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.

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.

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.

The cause was traced to the consumption of colza oil that had been intended for industrial rather than food use. To discourage human consumption, the oil was denatured by the addition of aniline to make it smell and taste bad. It was then imported as cheap industrial oil by the company RAPSA at San Sebastián, handled by RAELCA, and illegally refined by ITH in Seville to remove the aniline, resulting in a palatable product that could then be illegally sold. It was sold as "olive oil" by street vendors at weekly street markets, and was used on salads and for cooking. The commonly accepted hypothesis states that toxic compounds derived during the refinement process were responsible.

Once the origin of the syndrome was realised, public health officials organized an exchange programme, whereby those who had bought the oil could exchange it for pure olive oil, thereby quickly ending the outbreak.

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.

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

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.

The conclusion of the Joint WHO/CISAT Scientific Committee for the Toxic Oil Syndrome from 2002, that oil was the cause for TOS, is based only on epidemiological evidence, since up to now, experimental studies performed in a variety of laboratory animals have failed to reproduce the symptoms of human TOS. None of the "in vivo" or "in vitro" studies performed with toxic-oil-specific components, such as fatty acid anilides, and esters of 3-(N-phenylamino)-1,2-propanediol (abbreviated as PAP), have provided evidence that these markers are causally involved in the pathogenesis of TOS.

Specifically, three possible causative agents of TOS are PAP (3-(N-phenylamino)-1,2-propanediol), the 1,2-dioleoyl ester of PAP (abbreviated OOPAP), and the 3-oleoyl ester of PAP (abbreviated OPAP). These three compounds are formed by means of similar chemical processes, and oil that contains one of the three substances is likely to contain the other two. Oil samples that are suspected to have been ingested by people who later developed TOS often contain all three of these contaminants (among other substances), but are most likely to contain OOPAP. However, when these three substances were given to laboratory animals, OOPAP was not acutely toxic, PAP was toxic only after injection, but not after oral administration, and OPAP was toxic only after injection of high doses. Therefore, none of these three substances is thought to cause TOS. Similar results were obtained after administration of fatty acid anilides.

The fact that the first cases of the syndrome were located in Madrid, near the U.S. military base in Torrejón de Ardoz, and the secrecy surrounding the huge investigations, spread the idea of a conspiracy. Several of those affected by the TOS claim they never consumed that oil. Although the oil was mainly sold on street markets, a considerable percentage of the patients was upper class. Another theory suggests the toxic reaction was triggered by organophosphate poisoning (e. g., from pesticide residues in tomatoes) and covered up by the Spanish government and the WHO.

Current antidotes for OP poisoning consist of a pretreatment with carbamates to protect AChE from inhibition by OP compounds and post-exposure treatments with anti-cholinergic drugs. Anti-cholinergic drugs work to counteract the effects of excess acetylcholine and reactivate AChE. Atropine can be used as an antidote in conjunction with pralidoxime or other pyridinium oximes (such as trimedoxime or obidoxime), though the use of "-oximes" has been found to be of no benefit, or possibly harmful, in at least two meta-analyses. Atropine is a muscarinic antagonist, and thus blocks the action of acetylcholine peripherally. These antidotes are effective at preventing lethality from OP poisoning, but current treatment lack the ability to prevent post-exposure incapacitation, performance deficits, or permanent brain damage. While the efficacy of atropine has been well-established, clinical experience with pralidoxime has led to widespread doubt about its efficacy in treatment of OP poisoning.

Enzyme bioscavengers are being developed as a pretreatment to sequester highly toxic OPs before they can reach their physiological targets and prevent the toxic effects from occurring. Significant advances with cholinesterases (ChEs), specifically human serum BChE (HuBChE) have been made. HuBChe can offer a broad range of protection for nerve agents including soman, sarin, tabun, and VX. HuBChE also possess a very long retention time in the human circulation system and because it is from a human source it will not produce any antagonistic immunological responses. HuBChE is currently being assessed for inclusion into the protective regimen against OP nerve agent poisoning. Currently there is potential for PON1 to be used to treat sarin exposure, but recombinant PON1 variants would need to first be generated to increase its catalytic efficiency.

One other agent that is being researched is the Class III anti-arrhythmic agents. Hyperkalemia of the tissue is one of the symptoms associated with OP poisoning. While the cellular processes leading to cardiac toxicity are not well understood, the potassium current channels are believed to be involved. Class III anti-arrhythmic agents block the potassium membrane currents in cardiac cells, which makes them a candidate for become a therapeutic of OP poisoning.

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

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.

Several health authorities have issued related guidance documents, which need to be considered for drug development:

- ICH (International Conference on Harmonisation of Technical Requirements for Registration of Pharmaceuticals for Human Use)

- M3(R2) "Guidance on Nonclinical Safety Studies for the Conduct of Human Clinical Trials and Marketing Authorization for Pharmaceuticals"

- S9 "Nonclinical Evaluation for Anticancer Pharmaceuticals"

- S10 "Photosafety Evaluation"

- EMA (European Medicines Agency)

- "Note for Guidance on Photosafety Testing" (revision on-hold)

- "Question & Answers on the Note for Guidance on Photosafety Testing"

- FDA (U.S. Food and Drug Administration)

- MHLW/PMDA (Japanese Ministry of Health, Labour and Welfare / Pharmaceuticals and Medical Devices Agency)

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.

3T3 Neutral Red Phototoxicity Test – An in vitro toxicological assessment test used to determine the cytotoxic and photo(cyto)toxicity effect of a test article to murine fibroblasts in the presence or absence of UVA light.

"The 3T3 Neutral Red Uptake Phototoxicity Assay (3T3 NRU PT) can be utilized to identify the phototoxic effect of a test substance induced by the combination of test substance and light and is based on the comparison of the cytotoxic effect of a test substance when tested after the exposure and in the absence of exposure to a non-cytotoxic dose of UVA/vis light. Cytotoxicity is expressed as a concentration-dependent reduction of the uptake of the vital dye - Neutral Red.

Substances that are phototoxic in vivo after systemic application and distribution to the skin, as well as compounds that could act as phototoxicants after topical application to the skin can be identified by the test. The reliability and relevance of the 3T3 NRU PT have been evaluated and has been shown to be predictive when compared with acute phototoxicity effects in vivo in animals and humans." Taken with permission from

The illness is generally self-limiting. Management on the whole is preventative, by limiting exposure to mouldy environments with ventilation, or by wearing respiratory protection such as facemasks.

Toxic abortion is a medical phenomenon of spontaneous abortion, miscarriage, or stillbirth caused by toxins in the environment of the mother during pregnancy, especially as caused by toxic environmental pollutants, though sometimes reported as caused by naturally occurring plant toxins.

Aerotoxic syndrome is a phrase coined by Chris Winder and Jean-Christophe Balouet in 2000, to describe their claims of short- and long-term ill-health effects caused by breathing airliner cabin air which was alleged to have been contaminated to toxic levels (exceeding known, parts per million, safe levels) with atomized engine oils or other chemicals. Repeated investigations of such claims have failed to document cabin air has ever contained contaminants which exceeded known safe levels. An assessment by the UK's House of Lords Science and Technology Committee found that claims of health effects were unsubstantiated.

An update in 2008 found no significant new evidence. this syndrome is not recognized in medicine.

It was recognised as a distinct clinical syndrome in the 1980s. Previously, cases had been reported and given various names such as pulmonary mycotoxicosis, silo unloader’s syndrome, grain fever, toxin fever, humidifier fever, mill fever, toxic alveolitis or allergic alveolitis. In 1994, the National Institute for Occupational Safety and Health published case reports and highlighted the urgency for study of the syndrome.

Research and data collection in the agricultural industry is difficult, as many workers are casual.

For staphylococcal toxic shock syndrome, the diagnosis is based strictly upon CDC criteria defined in 2011, as follows:

1. Body temperature > 38.9 °C (102.02 °F)

2. Systolic blood pressure < 90 mmHg

3. Diffuse macular erythroderma

4. Desquamation (especially of the palms and soles) 1–2 weeks after onset

5. Involvement of three or more organ systems:

- Gastrointestinal (vomiting, diarrhea)

- Muscular: severe myalgia or creatine phosphokinase level at least twice the upper limit of normal for laboratory

- Mucous membrane hyperemia (vaginal, oral, conjunctival)

- Kidney failure (serum creatinine > 2 times normal)

- Liver inflammation (bilirubin, AST, or ALT > 2 times normal)

- Low platelet count (platelet count < 100,000 / mm)

- Central nervous system involvement (confusion without any focal neurological findings)

6. Negative results of:

- Blood, throat, and CSF cultures for other bacteria (besides "S. aureus")

- Negative serology for "Rickettsia" infection, leptospirosis, and measles

Cases are classified as confirmed or probable based on:

- Confirmed: All six of the criteria above are met (unless the patient dies before desquamation can occur)

- Probable: Five of the six criteria above are met

The term "toxic abortion" was first used to identify this phenomenon in humans in the earliest studies of the effects of pollutants on pregnancy in 1928, "An Experimental Investigation Concerning Toxic Abortion Produced by Chemical Agents" by Morris M. Datnow M.D.

Toxic abortion chemicals studied at that time were:

Petrochemicals,

Heavy metals,

Organic solvents,

Tetrachloroethylene,

Glycol ethers,

2-Bromopropane,

Ethylene oxide,

Anesthetic gases, and

Antineoplastic drugs.

In 1932, the "Journal of State Medicine" reported on a natural variation, with the occurrence of "a considerable number of cases of toxic abortion" being caused by untreated dental caries.

Study of pollution-caused abortion in humans ceased for a considerable time, interest renewing in the 2000s. A 2009 study found that fossil fuels play a role, as "pregnant African-American women who live within a half mile of freeways and busy roads were three times more likely to have miscarriages than women who don't regularly breathe exhaust fumes." A 2011 study found a correlation between exposure to workplace toxins and spontaneous abortion, and called for further study. "Newsweek" magazine reported in May 2014 that a spike in stillborn babies in the town of Vernal, in Utah, had correlated with an increase in pollution from new gas and oil drilling. "Newsweek" reported that "Vernal’s rate of neonatal mortality appears to have climbed from about average in 2010 (relative to national figures) to six times the normal rate three years later." "Newsweek" quoted one expert's observation that "We know that pregnant women who breathe more air pollution have much higher rates of virtually every adverse pregnancy outcome that exists." A study published in the "Journal of Environmental Health" in October 2014 found tetrachloroethylene or PCE, to be "linked to increased risk for stillbirths and other pregnancy complications."

The PCE study found that "pregnancies with high exposure to PCE were 2.4 times more likely to end with stillborn babies and 1.4 times more likely to experience placental abruption — when the placenta peels away from uterine wall before delivery, causing the mother to bleed and the baby to lose oxygen — compared with pregnancies never exposed to PCE." Higher exposure lead to a 35 percent higher risk of abruption. PCE has also been tied to an increased risk for cancer. Children exposed to PCE as fetuses and toddlers are more likely to use drugs later in life. The toxin has been linked to mental illness, an increased risk of breast cancer and some birth defects. It has been tied to anxiety, depression, and impairments in cognition, memory and attention. PCE contamination has been found in the Massachusetts water supply and "on military bases across the country," and "water systems in California and Pennsylvania and have also been found to be contaminated with PCE."

In 2015, "Newsweek" reported that chemicals found in fast food wrappers multiply miscarriage risk by sixteen times.

Some instances have been reported of women intentionally seeking to induce toxic abortion, where circumstances make medical abortion difficult to obtain, by exposing themselves to environmental toxins.

In 1955, the Ministry of International Trade and Industry began its policy to transition Japan's primary fossil fuel source from coal to petroleum. To accomplish that goal, construction of the Daichi Petrochemical Complex was begun in 1956. The complex contained an oil refinery, a petrochemical plant, and a power station. This was the first petrochemical complex constructed in Japan.

In 1960, the government of Prime Minister Hayato Ikeda accelerated the growth of petrochemical production as part of its goal to double individual incomes of Japanese citizens over a 10-year period. Also in 1960, MITI announced that a second complex was to be constructed on reclaimed land in northern Yokkaichi. The second complex went online in 1963. As demand for ethylene and other petrochemicals rose, a third complex was constructed which began production in 1972. Yokkaichi transferred its energy production from coal to oil more quickly than the rest of the nation. The oil used in Yokkaichi was primarily imported from the Middle East, which contained 2% sulfur in sulfur containing compounds, resulting in a white-colored smog developing over the city.

A class action court case was brought against Showa Yokkaichi Oil and initially adjudicated in September 1970. The class was ruled to contain 544 individuals, but that number has increased over the ensuing years.

A 2008 study by researchers from the Mie University Graduate School of Medicine and the Hiroshima University Natural Science Center for Basic Research and Development indicated a 10 to 20-fold higher mortality rates as a result of COPD and asthma in the affected populations of Yokkaichi versus the general population of Mie Prefecture.

Initial attempts to alleviate the problem by raising the height of smokestacks to disperse the pollutants over a larger area proved ineffective. Eventually flue-gas desulfurization was implemented on a large scale, leading to an improvement in the health of local populace.

Yokkaichi asthma has been identified in rapidly industrializing areas in the rest of the world, including Mexico City and mainland China.

The severity of this disease frequently warrants hospitalization. Admission to the intensive care unit is often necessary for supportive care (for aggressive fluid management, ventilation, renal replacement therapy and inotropic support), particularly in the case of multiple organ failure. The source of infection should be removed or drained if possible: abscesses and collections should be drained. Anyone wearing a tampon at the onset of symptoms should remove it immediately. Outcomes are poorer in patients who do not have the source of infection removed.

Antibiotic treatment should cover both "S. pyogenes" and "S. aureus". This may include a combination of cephalosporins, penicillins or vancomycin. The addition of clindamycin or gentamicin reduces toxin production and mortality.

In 1986, the United States Congress commissioned a report by the National Research Council (NRC) into cabin air quality. The report recommended a ban on smoking on aircraft in order to improve air quality. In 1988, the FAA banned smoking on domestic flights of less than two hours, and in 2000 extended the ban to all domestic and international flights.

Research commissioned by the UK government's Department for Transport (DfT) and published in 2000 found no link to long term health. The UK Parliament's Select Committee on Science and Technology concluded in its response to the many complaints received "from a number of witnesses, particularly the Organophosphate Information Network, BALPA, and the International Association of Flight Attendants, expressing concerns about the risk of tricresyl phosphate (TCP or TOCP) poisoning for cabin occupants, particularly for crew who might be subjected to repeated exposure in some aircraft types, as a result of oil leaking into the cabin air supply."

In 2009 the UK House of Commons Library service to Members of Parliament summarized the research into a "relationship between the [engine oil chemical] leaks and these health symptoms" as inconclusive, citing "problems with identifying the exact chemical that might be entering the air supply and therefore identifying what impact it may have on health" and "reports of problems with fumes and/or health symptoms not being reported correctly".

According to a 2008 report by Michael Bagshaw, Aviation Medicine Director at King's College London, there have been no peer-reviewed recorded cases of neurological harm in humans following TCP exposure. He pointed to an unpublished report from the Medical Toxicology Unit at Guy's Hospital in 2001 which looked at all exposures dating back to 1943 that showed that all documented exposures were to high concentrations greatly in excess of the amount present in jet oil.

In his 2013 paper, "Cabin Air Quality: A review of current aviation medical understanding," Bagshaw noted further: "A German study in 2013 of 332 crew members who had reported fume/odour during their last flight, failed to detect metabolites of TCP in urine samples. The authors concluded that health complaints could not be linked to TCP exposure in cabin air...A syndrome is a symptom complex, consistent and common to a given condition. Sufferers of the ‘aerotoxic syndrome’ describe a wide range of inconsistent symptoms and signs with much individual variability."

The evidence was independently reviewed by the Aerospace Medical Association, the US National Academy of Sciences and the Australian Civil Aviation Safety Authority (CASA) Expert Panel. All concluded there is insufficient consistency to establish a medical syndrome, and the ‘aerotoxic syndrome’ is not recognised in aviation medicine."

The 'nocebo effect' was among the conclusions published in a 2013 COT (Committee on Toxicity) position paper: "The acute illness which has occurred in relation to perceived episodes of contamination might reflect a toxic effect of one or more chemicals, but it could also have occurred through nocebo effects. There is strong scientific evidence that nocebo effects can lead to (sometimes severely disabling) illness from environmental exposures that are perceived as hazardous."

The condition can be prevented by using chloramphenicol at the recommended doses and monitoring blood levels, or alternatively, third generation cephalosporins can be effectively substituted for the drug, without the associated toxicity.