Respiratory infection in humans is relatively rare and presents as two stages. It infects the lymph nodes in the chest first, rather than the lungs themselves, a condition called hemorrhagic mediastinitis, causing bloody fluid to accumulate in the chest cavity, therefore causing shortness of breath. The first stage causes cold and flu-like symptoms. Symptoms include fever, shortness of breath, cough, fatigue, and chills. This can last hours to days. Often, many fatalities from inhalational anthrax are when the first stage is mistaken for the cold or flu and the victim does not seek treatment until the second stage, which is 90% fatal. The second (pneumonia) stage occurs when the infection spreads from the lymph nodes to the lungs. Symptoms of the second stage develop suddenly after hours or days of the first stage. Symptoms include high fever, extreme shortness of breath, shock, and rapid death within 48 hours in fatal cases. Historical mortality rates were over 85%, but when treated early (seen in the 2001 anthrax attacks), observed case fatality rate dropped to 45%. Distinguishing pulmonary anthrax from more common causes of respiratory illness is essential to avoiding delays in diagnosis and thereby improving outcomes. An algorithm for this purpose has been developed.

Cutaneous anthrax, also known as Hide porter's disease, is when anthrax occurs on the skin. It is the most common form (>90% of anthrax cases). Cutaneous anthrax is also the least dangerous form of anthrax (less than 1% mortality rate with treatment). Cutaneous anthrax presents as a boil-like skin lesion that eventually forms an ulcer with a black center (eschar). The black eschar often shows up as a large, painless, necrotic ulcer (beginning as an irritating and itchy skin lesion or blister that is dark and usually concentrated as a black dot, somewhat resembling bread mold) at the site of infection. In general, cutaneous infections form within the site of spore penetration between two and five days after exposure. Unlike bruises or most other lesions, cutaneous anthrax infections normally do not cause pain. Nearby lymph nodes may become infected, reddened, swollen, and painful. A scab forms over the lesion soon, and falls off in a few weeks. Complete recovery may take longer.

Cutaneous anthrax is typically caused when "B. anthracis" spores enter through cuts on the skin. This form is found most commonly when humans handle infected animals and/or animal products.

Cutaneous anthrax is rarely fatal if treated, because the infection area is limited to the skin, preventing the lethal factor, edema factor, and protective antigen from entering and destroying a vital organ. Without treatment, about 20% of cutaneous skin infection cases progress to toxemia and death.

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.

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.

An airborne disease is any disease that is caused by pathogens that can be transmitted through the air. Such diseases include many of considerable importance both in human and veterinary medicine. The relevant pathogens may be viruses, bacteria, or fungi, and they may be spread through breathing, talking, coughing, sneezing, raising of dust, spraying of liquids, toilet flushing or any activities which generates aerosol particles or droplets. Human airborne diseases do not include conditions caused by air pollution such as volatile organic compounds (VOCs), gasses and any airborne particles, though their study and prevention may help inform the science of airborne disease transmission.

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.

Prodromal symptoms are flu-like ones, such as fever, cough, myalgia, headache, lethargy, and shortness of breath, which rapidly deteriorates into acute respiratory failure. It is characterized by the sudden onset of shortness of breath with rapidly evolving pulmonary edema; it is often fatal despite mechanical ventilation and intervention with potent diuretics. It has a fatality rate of 36%.

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).

Chalicosis (Greek, χάλιξ, gravel), sometimes called flint disease, is a form of pneumoconiosis affecting the lungs or bronchioles, found chiefly among stonecutters.

The disease is caused by the inhalation of fine particles of stone.

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.

Berylliosis, or chronic beryllium disease (CBD), is a chronic allergic-type lung response and chronic lung disease caused by exposure to beryllium and its compounds, a form of beryllium poisoning. It is distinct from acute beryllium poisoning, which became rare following occupational exposure limits established around 1950. Berylliosis is an occupational lung disease.

The condition is incurable, but symptoms can be treated.

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.

Airborne diseases include any that are caused via transmission through the air. Many airborne diseases are of great medical importance. The pathogens transmitted may be any kind of microbe, and they may be spread in aerosols, dust or liquids. The aerosols might be generated from sources of infection such as the bodily secretions of an infected animal or person, or biological wastes such as accumulate in lofts, caves, garbage and the like. Such infected aerosols may stay suspended in air currents long enough to travel for considerable distances, though the rate of infection decreases sharply with the distance between the source and the organism infected.

Airborne pathogens or allergens often cause inflammation in the nose, throat, sinuses and the lungs. This is caused by the inhalation of these pathogens that affect a person's respiratory system or even the rest of the body. Sinus congestion, coughing and sore throats are examples of inflammation of the upper respiratory air way due to these airborne agents. Air pollution plays a significant role in airborne diseases which is linked to asthma. Pollutants are said to influence lung function by increasing air way inflammation.

Many common infections can spread by airborne transmission at least in some cases, including: Anthrax (inhalational), Chickenpox, Influenza, Measles, Smallpox, Cryptococcosis, and Tuberculosis.

Airborne diseases can also affect non-humans. For example, Newcastle disease is an avian disease that affects many types of domestic poultry worldwide which is transmitted via airborne contamination.

Often, airborne pathogens or allergens cause inflammation in the nose, throat, sinuses, and the upper airway lungs. Upper airway inflammation causes coughing congestion, and sore throat. This is caused by the inhalation of these pathogens that affect a person's respiratory system or even the rest of the body. Sinus congestion, coughing and sore throats are examples of inflammation of the upper respiratory air way due to these airborne agents.

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.

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.

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

Hantavirus pulmonary syndrome (HPS) is one of two potentially fatal syndromes of zoonotic origin caused by species of hantavirus. These include

Black Creek Canal virus (BCCV), New York virus (NYV), Sin Nombre virus (SNV), and certain other members of Hantavirus genera that are native to the United States and Canada. Specific rodents are the principal hosts of the hantaviruses including the hispid cotton rat ("Sigmodon hispidus") in southern Florida, which is the principal host of Black Creek Canal virus., the rice rat also in the south east, the deer mouse ("Peromyscus maniculatus") in Canada and the Western United States is the principal host of Sin Nombre virus. The white-footed mouse ("Peromyscus leucopus") in the eastern United States is the principal host of New York virus.

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.

Polymer fume fever or fluoropolymer fever, also informally called Teflon flu, is an inhalation fever caused by the fumes released when polytetrafluoroethylene (PTFE, known under the trade name Teflon) reaches temperatures of 300 °C (572 °F) to 450 °C (842 °F). When PTFE is heated above 450 °C the pyrolysis products are different and inhalation may cause acute lung injury. Symptoms are flu-like (chills, headaches and fevers) with chest tightness and mild cough. Onset occurs about 4 to 8 hours after exposure to the pyrolysis products of PTFE. A high white blood cell count may be seen and chest x-ray findings are usually minimal.

The polymer fumes are especially harmful to certain birds whose breathing, optimized for rapidity, allows toxins which are excluded by human lungs. Fumes from Teflon in very high heat are fatal to parrots, as well as some other birds (PTFE Toxicosis).

A "vaccine-preventable disease" is an infectious disease for which an effective preventive vaccine exists. If a person acquires a vaccine-preventable disease and dies from it, the death is considered a vaccine-preventable death.

The most common and serious vaccine-preventable diseases tracked by the World Health Organization (WHO) are: diphtheria, "Haemophilus influenzae" serotype b infection, hepatitis B, measles, meningitis, mumps, pertussis, poliomyelitis, rubella, tetanus, tuberculosis, and yellow fever. The WHO reports licensed vaccines being available to prevent, or contribute to the prevention and control of, 25 vaccine-preventable infections.

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.

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.

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.