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.

Strong evidence links pesticide exposure to birth defects, fetal death and altered fetal growth. Agent Orange, a 50:50 mixture of 2,4,5-T and 2,4-D, has been associated with bad health and genetic effects in Malaya and Vietnam. It was also found that offspring that were at some point exposed to pesticides had a low birth weight and had developmental defects.

Evidence links pesticide exposure to worsened neurological outcomes.

The United States Environmental Protection Agency finished a 10-year review of the organophosphate pesticides following the 1996 Food Quality Protection Act, but did little to account for developmental neurotoxic effects, drawing strong criticism from within the agency and from outside researchers. Comparable studies have not been done with newer pesticides that are replacing organophosphates.

Studies suggest that smoking decreases appetite, but did not conclude that overweight people should smoke or that their health would improve by smoking. This is also a cause of heart diseases. Smoking also decreases weight by overexpressing the gene AZGP1 which stimulates lipolysis.

Smoking causes about 10% of the global burden of fire deaths, and smokers are placed at an increased risk of injury-related deaths in general, partly due to also experiencing an increased risk of dying in a motor vehicle crash.

Smoking increases the risk of symptoms associated with Crohn's disease (a dose-dependent effect with use of greater than 15 cigarettes per day). There is some evidence for decreased rates of endometriosis in infertile smoking women, although other studies have found that smoking increases the risk in infertile women. There is little or no evidence of a protective effect in fertile women. Some preliminary data from 1996 suggested a reduced incidence of uterine fibroids, but overall the evidence is unconvincing.

Current research shows that tobacco smokers who are exposed to residential radon are twice as likely to develop lung cancer as non-smokers. As well, the risk of developing lung cancer from asbestos exposure is twice as likely for smokers than for non-smokers.

New research has found that women who smoke are at significantly increased risk of developing an abdominal aortic aneurysm, a condition in which a weak area of the abdominal aorta expands or bulges, and is the most common form of aortic aneurysm.

Smoking leads to an increased risk of bone fractures, especially hip fractures. It also leads to slower wound-healing after surgery, and an increased rate of postoperative healing complication.

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.

Smoking has a supra-additive effect in increasing the risk of lung cancer in those exposed to asbestos. Studies have shown an increased risk of lung cancer among smokers who are exposed to asbestos compared to nonsmokers.

Lead: The exposure of lead in coal ash can cause major damage to the nervous system. Lead exposure can lead to kidney disease, hearing impairment, high blood pressure, delays in development, swelling of the brain, hemoglobin damage, and male reproductive problems. Both low levels and high levels of lead exposure can cause harm to the human body.

Cadmium: When coal ash dust is inhaled, high levels of cadmium is absorbed into the body. More specifically, the lungs directly absorb cadmium into the bloodstream. When humans are exposed to cadmium over a long period of time, kidney disease and lung disease can occur. In addition, cadmium exposure can be associated with hypertension. Lastly, chronic exposure of cadmium can cause bone weakness which increases the risk of bone fractures and osteoporosis.

Chromium: The exposure of chromium (IV) in coal ash can cause lung cancer and asthma when inhaled. When coal ash waste pollutes drinking water, chromium (IV) can cause ulcers in the small intestine and stomach when ingested. Lastly, skin ulcers can also occur when the exposure chromium (IV) in coal ash comes in contact with the skin.

Arsenic: When high amounts of arsenic is inhaled or ingested through coal ash waste, diseases such as bladder cancer, skin cancer, kidney cancer and lung cancer can develop. Ultimately, exposure of arsenic over a long period of time can cause mortality. Furthermore, low levels of arsenic exposure can cause irregular heartbeats, nausea, diarrhea, vomiting, peripheral neuropathy and vision impairment.

Mercury: Chronic exposure of mercury from coal ash can cause harm to the nervous system. When mercury is inhaled or ingested various health effects can occur such as vision impairment, seizures, numbness, memory loss and sleeplessness.

Boron: When coal ash dust is inhaled, the exposure of boron can cause discomfort in the throat, nose and eye. Moreover, when coal ash waste is ingested, boron exposure can be associated with kidney, liver, brain, and intestine impairment.

Molybdenum: When molybdenum is inhaled from coal ash dust, discomfort of the nose, throat, skin and eye can occur. As a result, short-term molybdenum exposure can cause an increase of wheezing and coughing. Furthermore, chronic exposure of molybdenum can cause loss of appetite, tiredness, headaches and muscle soreness.

Thallium: The exposure of thallium in coal ash dust can cause peripheral neuropathy when inhaled. Furthermore, when coal ash is ingested, thallium exposure can cause diarrhea and vomiting. In addition, thallium exposure is also associated with heart, liver, lung and kidney complications.

Silica: When silica is inhaled from coal ash dust, fetal lung disease or silicosis can develop. Furthermore, chronic exposure of silica can cause lung cancer. In addition, exposure to silica over a period of time can cause loss of appetite, poor oxygen circulation, breathing complications and fever.

Exposure to asbestos in the form of fibers is always considered dangerous. Working with, or exposure to, material that is friable, or materials or works that could cause release of loose asbestos fibers, is considered high risk. However, in general, people who become ill from inhaling asbestos have been regularly exposed in a job where they worked directly with the material.

According to the National Cancer Institute, "A history of asbestos exposure at work is reported in about 70 percent to 80 percent of all cases. However, mesothelioma has been reported in some individuals without any known exposure to asbestos." A paper published in 1998, in the American Journal of Respiratory and Critical Care Medicine, concurs, and comments that asbestosis has been reported primarily in asbestos workers, and appears to require long-term exposure, high concentration for the development of the clinical disease. There is also a long latency period (the time taken between harmful contact and emergence of the actual resulting illness) of about 12 to 20 years, and potentially up to 40 years.

The most common diseases associated with chronic exposure to asbestos are asbestosis and mesothelioma.

According to OSHA, "there is no 'safe' level of asbestos exposure for any type of asbestos fiber. Asbestos exposures as short in duration as a few days have caused mesothelioma in humans. Every occupational exposure to asbestos can cause injury or disease; every occupational exposure to asbestos contributes to the risk of getting an asbestos related disease."

Infants may develop respiratory symptoms as a result of exposure to a specific type of fungal mold, called Penicillium. Signs that an infant may have mold-related respiratory problems include (but are not limited to) a persistent cough and/or wheeze. Increased exposure increases the probability of developing respiratory symptoms during their first year of life. Studies have shown that a correlation exists between the probability of developing asthma and increased exposure to "Penicillium". The levels are deemed ‘no mold’ to ‘low level’ , from ‘low’ to ‘intermediate’ , and from ‘intermediate’ to ‘high’.

Mold exposures have a variety of health effects depending on the person. Some people are more sensitive to mold than others. Exposure to mold can cause a number of health issues such as; throat irritation, nasal stuffiness, eye irritation, cough and wheezing, as well as skin irritation in some cases. Exposure to mold may also cause heightened sensitivity depending on the time and nature of exposure. People at higher risk for mold allergies are people with chronic lung illnesses, which will result in more severe reactions when exposed to mold.

There has been sufficient evidence that damp indoor environments are correlated with upper respiratory tract symptoms such as coughing, and wheezing in people with asthma.

Symptoms of mold exposure can include:

- Nasal and sinus congestion, runny nose

- Respiratory problems, such as wheezing and difficulty breathing, chest tightness

- Cough

- Throat irritation

- Sneezing / Sneezing fits

Coal ash contains many toxic substances that can negatively impact the human body. Employees working in coal-fired power plants or near coal ash waste sites are at major risk of inhaling coal ash dust. Coal ash dust is generally known as particulate matter (particle pollution) and the dust particles can harm the lungs when inhaled. Workers increase their risk of harmful side effects when they inhale the smallest coal ash dust particles. The smaller the coal ash dust particle, the deeper the particle will be inhaled into the lungs. As a result, the toxic particles can inflame the lungs causing severe damage to the body. Furthermore, coal ash dust can enter the body through the nose causing damage to the brain directly. However, regardless of particle entry, the toxicity from coal ash can cause harm to major body parts such as the brain, lungs, heart, liver, kidneys, stomach and intestines. Thus, individuals working near coal ash surface impoundments or landfills are at increased risk for many serious health problems.

OP pesticide exposure occurs through inhalation, ingestion and dermal contact. Because OP pesticides disintegrate quickly in air and light, they have been considered relatively safe to consumers. However, OP residues linger on fruits and vegetables. Certain OP pesticides have been banned for use on some crops, for example methyl parathion is banned from use on some crops while permitted on others.

The Environmental Working Group has developed lists for concerned consumers, identifying crops with the highest pesticide residue quantities and the lowest. The "Dirty Dozen" crops are updated yearly and in 2012 included apples, celery, sweet bell peppers, peaches, strawberries, imported nectarines, grapes, spinach, lettuce, cucumbers, domestic blueberries and potatoes. Forty-five fruits and vegetables are listed by the Environmental Working Group as being regularly found with pesticide residue associated with OPs.

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.

The International Agency for Research on Cancer (IARC), found that organophosphates may possibly increased cancer risk. Tetrachlorvinphos and parathion were classified as "possibly carcinogenic", malathion, and diazinon.

Some research has suggested that high levels of fluoride exposure may adversely affect neurodevelopment in children, but the evidence is of insufficient quality to allow any firm conclusions to be drawn.

Co-carcinogens can be a lifestyle like cigarette-smoking, alcohol-drinking or even areca nut tobacco-chewing, which is an Asian tradition, because those activities promote the cytopathic effect (CPE). Also, some virus are co-carcinogens like Herpesviruses, Epstein–Barr virus (EBV) and human herpesvirus 4 (HHV-4) Epstein–Barr virus destroy immune system for human body and then increase the risk of cancer such as Hodgkin’s lymphoma and human immunodeficiency virus because they cause a long term-chronic inflammation for lymphocytes and epithelial cells. Moreover, Over intake beta carotene for a long period of time increased the risk of lung cancer, prostate cancer and many other kind of malignant tumor for cigarette smoker and worker having high contact with asbestos. Generally, co-carcinogen can be irregular eating habits and disease virus and co-carcinogen not only help cancer cell make malignant tumor but also increase the risk of cardiovascular disease and mortality rate.

Excess fluoride consumption has been studied as a factor in the following:

Experiments for human toxicology require a long term following and a large amount of investment in order to classify a chemical as co-carcinogens, carcinogens or anti-carcinogenic. In recent years, people substitutes health supplement for healthy meal. Some myths even state beta carotene as elixir in developing country(The Third World).

With rising health consciousness, people rely on food supplements like vitamins A, B, C, D, E etc. these vitamins act as anti-oxidants chemical in the human body. Antioxidants is a good chemical in the appropriate consumption but a large overdose can cause cellular oxidation and cause cytopathic. Also, the industries can not strictly control the concentration and dose for supplement that extracted from natural food resources. A long-term consumption of those supplement can cause physical burden and also a significant hard work for organ to metabolize. Many health organization and government have published a maximum daily consumption for supplement called Tolerable Upper Intake Levels (UL), for example World Health Organization suggest the Tolerable Upper Intake Levels of Vitamin C is 2000 mg/d for adult men from age 31 to 50. Tolerable Upper Intake Levels is different for different gender and age. These suggested intake level can be followed in order to maintain the public health and safety.

Both animal and human experiment research shows that supplement cannot be the substitution to replace the daily food diet. Having a diverse diet and healthy habits is the better way to stay healthy instead of taking a lots of supplement that might be a co-carcinogen.

Since lead has been used widely for centuries, the effects of exposure are worldwide. Environmental lead is ubiquitous, and everyone has some measurable blood lead level. Atmospheric lead pollution increased dramatically beginning in the 1950s as a result of the widespread use of leaded gasoline. Lead is one of the largest environmental medicine problems in terms of numbers of people exposed and the public health toll it takes. Lead exposure accounts for about 0.2% of all deaths and 0.6% of disability adjusted life years globally.

Although regulation reducing lead in products has greatly reduced exposure in the developed world since the 1970s, lead is still allowed in products in many developing countries. In all countries that have banned leaded gasoline, average blood lead levels have fallen sharply. However, some developing countries still allow leaded gasoline, which is the primary source of lead exposure in most developing countries. Beyond exposure from gasoline, the frequent use of pesticides in developing countries adds a risk of lead exposure and subsequent poisoning. Poor children in developing countries are at especially high risk for lead poisoning. Of North American children, 7% have blood lead levels above 10 μg/dL, whereas among Central and South American children, the percentage is 33 to 34%. About one fifth of the world's disease burden from lead poisoning occurs in the Western Pacific, and another fifth is in Southeast Asia.

In developed countries, people with low levels of education living in poorer areas are most at risk for elevated lead. In the US, the groups most at risk for lead exposure are the impoverished, city-dwellers, and immigrants. African-American children and those living in old housing have also been found to be at elevated risk for high blood lead levels in the US. Low-income people often live in old housing with lead paint, which may begin to peel, exposing residents to high levels of lead-containing dust.

Risk factors for elevated lead exposure include alcohol consumption and smoking (possibly because of contamination of tobacco leaves with lead-containing pesticides). Adults with certain risk factors might be more susceptible to toxicity; these include calcium and iron deficiencies, old age, disease of organs targeted by lead (e.g. the brain, the kidneys), and possibly genetic susceptibility.

Differences in vulnerability to lead-induced neurological damage between males and females have also been found, but some studies have found males to be at greater risk, while others have found females to be.

In adults, blood lead levels steadily increase with increasing age. In adults of all ages, men have higher blood lead levels than women do. Children are more sensitive to elevated blood lead levels than adults are. Children may also have a higher intake of lead than adults; they breathe faster and may be more likely to have contact with and ingest soil. Children of ages one to three tend to have the highest blood lead levels, possibly because at that age they begin to walk and explore their environment, and they use their mouths in their exploration. Blood levels usually peak at about 18–24 months old. In many countries including the US, household paint and dust are the major route of exposure in children.

Outcome is related to the extent and duration of lead exposure. Effects of lead on the physiology of the kidneys and blood are generally reversible; its effects on the central nervous system are not. While peripheral effects in adults often go away when lead exposure ceases, evidence suggests that most of lead's effects on a child's central nervous system are irreversible. Children with lead poisoning may thus have adverse health, cognitive, and behavioral effects that follow them into adulthood.

Occupational exposure to chemicals, dusts, radiation, and certain industrial processes have been tied to occupational cancer. Exposure to cancer-causing chemicals, also called Carcinogens, may cause mutations that allow cells to grow out of control, causing cancer. Carcinogens in the workplace may include chemicals like anilines, chromates, dinitrotoluenes, arsenic and inorganic arsenic compounds, beryllium and beryllium compounds, cadmium compounds, and nickel compounds. Dusts that can cause cancer leather or wood dusts, asbestos, crystalline forms of silica, coal tar pitch volatiles, coke oven emissions, diesel exhaust and environmental tobacco smoke. sunlight; radon gas; and industrial, medical, or other exposure to ionizing radiation can all cause cancer in the workplace. Industrial processes associated with cancer include aluminum production; iron and steel founding; and underground mining with exposure to uranium or radon.

Other factors that play a role in cancer include:

- Personal characteristics such as age, sex, and race

- Family history of cancer

- Diet and personal habits such as cigarette smoking and alcohol consumption

- The presence of certain medical conditions or past medical treatments, including chemotherapy, radiation treatment, or some immune-system suppressing drugs.

- Exposure to cancer-causing agents in the environment (for example, sunlight, radon gas, air pollution, and infectious agents)

Aerotoxic syndrome is a phrase coined by Chris Winder and Jean-Christophe Balouet in 2000, to describe their claims of short- and long-term ill-health effects caused by breathing airliner cabin air which was alleged to have been contaminated to toxic levels (exceeding known, parts per million, safe levels) with atomized engine oils or other chemicals. Repeated investigations of such claims have failed to document cabin air has ever contained contaminants which exceeded known safe levels. An assessment by the UK's House of Lords Science and Technology Committee found that claims of health effects were unsubstantiated.

An update in 2008 found no significant new evidence. this syndrome is not recognized in medicine.

An estimated 48,000 cancers are diagnosed yearly in the US that come from occupational causes; this represents approximately 4-10% of total cancer in the United States. It is estimated that 19% of cancers globally are attributed to environmental exposures (including work-related exposures).

Sick building syndrome can also occur due to factors of the home. Laminated flooring can cause more exposure to chemicals and more resulting SBS symptoms compared to stone, tile, and cement flooring. Recent redecorating and new furnishings within the last year were also found to be associated with increased symptoms, along with dampness and related factors, having pets, and the presence of cockroaches. The presence of mosquitoes was also a factor related to more symptoms, though it is unclear whether it was due to the presence of mosquitoes or the use of repellents.