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.

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.

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.

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.

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.

As many of the clinical signs and symptoms of ethylene glycol poisoning are nonspecific and occur in many poisonings the diagnosis is often difficult. It is most reliably diagnosed by the measurement of the blood ethylene glycol concentration. Ethylene glycol in biological fluids can be determined by gas chromatography. Many hospital laboratories do not have the ability to perform this blood test and in the absence of this test the diagnosis must be made based on the clinical presentation of the patient. In this situation a helpful test to diagnose poisoning is the measurement of the osmolal gap. The patients' serum osmolality is measured by freezing point depression and then compared with the predicted osmolality based on the patients' measured sodium, glucose, blood urea nitrogen, and any ethanol that may have been ingested. The presence of a large osmolal gap supports a diagnosis of ethylene glycol poisoning. However, a normal osmolar gap does not rule out ethylene glycol exposure because of wide individual variability.

The increased osmolal gap is caused by the ethylene glycol itself. As the metabolism of ethylene glycol progresses there will be less ethylene glycol and this will decrease the blood ethylene glycol concentration and the osmolal gap making this test less useful. Additionally, the presence of other alcohols such as ethanol, isopropanol, or methanol or conditions such as alcoholic or diabetic ketoacidosis, lactic acidosis, or kidney failure may also produce an elevated osmolal gap leading to a false diagnosis.

Other laboratory abnormalities may suggest poisoning, especially the presence of a metabolic acidosis, particularly if it is characterized by a large anion gap. Large anion gap acidosis is usually present during the initial stage of poisoning. However, acidosis has a large number of differential diagnosis, including poisoning from methanol, salicylates, iron, isoniazid, paracetamol, theophylline, or from conditions such as uremia or diabetic and alcoholic ketoacidosis. The diagnosis of ethylene glycol poisoning should be considered in any patient with a severe acidosis. Urine microscopy can reveal needle or envelope-shaped calcium oxalate crystals in the urine which can suggest poisoning; although these crystals may not be present until the late stages of poisoning. Finally, many commercial radiator antifreeze products have fluorescein added to enable radiator leaks to be detected using a Wood's lamp. Following ingestion of antifreeze products containing ethylene glycol and fluorescein, a Wood's lamp may reveal fluorescence of a patient’s mouth area, clothing, vomitus, or urine which can help to diagnose poisoning.

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.

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.

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.

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%.

Antifreeze products for automotive use containing propylene glycol in place of ethylene glycol are available, and are generally considered safer to use, as it possesses an unpleasant taste in contrast to the perceived "sweet" taste of toxic ethylene glycol-based coolants, and only produces lactic acid in an animal's body, as their muscles do when exercised.

When using antifreeze products containing ethylene glycol, recommended safety measures include:

- Cleaning up any spill immediately and thoroughly. Spills may be cleaned by sprinkling cat litter, sand or other absorbent material directly on the spill. Once fully absorbed, while wearing protective gloves, the material may be scooped into a plastic bag, sealed and disposed. The spill area may be scrubbed with a stiff brush and warm, soapy water. The soapy water is not recommended to be drained in a storm drain.

- Checking vehicles regularly for leaks.

- Storing antifreeze in clearly marked original sealed containers, in areas that are inaccessible to pets or small children.

- Keeping pets and small children away from the area when draining the car radiator.

- Disposing of used antifreeze only by taking to a service station.

- If antifreeze is placed in toilets, ensuring the lid is down and the door closed.

Overexposure to chromium can occur in welders and other workers in the metallurgical industry, persons taking chromium-containing dietary supplements, patients who have received metallic surgical implants, and individuals who ingest chromium salts. Chromium concentrations in whole blood, plasma, serum or urine may be measured to monitor for safety in exposed workers, to confirm the diagnosis in potential poisoning victims, or to assist in the forensic investigation in a case of fatal overdosage.

The current mainstay of manganism treatment is levodopa and chelation with EDTA. Both have limited and at best transient efficacy. Replenishing the deficit of dopamine with levodopa has been shown to initially improve extrapyramidal symptoms, but the response to treatment goes down after 2 or 3 years, with worsening condition of the same patients noted even after 10 years since last exposure to manganese. Enhanced excretion of manganese prompted by chelation therapy brings its blood levels down but the symptoms remain largely unchanged, raising questions about efficacy of this form of treatment.

Increased ferroportin protein expression in human embryonic kidney (HEK293) cells is associated with decreased intracellular manganese concentration and attenuated cytotoxicity, characterized by the reversal of Mn-reduced glutamate uptake and diminished lactate dehydrogenase (LDH) leakage.

In cases of suspected copper poisoning, penicillamine is the drug of choice, and dimercaprol, a heavy metal chelating agent, is often administered. Vinegar is not recommended to be given, as it assists in solubilizing insoluble copper salts. The inflammatory symptoms are to be treated on general principles, as are the nervous ones.

There is some evidence that alpha-lipoic acid (ALA) may work as a milder chelator of tissue-bound copper. Alpha lipoic acid is also being researched for chelating other heavy metals, such as mercury.

For precious animals ;

- Repeat screening, case management to abate sources

- Medical and environmental evaluation,

- veterinary evaluation, chelation, case management

- If necessary, veterinary hospitalization, immediate chelation, case management.

The mainstays of treatment are removal from the source of lead and, for precious animals who have significantly high blood lead levels or who have symptoms of poisoning, chelation therapy with a chelating agent.

DIagnosis - I'm guessing in addition to evaluation (and rule out of) symptoms mentioned previously, there should maybe be mention of a blood test here since it's already been described as a way to gauge concentration -- "high blood concentrations lead to ____" stated in previous section so we can conclude that it can be measured in the blood and there's some existing accepted level of what level equals "high" as opposed to "normal".

Please delete, thank you and my apologies, logic is all I've got.

The only generally accepted adverse effect of fluoride at levels used for water fluoridation is dental fluorosis, which can alter the appearance of children's teeth during tooth development; this is mostly mild and usually only an aesthetic concern. Compared to unfluoridated water, fluoridation to 1 mg/L is estimated to cause fluorosis in one of every 6 people (range 4–21), and to cause fluorosis of aesthetic concern in one of every 22 people (range 13.6–∞).

Some research has suggested that high levels of fluoride exposure may adversely affect neurodevelopment in children, but the evidence is of insufficient quality to allow any firm conclusions to be drawn.

Thallium may be quantitated in blood or urine as a diagnostic tool in clinical poisoning situations or to aid in the medicolegal investigation of suspicious deaths. Normal background blood and urine concentrations in healthy persons are usually less than 1 μg/litre, but they are often in the 1–10 mg/litre range in survivors of acute intoxication.

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.

Currently, more research is being done on animal fetuses to determine the effects of OP's during critical periods of development. Due to children's decreased size, faster rate of respiration, and continuing organ development, this area is important to research. Research to determine the variability on the PON1 enzyme in humans is also currently being researched.

The use of the organophosphates in aviation lubricating oils and hydraulic fluids and its impact on health and flight safety is currently being researched. Aerotoxic syndrome is a medical condition allegedly caused by exposure to contaminated bleed air.

Purdey (1998) suggested that organophosphates, in particular Phosmet, induced the transmissible spongiform encephalopathy epidemic of BSE. A European Union food safety Scientific Steering Committee examined the evidence and did not find a link.

There are two main methods of removing both radioactive and stable isotopes of thallium from humans. First known was to use Prussian blue, which is a solid ion exchange material, which absorbs thallium. Up to 20 g per day of Prussian blue is fed by mouth to the person, and it passes through their digestive system and comes out in the stool. Hemodialysis and hemoperfusion are also used to remove thallium from the blood serum. At later stage of the treatment additional potassium is used to mobilize thallium from the tissue.

The management of AAlPP remains purely supportive because no specific antidote exists. Mortality rates approach 60%. Correction of metabolic acidosis is a cornerstone of treatment. The role of magnesium sulfate as a potential therapy in AlP poisoning may decrease the likelihood of a fatal outcome, and has been described in many studies. After ingestion, removal of unabsorbed poison from the gut ("gut decontamination"), especially if administered within 1–2 hours, can be effective. Potassium permanganate (1:10,000) gastric lavage can decompose the toxin. All patients of severe AlP poisoning require continuous invasive hemodynamic monitoring and early resuscitation with fluid and vasoactive agents.