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.

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.

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.

Estrogen birth control pills may increase the amount of copper in humans, but was not shown to increase absorption. Copper Intrauterine devices (IUDs) have been questioned anecdotally, with people claiming copper toxicity, but there is currently no scientific evidence to substantiate this claim. Estrogen increases the absorption of copper, making women more likely to carry excess copper even when no birth control is used.

The amount of estrogen (or copper) contained in these modern forms of contraception are generally considered safe, and the former restrictions for estrogen use (not to be used by women older than 40, 35 for smokers) were lifted in 1989.

There are conditions in which an individual's copper metabolism is compromised to such an extent that birth control may cause an issue with copper accumulation. They include toxicity or just increased copper from other sources, as well as the increased copper level of the individual's mother via the placenta before birth. The two hormones commonly used in birth control, estrogen and progestin, protect from each other's complications, so a combination method may work best. At least when existing imbalances have been treated.

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.

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)

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.

The EPA lists no evidence for human cancer incidence connected with copper, and lists animal evidence linking copper to cancer as "inadequate". Two studies in mice have shown no increased incidence of cancer. One of these used regular injections of copper compounds, including cupric oxide. One study of two strains of mice fed copper compounds found a varying increased incidence of reticulum cell sarcoma in males of one strain, but not the other (there was a slightly increased incidence in females of both strains). These results have not been repeated.

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.

Tin has no known natural biological role in living organisms. It is not easily absorbed by animals and humans. The low toxicity is relevant to the widespread use of tin in dinnerware and canned food. Nausea, vomiting and diarrhea have been reported after ingesting canned food containing 200 mg/kg of tin. This observation led, for example, the Food Standards Agency in the UK to propose upper limits of 200 mg/kg. A study showed that 99.5% of the controlled food cans contain tin in an amount below that level. However un-lacquered tin cans with food of a low pH for example fruits and pickled vegetables can contain elevated concentrations of tin.

The toxic effects of tin compounds is based on the interference with the iron and copper metabolism. For example, it affects heme and cytochrome P450, and decreases their effectiveness.

Organotin compounds can be very toxic. "Tri-"n"-alkyltins" are phytotoxic and, depending on the organic groups, can be powerful bactericides and fungicides. Other triorganotins are used as miticides and acaricides.

Tributyltin (TBT) was extensively used in marine antifouling paints, until discontinued for leisure craft due to concerns over longer term marine toxicity in high traffic areas such as marinas with large numbers of static boats.

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.

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.

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.

Tin poisoning refers to the toxic effects of tin and its compounds. Cases of poisoning from tin metal, its oxides, and its salts are "almost unknown"; on the other hand certain organotin compounds are almost as toxic as cyanide.

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.

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.

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.

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.

Those routes include contaminated air, water, soil, and food, and also, for birds ingestion of grit (lead shots, lead bullets).ingestion of paints,materials that are left out from the factories like batteries etc.

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.

A toxic heavy metal is any relatively dense metal or metalloid that is noted for its potential toxicity, especially in environmental contexts. The term has particular application to cadmium, mercury, lead and arsenic, all of which appear in the World Health Organisation's list of 10 chemicals of major public concern. Other examples include manganese, chromium, cobalt, nickel, copper, zinc, selenium, silver, antimony and thallium.

Heavy metals are found naturally in the earth. They become concentrated as a result of human caused activities and can enter plant, animal, and human tissues via inhalation, diet, and manual handling. Then, they can bind to and interfere with the functioning of vital cellular components. The toxic effects of arsenic, mercury, and lead were known to the ancients, but methodical studies of the toxicity of some heavy metals appear to date from only 1868. In humans, heavy metal poisoning is generally treated by the administration of chelating agents. Some elements otherwise regarded as toxic heavy metals are essential, in small quantities, for human health.

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.

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

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.

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".