Clinically, the most serious and immediate complication is acute respiratory distress syndrome (ARDS), which usually occurs within 24 h. Those with significant lower airway involvement may develop bacterial infection. Importantly, victims suffering body surface burn and smoke inhalation are the most susceptible. Thermal injury combined with inhalation injury compromises pulmonary function, producing microvascular hyperpermeability that leads to a significant increase in lung lymph flow and pulmonary edema. The terrorist attack on the World Trade Center on September 11, 2001 left many people with impaired lung function. A study of firefighters and EMS workers enrolled in the FDNY WTC Medical Monitoring and Treatment Program, whose lung function was tested prior to 9/11, documented a steep decline in lung function in the first year after 9/11. A new study that includes a thousand additional workers shows that the declines have persisted over time. Prior to 9/11, 3% of firefighters had below-normal lung function, one year after 9/11 nearly 19% did, and six years later it stabilized at 13%. Ten to 14 days after acute exposure to some agents (e.g. ammonia, nitrogen oxides, sulfur dioxide, mercury), some patients develop bronchiolitis obliterans progressing to ARDS. Bronchiolitis obliterans with organized pneumonia can ensue when granulation tissue accumulates in the terminal airways and alveolar ducts during the body's reparative process. A minority of these patients develop late pulmonary fibrosis. Also at enhanced risk are persons with co-morbidities. Several studies report that both aged persons and smokers are especially vulnerable to the adverse effects of inhalation injury.

Sulfur mustard was used as a chemical weapon in World War I and more recently in the Iran–Iraq War. Sulfur mustard is a vesicant alkylating agent with strong cytotoxic, mutagenic, and carcinogenic properties. After exposure, victims show skin irritations and blisters. This agent also causes respiratory tract lesions, bone marrow depression, and eye damage, the epithelial tissues of these organs being predominately affected. Inhalation of high doses of this gas causes lesions in the larynx, trachea, and large bronchi with inflammatory reactions and necrosis. The alkylating agent affects more the upper parts of the respiratory tract, and only intensely exposed victims showed signs like bronchiolitis obliterans in the distal part. Secondary effects of sulfur mustard exposure lead to chronic lung diseases such as chronic bronchitis.

VALI is most common in patients receiving mechanical ventilation for acute lung injury or acute respiratory distress syndrome (ALI/ARDS).

Possible reasons for predisposition to VALI include:

- An injured lung may be at risk for further injury

- Cyclic atelectasis is particularly common in an injured lung

24 percent of all patients mechanically ventilated will develop VALI for reasons other than ALI or ARDS. The incidence is probably higher among patients who already have ALI/ARDS, but estimates vary widely. The variable estimates reflect the difficulty in distinguishing VALI from progressive ALI/ARDS.

There are many industrial inhalants that are known to cause various types of bronchiolitis, including bronchiolitis obliterans.

Industrial workers who have presented with bronchiolitis:

- nylon-flock workers

- workers who spray prints onto textiles with polyamide-amine dyes

- battery workers who are exposed to thionyl chloride fumes

- workers at plants that use or manufacture flavorings, e.g. diacetyl butter-like flavoring

Bronchiolitis obliterans has many possible causes, including collagen vascular disease, transplant rejection in organ transplant patients, viral infection (respiratory syncytial virus, adenovirus, HIV, cytomegalovirus), Stevens-Johnson syndrome, Pneumocystis pneumonia, drug reaction, aspiration and complications of prematurity (bronchopulmonary dysplasia), and exposure to toxic fumes, including diacetyl, sulfur dioxide, nitrogen dioxide, ammonia, chlorine, thionyl chloride, methyl isocyanate, hydrogen fluoride, hydrogen bromide, hydrogen chloride, hydrogen sulfide, phosgene, polyamide-amine dyes, mustard gas and ozone. It can also be present in patients with rheumatoid arthritis. Certain orally administrated emergency medications, such as activated charcoal, have been known to cause it when aspirated. The ingestion of large doses of papaverine in the vegetable Sauropus androgynus has caused it. Additionally, the disorder may be idiopathic (without known cause).

Carbon monoxide (CO) is presumed to be a complication in smoke inhalation. The initial approach to presumed CO poisoning involves administering supplemental oxygen at a fraction of inspired oxygen (FiO2) of 100 percent and then the use of hyperbaric oxygen (HBO) therapy is evaluated by physicians.

Fire breathing is typically performed with a high flash point fuel, such as lamp oil (liquid paraffin), while fire eating is performed with low flash point fuels, such as white gas or naphtha. Highly purified fuels are preferred by fire performers due to their minimized toxicity, but other, more dangerous fuels may sometimes be used, such as ethanol, isopropanol, kerosene, gasoline, or charcoal lighter fluid. All fuels run the risk of causing pneumonitis if inhaled, however longer chain oils are more persistent than smaller molecules. Alcohols and volatile naphthas are likely to be absorbed or expelled from the body by evaporation and respiration.

Tobacco smoke is a known carcinogen. Workers in the hospitality industry may be exposed to tobacco smoke in the workplace, especially in environments like casinos and bars/restaurants.

Polycyclic aromatic hydrocarbons (PAHs), fused-ring chemicals formed during the combustion of fossil fuels, are metabolized by the cytochrome P450 complex to highly reactive carbocations, which can mutate DNA and cause cancer. Workers may be exposed to PAHs while working in a foundry, in the roofing industry, or due to environmental tobacco smoke.

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.

Fire breather’s pneumonia is caused by the entrance of hydrocarbon fuels into the bronchial tree, usually due to accidental aspiration or inhalation during a fire performance show. Fire breathing, or fire blowing, is the act of creating a plume of fire by blowing a mouthful of fuel in a fine mist (atomization) over a source of ignition. Fire eating, or fire swallowing, is the act of putting a flaming object into the mouth and extinguishing it.

In both disciplines, the performer holds their breath until the air is clear of vapors, so as to not inhale the hazardous fumes. However, improper technique or an accident can lead to ingestion, inhalation, or aspiration of fine droplets or vapors. Fire breathing and fire eating are separate acts, but the terms are sometimes erroneously used interchangeably in the literature.

Fuel ingestion can also occur due to siphoning by mouth of fuel products.

Once inhaled, these fuels induce an inflammatory reaction in lung tissue. They are not metabolized by tissue enzymes, but undergo emulsification and become engulfed by macrophages which, with time, may disintegrate and release oily substances surrounded by fibrous tissue and giant cells.

The annual incidence of ARDS is 13–23 people per 100,000 in the general population. Its incidence in the mechanically ventilated population in intensive care units is much higher. According to Brun-Buisson "et al" (2004), there is a prevalence of acute lung injury (ALI) of 16.1% percent in ventilated patients admitted for more than 4 hours.

Worldwide, severe sepsis is the most common trigger causing ARDS. Other triggers include mechanical ventilation, sepsis, pneumonia, Gilchrist's disease, drowning, circulatory shock, aspiration, traumaespecially pulmonary contusionmajor surgery, massive blood transfusions, smoke inhalation, drug reaction or overdose, fat emboli and reperfusion pulmonary edema after lung transplantation or pulmonary embolectomy. Pneumonia and sepsis are the most common triggers, and pneumonia is present in up to 60% of patients and may be either causes or complications of ARDS. Alcohol excess appears to increase the risk of ARDS. Diabetes was originally thought to decrease the risk of ARDS, but this has shown to be due to an increase in the risk of pulmonary edema. Elevated abdominal pressure of any cause is also probably a risk factor for the development of ARDS, particularly during mechanical ventilation.

The death rate varies from 25–40% in centers using up-to-date ventilatory strategies and up to 58% in all centers.

Since ARDS is an extremely serious condition which requires invasive forms of therapy it is not without risk. Complications to be considered include the following:

- Pulmonary: barotrauma (volutrauma), pulmonary embolism (PE), pulmonary fibrosis, ventilator-associated pneumonia (VAP)

- Gastrointestinal: bleeding (ulcer), dysmotility, pneumoperitoneum, bacterial translocation

- Cardiac: abnormal heart rhythms, myocardial dysfunction

- Kidney: acute kidney failure, positive fluid balance

- Mechanical: vascular injury, pneumothorax (by placing pulmonary artery catheter), tracheal injury/stenosis (result of intubation and/or irritation by endotracheal tube

- Nutritional: malnutrition (catabolic state), electrolyte deficiency.

"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.

Pneumonia is a form of acute respiratory infection that affects the lung parenchyma and oxygenation. When a patient with pneumonia is an alcoholic, the mortality rate exceeds by 50% if they are placed into intensive care (ICU). According to Kershaw, C 2008 page 1, "[a]s of 2001, pneumonia was the sixth most common cause of death in the United States". Alcoholics are at an increased risk for infection with tissue-damaging gram-negative pathogens or for the spread of bacteria in the blood.

FLD affects approximately .5%-3% of farmers. In some regions of the world such as Asia, the infection rate is more around 6%.

General treatment principles are removal from exposure, protection of the airway (i.e., preemptive intubation), and treatment of hypoxemia. Concomitant airway injury with acute bronchospasm often warrants treatment with bronchodilators because of the airway obstruction.

A beneficial role for corticosteroids has not been established by controlled trials in humans. Despite the lack of controlled evidence of efficacy, anecdotal reports of benefits from systemic corticosteroid use continue to appear.

Prophylactic antibiotic drugs have not proved to be efficacious in toxic lung injury. Antibiotics should be reserved for those patients with clinical evidence of infection.

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

The mechanisms of alcoholic lung disease are:

- Metabolism of alcohol reduces glutathione anti-oxidant levels in the lungs.

- Oxidation damage to the cells impairs the ability of the lungs to remove fluid.

- Oxidative damage to cells reduces immune response.

- Oxidative damage to cells results in a reduced ability to recover from injury.

These chemical changes compound the negative mechanical and microbiological effects of alcoholism on the respiratory system. These include impaired gag reflex and cilia function and greater likelihood of colonies of pneumococcal bacteria in the upper respiratory system.

Although lung damage from concurrent smoking and drug use is often indistinguishable from alcoholic lung disease, there is support for considering alcoholic lung disease as an independent syndrome. Over the last decade, evidence from epistemological studies show that alcohol abuse alone can increase by as much as fourfold the risk for acute respiratory distress syndrome.

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.

The best way to prevent silicosis is to identify work-place activities that produce respirable crystalline silica dust and then to eliminate or control the dust ("primary prevention"). Water spray is often used where dust emanates. Dust can also be controlled through dry air filtering.

Following observations on industry workers in Lucknow (India), experiments on rats found that jaggery (a traditional sugar) had a preventive action against silicosis.

In 2013 pneumoconiosis 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.

The number of workers in the United States exposed to beryllium vary but has been estimated to be as high as 800,000 during the 1960s and 1970s. A more recent study estimated the number of exposed workers in the United States from in 1996 to be around 134,000.

The rate of workers becoming sensitized to beryllium varies based on genetics and exposure levels. In one study researchers found the prevalence of beryllium sensitization to range from 9 - 19% depending on the industry. Many workers who are found to be sensitive to beryllium also meet the diagnostic criteria for CBD. In one study of nuclear workers, among those who were sensitized to beryllium, 66% were found to have CBD as well. The rate of progression from beryllium sensitization to CBD has been estimated to be approximately 6-8% per year. Stopping exposure to beryllium in those sensitized has not been definitively shown to stop the progression to CBD.

The overall prevalence of CBD among workers exposed to beryllium has ranged from 1 – 5% depending on industry and time period of study.

The general population is unlikely to develop acute or chronic beryllium disease because ambient air levels of beryllium are normally very low (<0.03 ng/m). However, a study found 1% of people living within 3/4 of a mile of a beryllium plant in Lorain, Ohio, had berylliosis after exposure to concentrations estimated to be less than 1 milligram per cubic metre of air. In the United States the Beryllium Case Registry contained 900 records, early cases relating to extraction and fluorescent lamp manufacture, later ones coming from the aerospace, ceramics and metallurgical industries.

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.