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.

According to the International Labour Office (ILO), PMF requires the presence of large opacity exceeding 1 cm (by x-ray). By pathology standards, the lesion in histologic section must exceed 2 cm to meet the definition of PMF. In PMF, lesions most commonly occupy the upper lung zone, and are usually bilateral. The development of PMF is usually associated with a restrictive ventilatory defect on pulmonary function testing. PMF can be mistaken for bronchogenic carcinoma and vice versa. PMF lesions tend to grow very slowly, so any rapid changes in size, or development of cavitation, should prompt a search for either alternative cause or secondary disease.

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.

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.

Progressive Massive Fibrosis (PMF), characterized by the development of large conglomerate masses of dense fibrosis (usually in the upper lung zones), can complicate silicosis and coal worker's pneumoconiosis. Conglomerate masses may also occur in other pneumoconioses, such as talcosis, berylliosis (CBD), kaolin pneumoconiosis, and pneumoconiosis from carbon compounds, such as carbon black, graphite, and oil shale. Conglomerate masses can also develop in sarcoidosis, but usually near the hilae and with surrounding paracitricial emphysema.

The disease arises firstly through the deposition of silica or coal dust (or other dust) within the lung, and then through the body's immunological reactions to the dust.

Pulmonary fibrosis (literally "scarring of the lungs") is a respiratory disease in which scars are formed in the lung tissues, leading to serious breathing problems. Scar formation, the accumulation of excess fibrous connective tissue (the process called fibrosis), leads to thickening of the walls, and causes reduced oxygen supply in the blood. As a consequence patients suffer from perpetual shortness of breath.

In some patients the specific cause of the disease can be diagnosed, but in others the probable cause cannot be determined, a condition called idiopathic pulmonary fibrosis. There is no known cure for the scars and damage in the lung due to pulmonary fibrosis.

Idiopathic pulmonary fibrosis (IPF) is a chronic irreversible and ultimately fatal disease characterized by a progressive decline in lung function. American Thoracic Society/European Respiratory Society International Multidisciplinary Consensus Classification of the Idiopathic Interstitial Pneumonias. This official statement of the American Thoracic Society (ATS), and the European Respiratory Society (ERS) was approved by the ATS board of directors, June 2013 and by the ERS Steering Committee, March 2013. "Am Respir Crit Care Med." 188 (6): 733–748. September 15, 2013. The term pulmonary fibrosis means scarring of lung tissue and is the cause of worsening dyspnea (shortness of breath). Fibrosis is usually associated with a poor prognosis.

IPF belongs to a large group of more than 200 lung diseases known as interstitial lung diseases (ILDs), characterized by the involvement of lung interstitium. The interstitium, the tissue between the air sacs in the lung, is the primary site of injury in ILDs. However, these disorders frequently affect not only the interstitium, but also the airspaces, peripheral airways, and vessels. Lung tissue from people with IPF shows a characteristic histopathologic pattern known as usual interstitial pneumonia (UIP). UIP is therefore the pathologic counterpart of IPF. The term 'idiopathic' is used because the cause of pulmonary fibrosis is still unknown. IPF usually occurs in adults of between 50 and 70 years of age, particularly those with a history of cigarette smoking, and affects more men than women. The diagnosis of IPF requires exclusion of other known causes of ILDs and the presence of a typical radiological pattern identified through high resolution computed tomography (HRCT). In the right clinical setting, it is possible to make the diagnosis of IPF by HRCT alone, obviating the need for surgical lung biopsy.

Treatment to slow down the progression of the disease may include nintedanib or pirfenidone.

Most common:

- Chest Pain

- Cough

- Fever

- Shortness of breath

- Joint pain, stiffness, swelling

- Skin nodules

People may not present with all these symptoms or non at all.

Clinically, IPH manifests as a triad of haemoptysis, diffuse parenchymal infiltrates on chest radiographs, and iron deficiency anaemia. It is diagnosed at an average age of 4.5 plus or minus 3.5 years, and it is twice as common in females. The clinical course of IPH is exceedingly variable, and most of the patients continue to have episodes of pulmonary haemorrhage despite therapy. Death may occur suddenly from acute pulmonary haemorrhage or after progressive pulmonary insufficiency resulting in chronic respiratory failure.

Idiopathic pulmonary haemosiderosis (or idiopathic pulmonary hemosiderosis; IPH) is a lung disease of unknown cause that is characterized by alveolar capillary bleeding and accumulation of haemosiderin in the lungs. It is rare, with an incidence between 0.24 and 1.23 cases per million people.

From most to lest common:

- Pleural involvement (pleurisy, effusions)

- Pulmonary parenchymal nodules, more common in men than in women

- Rheumatoid-associated interstitial lung disease

- Bronchiolitis obliterans organizing pneumonia

- Obliterative bronchiolitis (obstructive lung disease/bronchiectasis)

- Rheumatoid-associated pulmonary hypertension

- Pulmonary vasculitis/arteritis

- Shrinking lung syndrome

- Miscellaneous: MTX, cricoarytenoid arthritis, infection, cancer

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.

May have no signs and symptoms or they may include:

- cough, but not prominent;

- chest pain (not common);

- breathing difficulty (fast and shallow);

- low oxygen saturation;

- pleural effusion (transudate type);

- cyanosis (late sign);

- increased heart rate.

It is a common misconception that atelectasis causes fever. A study of 100 post-op patients followed with serial chest X-rays and temperature measurements showed that the incidence of fever decreased as the incidence of atelectasis increased. A recent review article summarizing the available published evidence on the association between atelectasis and post-op fever concluded that there is no clinical evidence supporting this doctrine.

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.

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.

Some people with bronchiectasis may have a cough productive of frequent green/yellow mucus (sputum), up to 240 ml (8 oz) daily. Bronchiectasis may also present with coughing up blood (hemoptysis) in the absence of sputum, called "dry bronchiectasis". Sputum production may also occur without coloration. People with bronchiectasis may have bad breath indicative of active infection. Frequent bronchial infections and breathlessness are two possible indicators of bronchiectasis.

Crepitations and expiratory rhonchi may be heard on auscultation. Nail clubbing is rare.

Caplan syndrome presents with cough and shortness of breath in conjunction with features of rheumatoid arthritis, such as painful joints and morning stiffness.

Examination should reveal tender, swollen metacarpophalangeal joints and rheumatoid nodules; auscultation of the chest may reveal diffuse râles that do not disappear on coughing or taking a deep breath.

Caplan syndrome is a nodular condition of the lung occurring in dust-exposed persons with either a history of rheumatoid arthritis (RA) or who subsequently develop RA within the following 5–10 years. The nodules in the lung typically occur bilaterally and peripherally, on a background of simple coal workers' pneumoconiosis. There are usually multiple nodules, varying in size from 0.5 to 5.0 cm. The nodules typically appear rapidly, often in only a few weeks. Nodules may grow, remain unchanged in size, resolve, or disappear and then reappear. They can cavitate, calcify, or develop air-fluid levels. Grossly, they can resemble a giant silicotic nodule. Histologically, they usually have a necrotic center surrounded by a zone of plasma cells and lymphocytes, and often with a peripheral inflammatory zone made of macrophages and neutrophils.

Atelectasis may be an acute or chronic condition. In acute atelectasis, the lung has recently collapsed and is primarily notable only for airlessness. In chronic atelectasis, the affected area is often characterized by a complex mixture of airlessness, infection, widening of the bronchi (bronchiectasis), destruction, and scarring (fibrosis).

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.

Caplan's syndrome (or Caplan disease or Rheumatoid pneumoconiosis) is a combination of rheumatoid arthritis (RA) and pneumoconiosis that manifests as intrapulmonary nodules, which appear homogenous and well-defined on chest X-ray.

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

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.

In chronic HP, patients often lack a history of acute episodes. They have an insidious onset of cough, progressive dyspnea, fatigue, and weight loss. This is associated with partial to complete but gradual reversibility. Avoiding any further exposure is recommended. Clubbing is observed in 50% of patients. Tachypnea, respiratory distress, and inspiratory crackles over lower lung fields often are present.

On chest radiographs, progressive fibrotic changes with loss of lung volume particularly affect the upper lobes. Nodular or ground-glass opacities are not present. Features of emphysema are found on significant chest films and CT scans.

Chronic forms reveal additional findings of chronic interstitial inflammation and alveolar destruction (honeycombing) associated with dense fibrosis. Cholesterol clefts or asteroid bodies are present within or outside granulomas.

In addition, many patients have hypoxemia at rest, and all patients desaturate with exercise.

Benign asbestos pleural effusion is an exudative pleural effusion (a buildup of fluid between the two pleural layers) following asbestos exposure. It is relatively uncommon and the earliest manifestation of disease following asbestos exposure, usually occurring within 10 years from exposure. Effusions may be asymptomatic but rarely, they can cause pain, fever, and breathlessness. Effusions usually last for 3–4 months and then resolve completely. They can also progress to diffuse pleural thickening. Diagnosis relies on a compatible history of asbestos exposure and exclusion of other probable causes.