Acute inhalation injury may result from frequent and widespread use of household cleaning agents and industrial gases (including chlorine and ammonia). The airways and lungs receive continuous first-pass exposure to non-toxic and irritant or toxic gases via inhalation. Irritant gases are those that, on inhalation, dissolve in the water of the respiratory tract mucosa and provoke an inflammatory response, usually from the release of acidic or alkaline radicals. Smoke, chlorine, phosgene, sulfur dioxide, hydrogen chloride, hydrogen sulfide, nitrogen dioxide, ozone, and ammonia are common irritants.

Depending on the type and amount of irritant gas inhaled, victims can experience symptoms ranging from minor respiratory discomfort to acute airway and lung injury and even death. A common response cascade to a variety of irritant gases includes inflammation, edema and epithelial sloughing, which if left untreated can result in scar formation and pulmonary and airway remodeling. Currently, mechanical ventilation remains the therapeutic mainstay for pulmonary dysfunction following acute inhalation injury.

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).

Smoke inhalation is the primary cause of death for victims of indoor fires. The inhalation or exposure to hot gaseous products of combustion can cause serious respiratory complications.

Some 50–80% of fire deaths are the result of smoke inhalation injuries, including burns to the respiratory system. The hot smoke injures or kills by a combination of thermal damage, poisoning and pulmonary irritation and swelling, caused by carbon monoxide, cyanide and other combustion products.

Oral ingestion of hydrocarbons often is associated with symptoms of mucous membrane irritation, vomiting, and central nervous system depression. Cyanosis, tachycardia, and tachypnea may appear as a result of aspiration, with subsequent development of chemical pneumonitis. Other clinical findings include albuminuria, hematuria, hepatic enzyme derangement, and cardiac arrhythmias. Doses as low as 10 ml orally have been reported to be potentially fatal, whereas some patients have survived the ingestion of 60 ml of petroleum distillates. A history of coughing or choking in association with vomiting strongly suggests aspiration and hydrocarbon pneumonia. Hydrocarbon pneumonia is an acute hemorrhagic necrotizing disease that can develop within 24 h after the ingestion. Pneumonia may require several weeks for complete resolution.

Symptoms of chemical (hydrocarbon) pneumonia may include:

- burning of the nose, eyes, lips, mouth, and throat

- dry cough

- wet cough producing clear, yellow, or green mucus

- cough producing blood or frothy pink matter

- nausea or abdominal pain

- chest pain

- shortness of breath

- painful breathing or pleuritis (an inflammation of the outside covering of the lungs)

- headache

- flu symptoms

Symptoms range from coughing and vomiting to nausea, sleepiness and confusion. Burns to the nose, mouth and face; singed nostril hairs; and difficulty breathing / carbonaceous sputum (burned saliva) are also signs of smoke inhalation injury. Approximately one third of patients admitted to burns units have pulmonary injury from hot smoke inhalation. The death rate of patients with both severe burns and smoke inhalation can be in excess of 50%.

Any person with apparent signs of smoke inhalation should be immediately evaluated by a medical professional such as a paramedic or physician. Advanced medical care may be necessary to save the life of the patient, including mechanical ventilation, even if the person is conscious and alert. Pending advanced intervention, the patient should be brought into fresh air and given medical oxygen if available.

Fire breather's pneumonia, also known as fire breather's lung or fire-eater's lung, is a distinct type of exogenous—that is, originating outside the body—lipoid pneumonia (chemical pneumonitis) that results from inhalation or aspiration of hydrocarbons of different types, such as lamp oil. Accidental inhalation of hydrocarbon fuels can occur during fire breathing, fire eating, or other fire performance, and may lead to pneumonitis.

Symptoms can vary significantly among individuals, ranging from asymptomatic to a severe, life-threatening disease. Onset usually occurs within hours, though symptoms may not appear for several days. Lipoid pneumonia is a rare condition, but is an occupational hazard of fire performers.

Smoke inhalation injury, either by itself but more so in the presence of body surface burn, can result in severe lung-induced morbidity and mortality. The most common cause of death in burn centers is now respiratory failure. The September 11 attacks in 2001 and forest fires in U.S. states such as California and Nevada are examples of incidents that have caused smoke inhalation injury. Injury to the lungs and airways is not only due to deposition of fine particulate soot but also due to the gaseous components of smoke, which include phosgene, carbon monoxide, and sulfur dioxide.

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 signs and symptoms of ARDS often begin within two hours of an inciting event, but can occur after 1–3 days. Signs and symptoms may include shortness of breath, fast breathing, and a low oxygen level in the blood due to abnormal ventilation.

"Fire-eater's lung" is an important variant of hydrocarbon pneumonitis, which typically involves adolescents or young adults who are exposed through mishap during flame-blowing performances using a variety of different flammable materials. The substances used overlap with some of the pediatric exposures (kerosene, gasoline) but can also include other hydrocarbons such as jet fuel and, in France, an aromatic hydrocarbon enriched petroleum-distillate called "kerdan". There has also been a case of citronella oil aspiration in a fire-eater. As with hydrocarbon pneumonitis in children, fire-eater's lung can also be complicated by pneumatocele. Although the term "acute lipoid pneumonia" has been used to refer to the "fire-eater's lung" syndrome, this is a misnomer.

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.

Acute respiratory distress syndrome (ARDS) is a medical condition occurring in critically ill patients characterized by widespread inflammation in the lungs. ARDS is not a particular disease; rather, it is a clinical phenotype which may be triggered by various pathologies such as trauma, pneumonia and sepsis.

The hallmark of ARDS is diffuse injury to cells which form the barrier of the microscopic air sacs of the lungs, surfactant dysfunction, activation of the innate immune system response, and dysfunction of the body's regulation of clotting and bleeding. In effect, ARDS impairs the lungs' ability to exchange oxygen and carbon dioxide with the blood across a thin layer of the lungs' microscopic air sacs known as alveoli.

The syndrome is associated with a death rate between 20 and 50%. The risk of death varies based on severity, the person's age, and the presence of other underlying medical conditions.

Although the terminology of "adult respiratory distress syndrome" has at times been used to differentiate ARDS from "infant respiratory distress syndrome" in newborns, the international consensus is that "acute respiratory distress syndrome" is the best term because ARDS can affect people of all ages.

The most common symptom of pulmonary edema is difficulty breathing, but may include other symptoms such as coughing up blood (classically seen as pink, frothy sputum), excessive sweating, anxiety, and pale skin. Shortness of breath can manifest as orthopnea (inability to lie down flat due to breathlessness) and/or paroxysmal nocturnal dyspnea (episodes of severe sudden breathlessness at night). These are common presenting symptoms of chronic pulmonary edema due to left ventricular failure. The development of pulmonary edema may be associated with symptoms and signs of "fluid overload"; this is a non-specific term to describe the manifestations of left ventricular failure on the rest of the body and includes peripheral edema (swelling of the legs, in general, of the "pitting" variety, wherein the skin is slow to return to normal when pressed upon), raised jugular venous pressure and hepatomegaly, where the liver is enlarged and may be tender or even pulsatile. Other signs include end-inspiratory crackles (sounds heard at the end of a deep breath) on auscultation and the presence of a third heart sound.

Ventilator-associated lung injury (VALI) is an acute lung injury that develops during mechanical ventilation and is termed ventilator-induced lung injury (VILI) if it can be proven that the mechanical ventilation caused the acute lung injury. In contrast, ventilator-associated lung injury (VALI) exists if the cause cannot be proven. VALI is the appropriate term in most situations because it is virtually impossible to prove what actually caused the lung injury in the hospital.

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.

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.

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.

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.

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.

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.

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.

It can be classified into acute interstitial pneumonitis, blood pneumonitis, lymphocytic interstitial pneumonitis, radiation pneumonitis, and uremic pneumonitis.

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.

Pulmonary edema is fluid accumulation in the tissue and air spaces of the lungs. It leads to impaired gas exchange and may cause respiratory failure. It is due to either failure of the left ventricle of the heart to remove blood adequately from the pulmonary circulation (cardiogenic pulmonary edema), or an injury to the lung parenchyma or vasculature of the lung (noncardiogenic pulmonary edema). Treatment is focused on three aspects: firstly improving respiratory function, secondly, treating the underlying cause, and thirdly avoiding further damage to the lung. Pulmonary edema, especially acute, can lead to fatal respiratory distress or cardiac arrest due to hypoxia. It is a cardinal feature of congestive heart failure. The term is from the Greek (oídēma, "swelling"), from οἰδέω (oidéō, "I swell").