The signs and symptoms of acute beryllium pneumonitis usually resolve over several weeks to months, but may be fatal in 10 percent of cases, and about 15–20% of cases may progress to CBD.

Acute beryllium poisoning approximately doubles the risk of getting lung cancer. The mechanism by which beryllium is carcinogenic is unclear, but may be due to ionic beryllium binding to nucleic acids; it is not mutagenic.

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”.

Acute beryllium poisoning is an occupational disease. Relevant occupations are those where beryllium is mined, processed or converted into metal alloys, or where machining of metals containing beryllium or recycling of scrap alloys occurs.

Beryllium is regarded extraordinarily hazardous to health upon enough amounts of dust, mists, or fumes consisting fragments little enough to inhale (typically 10µm or less). Metallographic preparation equipment and laboratory work surfaces must be damp wiped occasionally to inhibit buildup of particles. Cutting, grinding, and polishing procedures which manufacture dusts or fumes must be handled within sufficiently vented coverings supplied with particular filters.

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.

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.

Increased concentrations of urinary beta-2 microglobulin can be an early indicator of renal dysfunction in persons chronically exposed to low but excessive levels of environmental cadmium. The urinary beta-2 microglobulin test is an indirect method of measuring cadmium exposure. Under some circumstances, the Occupational Health and Safety Administration requires screening for renal damage in workers with long-term exposure to high levels of cadmium. Blood or urine cadmium concentrations provide a better index of excessive exposure in industrial situations or following acute poisoning, whereas organ tissue (lung, liver, kidney) cadmium concentrations may be useful in fatalities resulting from either acute or chronic poisoning. Cadmium concentrations in healthy persons without excessive cadmium exposure are generally less than 1 μg/L in either blood or urine. The ACGIH biological exposure indices for blood and urine cadmium levels are 5 μg/L and 5 μg/g creatinine, respectively, in random specimens. Persons who have sustained renal damage due to chronic cadmium exposure often have blood or urine cadmium levels in a range of 25-50 μg/L or 25-75 μg/g creatinine, respectively. These ranges are usually 1000-3000 μg/L and 100-400 μg/g, respectively, in survivors of acute poisoning and may be substantially higher in fatal cases.

Studies have shown that people who are atopic (sensitive), already suffer from allergies, asthma, or compromised immune systems and occupy damp or moldy buildings are at an increased risk of health problems such as inflammatory and toxic responses to mold spores, metabolites and other components. The most common health problem is an allergic reaction. Other problems are respiratory and/or immune system responses including respiratory symptoms, respiratory infections, exacerbation of asthma, and rarely hypersensitivity pneumonitis, allergic alveolitis, chronic rhinosinusitis and allergic fungal sinusitis. Severe reactions are rare but possible. A person's reaction to mold depends on their sensitivity and other health conditions, the amount of mold present, length of exposure and the type of mold or mold products.

Some molds also produce mycotoxins that can pose serious health risks to humans and animals. The term "toxic mold" refers to molds that produce mycotoxins, such as "Stachybotrys chartarum", not to all molds. Exposure to high levels of mycotoxins can lead to neurological problems and in some cases death. Prolonged exposure, e.g., daily workplace exposure, can be particularly harmful.

The five most common genera of indoor molds are "Cladosporium", "Penicillium", "Aspergillus", "Alternaria" and "Trichoderma".

Damp environments which allow mold to grow can also produce bacteria and help release volatile organic compounds.

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.

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

Cadmium is a naturally occurring toxic heavy metal with common exposure in industrial workplaces, plant soils, and from smoking. Due to its low permissible exposure to humans, overexposure may occur even in situations where trace quantities of cadmium are found. Cadmium is used extensively in electroplating, although the nature of the operation does not generally lead to overexposure. Cadmium is also found in some industrial paints and may represent a hazard when sprayed. Operations involving removal of cadmium paints by scraping or blasting may pose a significant hazard. Cadmium is also present in the manufacturing of some types of batteries. Exposures to cadmium are addressed in specific standards for the general industry, shipyard employment, construction industry, and the agricultural industry.

Metal fume fever is due to the inhalation of certain metals, either as fine dust or most commonly as fumes. Simple metal compounds such as oxides are equally capable of causing it. The effects of particularly toxic compounds, such as nickel carbonyl, are not considered merely metal fume fever.

Exposure usually arises through hot metalworking processes, such as smelting and casting of zinc alloys, welding of galvanized metals, brazing, or soldering. If the metal concerned is particularly high-risk, the residue from cold sanding processes may also cause fume fever, even if the dose is lower. It may also be caused by electroplated surfaces or metal-rich anti-corrosion paint, such as cadmium passivated steel or zinc chromate primer on aluminium aircraft parts. Exposure has also been reported in use of lead-free ammunition, by the harder steel core stripping excess metal from the jacket of the bullet and barrel of the rifle.

The most plausible metabolic source of the symptoms is a dose-dependent release of certain cytokines, an event which occurs by inhaling metal oxide fumes that injure the lung cells. This is not an allergic reaction, though allergic reactions to metal fumes can occur.

Prevention of metal fume fever in workers who are at risk (such as welders) involves avoidance of direct contact with potentially toxic fumes, improved engineering controls (exhaust ventilation systems), personal protective equipment (respirators), and education of workers regarding the features of the syndrome itself and proactive measures to prevent its development.

In some cases, the product's design may be changed so as to eliminate the use of risky metals. NiCd rechargeable batteries are being replaced by NiMH. These contain other toxic metals, such as chromium, vanadium and cerium. Cadmium is often replaced by other metals. Zinc or nickel plating can be used instead of cadmium plating, and brazing filler alloys now rarely contain cadmium.

Coal ash, also known as coal combustion residuals (CCRs), is the particulate residue that remains from burning coal. Depending on the chemical composition of the coal burned, this residue may contain toxic substances and pose a health risk to workers in coal-fired power plants.

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.

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.

In epidemiology, environmental diseases are diseases that can be directly attributed to environmental factors (as distinct from genetic factors or infection). Apart from the true monogenic genetic disorders, environmental diseases may determine the development of disease in those genetically predisposed to a particular condition. Stress, physical and mental abuse, diet, exposure to toxins, pathogens, radiation, and chemicals found in almost all personal care products and household cleaners are possible causes of a large segment of non-hereditary disease. If a disease process is concluded to be the result of a combination of genetic and "environmental factor" influences, its etiological origin can be referred to as having a multifactorial pattern.

There are many different types of environmental disease including:

- Lifestyle disease such as cardiovascular disease, diseases caused by substance abuse such as alcoholism, and smoking-related disease

- Disease caused by physical factors in the environment, such as skin cancer caused by excessive exposure to ultraviolet radiation in sunlight

- Disease caused by exposure to toxic or irritant chemicals in the environment such as toxic metals

==Environmental Diseases vs. Pollution-

Related Diseases==

Environmental diseases are a direct result from the environment. This includes diseases caused by substance abuse, exposure to toxic chemicals, and physical factors in the environment, like UV radiation from the sun, as well as genetic predisposition. Meanwhile, pollution-related diseases are attributed to exposure to toxins in the air, water, and soil. Therefore all pollution-related disease are environmental diseases, but not all environmental diseases are pollution-related diseases.

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.

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.

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.

Additionally, there are environmental diseases caused by the aromatic carbon compounds including : benzene, hexachlorocyclohexane, toluene diisocyanate, phenol, pentachlorophenol, quinone and hydroquinone.

Also included are the aromatic nitro-, amino-, and pyridilium-deratives: nitrobenzene, dinitrobenzene, trinitrotoluene, paramethylaminophenol sulfate (Metol), dinitro-ortho-cresol, aniline, trinitrophenylmethylnitramine (tetryl), hexanitrodiphenylamine (aurantia), phenylenediamines, and paraquat.

The aliphatic carbon compounds can also cause environmental disease. Included in these are methanol, nitroglycerine, nitrocellulose, dimethylnitrosamine, and the halogenated hydrocarbons: methyl chloride, methyl bromide, trichloroethylene, carbon tetrachloride, and the chlorinated naphthalenes. Also included are glycols: ethylene chlorhydrin and diethylene dioxide as well as carbon disulfide, acrylonitrile, acrylamide, and vinyl chloride.

It is difficult to differentiate the effects of low level metal poisoning from the environment with other kinds of environmental harms, including nonmetal pollution. Generally, increased exposure to heavy metals in the environment increases risk of developing cancer.

Without a diagnosis of metal toxicity and outside of evidence-based medicine, but perhaps because of worry about metal toxicity, some people seek chelation therapy to treat autism, cardiovascular disease, Alzheimer's disease, or any sort of neurodegeneration. Chelation therapy does not improve outcomes for those diseases.

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."

Nickel is classified by the IARC as a Group 1 carcinogen; nickel compound exposure is associated with nasal cancer as well as lung cancer. Workers may be exposed to nickel in machining/grinding industry, nickel extraction/production, welding, and electroplating.

Heavy metals "can bind to vital cellular components, such as structural proteins, enzymes, and nucleic acids, and interfere with their functioning". Symptoms and effects can vary according to the metal or metal compound, and the dose involved. Broadly, long-term exposure to toxic heavy metals can have carcinogenic, central and peripheral nervous system and circulatory effects. For humans, typical presentations associated with exposure to any of the "classical" toxic heavy metals, or chromium (another toxic heavy metal) or arsenic (a metalloid), are shown in the table.

Even though zinc is an essential requirement for a healthy body, excess zinc can be harmful, and cause zinc toxicity. Such toxicity levels have been seen to occur at ingestion of greater than 225 mg of Zinc. Excessive absorption of zinc can suppress copper and iron absorption. The free zinc ion in solution is highly toxic to bacteria, plants, invertebrates, and even vertebrate fish.