exertional dyspnea (shortness of breath) are common findings. Radiographically, chronic simple silicosis reveals a profusion of small (<10 mm in diameter) opacities, typically rounded, and predominating in the upper lung zones.

- Accelerated silicosis: Silicosis that develops 5–10 years after first exposure to higher concentrations of silica dust. Symptoms and x-ray findings are similar to chronic simple silicosis, but occur earlier and tend to progress more rapidly. Patients with accelerated silicosis are at greater risk for complicated disease, including progressive massive fibrosis (PMF).

- Complicated silicosis: Silicosis can become "complicated" by the development of severe scarring (progressive massive fibrosis, or also known as conglomerate silicosis), where the small nodules gradually become confluent, reaching a size of 1 cm or greater. PMF is associated with more severe symptoms and respiratory impairment than simple disease. Silicosis can also be complicated by other lung disease, such as tuberculosis, non-tuberculous mycobacterial infection, and fungal infection, certain autoimmune diseases, and lung cancer. Complicated silicosis is more common with accelerated silicosis than with the chronic variety.

- Acute silicosis: Silicosis that develops a few weeks to 5 years after exposure to high concentrations of respirable silica dust. This is also known as silicoproteinosis. Symptoms of acute silicosis include more rapid onset of severe disabling shortness of breath, cough, weakness, and weight loss, often leading to death. The x-ray usually reveals a diffuse alveolar filling with air bronchograms, described as a ground-glass appearance, and similar to pneumonia, pulmonary edema, alveolar hemorrhage, and alveolar cell lung cancer.

Occupational lung diseases are occupational diseases affecting the respiratory system, including occupational asthma, black lung disease (coalworker's pneumoconiosis), chronic obstructive pulmonary disease (COPD), mesothelioma, and silicosis. Infectious lung diseases can also be acquired in an occupational context. Exposure to substances like flock and silica can cause fibrosing lung disease, whereas exposure to carcinogens like asbestos and beryllium can cause lung cancer. Occupational cases of interstitial lung disease may be misdiagnosed as COPD, idiopathic pulmonary fibrosis, or a myriad of other diseases; leading to a delay in identification of the causative agent.

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.

Flock worker's lung is an occupational lung disease caused by exposure to flock, small fibers that are glued to a backing in order to create a specific texture. People who work in flocking are at risk of inhaling the small fibers, which causes interstitial lung disease. The disease was initially described in 1998, when a group of workers at a flocking plant developed interstitial lung disease of unknown cause.

Coal workers' pneumoconiosis (CWP), also known as black lung disease or black lung, is caused by long exposure to coal dust. It is common in coal miners and others who work with coal. It is similar to both silicosis from inhaling silica dust and to the long-term effects of tobacco smoking. Inhaled coal dust progressively builds up in the lungs and cannot be removed by the body; this leads to inflammation, fibrosis, and in worse cases, necrosis.

Coal workers' pneumoconiosis, severe state, develops after the initial, milder form of the disease known as anthracosis ("anthrac" — coal, carbon). This is often asymptomatic and is found to at least some extent in all urban dwellers due to air pollution. Prolonged exposure to large amounts of coal dust can result in more serious forms of the disease, "simple coal workers' pneumoconiosis" and "complicated coal workers' pneumoconiosis" (or progressive massive fibrosis, or PMF). More commonly, workers exposed to coal dust develop industrial bronchitis, clinically defined as chronic bronchitis (i.e. productive cough for 3 months per year for at least 2 years) associated with workplace dust exposure. The incidence of industrial bronchitis varies with age, job, exposure, and smoking. In nonsmokers (who are less prone to develop bronchitis than smokers), studies of coal miners have shown a 16% to 17% incidence of industrial bronchitis.

In 2013 CWP resulted in 25,000 deaths down from 29,000 deaths in 1990.

Brown lung can ultimately result in narrowing of the airways, lung scarring and death from infection or respiratory failure.

Pneumoconiosis is an occupational lung disease and a restrictive lung disease caused by the inhalation of dust, often in mines and from agriculture.

In 2013, it resulted in 260,000 deaths, up from 251,000 deaths in 1990. Of these deaths, 46,000 were due to silicosis, 24,000 due to asbestosis and 25,000 due to coal workers pneumoconiosis.

Asbestosis is a fibrosing interstitial lung disease caused by exposure to forms of the mineral asbestos.

The major signs of indium lung are pulmonary alveolar proteinosis and pulmonary fibrosis. Symptoms include dyspnea (shortness of breath), cough, and increased sputum production. Hemoptysis has also been seen in people with indium lung. Other symptoms seen in some but not all cases include digital clubbing, low DLCO (capacity to move oxygen from the alveoli into the blood), and lowered forced expiratory volume. Emphysema has been associated with indium lung, but may not be part of the syndrome.

Bronchiolitis obliterans (BO), informally known as popcorn lung, is a disease that results in obstruction of the smallest airways of the lungs (bronchioles) due to inflammation. Symptoms include a dry cough, shortness of breath, wheezing, and feeling tired. These symptoms generally get worse over weeks to months. It is not related to organizing pneumonia.

Causes include breathing in toxic fumes, respiratory infections, connective tissue disorder, or following a bone marrow or heart-lung transplant. Symptoms may not occur until two to eight weeks following toxic exposure or infection. The underlying mechanism involves inflammation that results in scar tissue formation. Diagnosis is by CT scan, pulmonary function tests, or lung biopsy. A chest X-ray is often normal.

While the disease is not reversible treatments can slow further worsening. This may include the use of corticosteroids or immunosuppressive medication. A lung transplant may be tried. Outcomes are often poor with most people dying in months to years.

Bronchiolitis obliterans is rare in the general population. It affects about 75% of people by ten years following a lung transplant and up to 10% of people who have received a bone marrow transplant from someone else. The condition was first clearly described in 1981. Prior descriptions occurred as early as 1956.

Positive indications on patient assessment:

- Shortness of breath

- Chest X-ray may show a characteristic patchy, subpleural, bibasilar interstitial infiltrates or small cystic radiolucencies called honeycombing.

Pneumoconiosis in combination with multiple pulmonary rheumatoid nodules in rheumatoid arthritis patients is known as Caplan's syndrome.

Silicosis (also known as pneumonoultramicroscopicsilicovolcanoconiosis, previously miner's phthisis, grinder's asthma, potter's rot and other occupation-related names) is a form of occupational lung disease caused by inhalation of crystalline silica dust, and is marked by inflammation and scarring in the form of nodular lesions in the upper lobes of the lungs. It is a type of pneumoconiosis.

Silicosis (particularly the acute form) is characterized by shortness of breath, cough, fever, and cyanosis (bluish skin). It may often be misdiagnosed as pulmonary edema (fluid in the lungs), pneumonia, or tuberculosis.

Silicosis resulted in 46,000 deaths globally in 2013 down from 55,000 deaths in 1990.

The name "silicosis" (from the Latin "silex", or flint) was originally used in 1870 by Achille Visconti (1836–1911), prosector in the Ospedale Maggiore of Milan. The recognition of respiratory problems from breathing in dust dates to ancient Greeks and Romans. Agricola, in the mid-16th century, wrote about lung problems from dust inhalation in miners. In 1713, Bernardino Ramazzini noted asthmatic symptoms and sand-like substances in the lungs of stone cutters. With industrialization, as opposed to hand tools, came increased production of dust. The pneumatic hammer drill was introduced in 1897 and sandblasting was introduced in about 1904, both significantly contributing to the increased prevalence of silicosis.

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.

The signs and symptoms of asbestosis typically manifest after a significant amount of time has passed following asbestos exposure, often several decades under current conditions in the US. The primary symptom of asbestosis is generally the slow onset of shortness of breath, especially with physical activity. Clinically advanced cases of asbestosis may lead to respiratory failure. When a physician listens with a stethoscope to the lungs of a person with asbestosis, they may hear inspiratory crackles.

The characteristic pulmonary function finding in asbestosis is a restrictive ventilatory defect. This manifests as a reduction in lung volumes, particularly the vital capacity (VC) and total lung capacity (TLC). The TLC may be reduced through alveolar wall thickening; however, this is not always the case. Large airway function, as reflected by FEV/FVC, is generally well preserved. In severe cases, the drastic reduction in lung function due to the stiffening of the lungs and reduced TLC may induce right-sided heart failure (cor pulmonale). In addition to a restrictive defect, asbestosis may produce reduction in diffusion capacity and a low amount of oxygen in the blood of the arteries.

Indium lung is a rare occupational lung disease caused by exposure to respirable indium in the form of indium tin oxide. It is classified as an interstitial lung disease (diffuse parenchymal lung disease).

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.

Byssinosis, also called "brown lung disease" or "Monday fever", is an occupational lung disease caused by exposure to cotton dust in inadequately ventilated working environments. Byssinosis commonly occurs in workers who are employed in yarn and fabric manufacture industries. It is now thought that the cotton dust directly causes the disease and some believe that the causative agents are endotoxins that come from the cell walls of gram-negative bacteria that grow on the cotton. Although bacterial endotoxin is a likely cause, the absence of similar symptoms in workers in other industries exposed to endotoxins makes this uncertain.

Of the 81 byssinosis-related fatalities reported in the United States between 1990 and 1999, 48% included an occupation in the yarn, thread, and fabric industry on the victim's death certificate. This disease often occurred in the times of the industrial revolution. Most commonly young girls working in mills or other textile factories would be afflicted with this disease. In the United States, from 1996 to 2005, North Carolina accounted for about 37% of all deaths caused by byssinosis, with 31, followed by South Carolina (8) and Georgia (7).

The term "brown lung" is a misnomer, as the lungs of affected individuals are not brown.

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.

Asbestosis is long term inflammation and scarring of the lungs due to asbestos. Symptoms may include shortness of breath, cough, wheezing, and chest pain. Complications may include lung cancer, mesothelioma, and pulmonary heart disease.

Asbestosis is caused by breathing in asbestos fibers. Generally it required a relatively large exposure over a long period of time. Such levels of exposure typically only occur in those who work with the material. All types of asbestos fibers are associated with concerns. It is generally recommended that currently existing asbestos be left undisturbed. Diagnosis is based upon a history of exposure together with medical imaging. It is a type of interstitial pulmonary fibrosis.

There is no specific treatment. Recommendations may include stopping smoking, influenza vaccination, pneumococcal vaccination, or oxygen therapy. Asbestosis affected about 157,000 people and resulted in 3,600 deaths in 2015. Asbestos use has been banned in a number of countries in an effort to prevent disease.

Shortness of breath is often the symptom that most bothers people. It is commonly described as: "my breathing requires effort," "I feel out of breath," or "I can't get enough air in". Different terms, however, may be used in different cultures. Typically the shortness of breath is worse on exertion of a prolonged duration and worsens over time. In the advanced stages, or end stage pulmonary disease it occurs during rest and may be always present. It is a source of both anxiety and a poor quality of life in those with COPD. Many people with more advanced COPD breathe through pursed lips and this action can improve shortness of breath in some.

Fire breather’s pneumonia usually presents with certain non-specific symptoms, and may vary significantly among individuals. The most common symptoms include:

- Cough

- Dyspnea (shortness of breath)

- Chest pain

- Fever

- Weakness

- Hemoptysis (coughing up blood)

Acute pneumonitis typically begins asymptomatic, with a worsening of symptoms over the course of hours or days. Following aspiration of fuel, there is often a period of latency from 8–24 hours before the symptoms occur. Patients may not recall a specific instance of aspiration. Severe cases may lead to acute respiratory distress syndrome (ARDS).

A chronic cough is often the first symptom to develop. When it persists for more than three months each year for at least two years, in combination with sputum production and without another explanation, it is by definition chronic bronchitis. This condition can occur before COPD fully develops. The amount of sputum produced can change over hours to days. In some cases, the cough may not be present or may only occur occasionally and may not be productive. Some people with COPD attribute the symptoms to a "smoker's cough". Sputum may be swallowed or spat out, depending often on social and cultural factors. Vigorous coughing may lead to rib fractures or a brief loss of consciousness. Those with COPD often have a history of "common colds" that last a long time.

The signs and symptoms of PAP include shortness of breath, a cough, low grade fever, and weight loss.

The clinical course of PAP is unpredictable. Spontaneous remission is recognized, and some patients have stable symptoms. Death may occur due to the progression of PAP or of any underlying associated disease. Individuals with PAP are more vulnerable to lung infections such as bacterial pneumonia, mycobacterium avium-intracellulare infection, or a fungal infection.

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.