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.

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.

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.

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

The toxicity of aluminium phosphide is attributed to the liberation of phosphine gas, a cytotoxic compound that causes free radical mediated injury, inhibits vital cellular enzymes and is directly corrosive to tissues. The following reaction releases phosphine when AlP reacts with water in the body:

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.

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.

Many over-the-counter and prescription-only medications contain paracetamol. Because of its wide availability paired with comparably high toxicity, (compared to ibuprofen and aspirin) there is a much higher potential for overdose. Paracetamol toxicity is one of the most common causes of poisoning worldwide. In the United States, the United Kingdom, Australia, and New Zealand, paracetamol is the most common cause of drug overdoses. Additionally, in both the United States and the United Kingdom it is the most common cause of acute liver failure.

In England and Wales an estimated 41,200 cases of paracetamol poisoning occurred in 1989 to 1990, with a mortality of 0.40%. It is estimated that 150 to 200 deaths and 15 to 20 liver transplants occur as a result of poisoning each year in England and Wales. Paracetamol overdose results in more calls to poison control centers in the US than overdose of any other pharmacological substance, accounting for more than 100,000 calls, as well as 56,000 emergency room visits, 2,600 hospitalizations, and 458 deaths due to acute liver failure per year. A study of cases of acute liver failure between November 2000 and October 2004 by the Centers for Disease Control and Prevention in the USA found that paracetamol was the cause of 41% of all cases in adults, and 25% of cases in children.

Treatment for antifreeze poisoning needs to be started as soon after ingestion as possible to be effective; the earlier treatment is started, the greater the chance of survival. Cats must be treated within 3 hours of ingesting of antifreeze to be effective, while dogs must be treated within 8–12 hours of ingestion. Once kidney failure develops, the prognosis is poor.

Generally, if the patient is treated and survives then a full recovery is expected. Patients who present early to medical facilities and have prompt medical treatment typically will have a favorable outcome. Alternatively, patients presenting late with signs and symptoms of coma, hyperkalemia, seizures, or severe acidosis have a poor prognosis. Patients who develop severe central nervous system manifestations or stroke who survive may have long term neurologic dysfunction; in some cases they may recover, although convalescence may be prolonged. The most significant long-term complication is related to the kidneys. Cases of permanent kidney damage, often requiring chronic dialysis or kidney transplantation, have been reported after severe poisoning.

The mortality rate from paracetamol overdose increases two days after the ingestion, reaches a maximum on day four, and then gradually decreases. Acidosis is the most important single indicator of probable mortality and the need for transplantation. A mortality rate of 95% without transplant was reported in patients who had a documented pH less than 7.30. Other indicators of poor prognosis include renal insufficiency (stage 3 or worse), hepatic encephalopathy, a markedly elevated prothrombin time, or an elevated blood lactic acid level (lactic acidosis). One study has shown that a factor V level less than 10% of normal indicated a poor prognosis (91% mortality), whereas a ratio of factor VIII to factor V of less than 30 indicated a good prognosis (100% survival). Patients with a poor prognosis are usually identified for likely liver transplantation. Patients that do not die are expected to fully recover and have a normal life expectancy and quality of life.

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.

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.

During the latter part of the 20th century, the number of poisonings from salicylates declined, mainly because of the increased popularity of other over-the-counter analgesics such as paracetamol (acetaminophen). Fifty-two deaths involving single-ingredient aspirin were reported in the United States in 2000; however, in all but three of these cases, the reason for the ingestion of lethal doses was intentional—predominantly suicidal.

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.

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.

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)

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.

Acute pesticide poisoning is a large-scale problem, especially in developing countries.

"Most estimates concerning the extent of acute pesticide poisoning have been based on data from hospital admissions which would include only the more serious cases. The latest estimate by a WHO task group indicates that there may be 1 million serious unintentional poisonings each year and in addition 2 million people hospitalized for suicide attempts with pesticides. This necessarily reflects only a fraction of the real problem. On the basis of a survey of self-reported minor poisoning carried out in the Asian region, it is estimated that there could be as many as 25 million agricultural workers in the developing world suffering an episode of poisoning each year." In Canada in 2007 more than 6000 cases of acute pesticide poisoning occurred.

Estimating the numbers of chronic poisonings worldwide is more difficult.

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.

Aspirin poisoning has controversially been cited as a possible cause of the high mortality rate during the 1918 flu pandemic, which killed 50 to 100 million people.

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.

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.

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.

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.