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.

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.

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.

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.

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.

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.

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.

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.

Efforts to prevent poisoning include child-resistant packaging and a lower number of pills per package.

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.

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)

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.

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.

Intravenous fluids containing dextrose such as D5W are recommended to keep a urinary output between 2 and 3 ml/kg/h.

Sodium bicarbonate is given in a significant aspirin overdose (salicylate level greater than 35 mg/dl 6 hours after ingestion) regardless of the serum pH, as it enhances elimination of aspirin in the urine. It is given until a urine pH between 7.5 and 8.0 is achieved.

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.

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%.

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.

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.

There are many conditions to be considered in the differential diagnosis of carbon monoxide poisoning. The earliest symptoms, especially from low level exposures, are often non-specific and readily confused with other illnesses, typically flu-like viral syndromes, depression, chronic fatigue syndrome, chest pain, and migraine or other headaches. Carbon monoxide has been called a "great mimicker" due to the presentation of poisoning being diverse and nonspecific. Other conditions included in the differential diagnosis include acute respiratory distress syndrome, altitude sickness, lactic acidosis, diabetic ketoacidosis, meningitis, methemoglobinemia, or opioid or toxic alcohol poisoning.

Increased nicotine or cotinine (the nicotine metabolite) is detected in urine or blood, or serum nicotine concentrations increase.

The prognosis is typically good when medical care is provided and patients adequately treated are unlikely to have any long-term sequelae. However, severely affected patients with prolonged seizures or respiratory failure may have ongoing impairments secondary to the hypoxia. It has been stated that if a patient survives nicotine poisoning during the first 4 hours, they usually recover completely. At least at "normal" levels, as nicotine in the human body is broken down, it has an approximate biological half-life of 1–2 hours. Cotinine is an active metabolite of nicotine that remains in the blood for 18–20 hours, making it easier to analyze due to its longer half-life.

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.

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.

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.

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.