6,530 patients were admitted to hospitals with poisoning, and 459 deaths reported. Cases reached a peak of hundreds per day in January, and had largely subsided by the beginning of March. The last admittance was on 27 March; admissions represented every age and gender stratum, although those under the age of ten represented a third of admitted cases. This number is "certainly an underestimate", because of the availability of hospital treatment, hospital overcrowding and lack of faith in treatment. In the most severely affected areas, prevalence was 28% and mortality was 21% of the cases. Some Iraqi doctors believe both the number of cases and fatalities are at least ten times too low, with perhaps 100,000 cases of brain damage. One suggested reason for the vast discrepancy between reported and estimated numbers of deaths is the Iraqi custom, common to large parts of the Middle East, for a person to die at home when possible. Home deaths would not have been recorded.

A large number of patients with minor symptoms recovered completely; those with more serious symptoms improved. This was in contrast to expected outcomes, largely based on analysis of Minamata disease in Japan. In boys with mercury levels below clinical poisoning, a reduction in school performance was noted, although this correlation could not be confirmed. In infants, the mercury poisoning caused central nervous system damage. Relatively low doses caused slower development in children, and abnormal reflexes. Different treatments for mercury poisoning have since been developed, and "quiet baby syndrome", characterised by a baby who never cries, is now a recognised symptom of methylmercury-induced brain damage. Ongoing recommendations of the food regulation authorities have focused on consumption by pregnant women and infant children, noting the particular susceptibility of fetuses and infants to methylmercury poisoning. Data from Iraq have confirmed that methylmercury can pass to a child "in utero", and mercury levels were equal to or higher in the newborn child than in the mother.

In 1974, a joint Food and Agriculture Organization (FAO) and World Health Organisation (WHO) meeting made several recommendations to prevent a similar outbreak. These included stressing the importance of labelling bags in the local language and with locally understood warning symbols. The possibility of an additive creating a strong bitter taste was studied. The meeting urged governments to strictly regulate methyl- and ethylmercury use in their respective countries, including limiting use to where no other reasonable alternative was available. It also recommended the involvement of the FAO and WHO in assisting national governments in regulation and enforcement, and the setting up of national poison control centres. Over 9–13 November, a Conference on Intoxication due to Alkylmercury-Treated Seed was held in Baghdad. It supported the recommendations of the FAO/WHO report and further suggested that local and national media should publicise outbreaks, including size and symptoms; it considered the distribution of this information crucial. It also laid out a general plan as to the collection of relevant information from the field and potential analysis for further investigation. It called on national governments to make use of WHO involvement whenever feasible, and absolved world governments in clear terms, saying that "No country should ever feel that any blame will attach to it for allowing an outbreak to occur".

Iraq now has the highest incidence of Parkinson's in the world. Parkinson's symptoms are very similar to mercury poisoning symptoms. Mercury that enters the brain has a half-life of 27.5 years and chelators are not able to remove it.

Some of grain (73,201 tonnes of wheat grain and 22,262 tonnes of barley), coloured a pink-orange hue, were shipped to Iraq from the United States and Mexico. The wheat arrived in Basra on SS "Trade Carrier" between 16 September and 15 October, barley between 22 October and 24 November 1971. Iraq's government chose Mexipak, a high-yield wheat seed developed in Mexico by Norman Borlaug. The seeds contained an average of 7.9 μg/g of mercury, with some samples containing up to nearly twice that. The decision to use mercury-coated grain has been reported as made by the Iraqi government, rather than the supplier, Cargill. The three Northern governorates of Ninawa, Kirkuk and Erbil together received more than half the shipments. Contributing factors to the epidemic included the fact that distribution started late, and much grain arrived after the October–November planting season.

Farmers holding grain ingested it instead, since their own planting had been completed. Distribution was hurried and open, with grain being distributed free of charge or with payment in kind. Some farmers sold their own grain lest this new grain devalue what they had. This left them dependent on tainted grain for the winter. Many Iraqis were either unaware of the significant health risk posed, or chose to ignore the warnings. Initially, farmers were to certify with a thumbprint or signature that they understood the grain was poison, but according to some sources, distributors did not ask for such an indication. Warnings on the sacks were in Spanish and English, not at all understood, or included the black-and-white skull and crossbones design, which meant nothing to Iraqis. The long latent period may have granted farmers a false sense of security, when animals fed the grain appeared to be fine. The red dye washed off the grain; the mercury did not. Hence, washing may have given only the appearance of removing the poison.

Mercury was ingested through the consumption of homemade bread, meat and other animal products obtained from livestock given treated barley, vegetation grown from soil contaminated with mercury, game birds that had fed on the grain and fish caught in rivers, canals, and lakes into which treated grain had been dumped by the farmers. Ground seed dust inhalation was a contributing factor in farmers during sowing and grinding. Consumption of ground flour through homemade bread is thought to have been the major cause, since no cases were reported in urban areas, where government flour supplies were commercially regulated.

When thinking of pesticide poisoning, one does not take into consideration the contribution that is made of their own household. The majority of households in Canada use pesticides while taking part in activities such as gardening. In Canada 96 percent of households report having a lawn or a garden. 56 percent of the households who have a lawn or a garden utilize fertilizer or pesticide. This form of pesticide use may contribute to the third type of poisoning, which is caused by long-term low-level exposure. As mentioned before, long-term low-level exposure affects individuals from sources such as pesticide residues in food as well as contact with pesticide residues in the air, water, soil, sediment, food materials, plants and animals.

Pesticide poisoning is an important occupational health issue because pesticides are used in a large number of industries, which puts many different categories of workers at risk. Extensive use puts agricultural workers in particular at increased risk for pesticide illnesses. Exposure can occur through inhalation of pesticide fumes, and often occurs in settings including greenhouse spraying operations and other closed environments like tractor cabs or while operating rotary fan mist sprayers in facilities or locations with poor ventilation systems.

Workers in other industries are at risk for exposure as well. For example, commercial availability of pesticides in stores puts retail workers at risk for exposure and illness when they handle pesticide products. The ubiquity of pesticides puts emergency responders such as fire-fighters and police officers at risk, because they are often the first responders to emergency events and may be unaware of the presence of a poisoning hazard. The process of aircraft disinsection, in which pesticides are used on inbound international flights for insect and disease control, can also make flight attendants sick.

Different job functions can lead to different levels of exposure. Most occupational exposures are caused by absorption through exposed skin such as the face, hands, forearms, neck, and chest. This exposure is sometimes enhanced by inhalation in settings including spraying operations in greenhouses and other closed environments, tractor cabs, and the operation of rotary fan mist sprayers.

Some elements otherwise regarded as toxic heavy metals are essential, in small quantities, for human health. These elements include vanadium, manganese, iron, cobalt, copper, zinc, selenium, strontium and molybdenum. A deficiency of these essential metals may increase susceptibility to heavy metal poisoning.

In humans, heavy metal poisoning is generally treated by the administration of chelating agents.

These are chemical compounds, such as (calcium disodium ethylenediaminetetraacetate) that convert heavy metals to chemically inert forms that can be excreted without further interaction with the body. Chelates are not without side effects and can also remove beneficial metals from the body. Vitamin and mineral supplements are sometimes co-administered for this reason.

Soils contaminated by heavy metals can be remediated by one or more of the following technologies: isolation; immobilization; toxicity reduction; physical separation; or extraction. "Isolation" involves the use of caps, membranes or below-ground barriers in an attempt to quarantine the contaminated soil. "Immobilization" aims to alter the properties of the soil so as to hinder the mobility of the heavy contaminants. "Toxicity reduction" attempts to oxidise or reduce the toxic heavy metal ions, via chemical or biological means into less toxic or mobile forms. "Physical separation" involves the removal of the contaminated soil and the separation of the metal contaminants by mechanical means. "Extraction" is an on or off-site process that uses chemicals, high-temperature volatization, or electrolysis to extract contaminants from soils. The process or processes used will vary according to contaminant and the characteristics of the site.

Thallium and its compounds are often highly toxic. Contact with skin is dangerous, and adequate ventilation should be provided when melting this metal. Many thallium(I) compounds are highly soluble in water and are readily absorbed through the skin. Exposure to them should not exceed 0.1 mg per m of skin in an 8-hour time-weighted average (40-hour work week). Thallium is a suspected human carcinogen.

Part of the reason for thallium's high toxicity is that, when present in aqueous solution as the univalent thallium(I) ion (Tl), it exhibits some similarities with essential alkali metal cations, particularly potassium (due to similar ionic radii). It can thus enter the body via potassium uptake pathways. Other aspects of thallium's chemistry differ strongly from that of the alkali metals, such as its high affinity for sulfur ligands. Thus, this substitution disrupts many cellular processes (for instance, thallium may attack sulfur-containing proteins such as cysteine residues and ferredoxins). Thallium's toxicity has led to its use (now discontinued in many countries) as a rat and ant poison.

Among the distinctive effects of thallium poisoning are hair loss (which led to its initial use as a depilatory before its toxicity was properly appreciated) and damage to peripheral nerves (victims may experience a sensation of walking on hot coals), although the loss of hair only generally occurs in low doses; in high doses the thallium kills before this can take effect. Thallium was once an effective murder weapon before its effects became understood and an antidote (Prussian blue) discovered. Indeed, thallium poisoning has been called the "poisoner's poison" since thallium is colorless, odorless and tasteless; its slow-acting, painful and wide-ranging symptoms are often suggestive of a host of other illnesses and conditions.

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 exact nature of the poison is still unclear. In the U.S. outbreak, the source of the fish was traced by the Centers for Disease Control and Prevention, and studies of other fish from the same sources showed a hexane-soluble (and hence non-polar lipid) substance that induced similar symptoms in mice; other food-borne poisons commonly found in fish could not be detected. It cannot be inactivated by cooking, as all six CDC cases had consumed cooked or fried fish. Palytoxin has been proposed as a disease model. It has also been suggested that the toxin may have thiaminase activity (i.e. it degrades thiamine, also known as vitamin B1).

Human milk sickness is uncommon today in the United States. Current practices of animal husbandry generally control the pastures and feed of cattle, and the pooling of milk from many producers lowers the risk of tremetol present in dangerous amounts. The poison tremetol is not inactivated by pasteurization. Although extremely rare, milk sickness can occur if a person drinks contaminated milk or eats dairy products gathered from a single cow or from a smaller herd that has fed on the white snakeroot plant. There is no cure, but treatment is available.

Chronic arsenic poisoning results from drinking contaminated well water over a long period of time. Many aquifers contain high concentration of arsenic salts. The World Health Organization (WHO) recommends a limit of 0.01 mg/L (10 parts per billion) of arsenic in drinking water. This recommendation was established based on the limit of detection for most laboratories' testing equipment at the time of publication of the WHO water quality guidelines. More recent findings show that consumption of water with levels as low as 0.00017 mg/L (0.17 parts per billion) over long periods of time can lead to arsenicosis.

From a 1988 study in China, the US protection agency quantified the lifetime exposure of arsenic in drinking water at concentrations of 0.0017 mg/L, 0.00017 mg/L, and 0.000017 mg/L are associated with a lifetime skin cancer risk of 1 in 10,000, 1 in 100,000, and 1 in 1,000,000 respectively. WHO asserts that a level of 0.01 mg/L poses a risk of 6 in 10000 chance of lifetime skin cancer risk and contends that this level of risk is acceptable.

One of the worst incidents of arsenic poisoning via well water occurred in Bangladesh, which the World Health Organization called the "largest mass poisoning of a population in history."

Mining techniques such as hydraulic fracturing may mobilize arsenic in groundwater and aquifers due to enhanced methane transport and resulting changes in redox conditions, and inject fluid containing additional arsenic.

Once kidney failure has developed in dogs and cats, the outcome is poor.

Historically, eating grain products, particularly rye, contaminated with the fungus "Claviceps purpurea" was the cause of ergotism.

The toxic ergoline derivatives are found in ergot-based drugs (such as methylergometrine, ergotamine or, previously, ergotoxine). The deleterious side-effects occur either under high dose or when moderate doses interact with potentiators such as erythromycin.

The alkaloids can pass through lactation from mother to child, causing ergotism in infants.

Organic arsenic is less harmful than inorganic arsenic. Seafood is a common source of the less toxic organic arsenic in the form of arsenobetaine. The arsenic reported in 2012 in fruit juice and rice by "Consumer Reports" was primarily inorganic arsenic.

The 1951 Pont-Saint-Esprit mass poisoning, also known as Le Pain Maudit, occurred on 15 August 1951, in the small town of Pont-Saint-Esprit in southern France. More than 250 people were involved, including 50 persons interned in asylums and resulted in 7 deaths. A foodborne illness was suspected, and among these it was originally believed to be a case of "cursed bread" ("pain maudit").

Most academic sources accept ergot poisoning as the cause of the epidemic, while a few theorize other causes such as poisoning by mercury, mycotoxins, or nitrogen trichloride.

Ethylene glycol poisoning is a relatively common occurrence worldwide. Human poisoning often occurs in isolated cases, but may also occur in epidemics. Many cases of poisoning are the result of using ethylene glycol as a cheap substitute for alcohol or intentional ingestions in suicide attempts. Less commonly it has been used as a means of homicide. Children or animals may be exposed by accidental ingestion; children and animals often consume large amounts due to ethylene glycol having a sweet taste. In the United States there were 5816 cases reported to poison centers in 2002. Additionally, ethylene glycol was the most common chemical responsible for deaths reported by US poison centers in 2003. In Australia there were 17 cases reported to the Victorian poison center and 30 cases reported to the New South Wales poison center in 2007. However, these numbers may underestimate actual numbers because not all cases attributable to ethylene glycol are reported to poison control centers. Most deaths from ethylene glycol are intentional suicides; deaths in children due to unintentional ingestion are extremely rare.

In an effort to prevent poisoning, often a bittering agent called denatonium benzoate, known by the trade name Bitrex, is added to ethylene glycol preparations as an adversant to prevent accidental or intentional ingestion. The bittering agent is thought to stop ingestion as part of the human defense against ingestion of harmful substances is rejection of bitter tasting substances. In the United States, eight states (Oregon, California, New Mexico, Virginia, Arizona, Maine, Tennessee, Washington) have made the addition of bittering agents to antifreeze compulsory. Three follow up studies targeting limited populations or suicidal persons to assess the efficacy of bittering agents in preventing toxicity or death have, however, shown limited benefit of bittering ethylene glycol preparations in these two populations. Specifically, Mullins finds that bittering of antifreeze does not reduce reported cases of poisoning of preschoolers in the US state of Oregon. Similarly, White found that adding bittering agents did not decrease the frequency or severity of antifreeze poisonings in children under the age of 5. Additionally, another study by White found that suicidal persons are not deterred by the bittered taste of antifreeze in their attempts to kill themselves. These studies did not focus on poisoning of domestic pets or livestock, for example, or inadvertent exposure to bittered antifreeze among a large population (of non-preschool age children).

Poisoning of a raccoon was diagnosed in 2002 in Prince Edward Island, Canada. An online veterinary manual provides information on lethal doses of ethylene glycol for chicken, cattle, as well as cats and dogs, adding that younger animals may be more susceptible.

Mushrooms may be rendered poisonous by insecticides or herbicides sprayed on lawns or reserves. At least one author recommends never picking them in non-natural landscapes for this reason.

Also, mushrooms are sometimes contaminated by concentrating pollutants, such as heavy metals or radioactive material (see Chernobyl disaster effects).

Rotten mushrooms may cause food poisoning. Mushrooms that are mushy, bad-smelling, or moldy (even of a choice edible species) may be toxic due to bacterial decay or mold.

Many mushrooms are high in fiber. Excessive consumption of mushrooms may lead to indigestion, which may be diagnosed as mushroom "poisoning".

Dark-purple or black grain kernels, known as ergot bodies, can be identifiable in the heads of cereal or grass just before harvest. In most plants the ergot bodies are larger than normal grain kernels, but can be smaller if the grain is a type of wheat. A larger separation between the bodies and the grain kernels show the removal of ergot bodies during grain cleaning.

New species of fungi are continuing to be discovered, with an estimated number of 800 new species registered annually. This, added to the fact that many investigations have recently reclassified some species of mushrooms from edible to poisonous has made older classifications insufficient at describing what now is known about the different species of fungi that are harmful to humans. Thus, contrary to what older registers state, it is now thought that of the approximately 100,000 known fungi species found worldwide, about 100 of them are poisonous to humans. However, by far the majority of mushroom poisonings are not fatal, and the majority of fatal poisonings are attributable to the "Amanita phalloides" mushroom.

A majority of these cases are due to mistaken identity. This is a common occurrence with "A. phalloides" in particular, due to its resemblance to the Asian paddy-straw mushroom, "Volvariella volvacea". Both are light-colored and covered with a universal veil when young.

"Amanita"s can be mistaken for other species, as well, in particular when immature. On at least one occasion they have been mistaken for "Coprinus comatus". In this case, the victim had some limited experience in identifying mushrooms, but did not take the time to correctly identify these particular mushrooms until after he began to experience symptoms of mushroom poisoning.

The author of "Mushrooms Demystified", David Arora cautions puffball-hunters to beware of "Amanita" "eggs", which are "Amanita"s still entirely encased in their universal veil. "Amanita"s at this stage are difficult to distinguish from puffballs. Foragers are encouraged to always cut the fruiting bodies of suspected puffballs in half, as this will reveal the outline of a developing "Amanita" should it be present within the structure.

A majority of mushroom poisonings in general are the result of small children, especially toddlers in the "grazing" stage, ingesting mushrooms found in the lawn. While this can happen with any mushroom, "Chlorophyllum molybdites" is often implicated due to its preference for growing in lawns. "C. molybdites" causes severe gastrointestinal upset but is not considered deadly poisonous.

A few poisonings are the result of misidentification while attempting to collect hallucinogenic mushrooms for recreational use. In 1981, one fatality and two hospitalizations occurred following consumption of "Galerina autumnalis", mistaken for a "Psilocybe" species. "Galerina" and "Psilocybe" species are both small, brown, and sticky, and can be found growing together. However, "Galerina" contains amatoxins, the same poison found in the deadly "Amanita" species. Another case reports kidney failure following ingestion of "Cortinarius orellanus", a mushroom containing orellanine.

It is natural that accidental ingestion of hallucinogenic species also occurs, but is rarely harmful when ingested in small quantities. Cases of serious toxicity have been reported in small children. "Amanita pantherina", while containing the same hallucinogens as "Amanita muscaria" (e.g., ibotenic acid and muscimol), has been more commonly associated with severe gastrointestinal upset than its better-known counterpart.

Although usually not fatal, "Omphalotus" spp., "Jack-o-lantern mushrooms," are another cause of sometimes significant toxicity. They are sometimes mistaken for chanterelles. Both are bright-orange and fruit at the same time of year, although "Omphalotus" grows on wood and has true gills rather than the veins of a "Cantharellus". They contain toxins known as illudins, which causes gastrointestinal symptoms.

Bioluminescent species are generally inedible and often mildly toxic.

"Clitocybe dealbata", which is occasionally mistaken for an oyster mushroom or other edible species contains muscarine.

Toxicities can also occur with collection of morels. Even true morels, if eaten raw, will cause gastrointestinal upset. Typically, morels are thoroughly cooked before eating. "Verpa bohemica", although referred to as "thimble morels" or "early morels" by some, have caused toxic effects in some individuals. "Gyromitra" spp., "false morels", are deadly poisonous if eaten raw. They contain a toxin called gyromitrin, which can cause neurotoxicity, gastrointestinal toxicity, and destruction of the blood cells. The Finns consume "Gyromitra esculenta" after parboiling, but this may not render the mushroom entirely safe, resulting in its being called the "fugu of the Finnish cuisine".

A more unusual toxin is coprine, a disulfiram-like compound that is harmless unless ingested within a few days of ingesting alcohol. It inhibits aldehyde dehydrogenase, an enzyme required for breaking down alcohol. Thus, the symptoms of toxicity are similar to being hung over—flushing, headache, nausea, palpitations, and, in severe cases, trouble breathing. "Coprinus" species, including "Coprinopsis atramentaria", contain coprine. "Coprinus comatus" does not, but it is best to avoid mixing alcohol with other members of this genus.

Recently, poisonings have also been associated with "Amanita smithiana". These poisonings may be due to orellanine, but the onset of symptoms occurs in 4 to 11 hours, which is much quicker than the 3 to 20 days normally associated with orellanine.

"Paxillus involutus" is also inedible when raw, but is eaten in Europe after pickling or parboiling. However, after the death of the German mycologist Dr Julius Schäffer, it was discovered that the mushroom contains a toxin that can stimulate the immune system to attack its own red blood cells. This reaction is rare, but can occur even after safely eating the mushroom for many years. Similarly, "Tricholoma equestre" was widely considered edible and good, until it was connected with rare cases of rhabdomyolysis.

In the fall of 2004, thirteen deaths were associated with consumption of "Pleurocybella porrigens" or "angel's wings". In general, these mushrooms are considered edible. All the victims died of an acute brain disorder, and all had pre-existing kidney disease. The exact cause of the toxicity was not known at this time and the deaths cannot be definitively attributed to mushroom consumption.

However, mushroom poisoning is not always due to mistaken identity. For example, the highly toxic ergot "Claviceps purpurea", which grows on rye, is sometimes ground up with rye, unnoticed, and later consumed. This can cause devastating, even fatal effects, which is called ergotism.

Cases of idiosyncratic or unusual reactions to fungi can also occur. Some are probably due to allergy, others to some other kind of sensitivity. It is not uncommon for an individual person to experience gastrointestinal upset associated with one particular mushroom species or genus.

Mold health issues are potentially harmful effects of molds.

Molds (US usage; British English "moulds") are ubiquitous in the biosphere, and mold spores are a common component of household and workplace dust. The United States Centers for Disease Control and Prevention reported in its June 2006 report, 'Mold Prevention Strategies and Possible Health Effects in the Aftermath of Hurricanes and Major Floods,' that "excessive exposure to mold-contaminated materials can cause adverse health effects in susceptible persons regardless of the type of mold or the extent of contamination." When mold spores are present in abnormally high quantities, they can present especially hazardous health risks to humans after prolonged exposure, including allergic reactions or poisoning by mycotoxins, or causing fungal infection (mycosis).

Infants may develop respiratory symptoms as a result of exposure to a specific type of fungal mold, called Penicillium. Signs that an infant may have mold-related respiratory problems include (but are not limited to) a persistent cough and/or wheeze. Increased exposure increases the probability of developing respiratory symptoms during their first year of life. Studies have shown that a correlation exists between the probability of developing asthma and increased exposure to "Penicillium". The levels are deemed ‘no mold’ to ‘low level’ , from ‘low’ to ‘intermediate’ , and from ‘intermediate’ to ‘high’.

Mold exposures have a variety of health effects depending on the person. Some people are more sensitive to mold than others. Exposure to mold can cause a number of health issues such as; throat irritation, nasal stuffiness, eye irritation, cough and wheezing, as well as skin irritation in some cases. Exposure to mold may also cause heightened sensitivity depending on the time and nature of exposure. People at higher risk for mold allergies are people with chronic lung illnesses, which will result in more severe reactions when exposed to mold.

There has been sufficient evidence that damp indoor environments are correlated with upper respiratory tract symptoms such as coughing, and wheezing in people with asthma.

The toxicological cause of the disease has been attributed to the neurotoxin ODAP which acts as a structural analogue of the neurotransmitter glutamate. Ingestion of legumes containing the toxin occurs, although knowledge of how to detoxify Lathyrus is present, but drought conditions can lead to fuel and water shortages preventing the necessary steps from being taken, particularly in impoverished countries. Lathyrism usually occurs where the despair of poverty and malnutrition leaves few other food options. Lathyrism can also be caused by food adulteration.

It was first described in 1924 in the vicinity of Königsberg, Germany (now Kaliningrad, Russia) on the Baltic coast, in people staying around the northern part of the Vistula Lagoon (German: "Frisches Haff").

Over the subsequent fifteen years, about 1000 cases were reported in people, birds and cats, usually in the summer and fall, and a link was made with the consumption of fish (burbot, eel and pike). Since that time, only occasional reports have appeared of the condition, mostly from the Soviet Union and Germany.

In 1997, six cases of Haff disease were reported in California and Missouri, all after the consumption of buffalo fish ("Ictiobus cyprinellus").

In July and August 2010, dozens of people contracted rhabdomyolysis after eating "Procambarus clarkii" in Nanjing, China. A month later, the Chinese authorities claimed they were victims of Haff disease.

An outbreak was reported in Brooklyn, New York on 18 November 2011, when two household members were stricken by the syndrome after eating buffalo fish. On February 4, 2014 two cases of Haff Disease were reported in Cook County, Illinois following the consumption of buffalo fish.

A group from Brazil has recently identified a Haff Disease outbreak in Bahia state with 71 cases identified.

Milk sickness, also known as tremetol vomiting or, in animals, as trembles, is a kind of poisoning, characterized by trembling, vomiting, and severe intestinal pain, that affects individuals who ingest milk, other dairy products, or meat from a cow that has fed on white snakeroot plant, which contains the poison tremetol.

Although very rare today, milk sickness claimed thousands of lives among migrants to the Midwest in the early 19th century in the United States, especially in frontier areas along the Ohio River Valley and its tributaries where white snakeroot was prevalent. New settlers were unfamiliar with the plant and its properties. A notable victim was Nancy Hanks Lincoln, the mother of Abraham Lincoln, who died in 1818. Nursing calves and lambs may have died from their mothers' milk contaminated with snakeroot, although the adult cows and sheep showed no signs of poisoning. Cattle, horses, and sheep are the animals most often poisoned.

Anna Pierce Hobbs Bixby, called Dr. Anna on the frontier, is credited today by the American medical community with having identified white snakeroot as the cause of the illness. Told about the plant's properties by an elderly Shawnee woman she befriended, Bixby did testing to observe and document evidence. She wrote up her findings to share the discovery in the medical world. The Shawnee woman's name has been lost to history.

Shortly after the incident, in September 1951, scientists writing in the "British Medical Journal" declared that “the outbreak of poisoning” was due to eating bread made from rye grain that was infected with the fungus. The victims appeared to have one common connection. They had eaten bread from the bakery of Roch Briand who was subsequently blamed for using flour made from rye.