There are relatively simple tests for radon gas. Radon test kits are commercially available. The short-term radon test kits used for screening purposes are inexpensive, in many cases free. Discounted test kits can be purchased online through The National Radon Program Services at Kansas State University or through state radon offices. Information about local radon zones and specific state contact information can be accessed through the EPA Map at https://www.epa.gov/radon/find-information-about-local-radon-zones-and-state-contact-information. The kit includes a collector that the user hangs in the lowest livable floor of the dwelling for 2 to 7 days. Charcoal canisters are another type of short-term radon test, and are designed to be used for 2 to 4 days. The user then sends the collector to a laboratory for analysis. Both devices are passive, meaning that they do not need power to function.

It should be noted that the accuracy of the residential radon test depends upon the lack of ventilation in the house when the sample is being obtained. Thus, the occupants will be instructed not to open windows, etc., for ventilation during the pendency of test, usually two days or more.

Long-term kits, taking collections for 3 months up to one year, are also available. An open-land test kit can test radon emissions from the land before construction begins. A Lucas cell is one type of long-term device. A Lucas cell is also an active device, or one that requires power to function. Active devices provide continuous monitoring, and some can report on the variation of radon and interference within the testing period. These tests usually require operation by trained testers and are often more expensive than passive testing. The National Radon Proficiency Program (NRPP) provides a list of radon measurement professionals.

Radon levels fluctuate naturally. An initial test might not be an accurate assessment of a home's average radon level. Transient weather can affect short term measurements. Therefore, a high result (over 4 pCi/L) justifies repeating the test before undertaking more expensive abatement projects. Measurements between 4 and 10 pCi/L warrant a long-term radon test. Measurements over 10 pCi/L warrant only another short-term test so that abatement measures are not unduly delayed. Purchasers of real estate are advised to delay or decline a purchase if the seller has not successfully abated radon to 4 pCi/L or less.

Since radon concentrations vary substantially from day to day, single grab-type measurements are generally not very useful, except as a means of identifying a potential problem area, and indicating a need for more sophisticated testing. The EPA recommends that an initial short-term test be performed in a closed building. An initial short-term test of 2 to 90 days allows residents to be informed quickly in case a home contains high levels of radon. Long-term tests provide a better estimate of the average annual radon level.

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.

Berylliosis 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 and recycling of scrap alloys occurs. It is associated with aerospace manufacturing, microwave semiconductor electronics, beryllium mining or manufacturing of fluorescent light bulbs (which once contained beryllium compounds in their internal phosphor coating). Beryllia was used in lamp manufacture because of ceramic's obvious virtues for insulation and heat resistance, and also because beryllia could be made transparent. Certain welding anodes along with other electrical contacts and even non-sparking tools are made of beryllium copper alloy and the subsequent machining of such materials would cause the disease as well.

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

Diagnosis is primarily anecdotal, that is, it depends upon a good occupational history. Diagnosis of metal fume fever can be easily missed because the complaints are non-specific, resemble a number of other common illnesses, and presentation occurs typically 2–4 hours after the exposure. When respiratory symptoms are prominent, metal fume fever may be confused with acute bronchitis or pneumonia. The diagnosis is based primarily upon a history of exposure to metal oxide fumes. Cain and Fletcher (2010) report a case of metal fume fever that was diagnosed only by taking a full occupational history and by close collaboration between primary and secondary health care personnel.

Physical symptoms vary among persons exposed, depending largely upon the stage in the course of the syndrome during which examination occurs. Patients may present with wheezing or crackles in the lungs. They typically have an increased white blood cell count, and urine, blood plasma and skin zinc levels may (unsurprisingly) be elevated. Chest X-ray abnormalities may also be present.

An interesting feature of metal fume fever involves rapid adaptation to the development of the syndrome following repeated metal oxide exposure. Workers with a history of recurrent metal fume fever often develop a tolerance to the fumes. This tolerance, however, is transient, and only persists through the work week. After a weekend hiatus, the tolerance has usually disappeared. This phenomenon of tolerance is what led to the name "Monday Fever".

In 2006, approximately 700 metal fume exposures were reported to the United States Poison control center. The American Welding Society estimated that 2500 employees in the steel industry develop metal fume fever in the US each year and that the majority of the cases are not reported.

When exposure to a carcinogenic substance is suspected, the cause/effect relationship on any given case can never be ascertained. Lung cancer occurs spontaneously, and there is no difference between a "natural" cancer and another one caused by radon (or smoking). Furthermore, it takes years for a cancer to develop, so that determining the past exposure of a case is usually very approximative. The health effect of radon can only be demonstrated through theory and statistical observation.

The study design for epidemiological methods may be of three kinds:

- The best proofs come from observations of cohorts (predetermined populations with known exposures and exhaustive follow-up), such as those on miners, or on Hiroshima and Nagasaki survivors. Such studies are efficient, but very costly when the population needs to be a large one. Such studies can only be used when the effect is strong enough, hence, for high exposures.

- Alternate proofs are case-control studies (the environment factors of a "case" population is individually determined, and compared to that of a "control″ population, to see what the difference might have been, and which factors may be significant), like the ones that have been used to demonstrate the link between lung cancer and smoking. Such studies can identify key factors when the signal/noise ratio is strong enough, but are very sensitive to selection bias, and prone to the existence of confounding factors.

- Lastly, ecological studies may be used (where the global environment variables and their global effect on two different populations are compared). Such studies are "cheap and dirty": they can be easily conducted on very large populations (the whole USA, in Dr Cohen's study), but are prone to the existence of confounding factors, and exposed to the ecological fallacy problem.

Furthermore, theory and observation must confirm each other for a relationship to be accepted as fully proven. Even when a statistical link between factor and effect appears significant, it must be backed by a theoretical explanation; and a theory is not accepted as factual unless confirmed by observations.

The current reference range for acceptable blood lead concentrations in healthy persons without excessive exposure to environmental sources of lead is less than 5 µg/dL for children. It was less than 25 µg/dL for adults. Previous to 2012 the value for children was 10 (µg/dl). The current biological exposure index (a level that should not be exceeded) for lead-exposed workers in the U.S. is 30 µg/dL in a random blood specimen.

In 2015, US HHS/CDC/NIOSH designated 5 µg/dL (five micrograms per deciliter) of whole blood, in a venous blood sample, as the reference blood lead level for adults. An elevated BLL is defined as a BLL ≥5 µg/dL. This case definition is used by the ABLES program, the Council of State and Territorial Epidemiologists (CSTE), and CDC’s National Notifiable Diseases Surveillance System (NNDSS). Previously (i.e. from 2009 until November 2015), the case definition for an elevated BLL was a BLL ≥10 µg/dL. The U.S. national BLL geometric mean among adults was 1.2 μg/dL in 2009–2010.

Blood lead concentrations in poisoning victims have ranged from 30->80 µg/dL in children exposed to lead paint in older houses, 77–104 µg/dL in persons working with pottery glazes, 90–137 µg/dL in individuals consuming contaminated herbal medicines, 109–139 µg/dL in indoor shooting range instructors and as high as 330 µg/dL in those drinking fruit juices from glazed earthenware containers.

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

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.

People are continually exposed to metals in the environment. Medical tests can detect metals often, but this is to be expected and alone is not evidence that a person is poisoned. Metal screening tests should not be used unless there is reason to believe that a person has had excessive exposure to metals. People should seek medical testing for poisoning only if they are concerned for a particular reason, and physicians should consider a patient's history and physical examination before conducting tests to detect metals.

A fiber cannot be identified or ruled out as asbestos, either using the naked eye or by simply looking at a fiber under a regular microscope. The most common methods of identifying asbestos fibers are by using polarized light microscopy (PLM) or transmission electron microscopy (TEM). PLM is less expensive, but TEM is more precise and can be used at lower concentrations of asbestos.

If asbestos abatement is performed, completion of the abatement is verified using visual confirmation and may also involve air sampling. Air samples are typically analyzed using phase contrast microscopy (PCM). PCM involves counting fibers on a filter using a microscope. Airborne occupational exposure limits for asbestos are based on using the PCM method.

The American Conference of Governmental Industrial Hygienists has a recommended Threshold Limit Value (TLV) for asbestos of 0.1 fibers/mL over an 8-hour shift. OSHA in the United States and occupational health and safety regulatory jurisdictions in Canada use 0.1 fibers/mL over an 8-hour shift as their exposure limits.

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.

There are three key elements to the diagnosis of silicosis. First, the patient history should reveal exposure to sufficient silica dust to cause this illness. Second, chest imaging (usually chest x-ray) that reveals findings consistent with silicosis. Third, there are no underlying illnesses that are more likely to be causing the abnormalities. Physical examination is usually unremarkable unless there is complicated disease. Also, the examination findings are not specific for silicosis. Pulmonary function testing may reveal airflow limitation, restrictive defects, reduced diffusion capacity, mixed defects, or may be normal (especially without complicated disease). Most cases of silicosis do not require tissue biopsy for diagnosis, but this may be necessary in some cases, primarily to exclude other conditions.

For uncomplicated silicosis, chest x-ray will confirm the presence of small ( 1 cm) occurs from coalescence of small opacities, particularly in the upper lung zones. With retraction of the lung tissue, there is compensatory emphysema. Enlargement of the hilum is common with chronic and accelerated silicosis. In about 5–10% of cases, the nodes will calcify circumferentially, producing so-called "eggshell" calcification. This finding is not pathognomonic (diagnostic) of silicosis. In some cases, the pulmonary nodules may also become calcified.

A computed tomography or CT scan can also provide a mode detailed analysis of the lungs, and can reveal cavitation due to concomitant mycobacterial infection.

Diagnosis includes determining the clinical signs and the medical history, with inquiry into possible routes of exposure. Clinical toxicologists, medical specialists in the area of poisoning, may be involved in diagnosis and treatment.

The main tool in diagnosing and assessing the severity of lead poisoning is laboratory analysis of the blood lead level (BLL).

Blood film examination may reveal basophilic stippling of red blood cells (dots in red blood cells visible through a microscope), as well as the changes normally associated with iron-deficiency anemia (microcytosis and hypochromasia). However, basophilic stippling is also seen in unrelated conditions, such as megaloblastic anemia caused by vitamin B12 (colbalamin) and folate deficiencies.

Exposure to lead also can be evaluated by measuring erythrocyte protoporphyrin (EP) in blood samples. EP is a part of red blood cells known to increase when the amount of lead in the blood is high, with a delay of a few weeks. Thus EP levels in conjunction with blood lead levels can suggest the time period of exposure; if blood lead levels are high but EP is still normal, this finding suggests exposure was recent. However, the EP level alone is not sensitive enough to identify elevated blood lead levels below about 35 μg/dL. Due to this higher threshold for detection and the fact that EP levels also increase in iron deficiency, use of this method for detecting lead exposure has decreased.

Blood lead levels are an indicator mainly of recent or current lead exposure, not of total body burden. Lead in bones can be measured noninvasively by X-ray fluorescence; this may be the best measure of cumulative exposure and total body burden. However this method is not widely available and is mainly used for research rather than routine diagnosis. Another radiographic sign of elevated lead levels is the presence of radiodense lines called lead lines at the metaphysis in the long bones of growing children, especially around the knees. These lead lines, caused by increased calcification due to disrupted metabolism in the growing bones, become wider as the duration of lead exposure increases. X-rays may also reveal lead-containing foreign materials such as paint chips in the gastrointestinal tract.

Fecal lead content that is measured over the course of a few days may also be an accurate way to estimate the overall amount of childhood lead intake. This form of measurement may serve as a useful way to see the extent of oral lead exposure from all the diet and environmental sources of lead.

Lead poisoning shares symptoms with other conditions and may be easily missed. Conditions that present similarly and must be ruled out in diagnosing lead poisoning include carpal tunnel syndrome, Guillain–Barré syndrome, renal colic, appendicitis, encephalitis in adults, and viral gastroenteritis in children. Other differential diagnoses in children include constipation, abdominal colic, iron deficiency, subdural hematoma, neoplasms of the central nervous system, emotional and behavior disorders, and intellectual disability.

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.

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.

Chelation therapy is a medical procedure that involves the administration of chelating agents to remove heavy metals from the body. Chelating agents are molecules that have multiple electron-donating groups, which can form stable coordination complexes with metal ions. Complexation prevents the metal ions from reacting with molecules in the body, and enable them to be dissolved in blood and eliminated in urine. It should only be used in people who have a diagnosis of metal intoxication. That diagnosis should be validated with tests done in appropriate biological samples.

Chelation therapy is administered under very careful medical supervision due to various inherent risks. When the therapy is administered properly, the chelation drugs have significant side effects. Chelation administered inappropriately can cause neurodevelopmental toxicity, increase risk of developing cancer, and cause death; chelation also removes essential metal elements and requires measures to prevent their loss.

Patient history should reveal exposure to cotton, flax, hemp, or jute dust. Diagnostic tests include a lung function test and a chest x ray or CT scan.

Measurable change in lung function before and after working shifts is key to diagnosis. Patients suffering from byssinosis show a significant drop in FEV1 over the course of work shift.

Chest radiographs show areas of opacity due to fibrosis of the pulmonary parenchyma.

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.

There are three basic criteria for the diagnosis of CWP:

1. Chest radiography consistent with CWP

2. An exposure history to coal dust (typically underground coal mining) of sufficient amount and latency

3. Exclusion of alternative diagnoses (mimics of CWP)

Symptoms and pulmonary function testing relate to the degree of respiratory impairment but are not part of the diagnostic criteria. As noted above, the chest X-ray appearance for CWP can be virtually indistinguishable from silicosis. Chest CT, particularly high-resolution scanning (HRCT), are more sensitive than plain X-ray for detecting the small round opacities.

Diagnosis of occupational asthma uses several techniques.

A non-specific bronchial hyperreactivity test can be used to help diagnose occupational asthma. It involves testing with methacholine, after which the forced expiratory volume in 1 second (FEV) of the patient is measured. This test is often used for measuring the intensity of a person's asthma and to confirm that the person needs to be treated for asthma.

Other non specific tests could require the patient to run for a few minutes at a continuous pace. In this case, the individual’s peak expiratory flow rate (PEFR) is measured, showing how fast a person can exhale. PEFR can also be measured at work to see if there is a difference from the PEFR in a controlled environment. Measuring PEFR at work is a highly reliable test for occupational asthma.

A skin prick test is usually performed on the inner forearm where a grid is marked and a drop of the allergens to be tested are placed on the arm in the grid. Once this has been done, the skin is pricked through the drop using a lancet. Reactions, if any, occur within 10 to 15 minutes and these results can then be analyzed.

Immunoglobulin E is an antibody found in human blood and is effective against toxins. Since it can also trigger allergic reactions to specific allergens like pollen, the IgE test is performed to evaluate whether the subject is allergic to these substances.

A spirometer is a device used to measure timed expired and inspired volumes, and can be used to help diagnose occupational asthma.

Specific inhalation challenges test for reactions to substances found in the workplace. One method is a whole body sealed chamber where the patient is exposed to articles that are present in their workplace. This method has the advantage of being able to assess, albeit highly subjectively, ocular and nasal symptoms as well as a reduction in FEV. Another test requires the patient to breathe aerosols of the suspected asthmagens through an oro-facial mask. These asthmagens are aerosolized using closed circuit chambers, and the quantities and concentrations administered are minute and extremely stable, to minimize the risk of exaggerated responses.

Prevention of occupational asthma can be accomplished through better education of workers, management, unions and medical professionals. This will enable them to identify the risk factors and put in place preventive measures, including respiratory protection and exposure limits.

In the United States, the only federal regulation regarding the disposal of coal ash is called “Disposal of Coal Combustion Residuals from Electric Utilities”, which was signed into law on December 19th, 2014. In addition, when coal ash is disposed into surface impoundments and landfills, coal ash is regulated as non-hazardous solid waste under the Resource Conservation and Recovery Act (RCRA). Thus, the requirements of the coal ash disposal law is regulated under subtitle D of the RCRA.

In order for this federal regulation to be effective, there are some major requirements that surface impoundments and landfill facilities must follow. This rule requires facilities to prevent and control coal ash dust from accumulating into the air. As a result, facilities must provide annual plans for coal ash dust control. Furthermore, there are location restrictions where new landfills and surface impoundments can be built. In addition, if regulations of coal ash dust control are not maintained, closure of the facility will occur under the federal law. The law also requires all coal ash waste facilities to create annual groundwater monitoring reports. Lastly, all coal ash waste surface impoundments and landfills must keep a written record of the federal regulations at the facility for five years. Ultimately, this recent federal regulation is trying to eliminate occupational health concerns and environmental health issues regarding coal ash toxicity.

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).