Most pesticide-related illnesses have signs and symptoms that are similar to common medical conditions, so a complete and detailed environmental and occupational history is essential for correctly diagnosing a pesticide poisoning. A few additional screening questions about the patient's work and home environment, in addition to a typical health questionnaire, can indicate whether there was a potential pesticide poisoning.

If one is regularly using carbamate and organophosphate pesticides, it is important to obtain a baseline cholinesterase test. Cholinesterase is an important enzyme of the nervous system, and these chemical groups kill pests and potentially injure or kill humans by inhibiting cholinesterase. If one has had a baseline test and later suspects a poisoning, one can identify the extent of the problem by comparison of the current cholinesterase level with the baseline level.

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.

Accidental poisonings can be avoided by proper labeling and storage of containers. When handling or applying pesticides, exposure can be significantly reduced by protecting certain parts of the body where the skin shows increased absorption, such as the scrotal region, underarms, face, scalp, and hands. Safety protocols to reduce exposure include the use of personal protective equipment, washing hands and exposed skin during as well as after work, changing clothes between work shifts, and having first aid trainings and protocols in place for workers.

Personal protective equipment for preventing pesticide exposure includes the use of a respirator, goggles, and protective clothing, which have all have been shown to reduce risk of developing pesticide-induced diseases when handling pesticides. A study found the risk of acute pesticide poisoning was reduced by 55% in farmers who adopted extra personal protective measures and were educated about both protective equiment and pesticide exposure risk. Exposure can be significantly reduced when handling or applying pesticides by protecting certain parts of the body where the skin shows increased absorption, such as the scrotal region, underarms, face, scalp, and hands. Using chemical-resistant gloves has been shown to reduce contamination by 33–86%.

A number of measurements exist to assess exposure and early biological effects for organophosphate poisoning. Measurements of OP metabolites in both the blood and urine can be used to determine if a person has been exposed to organophosphates. Specifically in the blood, metabolites of cholinesterases, such as butyrylcholinesterase (BuChE) activity in plasma, neuropathy target esterase (NTE) in lymphocytes, and of acetylcholinesterase (AChE) activity in red blood cells. Due to both AChE and BuChE being the main targets of organophosphates, their measurement is widely used as an indication of an exposure to an OP. The main restriction on this type of diagnosis is that depending on the OP the degree to which either AChE or BuChE are inhibited differs; therefore, measure of metabolites in blood and urine do not specify for a certain OP. However, for fast initial screening, determining AChE and BuChE activity in the blood are the most widely used procedures for confirming a diagnosis of OP poisoning. The most widely used portable testing device is the Test-mate ChE field test, which can be used to determine levels of Red Blood Cells (RBC), AChE and plasma (pseudo) cholinesterase (PChE) in the blood in about four minutes. This test has been shown to be just as effective as a regular laboratory test and because of this, the portable ChE field test is frequently used by people who work with pesticides on a daily basis.

Diagnosis is typically made based on a history of significant radiation exposure and suitable clinical findings. An absolute lymphocyte count can give a rough estimate of radiation exposure. Time from exposure to vomiting can also give estimates of exposure levels if they are less than 1000 rad.

Pesticides exposure cannot be studied in placebo controlled trials as this would be unethical. A definitive cause effect relationship therefore cannot be established. Consistent evidence can and has been gathered through other study designs. The precautionary principle is thus frequently used in environmental law such that absolute proof is not required before efforts to decrease exposure to potential toxins are enacted.

The American Medical Association recommend limiting exposure to pesticides. They came to this conclusion due to the fact that surveillance systems currently in place are inadequate to determine problems related to exposure. The utility of applicator certification and public notification programs are also of unknown value in their ability to prevent adverse outcomes.

Many studies have examined the effects of pesticide exposure on the risk of cancer. Associations have been found with: leukemia, lymphoma, brain, kidney, breast, prostate, pancreas, liver, lung, and skin cancers. This increased risk occurs with both residential and occupational exposures. Increased rates of cancer have been found among farm workers who apply these chemicals. A mother's occupational exposure to pesticides during pregnancy is associated with an increases in her child's risk of leukemia, Wilms' tumor, and brain cancer. Exposure to insecticides within the home and herbicides outside is associated with blood cancers in children.

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.

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.

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.

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.

Mercury thermometers and mercury light bulbs are not as common as they used to be, and the amount of mercury they contain is unlikely to be a health concern if handled carefully. However, broken items still require careful cleanup, as mercury can be hard to collect and it is easy to accidentally create a much larger exposure problem.

The longer that humans are subjected to radiation the larger the dose will be. The advice in the nuclear war manual entitled "Nuclear War Survival Skills" published by Cresson Kearny in the U.S. was that if one needed to leave the shelter then this should be done as rapidly as possible to minimize exposure.

In chapter 12, he states that ""[q]uickly putting or dumping wastes outside is not hazardous once fallout is no longer being deposited. For example, assume the shelter is in an area of heavy fallout and the dose rate outside is 400 roentgen (R) per hour, enough to give a potentially fatal dose in about an hour to a person exposed in the open. If a person needs to be exposed for only 10 seconds to dump a bucket, in this 1/360 of an hour he will receive a dose of only about 1 R. Under war conditions, an additional 1-R dose is of little concern."" In peacetime, radiation workers are taught to work as quickly as possible when performing a task which exposes them to radiation. For instance, the recovery of a lost radiography source should be done as quickly as possible.

Diagnosis of elemental or inorganic mercury poisoning involves determining the history of exposure, physical findings, and an elevated body burden of mercury. Although whole-blood mercury concentrations are typically less than 6 μg/L, diets rich in fish can result in blood mercury concentrations higher than 200 μg/L; it is not that useful to measure these levels for suspected cases of elemental or inorganic poisoning because of mercury's short half-life in the blood. If the exposure is chronic, urine levels can be obtained; 24-hour collections are more reliable than spot collections. It is difficult or impossible to interpret urine samples of patients undergoing chelation therapy, as the therapy itself increases mercury levels in the samples.

Diagnosis of organic mercury poisoning differs in that whole-blood or hair analysis is more reliable than urinary mercury levels.

Nickel allergy can be confirmed by a properly trained health care provider based on the medical history, physical exam and a painless specialized patch test— when necessary. A significant number of people may self-diagnose, and not contact medical professionals, which could result in massive underreporting of the problem by scientific researchers.

Confirming the diagnosis of Ni-ACD specifically involves inducing the skin to demonstrate a rash where the chemicals are applied (a delayed type hypersensitivity reaction), evidence that the patient is exposed to nickel, and establishing that the reaction and the exposure explain the current rash/symptoms under question. The patch test plays a significant role in diagnosing ACD.

The patch test evokes a delayed, Type IV hypersensitivity reaction, which is a cell-mediated, antibody independent, immune response. Patch testing is the "gold standard" diagnostic tool for Ni-ACD. In this sense, a positive patch test to nickel establishes that the subject has been previously exposed and is therefore sensitized to nickel. It does not necessarily indicate that the patch reaction is the cause of the current clinical disease. A negative test demonstrates that the patient is sub-threshold, either minimally or not sensitized. Cumulatively, clinical reasoning and a patch test help determine if nickel could be the cause of a current dermatitis reaction.

People may be exposed to toxic chemicals or similar dangerous substances from pharmaceutical products, consumer products, the environment, or in the home or at work. Many toxic tort cases arise either from the use of medications, or through exposure at work.

Organophosphate pesticides are one of the top causes of poisoning worldwide, with an annual incidence of poisonings among agricultural workers varying from 3-10% per country.

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.

There have also been many occupational toxic tort cases, because industrial and other workers are often chronically exposed to toxic chemicals - more so than consumers and residents. Thousands of toxic chemicals are used in industry and workers in these areas can experience a variety of toxic injuries. Unlike the general population, which is exposed to trace amounts of thousands of different chemicals in the environment, industrial workers may be regularly exposed to much higher levels of chemicals and therefore have a greater risk of developing disease from particular chemical exposures than the general population.

An occupational toxic injury case may result in a workers' compensation claim, which is made against the worker's employer. The same injury can potentially support a toxic tort case against "third parties", that is, people or entities other than the employer, such as manufacturers or distributors of chemicals, substancees or equipment that exposed the worker to the chemicals, or the people or entities in control of the premises where the worker was exposed to the toxic chemicals.

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.

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.

Nickel has wide utility of application in manufactured metals, because it is both strong and malleable, leading to ubiquitous presence and the potential for consumers to be in contact with it daily. However, for those that have the rash of allergic contact dermatitis (ACD) due to a nickel allergy, it can be a challenge to avoid. Foods, common kitchen utensils, cell phones, jewelry and many other items may contain nickel and be a source of irritation due to the allergic reaction caused by the absorption of free released nickel through direct and prolonged contact. The most appropriate measure for nickel allergic persons is to prevent contact with the allergen.

In 2011, researchers showed that applying a thin layer of glycerine emollient containing nanoparticles of either calcium carbonate or calcium phosphate on an isolated piece of pig skin (in vitro) and on the skin of mice (in vivo) prevents the penetration of nickel ions into the skin. The nanoparticles capture nickel ions by cation exchange, and remain on the surface of the skin, allowing them to be removed by simple washing with water. Approximately 11-fold fewer nanoparticles by mass are required to achieve the same efficacy as the chelating agent ethylenediamine tetraacetic acid. Using nanoparticles with diameters smaller than 500 nm in topical creams may be an effective way to limit the exposure to metal ions that can cause skin irritation'.

Pre-emptive avoidance strategies (PEAS) might ultimately lower the sensitization rates of children who would suffer from ACD In an expert review of clinical immunology from "Taylor & Francis Online", it is theorized that prevention of exposure to nickel early on could reduce the number of those that are sensitive to nickel by one-quarter to one-third. Identification of the many sources of nickel is vital to understanding the nickel sensitization story, food like chocolate and fish, zippers, buttons, cells phones and even orthodontic braces and eyeglass frames might contain nickel. Items that contain sentimental value (heirlooms, wedding rings) could be treated with an enamel or rhodium plating.

Sensitized individuals may check product labels or contact the manufacturer or retailer regarding possible nickel content. The Dermatitis Academy has created an educational website to provide more information about nickel, including information about prevention, exposure, sources, and general information about nickel allergy. These resources provide guidance in a prevention initiative for children worldwide.

Electromagnetic hypersensitivity is not an accepted diagnosis; medically there is no case definition or clinical practice guideline and there is no specific test to identify it, nor is there an agreed-upon definition with which to conduct clinical research.

Complaints of electromagnetic hypersensitivity may mask organic or psychiatric illness. Diagnosis of those underlying conditions involves investigating and identifying possible known medical causes of any symptoms observed. It may require both a thorough medical evaluation to identify and treat any specific conditions that may be responsible for the symptoms, and a psychological evaluation to identify alternative psychiatric/psychological conditions that may be responsible or contribute to the symptoms.

Symptoms may also be brought on by imagining that exposure is causing harm, an example of the nocebo effect. Studies have shown that reports of symptoms are more closely associated with belief that one is being exposed than with any actual exposure.

Chronic exposure to human nail dust is a serious occupational hazard that can be minimized by not producing such dust. Best practice is to avoid electrical debridement or burring of mycotic nails unless the treatment is necessary. When the procedure is necessary, it is possible to reduce exposure by using nail dust extractors, local exhaust, good housekeeping techniques, personal protective equipment such as gloves, glasses or goggles, face shields, and an appropriately fitted disposable respirators to protect against the hazards of nail dust and flying debris.

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).