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.

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.

Some of the toxic effects of mercury are partially or wholly reversible, either through specific therapy or through natural elimination of the metal after exposure has been discontinued. Autopsy findings point to a half-life of inorganic mercury in human brains of 27.4 years. Heavy or prolonged exposure can do irreversible damage, in particular in fetuses, infants, and young children. Young's syndrome is believed to be a long-term consequence of early childhood mercury poisoning.

Mercuric chloride may cause cancer as it has caused increases in several types of tumors in rats and mice, while methyl mercury has caused kidney tumors in male rats. The EPA has classified mercuric chloride and methyl mercury as possible human carcinogens (ATSDR, EPA)

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.

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.

Methylmercury is the major source of organic mercury for all individuals. Due to bioaccumulation it works its way up through the food web and thus biomagnifies, resulting in high concentrations among populations of some species. Top predatory fish, such as tuna or swordfish, are usually of greater concern than smaller species. The US FDA and the EPA advise women of child-bearing age, nursing mothers, and young children to completely avoid swordfish, shark, king mackerel and tilefish from the Gulf of Mexico, and to limit consumption of albacore ("white") tuna to no more than per week, and of all other fish and shellfish to no more than per week. A 2006 review of the risks and benefits of fish consumption found, for adults, the benefits of one to two servings of fish per week outweigh the risks, even (except for a few fish species) for women of childbearing age, and that avoidance of fish consumption could result in significant excess coronary heart disease deaths and suboptimal neural development in children.

The period between exposure to methylmercury and the appearance of symptoms in adult poisoning cases is long. The longest recorded latent period is five months after a single exposure, in the Dartmouth case (see History); other latent periods in the range of weeks to months have also been reported. No explanation for this long latent period is known. When the first symptom appears, typically paresthesia (a tingling or numbness in the skin), it is followed rapidly by more severe effects, sometimes ending in coma and death. The toxic damage appears to be determined by the peak value of mercury, not the length of the exposure.

Methylmercury exposure during rodent gestation, a developmental period that approximately models human neural development during the first two trimesters of gestation, has long-lasting behavioral consequences that appear in adulthood and, in some cases, may not appear until aging. Prefrontal cortex or dopamine neurotransmission could be especially sensitive to even subtle gestational methylmercury exposure and suggests that public health assessments of methylmercury based on intellectual performance may underestimate the impact of methylmercury in public health.

Ethylmercury is a breakdown product of the antibacteriological agent ethylmercurithiosalicylate, which has been used as a topical antiseptic and a vaccine preservative (further discussed under Thiomersal below). Its characteristics have not been studied as extensively as those of methylmercury. It is cleared from the blood much more rapidly, with a half-life of seven to 10 days, and it is metabolized much more quickly than methylmercury. It is presumed not to have methylmercury's ability to cross the blood–brain barrier via a transporter, but instead relies on simple diffusion to enter the brain. Other exposure sources of organic mercury include phenylmercuric acetate and phenylmercuric nitrate. These compounds were used in indoor latex paints for their antimildew properties, but were removed in 1990 because of cases of toxicity.

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.

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.

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.

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.

Heavy metals "can bind to vital cellular components, such as structural proteins, enzymes, and nucleic acids, and interfere with their functioning". Symptoms and effects can vary according to the metal or metal compound, and the dose involved. Broadly, long-term exposure to toxic heavy metals can have carcinogenic, central and peripheral nervous system and circulatory effects. For humans, typical presentations associated with exposure to any of the "classical" toxic heavy metals, or chromium (another toxic heavy metal) or arsenic (a metalloid), are shown in the table.

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.

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.

It is difficult to differentiate the effects of low level metal poisoning from the environment with other kinds of environmental harms, including nonmetal pollution. Generally, increased exposure to heavy metals in the environment increases risk of developing cancer.

Without a diagnosis of metal toxicity and outside of evidence-based medicine, but perhaps because of worry about metal toxicity, some people seek chelation therapy to treat autism, cardiovascular disease, Alzheimer's disease, or any sort of neurodegeneration. Chelation therapy does not improve outcomes for those diseases.

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.

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.

Even though zinc is an essential requirement for a healthy body, excess zinc can be harmful, and cause zinc toxicity. Such toxicity levels have been seen to occur at ingestion of greater than 225 mg of Zinc. Excessive absorption of zinc can suppress copper and iron absorption. The free zinc ion in solution is highly toxic to bacteria, plants, invertebrates, and even vertebrate fish.

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.

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.

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.

Decontamination of people exposed to hydrogen cyanide gas only requires removal of the outer clothing and the washing of their hair. Those exposed to liquids or powders generally require full decontamination.

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.

Acute hydrogen cyanide poisoning can result from inhalation of fumes from burning polymer products that use nitrile in their production, such as polyurethane, or vinyl. It can also be caused by breakdown of nitroprusside into nitric oxide and cyanide. Nitroprusside may be used during treatment of hypertensive crisis.

In addition to its uses as a pesticide and insecticide, cyanide is contained in tobacco smoke and smoke from building fires, and is present in many seeds or kernels such as those of almonds, apricots, apples, oranges, and in foods including cassava (also known as yuca or manioc), and bamboo shoots. Vitamin B12, in the form of hydroxocobalamin (also spelled hydroxycobalamin), may reduce the negative effects of chronic exposure, and a deficiency can lead to negative health effects following exposure.

Cows and horses as well as pet animals are also susceptible to the effects of lead toxicity. Sources of lead exposure in pets can be the same as those that present health threats to humans sharing the environment, such as paint and blinds, and there is sometimes lead in toys made for pets. Lead poisoning in a pet dog may indicate that children in the same household are at increased risk for elevated lead levels.

Increased concentrations of urinary beta-2 microglobulin can be an early indicator of renal dysfunction in persons chronically exposed to low but excessive levels of environmental cadmium. The urinary beta-2 microglobulin test is an indirect method of measuring cadmium exposure. Under some circumstances, the Occupational Health and Safety Administration requires screening for renal damage in workers with long-term exposure to high levels of cadmium. Blood or urine cadmium concentrations provide a better index of excessive exposure in industrial situations or following acute poisoning, whereas organ tissue (lung, liver, kidney) cadmium concentrations may be useful in fatalities resulting from either acute or chronic poisoning. Cadmium concentrations in healthy persons without excessive cadmium exposure are generally less than 1 μg/L in either blood or urine. The ACGIH biological exposure indices for blood and urine cadmium levels are 5 μg/L and 5 μg/g creatinine, respectively, in random specimens. Persons who have sustained renal damage due to chronic cadmium exposure often have blood or urine cadmium levels in a range of 25-50 μg/L or 25-75 μg/g creatinine, respectively. These ranges are usually 1000-3000 μg/L and 100-400 μg/g, respectively, in survivors of acute poisoning and may be substantially higher in fatal cases.