While radon presents the aforementioned risks in adults, exposure in children leads to a unique set of health hazards that are still being researched. The physical composition of children leads to faster rates of exposure through inhalation given that their respiratory rate is higher than that of adults, resulting in more gas exchange and more potential opportunities for radon to be inhaled. In addition to this potentially higher dose of radon inhalation, children have smaller lungs, which can become damaged much more quickly than adults’ lungs. For example, children who are exposed to radon and who live in a household where they are exposed to tobacco smoke have a 20 times greater risk of developing lung cancer.

The resulting health effects in children are similar to those of adults, predominantly including lung cancer and respiratory illnesses such as asthma, bronchitis, and pneumonia. While there have been numerous studies assessing the link between radon exposure and childhood leukemia, the results are largely varied. Many ecological studies show a positive association between radon exposure and childhood leukemia; however, most case control studies have produced a weak correlation. Genotoxicity has been noted in children exposed to high levels of radon, specifically a significant increase of frequency of aberrant cells was noted, as well as an “increase in the frequencies of single and double fragments, chromosome interchanges, [and] number of aberrations chromatid and chromosome type”.

UNSCEAR recommends a reference value of 9 nSv (Bq·h/m).

For example, a person living (7000 h/year) in a concentration of 40 Bq/m receives an effective dose of 1 mSv/year.

Studies of miners exposed to radon and its decay products provide a direct basis for assessing their lung cancer risk. The BEIR VI report, entitled "Health Effects of Exposure to Radon", reported an excess relative risk from exposure to radon that was equivalent to 1.8% per megabecquerel hours per cubic meter (MBq·h/m) (95% confidence interval: 0.3, 35) for miners with cumulative exposures below 30 MBq·h/m. Estimates of risk per unit exposure are 5.38×10 per WLM; 9.68×10/WLM for ever smokers; and 1.67×10 per WLM for never smokers.

According to the UNSCEAR modeling, based on these miner's studies, the excess relative risk from long-term residential exposure to radon at 100 Bq/m is considered to be about 0.16 (after correction for uncertainties in exposure assessment), with about a threefold factor of uncertainty higher or lower than that value.

In other words, the absence of ill effects (or even positive hormesis effects) at 100 Bq/m are compatible with the known data.

The ICPR 65 model follows the same approach, and estimates the relative lifelong risk probability of radon-induced cancer death to 1.23 × 10 per Bq/(m·year). This relative risk is a global indicator; the risk estimation is independent of sex, age, or smoking habit. Thus, if a smoker's chances of dying of lung cancer are 10 times that of a nonsmoker's, the relative risks for a given radon exposure will be the same according to that model, meaning that the absolute risk of a radon-generated cancer for a smoker is (implicitly) tenfold that of a nonsmoker.

The risk estimates correspond to a unit risk of approximately 3–6 × 10 per Bq/m, assuming a lifetime risk of lung cancer of 3%. This means that a person living in an average European dwelling with 50 Bq/m has a lifetime excess lung cancer risk of 1.5–3 × 10. Similarly, a person living in a dwelling with a high radon concentration of 1000 Bq/m has a lifetime excess lung cancer risk of 3–6%, implying a doubling of background lung cancer risk.

The BEIR VI model proposed by the National Academy of Sciences of the USA is more complex. It is a multiplicative model that estimates an excess risk per exposure unit. It takes into account age, elapsed time since exposure, and duration and length of exposure, and its parameters allow for taking smoking habits into account.

In the absence of other causes of death, the absolute risks of lung cancer by age 75 at usual radon concentrations of 0, 100, and 400 Bq/m would be about 0.4%, 0.5%, and 0.7%, respectively, for lifelong nonsmokers, and about 25 times greater (10%, 12%, and 16%) for cigarette smokers.

There is great uncertainty in applying risk estimates derived from studies in miners to the effects of residential radon, and direct estimates of the risks of residential radon are needed.

As with the miner data, the same confounding factor of other carcinogens such as dust applies. Radon concentration is high in poorly ventilated homes and buildings and such buildings tend to have poor air quality, larger concentrations of dust etc. BEIR VI did not consider that other carcinogens such as dust might be the cause of some or all of the lung cancers, thus omitting a possible spurious relationship.

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.

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.

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.

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.

Smoking is the cause of about 5 million deaths per year. This makes it the most common cause of preventable early death. One study found that male and female smokers lose on average of 13.2 and 14.5 years of life, respectively. Another found a loss of life of 6.8 years. Each cigarette that is smoked is estimated to shorten life by an average of 11 minutes. At least half of all lifelong smokers die earlier as a result of smoking. Smokers are three times as likely to die before the age of 60 or 70 as non-smokers.

In the United States, cigarette smoking and exposure to tobacco smoke accounts for roughly one in five, or at least 443,000 premature deaths annually. To put this into context, ABC's Peter Jennings famously reported that in the US alone, tobacco kills the equivalent of three jumbo jets full of people crashing every day, with no survivors. On a worldwide basis, this equates to a single jumbo jet every hour.

A 2015 study found that about 17% of mortality due to cigarette smoking in the United States is due to diseases other than those usually believed to be related.

A study of an outbreak of an (H1N1) influenza in an Israeli military unit of 336 healthy young men to determine the relation of cigarette smoking to the incidence of clinically apparent influenza, revealed that, of 168 smokers, 68.5 percent had influenza, as compared with 47.2 percent of nonsmokers. Influenza was also more severe in the smokers; 50.6 percent of the smokers lost work days or required bed rest, or both, as compared with 30.1 percent of the nonsmokers.

According to a study of 1,900 male cadets after the 1968 Hong Kong A2 influenza epidemic at a South Carolina military academy, compared with nonsmokers, heavy smokers (more than 20 cigarettes per day) had 21% more illnesses and 20% more bed rest, light smokers (less than 20 cigarettes per day) had 10% more illnesses and 7% more bed rest.

The effect of cigarette smoking upon epidemic influenza was studied prospectively among 1,811 male college students. Clinical influenza incidence among those who daily smoked 21 or more cigarettes was 21% higher than that of non-smokers. Influenza incidence among smokers of 1 to 20 cigarettes daily was intermediate between non-smokers and heavy cigarette smokers.

Surveillance of a 1979 influenza outbreak at a military base for women in Israel revealed that influenza symptoms developed in 60.0% of the current smokers vs. 41.6% of the nonsmokers.

Smoking seems to cause a higher relative influenza-risk in older populations than in younger populations. In a prospective study of community-dwelling people 60–90 years of age, during 1993, of unimmunized people 23% of smokers had clinical influenza as compared with 6% of non-smokers.

Smoking may substantially contribute to the growth of influenza epidemics affecting the entire population. However the proportion of influenza cases in the general non-smoking population attributable to smokers has not yet been calculated.

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

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 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).

Chlorine is a relatively common gas in industry with a variety of uses. It is used to disinfect water as well as being a part of the sanitation process for sewage and industrial waste. Chlorine is also used as a bleaching agent during the production of paper and cloth. Many household cleaning products, including bleach, contain chlorine. Given the volume and ease of chlorine for industrial and commercial use, exposure could occur from an accidental spill or a deliberate attack. The National Institute for Occupational Safety and Health recommends that a person wear splash proof goggles, a face shield and a respirator mask when working in the vicinity of chlorine gas. Because chlorine is a gas at room temperature, most exposure occurs via inhalation. Exposure may also occur through skin or eye contact or by ingesting chlorine-contaminated food or water. Chlorine is a strong oxidizing element causing the hydrogen to split from water in moist tissue, resulting in nascent oxygen and hydrogen chloride that cause corrosive tissue damage. Additionally oxidation of chlorine may form hypochlorous acid, which can penetrate cells and react with cytoplasmic proteins destroying cell structure. Chlorine’s odor provides early warning signs of exposure but causes olfactory fatigue or adaptations, reducing awareness of exposure at low concentrations. With increased exposure, symptoms may progress to labored respirations, severe coughing, chest tightness, wheezing, dyspnea, and broncospasm associated with a decrease in oxygen saturation level. . Severe exposure may result in changes in upper and lower airways resulting in an acute lung injury, which may not be present until several hours after exposure. A recent chlorine gas leak in Pune, India, landed 20 individuals in the hospital. Though that was an accidental exposure, chlorine gas has been used as a weapon of warfare since World War I, most recently in 2007 in Iraq.

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 primary risk factor for COPD globally is tobacco smoking. Of those who smoke, about 20% will get COPD, and of those who are lifelong smokers, about half will get COPD. In the United States and United Kingdom, of those with COPD, 80–95% are either current smokers or previously smoked. The likelihood of developing COPD increases with the total smoke exposure. Additionally, women are more susceptible to the harmful effects of smoke than men. In nonsmokers, secondhand smoke is the cause of about 20% of cases. Other types of smoke, such as, marijuana, cigar, and water-pipe smoke, also confer a risk. Water-pipe smoke appears to be as harmful as smoking cigarettes. Problems from marijuana smoke may only be with heavy use. Women who smoke during pregnancy may increase the risk of COPD in their child. For the same amount of cigarette smoking, women have a higher risk of COPD than men.

Intense and prolonged exposure to workplace dusts, chemicals, and fumes increases the risk of COPD in both smokers and nonsmokers. Workplace exposures are believed to be the cause in 10–20% of cases. In the United States, they are believed to be related to more than 30% of cases among those who have never smoked and probably represent a greater risk in countries without sufficient regulations.

A number of industries and sources have been implicated, including high levels of dust in coal mining, gold mining, and the cotton textile industry, occupations involving cadmium and isocyanates, and fumes from welding. Working in agriculture is also a risk. In some professions, the risks have been estimated as equivalent to that of one-half to two packs of cigarettes a day. Silica dust and fiberglass dust exposure can also lead to COPD, with the risk unrelated to that for silicosis. The negative effects of dust exposure and cigarette smoke exposure appear to be additive or possibly more than additive.

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.

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.

Typical levels of beryllium that industries may release into the air are of the order of , averaged over a 30-day period, or of workroom air for an 8-hour work shift. Compliance with the current U.S. Occupational Safety and Health Administration (OSHA) permissible exposure limit for beryllium of has been determined to be inadequate to protect workers from developing beryllium sensitization and CBD. The American Conference of Governmental Industrial Hygienists (ACGIH), which is an independent organization of experts in the field of occupational health, has proposed a threshold limit value (TLV) of in a 2006 Notice of Intended Change (NIC). This TLV is 40 times lower than the current OSHA permissible exposure limit, reflecting the ACGIH analysis of best available peer-reviewed research data concerning how little airborne beryllium is required to cause sensitization and CBD.

Because it can be difficult to control industrial exposures to beryllium, it is advisable to use any methods possible to reduce airborne and surface contamination by beryllium, to minimize the use of beryllium and beryllium-containing alloys whenever possible, and to educate people about the potential hazards if they are likely to encounter beryllium dust or fumes. It is important to damp wipe meallographic preparation equipment to prevent accumulation of dry particles. Sectioning, grinding, and polishing must be performed under sufficiently vented hoods equipped with special filters.

On 29 January 2009, the Los Alamos National Laboratory announced it was notifying nearly 2,000 current and former employees and visitors that they may have been exposed to beryllium in the lab and may be at risk of disease. Concern over possible exposure to the material was first raised in November 2008, when a box containing beryllium was received at the laboratory's short-term storage facility.

Acute bronchitis is one of the most common diseases. About 5% of adults are affected and about 6% of children have at least one episode a year. It occurs more often in the winter. More than 10 million people in the United States visit a doctor each year for this condition with about 70% receiving antibiotics which are mostly not needed. There are efforts to decrease the use of antibiotics in acute bronchitis.

Most cases of chronic bronchitis are caused by smoking cigarettes or other forms of tobacco. Additionally, chronic inhalation of air pollution or irritating fumes or dust from hazardous exposures in occupations such as coal mining, grain handling, textile manufacturing, livestock farming, and metal moulding may also be a risk factor for the development of chronic bronchitis. Protracted bacterial bronchitis is usually caused by "Streptococcus pneumoniae", "Non-typable Haemophilus influenzae", or "Moraxella catarrhalis".

There is no cure available for asbestosis. Oxygen therapy at home is often necessary to relieve the shortness of breath and correct underlying low blood oxygen levels. Supportive treatment of symptoms includes respiratory physiotherapy to remove secretions from the lungs by postural drainage, chest percussion, and vibration. Nebulized medications may be prescribed in order to loosen secretions or treat underlying chronic obstructive pulmonary disease. Immunization against pneumococcal pneumonia and annual influenza vaccination is administered due to increased sensitivity to the diseases. Those with asbestosis are at increased risk for certain cancers. If the person smokes, quitting the habit reduces further damage. Periodic pulmonary function tests, chest x-rays, and clinical evaluations, including cancer screening/evaluations, are given to detect additional hazards.

Modern jetliners have an environmental control system (ECS) that manages the flow of cabin air. Outside air enters the engines and is compressed in the forward section, prior to the combustion section, ensuring no combustion products can enter the cabin. A portion of that compressed bleed air is used to pressurize the cabin. The ECS then recirculates some of that cabin air through HEPA filters, while the rest is directed to outflow valves, ensuring there is a constant supply of fresh, clean air coming into the cabin pressurization system at all times.

It is possible for contaminants to enter the cabin through the air-supply system and through other means. Substances used in the maintenance and treatment of aircraft, including aviation engine oil, hydraulic fluid, cleaning compounds and de-icing fluids, can contaminate the ECS. Ground and flight crews, as well as passengers themselves can be sources of contaminants such as pesticides, bioeffluents, viruses, bacteria, allergens, and fungal spores.

Possible sources of poor-quality cabin air include exposures related to normal operations of the aircraft:

- Ozone (O)

- Carbon dioxide (passengers exhaling CO)

- Carbon monoxide (CO - Jet exhaust fumes, Ambient airport air)

- Temperature

- Relative humidity

- Off-gassing from interior material and cleaning agents

- Bioeffluents

- Personal-care products

- Allergens

- Infectious or inflammatory agents

- Cabin pressure/partial pressure of oxygen

- Alcohol

- Formaldehyde

- Deicing fluid

- Particulate matter (including dust which contains microbes)

- Dry ice used to keep food cold

- Toilet fluid, leaked or spilled

- Rain repellent fluid

- Pyrethroid pesticides

- Pre-existing illness—such as anemia, asthma, COPD, and coronary arterial disease—the stresses of flight could exacerbate symptoms.

- Nocebo effects can lead to serious health problems too.

Jet engines require synthetic oils for lubrication. These oils contain ingredients such as tricresyl phosphate (TCP or TOCP), an organophosphate, which can be toxic to humans in quantities much larger than are found in aviation engine oil.

Engine bearing seals are installed to ensure that critical engine bearings are continuously lubricated, and to prevent engine oil from leaking into the compressed air stream. If a bearing seal fails and begins to leak, depending on the location of the seal, some amount of engine oil may be released into the compressed air stream. Oil leaks may be detected by an odour akin to hot frying-pan fume, or, in more serious cases, by smoke in the cabin. This is known in the industry as a fume event.

Many environmental factors have been associated with asthma's development and exacerbation including allergens, air pollution, and other environmental chemicals. Smoking during pregnancy and after delivery is associated with a greater risk of asthma-like symptoms. Low air quality from factors such as traffic pollution or high ozone levels has been associated with both asthma development and increased asthma severity. Over half of cases in children in the United States occur in areas with air quality below EPA standards. Low air quality is more common in low-income and minority communities.

Exposure to indoor volatile organic compounds may be a trigger for asthma; formaldehyde exposure, for example, has a positive association. Also, phthalates in certain types of PVC are associated with asthma in children and adults. While exposure to pesticides is linked to the development of asthma it is unclear if this is a cause and effect relationship.

There is an association between acetaminophen (paracetamol) use and asthma. The majority of the evidence does not, however, support a causal role. A 2014 review found that the association disappeared when respiratory infections were taken into account. Use by a mother during pregnancy is also associated with an increased risk as is psychological stress during pregnancy.

Asthma is associated with exposure to indoor allergens. Common indoor allergens include dust mites, cockroaches, animal dander (fragments of fur or feathers), and mold. Efforts to decrease dust mites have been found to be ineffective on symptoms in sensitized subjects. Certain viral respiratory infections, such as respiratory syncytial virus and rhinovirus, may increase the risk of developing asthma when acquired as young children. Certain other infections, however, may decrease the risk.

A 2015 SBU-report including a systematic review of non-chemical riskfactors for occupation cardiovascular disease found an association between certain occupational risk factors and developing cardiovascular disease in those:

- With mentally stressfull work with a lack of control of their own working situation — with a effort-reward imbalance

- Who experience low social support at work; who experience injustice or experience insufficient opportunities for personal development; or those who experience job insecurity

- Those who work night schedules; or have long working weeks

- Those who are exposed to noise

Specifically the risk of stroke was also increased by:

- Exposure to ionizing radiation

Hypertension develops more often in those who experience job strain and who have shift-work. Differences between women and men in risk are small, however men risk suffering and dieing of heart attacks or stroke twice as often as women during working life.

When humans breathe in an asphyxiant gas, such as pure nitrogen, helium, neon, argon, sulfur hexafluoride, methane, or any other physiologically inert gas(es), they exhale carbon dioxide without re-supplying oxygen. Physiologically inert gases (those that have no toxic effect, but merely dilute oxygen) are generally free of odor and taste. As such, the human subject detects little abnormal sensation as the oxygen level falls. This leads to asphyxiation (death from lack of oxygen) without the painful and traumatic feeling of suffocation (the hypercapnic alarm response, which in humans arises mostly from carbon dioxide levels rising), or the side effects of poisoning. In scuba diving rebreather accidents, there is often little sensation but euphoria—however, a slow decrease in oxygen breathing gas content has effects which are quite variable. By contrast, suddenly breathing pure inert gas causes oxygen levels in the blood to fall precipitously, and may lead to unconsciousness in only a few breaths, with no symptoms at all.

Some animal species are better equipped than humans to detect hypoxia, and these species are more uncomfortable in low-oxygen environments that result from inert gas exposure.