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.

Therapy is supportive and includes removal from further beryllium exposure. For very severe cases mechanical ventilation may be required.

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.

Treatment of mild metal fume fever consists of bedrest, keeping the patient well hydrated, and symptomatic therapy (e.g. aspirin for headaches) as indicated. In the case of non-allergic acute lung injury, standard or recommended approaches to treatment have not been defined.

The consumption of large quantities of cow's milk, either before or immediately after exposure is a traditional remedy. However, the United Kingdom Health and Safety Executive challenges this advice, warning, "Don’t believe the stories about drinking milk before welding. It does not prevent you getting metal fume fever."

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.

There is no cure for berylliosis; the goals of treatment are to reduce symptoms and slow the progression of disease.

Although the evidence that stopping exposure to beryllium decreases progression of the disease, it is still considered to be an accepted approach to treatment in any stage of disease.

People with early stages of disease, without lung function abnormalities or clinical symptoms, are periodically monitored with physical exams, pulmonary function testing and radiography.

Once clinical symptoms or significant abnormalities in pulmonary function testing appear, treatments include oxygen and oral corticosteroids and whatever supportive therapy is required.

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.

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.

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.

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.

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.

Coal ash is found in coal-fired power plants. Coal is burned in coal-fired plants to produce electricity. More specifically, the coal is pulverized and then burned to generate energy. The particles that remain after burning coal is called coal ash. The production of coal combustion produces many by-products of coal ash. Some of these by-products are boiler slag, flue gas desulfurization material, bottom ash, fly ash, scrubber residues, cenospheres and fluidized bed combustion ash. Depending on the coal that was burned, the chemical composition found in coal ash can vary. However, most coal ash will contain aluminum oxide (AlO), calcium oxide (CaO) and silicon dioxide (SiO). Regardless of the by-product produced, there are many toxic substances that are present in coal ash that can cause major health problems in humans. Some toxic constituents that are found in coal ash are arsenic, boron, cadmium, chromium, cobalt, copper, lead, mercury, molybdenum, selenium, thallium and uranium.

In the United States, approximately 44.6 percent of electricity is produced from over 450 coal-fired power plants. In 2012, approximately 110 million tons of coal ash was produced from the coal that was burned in the United States. However, more than half of the coal ash produced is dumped into surface impoundments (wet storage) or landfills (dry storage). Specifically, there are approximately 1,070 coal ash waste ponds and about 435 landfill sites located throughout the United States. The major problem of these disposal sites is the toxicity of coal ash escaping and causing harm to humans and the environment. When coal ash waste is not properly controlled, the toxic substances can affect drinking water, food and air.

A toxic heavy metal is any relatively dense metal or metalloid that is noted for its potential toxicity, especially in environmental contexts. The term has particular application to cadmium, mercury, lead and arsenic, all of which appear in the World Health Organisation's list of 10 chemicals of major public concern. Other examples include manganese, chromium, cobalt, nickel, copper, zinc, selenium, silver, antimony and thallium.

Heavy metals are found naturally in the earth. They become concentrated as a result of human caused activities and can enter plant, animal, and human tissues via inhalation, diet, and manual handling. Then, they can bind to and interfere with the functioning of vital cellular components. The toxic effects of arsenic, mercury, and lead were known to the ancients, but methodical studies of the toxicity of some heavy metals appear to date from only 1868. In humans, heavy metal poisoning is generally treated by the administration of chelating agents. Some elements otherwise regarded as toxic heavy metals are essential, in small quantities, for human health.

In humans, heavy metal poisoning is generally treated by the administration of chelating agents.

These are chemical compounds, such as (calcium disodium ethylenediaminetetraacetate) that convert heavy metals to chemically inert forms that can be excreted without further interaction with the body. Chelates are not without side effects and can also remove beneficial metals from the body. Vitamin and mineral supplements are sometimes co-administered for this reason.

Soils contaminated by heavy metals can be remediated by one or more of the following technologies: isolation; immobilization; toxicity reduction; physical separation; or extraction. "Isolation" involves the use of caps, membranes or below-ground barriers in an attempt to quarantine the contaminated soil. "Immobilization" aims to alter the properties of the soil so as to hinder the mobility of the heavy contaminants. "Toxicity reduction" attempts to oxidise or reduce the toxic heavy metal ions, via chemical or biological means into less toxic or mobile forms. "Physical separation" involves the removal of the contaminated soil and the separation of the metal contaminants by mechanical means. "Extraction" is an on or off-site process that uses chemicals, high-temperature volatization, or electrolysis to extract contaminants from soils. The process or processes used will vary according to contaminant and the characteristics of the site.

Radon has been produced commercially for use in radiation therapy, but for the most part has been replaced by radionuclides made in accelerators and nuclear reactors. Radon has been used in implantable seeds, made of gold or glass, primarily used to treat cancers.

The gold seeds were produced by filling a long tube with radon pumped from a radium source, the tube being then divided into short sections by crimping and cutting. The gold layer keeps the radon within, and filters out the alpha and beta radiations, while allowing the gamma rays to escape (which kill the diseased tissue). The activities might range from 0.05 to 5 millicuries per seed (2 to 200 MBq). The gamma rays are produced by radon and the first short-lived elements of its decay chain (Po, Pb, Bi, Po).

Radon and its first decay products being very short-lived, the seed is left in place. After 12 half-lives (43 days), radon radioactivity is at 1/2000 of its original level. At this stage, the predominant residual activity is due to the radon decay product Pb, whose half-life (22.3 year) is 2000 times that of radon (and whose activity is thus 1/2000 or radon's), and its descendants Bi and Po, totalizing 0.03% of the initial seed activity.

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.

Exposure to lead may also decrease lifespan and have health effects in the long term. Death rates from a variety of causes have been found to be higher in people with elevated blood lead levels; these include cancer, stroke, and heart disease, and general death rates from all causes. Lead is considered a possible human carcinogen based on evidence from animal studies. Evidence also suggests that age-related mental decline and psychiatric symptoms are correlated with lead exposure. Cumulative exposure over a prolonged period may have a more important effect on some aspects of health than recent exposure. Some health effects, such as high blood pressure, are only significant risks when lead exposure is prolonged (over about one year).

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.

Mold health issues are potentially harmful effects of molds.

Molds (US usage; British English "moulds") are ubiquitous in the biosphere, and mold spores are a common component of household and workplace dust. The United States Centers for Disease Control and Prevention reported in its June 2006 report, 'Mold Prevention Strategies and Possible Health Effects in the Aftermath of Hurricanes and Major Floods,' that "excessive exposure to mold-contaminated materials can cause adverse health effects in susceptible persons regardless of the type of mold or the extent of contamination." When mold spores are present in abnormally high quantities, they can present especially hazardous health risks to humans after prolonged exposure, including allergic reactions or poisoning by mycotoxins, or causing fungal infection (mycosis).

In the late 20th century and early 21st century, some "health mines" were established in Basin, Montana, which attracted people seeking relief from health problems such as arthritis through limited exposure to radioactive mine water and radon. The practice is controversial because of the "well-documented ill effects of high-dose radiation on the body." Radon has nevertheless been found to induce beneficial long-term effects.

Silicosis is a permanent disease with no cure. Treatment options currently available focus on alleviating the symptoms and preventing any further progress of the condition. These include:

- Stopping further exposure to airborne silica, silica dust and other lung irritants, including tobacco smoking.

- Cough suppressants.

- Antibiotics for bacterial lung infection.

- TB prophylaxis for those with positive tuberculin skin test or IGRA blood test.

- Prolonged anti-tuberculosis (multi-drug regimen) for those with active TB.

- Chest physiotherapy to help the bronchial drainage of mucus.

- Oxygen administration to treat hypoxemia, if present.

- Bronchodilators to facilitate breathing.

- Lung transplantation to replace the damaged lung tissue is the most effective treatment, but is associated with severe risks of its own.

- For acute silicosis, bronchoalveolar lavage may alleviate symptoms, but does not decrease overall mortality.

Experimental treatments include:

- Inhalation of powdered aluminium, d-penicillamine and polyvinyl pyridine-N-oxide.

- Corticosteroid therapy.

- Chinese Herbal Kombucha

- The herbal extract tetrandrine may slow progression of silicosis.

Humans are not alone in suffering from lead's effects; plants and animals are also affected by lead toxicity to varying degrees depending on species. Animals experience many of the same effects of lead exposure as humans do, such as abdominal pain, peripheral neuropathy, and behavioral changes such as increased aggression. Much of what is known about human lead toxicity and its effects is derived from animal studies. Animals are used to test the effects of treatments, such as chelating agents, and to provide information on the pathophysiology of lead, such as how it is absorbed and distributed in the body.

Farm animals such as cows and horses as well as pet animals are also susceptible to the effects of lead toxicity. Sources of lead exposure in pets can be the same as those that present health threats to humans sharing the environment, such as paint and blinds, and there is sometimes lead in toys made for pets. Lead poisoning in a pet dog may indicate that children in the same household are at increased risk for elevated lead levels.

Noxious gases can be categorized as : Simple asphyxiants, chemical asphyxiants, and irritant gases. The simple asphixiants are nitrogen, methane, and carbon dioxide.

The chemical asphyxiants are carbon monoxide, sulfuretted hydrogen and hydrogen cyanide.

The irritant gases are sulfur dioxide, ammonia, nitrogen dioxide, chlorine, phosgene, and fluorine and its compounds, which include luroine and hydrofluoric acid, fluorspar, fluorapatite, cryolite, and organic fluorine compounds.

Affected workers should be offered alternative employment. Continued exposure leads to development of persistent symptoms and progressive decline in FEV1.

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.