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.

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.

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.

Old methods of detection involve colorimetric assays such as the Prussian Blue test, the pyridine-barbiturate assay and the taurine fluorescence-HPLC but like all colorimetric assays these can be prone to false positives. Lipid peroxidation, an artifact of heart attack produces dialdehydes that cross-react with the pyridine-barbiturate assay. Meanwhile, the taurine-fluorescence-HPLC assay used for cyanide detection is identical to the assay used to detect glutathione in spinal fluid. Recently, cyanide and thiocyanate assays have been run with mass spectrometry (LC/MS/MS), which are considered specific tests. Since cyanide has such a short half-life, the main metabolite, thiocyanate is typically measured to determine exposure.

Decontamination of people exposed to hydrogen cyanide gas only requires removal of the outer clothing and the washing of their hair. Those exposed to liquids or powders generally require full decontamination.

Arsenic may be measured in blood or urine to monitor excessive environmental or occupational exposure, confirm a diagnosis of poisoning in hospitalized victims or to assist in the forensic investigation in a case of fatal over dosage. Some analytical techniques are capable of distinguishing organic from inorganic forms of the element. Organic arsenic compounds tend to be eliminated in the urine in unchanged form, while inorganic forms are largely converted to organic arsenic compounds in the body prior to urinary excretion. The current biological exposure index for U.S. workers of 35 µg/L total urinary arsenic may easily be exceeded by a healthy person eating a seafood meal.

Tests are available to diagnose poisoning by measuring arsenic in blood, urine, hair, and fingernails. The urine test is the most reliable test for arsenic exposure within the last few days. Urine testing needs to be done within 24–48 hours for an accurate analysis of an acute exposure. Tests on hair and fingernails can measure exposure to high levels of arsenic over the past 6–12 months. These tests can determine if one has been exposed to above-average levels of arsenic. They cannot predict, however, whether the arsenic levels in the body will affect health. Chronic arsenic exposure can remain in the body systems for a longer period of time than a shorter term or more isolated exposure and can be detected in a longer time frame after the introduction of the arsenic, important in trying to determine the source of the exposure.

Hair is a potential bioindicator for arsenic exposure due to its ability to store trace elements from blood. Incorporated elements maintain their position during growth of hair. Thus for a temporal estimation of exposure, an assay of hair composition needs to be carried out with a single hair which is not possible with older techniques requiring homogenization and dissolution of several strands of hair. This type of biomonitoring has been achieved with newer microanalytical techniques like Synchrotron radiation based X ray fluorescence (SXRF) spectroscopy and Microparticle induced X ray emission (PIXE).The highly focused and intense beams study small spots on biological samples allowing analysis to micro level along with the chemical speciation. In a study, this method has been used to follow arsenic level before, during and after treatment with Arsenious oxide in patients with Acute Promyelocytic Leukemia.

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.

Dimercaprol and dimercaptosuccinic acid are chelating agents that sequester the arsenic away from blood proteins and are used in treating acute arsenic poisoning. The most important side effect is hypertension. Dimercaprol is considerably more toxic than succimer.

DMSA monoesters, e.g. MiADMSA, are promising antidotes for arsenic poisoning. Calcium sodium edetate is also used.

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.

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.

Tin has no known natural biological role in living organisms. It is not easily absorbed by animals and humans. The low toxicity is relevant to the widespread use of tin in dinnerware and canned food. Nausea, vomiting and diarrhea have been reported after ingesting canned food containing 200 mg/kg of tin. This observation led, for example, the Food Standards Agency in the UK to propose upper limits of 200 mg/kg. A study showed that 99.5% of the controlled food cans contain tin in an amount below that level. However un-lacquered tin cans with food of a low pH for example fruits and pickled vegetables can contain elevated concentrations of tin.

The toxic effects of tin compounds is based on the interference with the iron and copper metabolism. For example, it affects heme and cytochrome P450, and decreases their effectiveness.

Organotin compounds can be very toxic. "Tri-"n"-alkyltins" are phytotoxic and, depending on the organic groups, can be powerful bactericides and fungicides. Other triorganotins are used as miticides and acaricides.

Tributyltin (TBT) was extensively used in marine antifouling paints, until discontinued for leisure craft due to concerns over longer term marine toxicity in high traffic areas such as marinas with large numbers of static boats.

Poisoning is a condition or a process in which an organism becomes chemically harmed (poisoned) by a toxic substance or venom of an animal.

Acute poisoning is exposure to a poison on one occasion or during a short period of time. Symptoms develop in close relation to the degree of exposure. Absorption of a poison is necessary for systemic poisoning (that is, in the blood throughout the body). In contrast, substances that destroy tissue but do not absorb, such as lye, are classified as corrosives rather than poisons. Furthermore, many common household medications are not labeled with skull and crossbones, although they can cause severe illness or even death. In the medical sense, toxicity and poisoning can be caused by less dangerous substances than those legally classified as a poison. Toxicology is the study and practice of the symptoms, mechanisms, diagnosis, and treatment of poisoning.

Chronic poisoning is long-term repeated or continuous exposure to a poison where symptoms do not occur immediately or after each exposure. The patient gradually becomes ill, or becomes ill after a long latent period. Chronic poisoning most commonly occurs following exposure to poisons that bioaccumulate, or are biomagnified, such as mercury, gadolinium, and lead.

Contact or absorption of poisons can cause rapid death or impairment. Agents that act on the nervous system can paralyze in seconds or less, and include both biologically derived neurotoxins and so-called nerve gases, which may be synthesized for warfare or industry.

Inhaled or ingested cyanide, used as a method of execution in gas chambers, almost instantly starves the body of energy by inhibiting the enzymes in mitochondria that make ATP. Intravenous injection of an unnaturally high concentration of potassium chloride, such as in the execution of prisoners in parts of the United States, quickly stops the heart by eliminating the cell potential necessary for muscle contraction.

Most biocides, including pesticides, are created to act as poisons to target organisms, although acute or less observable chronic poisoning can also occur in non-target organisms (secondary poisoning), including the humans who apply the biocides and other beneficial organisms. For example, the herbicide 2,4-D imitates the action of a plant hormone, which makes its lethal toxicity specific to plants. Indeed, 2,4-D is not a poison, but classified as "harmful" (EU).

Many substances regarded as poisons are toxic only indirectly, by toxication. An example is "wood alcohol" or methanol, which is not poisonous itself, but is chemically converted to toxic formaldehyde and formic acid in the liver. Many drug molecules are made toxic in the liver, and the genetic variability of certain liver enzymes makes the toxicity of many compounds differ between individuals.

Exposure to radioactive substances can produce radiation poisoning, an unrelated phenomenon.

The following guideline values (ppm values rounded) and periods of time-weighted average exposures have been determined in such a way that the carboxyhaemoglobin (COHb) level of 2.5% is not exceeded, even when a normal subject engages in light or moderate exercise:

- 100 mg/m3 (87 ppm) for 15 min

- 60 mg/m3 (52 ppm) for 30 min

- 30 mg/m3 (26 ppm) for 1 h

- 10 mg/m3 (9 ppm) for 8 h

For indoor air quality 7 mg/m3 (6 ppm) for 24 h (so as not to exceed 2% COHb for chronic exposure)

In Belgium, the Conseil Supérieur de la Santé gives a scientific advisory report on public health policy, the Superior Health Council of Belgium provides an overview of products that are authorized in Belgium for consumer use and that contain caustic substances, as well as of the risks linked to exposure to these products. This report aims at suggesting protection measures for the consumers, and formulates recommendations that apply to the different stages of the chain, which begins with the formulation of the product, followed by its regulation / marketing / application and post-application and ends with its monitoring.

Nitric acid test and paper chromatography test are used in the detection of argemone oil.Paper chromatography test is the most sensitive test.

Tin poisoning refers to the toxic effects of tin and its compounds. Cases of poisoning from tin metal, its oxides, and its salts are "almost unknown"; on the other hand certain organotin compounds are almost as toxic as cyanide.

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.

The NFPA standard is not necessarily enforced by law. As of April 2006, the U.S. state of Massachusetts requires detectors to be present in all residences with potential CO sources, regardless of building age and whether they are owner-occupied or rented. This is enforced by municipal inspectors, and was inspired by the death of 7-year-old Nicole Garofalo in 2005 due to snow blocking a home heating vent. Other jurisdictions may have no requirement or only mandate detectors for new construction or at time of sale.

Despite similar deaths in vehicles with clogged exhaust pipes (for example in the Northeastern United States blizzard of 1978 and February 2013 nor'easter) and the commercial availability of the equipment, there is no legal requirement for automotive CO detectors.

Some medications that can be used for erethism are Traid and Ritalin. Methylphenidate (Ritalin) is a stimulant drug approved for therapy of attention-deficit hyperactivity disorder, postural orthostatic tachycardia syndrome and narcolepsy. It may also be prescribed for off-label use in treatment-resistant cases of lethargy, depression (mood), or neural insult.

One treatment of mercury poisoning was to admit fresh air to the patient by having him go outside daily as much as possible. Stimulants such as ammonia have also been documented to help restore pulse to a normal rhythm. For a more comprehensive reading of treatment, see Mercury poisoning, 'Treatment' section.

Erethism or erethism mercurialis is a neurological disorder which affects the whole central nervous system, as well as a symptom complex derived from mercury poisoning. This is also sometimes known as the mad hatter disease. Historically, this was common among old England felt-hatmakers who used mercury to stabilize the wool in a process called felting, where hair was cut from a pelt of an animal such as a rabbit. The industrial workers were exposed to the mercury vapors, giving rise to the expression “mad as a hatter.” Some believe that the character the Mad Hatter in Lewis Carroll's Alice in Wonderland is an example of someone suffering from erethism, but the origin of this account is unclear. The character was almost certainly based on Theophilus Carter, an eccentric furniture dealer who was well known to Carroll.

Mad hatter disease, or mad hatter syndrome, was an occupational disease among hatmakers, caused by chronic mercury poisoning. It affected those whose felting work involved prolonged exposure to mercury vapors. The neurotoxic effects included tremor and the pathological shyness and irritability characteristic of erethism.

Erethism is due to mercury poisoning. Mercury is an element that is found all over the earth in soil, rocks, and water. People who get erethism are usually exposed to jobs that have something to do with these elements, such as construction. People who work in factory jobs tend to have a higher chance of getting erethism. The problem with mercury is that if humans are exposed to any of the forms of mercury, depending on the amount (dose), route (ingestion, skin contact, inhalation), duration (time) of exposure, it can be toxic. Some elemental and chemical forms of mercury (vapor, methylmercury, inorganic mercury) are more toxic than other forms. The human fetus and medically compromised people (for example, patients with lung or kidney problems) are the most susceptible to the toxic effects of mercury.

It is commonly characterized through behavioral changes such as irritability, low self-confidence, depression, apathy, shyness and timidity, and in some extreme cases with prolonged exposure to mercury vapors, delirium, personality changes and memory loss occur as a result. People with erethism find it difficult to interact socially with others, with behaviors similar to that of a social phobia. Although most of the effects of erethism are neurological, some physical problems arise as well, including a decrease in physical strength, “headaches, general pain, and tremors after exposure to metallic mercury” as well as irregular heartbeat. It has been documented that “the tremor in the hands can be so severe that the victim is unable to hold a glass of water without spilling its contents.”

The primary risk factor for erethism is long-term exposure to mercury vapors and gasses at high levels. One group at risk for mercury poisoning is industrial workers and those exposed to high levels of mercury residing naturally in the environment. Erethism is not as serious an issue as it was back before acceptable working condition regulations were enforced. Preventing mercury levels from getting too high limits the amount available for inhalation.

There is a risk of mercury poisoning in the home in some cases. Exposure to mercury vapor may stem from cultural and religious reasons where mercury is sprinkled on the floor of a home or car, burned in a candle, or mixed with perfume. Due to widespread use and popular concern, the risk of toxicity from dental amalgam has been exhaustively investigated. Many studies have not revealed convincing evidence of toxicity . However, in 2015 research showed that an increased mercury release from dental amalgam restorations after exposure to electromagnetic fields is a potential hazard for hypersensitive people and pregnant women.

The exact symptoms of a chemical burn depend on the chemical involved. Symptoms include itching, bleaching or darkening of skin, burning sensations, trouble breathing, coughing blood and/or tissue necrosis. Common sources of chemical burns include sulfuric acid (HSO), hydrochloric acid (HCl), sodium hydroxide (NaOH), lime (CaO), silver nitrate (AgNO), and hydrogen peroxide (HO). Effects depend on the substance; hydrogen peroxide removes a bleached layer of skin, while nitric acid causes a characteristic color change to yellow in the skin, and silver nitrate produces noticeable black stains. Chemical burns may occur through direct contact on body surfaces, including skin and eyes, via inhalation, and/or by ingestion. Lipophilic substances that diffuse efficiently in human tissue, e.g., hydrofluoric acid, sulfur mustard, and dimethyl sulfate, may not react immediately, but instead produce the burns and inflammation hours after the contact. Chemical fabrication, mining, medicine, and related professional fields are examples of occupations where chemical burns may occur. Hydrofluoric acid leaches into the bloodstream and reacts with calcium and magnesium, and the resulting salts can cause cardiac arrest after eating through skin.

Poisoning by lead and mercury has been know since antiquity. Other toxic metals or metals that are known to evoke adverse immune reactions are arsenic, phosphorus, zinc, beryllium, cadmium, chromium, manganese, nickel, cobalt, osmium, platinum, selenium, tellurium, thallium, uranium, and vanadium.

Withdrawal of the contaminated cooking oil is the most important initial step. Bed rest with leg elevation and a protein-rich diet are useful. Supplements of calcium, antioxidants (vitamin C and E), and thiamine and other B vitamins are commonly used. Corticosteroids and antihistaminics such as promethazine have been advocated by some investigators, but demonstrated efficacy is lacking. Diuretics are used universally but caution must be exercised not to deplete the intravascular volume unless features of frank congestive cardiac failure are present, as oedema is mainly due to increased capillary permeability. Cardiac failure is managed by bed rest, salt restriction, digitalis and diuretics. Pneumonia is treated with appropriate antibiotics. Renal failure may need dialysis therapy and complete clinical recovery is seen. Glaucoma may need operative intervention, but generally responds to medical management.

Acute inhalation injury may result from frequent and widespread use of household cleaning agents and industrial gases (including chlorine and ammonia). The airways and lungs receive continuous first-pass exposure to non-toxic and irritant or toxic gases via inhalation. Irritant gases are those that, on inhalation, dissolve in the water of the respiratory tract mucosa and provoke an inflammatory response, usually from the release of acidic or alkaline radicals. Smoke, chlorine, phosgene, sulfur dioxide, hydrogen chloride, hydrogen sulfide, nitrogen dioxide, ozone, and ammonia are common irritants.

Depending on the type and amount of irritant gas inhaled, victims can experience symptoms ranging from minor respiratory discomfort to acute airway and lung injury and even death. A common response cascade to a variety of irritant gases includes inflammation, edema and epithelial sloughing, which if left untreated can result in scar formation and pulmonary and airway remodeling. Currently, mechanical ventilation remains the therapeutic mainstay for pulmonary dysfunction following acute inhalation injury.

Carbon monoxide (CO) is presumed to be a complication in smoke inhalation. The initial approach to presumed CO poisoning involves administering supplemental oxygen at a fraction of inspired oxygen (FiO2) of 100 percent and then the use of hyperbaric oxygen (HBO) therapy is evaluated by physicians.