Zhu Ling (, born 1973) is best known as the victim of an unsolved 1995 thallium poisoning case in Beijing, China. Her symptoms were posted to the Internet via a Usenet newsgroup by her friend from Peking University, Bei Zhicheng and were subsequently proven to be caused by thallium poisoning. Her case was then reviewed by physicians in many different countries who examined her symptoms and made suggestions as to diagnoses and treatment. This effort was recognized as the first large scale tele-medicine trial. Her life was ultimately saved, but she suffered serious neurological damage and permanent physical impairment.

This case drew great attention in the Chinese media, because the victim and the suspect were living in the same dormitory in the most prestigious university of China, and the case was never solved. Internet discussion of the crime has continued since then and became a hot topic on major online Chinese communities very frequently as a high-profile cold case.

In Chinese alchemy, elixir poisoning refers to the toxic effects from elixirs of immortality that contained metals and minerals such as mercury and arsenic. The official "Twenty-Four Histories" record numerous Chinese emperors, nobles, and officials who ironically died from taking elixirs in order to prolong their lifespans. The first emperor to die from elixir poisoning was likely Qin Shi Huang (d. 210 BCE) and the last was Yongzheng (d. 1735). Despite common knowledge that immortality potions could be deadly, fangshi and Daoist alchemists continued the elixir-making practice for two millennia.

, sometimes referred to as , is a neurological syndrome caused by severe mercury poisoning. Symptoms include ataxia, numbness in the hands and feet, general muscle weakness, loss of peripheral vision, and damage to hearing and speech. In extreme cases, insanity, paralysis, coma, and death follow within weeks of the onset of symptoms. A congenital form of the disease can also affect fetuses in the womb.

Minamata disease was first discovered in Minamata city in Kumamoto prefecture, Japan, in 1956. It was caused by the release of methylmercury in the industrial wastewater from the Chisso Corporation's chemical factory, which continued from 1932 to 1968. This highly toxic chemical bioaccumulated in shellfish and fish in Minamata Bay and the Shiranui Sea, which, when eaten by the local populace, resulted in mercury poisoning. While cat, dog, pig, and human deaths continued for 36 years, the government and company did little to prevent the pollution. The animal effects were severe enough in cats that they came to be named as having "dancing cat fever".

As of March 2001, 2,265 victims had been officially recognised as having Minamata disease (1,784 of whom had died) and over 10,000 had received financial compensation from Chisso. By 2004, Chisso Corporation had paid $86 million in compensation, and in the same year was ordered to clean up its contamination. On March 29, 2010, a settlement was reached to compensate as-yet uncertified victims.

A second outbreak of Minamata disease occurred in Niigata Prefecture in 1965. The original Minamata disease and Niigata Minamata disease are considered two of the four big pollution diseases of Japan.

The outbreak began in July 1518 when a woman, Mrs. Troffea, began to dance fervently in a street in Strasbourg. This lasted somewhere between four and six days. Within a week, 34 others had joined, and within a month, there were around 400 dancers, predominantly female. Some of these people would die from heart attacks, strokes, or exhaustion. One report indicates that for a period, the plague killed around fifteen people per day.

Historical documents, including "physician notes, cathedral sermons, local and regional chronicles, and even notes issued by the Strasbourg city council" are clear that the victims danced. It is not known why these people danced, some even to their deaths.

As the dancing plague worsened, concerned nobles sought the advice of local physicians, who ruled out astrological and supernatural causes, instead announcing that the plague was a "natural disease" caused by "hot blood". However, instead of prescribing bleeding, authorities encouraged more dancing, in part by opening two guildhalls and a grain market, and even constructing a wooden stage. The authorities did this because they believed that the dancers would recover only if they danced continuously night and day. To increase the effectiveness of the cure, authorities even paid for musicians to keep the afflicted moving.

Historian John Waller stated that a marathon runner could not have lasted the intense workout that these men and women did hundreds of years ago.

The 1858 Bradford sweets poisoning was the arsenic poisoning of more than 200 people in Bradford, England, when sweets accidentally made with arsenic were sold from a market stall. Twenty-one victims died as a result. The event contributed to the passage of the Pharmacy Act 1868 in the United Kingdom and legislation regulating the adulteration of foodstuffs.

The Dancing Plague (or Dance Epidemic) of 1518 was a case of dancing mania that occurred in Strasbourg, Alsace, (then part of the Holy Roman Empire) in July 1518. Around 400 people took to dancing for days without rest and, over the period of about one month, some of those affected collapsed or even died of heart attack, stroke, or exhaustion.

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.

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.

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.

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.

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

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

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

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

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

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

Yunnan sudden death syndrome is a label used to define unexplained cases of cardiac arrest, which afflicted significant numbers of rural villagers in Yunnan province, in southwest China. Cases occurred almost always during the midsummer rainy season (from June to August), at an altitude of . The cause turned out to be a mushroom now blamed for an estimated 400 deaths in the past three decades.

The mysterious fatalities were recorded for decades before researchers from the Chinese Center for Disease Control and Prevention isolated a significant factor common in every case: a tiny unknown mushroom which was unintentionally gathered and consumed during wild mushroom harvests in the region. Previously the syndrome was thought to be caused by Keshan disease, caused by the Coxsackie virus.

The mushroom, "Trogia venenata", is also known as 'Little White'. It has been determined that families collecting fungi to sell have been eating these Little White mushrooms as they have no commercial value. Three amino acids present in the mushrooms have been shown to be toxic. The mushrooms have also been shown to contain very high quantities of barium, and it may be that some of the deaths are simply from barium poisoning.

In the hours before death, about two-thirds of the victims had such symptoms as nausea, dizziness, heart palpitations, seizures and fatigue.

However, in December 2012 it was announced that Dr Xu Jianping (徐建平) has been collecting samples of "Trogia venenata" in Yunnan for the past three years, and his research now shows that barium levels in the wild mushroom are no higher than those of common foods such as poultry and fish. Nonetheless, it appears the mushroom will still likely play a role. Since publication of the widely circulated 2010 "Science" article, no instances of Yunnan sudden death syndrome have been reported.

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

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

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.

Since lead has been used widely for centuries, the effects of exposure are worldwide. Environmental lead is ubiquitous, and everyone has some measurable blood lead level. Atmospheric lead pollution increased dramatically beginning in the 1950s as a result of the widespread use of leaded gasoline. Lead is one of the largest environmental medicine problems in terms of numbers of people exposed and the public health toll it takes. Lead exposure accounts for about 0.2% of all deaths and 0.6% of disability adjusted life years globally.

Although regulation reducing lead in products has greatly reduced exposure in the developed world since the 1970s, lead is still allowed in products in many developing countries. In all countries that have banned leaded gasoline, average blood lead levels have fallen sharply. However, some developing countries still allow leaded gasoline, which is the primary source of lead exposure in most developing countries. Beyond exposure from gasoline, the frequent use of pesticides in developing countries adds a risk of lead exposure and subsequent poisoning. Poor children in developing countries are at especially high risk for lead poisoning. Of North American children, 7% have blood lead levels above 10 μg/dL, whereas among Central and South American children, the percentage is 33 to 34%. About one fifth of the world's disease burden from lead poisoning occurs in the Western Pacific, and another fifth is in Southeast Asia.

In developed countries, people with low levels of education living in poorer areas are most at risk for elevated lead. In the US, the groups most at risk for lead exposure are the impoverished, city-dwellers, and immigrants. African-American children and those living in old housing have also been found to be at elevated risk for high blood lead levels in the US. Low-income people often live in old housing with lead paint, which may begin to peel, exposing residents to high levels of lead-containing dust.

Risk factors for elevated lead exposure include alcohol consumption and smoking (possibly because of contamination of tobacco leaves with lead-containing pesticides). Adults with certain risk factors might be more susceptible to toxicity; these include calcium and iron deficiencies, old age, disease of organs targeted by lead (e.g. the brain, the kidneys), and possibly genetic susceptibility.

Differences in vulnerability to lead-induced neurological damage between males and females have also been found, but some studies have found males to be at greater risk, while others have found females to be.

In adults, blood lead levels steadily increase with increasing age. In adults of all ages, men have higher blood lead levels than women do. Children are more sensitive to elevated blood lead levels than adults are. Children may also have a higher intake of lead than adults; they breathe faster and may be more likely to have contact with and ingest soil. Children of ages one to three tend to have the highest blood lead levels, possibly because at that age they begin to walk and explore their environment, and they use their mouths in their exploration. Blood levels usually peak at about 18–24 months old. In many countries including the US, household paint and dust are the major route of exposure in children.

Outcome is related to the extent and duration of lead exposure. Effects of lead on the physiology of the kidneys and blood are generally reversible; its effects on the central nervous system are not. While peripheral effects in adults often go away when lead exposure ceases, evidence suggests that most of lead's effects on a child's central nervous system are irreversible. Children with lead poisoning may thus have adverse health, cognitive, and behavioral effects that follow them into adulthood.

The distinction between Hua () and Yi (), also known as Sino–barbarian dichotomy, is an ancient Chinese concept that differentiated a culturally defined "China" (called Hua, Huaxia 華夏, or Xia 夏) from cultural or ethnic outsiders (Yi "barbarians"). Although Yi is often translated as "barbarian", other translations of this term in English include "foreigners",

"ordinary others" "wild tribes", and "uncivilized tribes."

The Hua–Yi distinction asserted Chinese superiority, but implied that outsiders could become "Hua" by adopting Chinese values and customs.

The etymology of English elixir derives from Medieval Latin "", from Arabic ("al-ʾiksīr"), probably from Ancient Greek ("xḗrion" "a desiccative powder for wounds"). "Elixir" originated in medieval European alchemy meaning "A preparation by the use of which it was sought to change metals into gold" (elixir stone or philosopher's stone) or "A supposed drug or essence with the property of indefinitely prolonging life" (elixir of life). The word was figuratively extended to mean "A sovereign remedy for disease. Hence adopted as a name for quack medicines" (e.g., Daffy's Elixir) and "The quintessence or soul of a thing; its kernel or secret principle". In modern usage, "elixir" is a pharmaceutical term for "A sweetened aromatic solution of alcohol and water, serving as a vehicle for medicine" ("Oxford English Dictionary", 2nd ed., 2009). Outside of Chinese cultural contexts, English "elixir poisoning" usually refers to accidental contamination, such as the 1937 Elixir sulfanilamide mass poisoning in the United States.

"Dān" 丹 "cinnabar; vermillion; elixir; alchemy" is the keyword for Chinese immortality elixirs. The red mineral cinnabar ("dānshā" 丹砂 lit. "cinnabar sand") was anciently used to produce the pigment vermilion ("zhūhóng" 朱紅) and the element mercury ("shuǐyín" 水銀 "watery silver" or "gǒng" 汞).

According to the "ABC Etymological Dictionary of Old Chinese", the etymology of Modern Standard Chinese "dān" from Old Chinese "*tān" (< *"tlan" ?) 丹 "red; vermillion; cinnabar", "gān" 矸 in "dāngān" 丹矸 from *"tân-kân" (< *"tlan-klan" ?) "cinnabar; vermillion ore", and "zhān" from *"tan" 旃 "a red flag" derive from Proto-Kam-Sui *"h-lan" "red" or Proto-Sino-Tibetan *"tja-n" or *"tya-n" "red". The *"t-" initial and *"t-" or *"k-" doublets indicate that Old Chinese borrowed this item. (Schuessler 2007: 204).

Although the word "dan" 丹 "cinnabar; red" frequently occurs in oracle script from the late Shang Dynasty (ca. 1600-1046 BCE) and bronzeware script and seal script from the Zhou Dynasty (1045-256 BCE), paleographers disagree about the graphic origins of the logograph 丹 and its ancient variants 𠁿 and 𠕑. Early scripts combine a 丶 dot or ⼀ stroke (depicting a piece of cinnabar) in the middle of a surrounding frame, which is said to represent:

- "jǐng" 井 "well" represents the mine from which the cinnabar is taken" ("Shuowen Jiezi")

- "the crucible of the Taoist alchemists" (Léon Wieger )

- "the contents of a square receptacle" (Bernhard Karlgren)

- "placed in a tray or palette to be used as red pigment" (Wang Hongyuan 王宏源)

- "mineral powder on a stretched filter-cloth" (Needham and Lu).

Many Chinese elixir names are compounds of "dan", such as "jīndān" 金丹 (with "gold") meaning "golden elixir; elixir of immortality; potable gold" and "xiāndān" 仙丹 (with "Daoist immortal") "elixir of immortality; panacea", and "shéndān" 神丹 (with "spirit; god") "divine elixir". "Bùsǐ zhī yào" 不死之藥 "drug of deathlessness" was another early name for the elixir of immortality. Chinese alchemists would "liàndān" 煉丹 (with "smelt; refine") "concoct pills of immortality" using a "dāndǐng" 丹鼎 (with "tripod cooking vessel; cauldron") "furnace for concocting pills of immortality". In addition, the ancient Chinese believed that other substances provided longevity and immortality, notably the "língzhī" 靈芝 ""Ganoderma" mushroom".

The transformation from chemistry-based "waidan" 外丹 "external elixir/alchemy" to physiology-based "neidan" 內丹 "internal elixir/alchemy" gave new analogous meanings to old terms. The human body metaphorically becomes a "ding" "cauldron" in which the adept forges the Three Treasures (essence, life-force, and spirit) within the "jindan" Golden Elixir within the "dāntián" 丹田 (with "field") "lower part of the abdomen".

In early China, alchemists and pharmacists were one in the same. Traditional Chinese Medicine also used less concentrated cinnabar and mercury preparations, and "dan" means "pill; medicine" in general, for example, "dānfāng" 丹方 semantically changed from "prescription for elixir of immortality" to "medical prescription". "Dan" was lexicalized into medical terms such as " dānjì" 丹劑 "pill preparation" and "dānyào" 丹藥 "pill medicine".

The Chinese names for immortality elixirs have parallels in other cultures and languages, for example, Indo-Iranian "soma" or "haoma", Sanskrit "amrita", and Greek "ambrosia".

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.

Ergotism (pron. ) is the effect of long-term ergot poisoning, traditionally due to the ingestion of the alkaloids produced by the "Claviceps purpurea" fungus that infects rye and other cereals, and more recently by the action of a number of ergoline-based drugs. It is also known as ergotoxicosis, ergot poisoning and Saint Anthony's Fire. Ergot poisoning is a proposed explanation of bewitchment.

OP pesticide exposure occurs through inhalation, ingestion and dermal contact. Because OP pesticides disintegrate quickly in air and light, they have been considered relatively safe to consumers. However, OP residues linger on fruits and vegetables. Certain OP pesticides have been banned for use on some crops, for example methyl parathion is banned from use on some crops while permitted on others.

The Environmental Working Group has developed lists for concerned consumers, identifying crops with the highest pesticide residue quantities and the lowest. The "Dirty Dozen" crops are updated yearly and in 2012 included apples, celery, sweet bell peppers, peaches, strawberries, imported nectarines, grapes, spinach, lettuce, cucumbers, domestic blueberries and potatoes. Forty-five fruits and vegetables are listed by the Environmental Working Group as being regularly found with pesticide residue associated with OPs.

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.

The International Agency for Research on Cancer (IARC), found that organophosphates may possibly increased cancer risk. Tetrachlorvinphos and parathion were classified as "possibly carcinogenic", malathion, and diazinon.

The mortality rates from AAlPP vary from 40 to 80 percent. The actual numbers of cases may be much larger, as less than five percent of those with AAlPP eventually reach a tertiary care center. Since 1992, when aluminium phosphide became freely available in the market, it had, reportedly, overtaken all other forms of deliberate poisoning, such as organophosphorus and barbiturate poisoning, in North India. In a 25-year-long study on 5,933 unnatural deaths in northwest India, aluminium phosphide poisoning was found to be the major cause of death among all cases of poisonings.

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.