Plants that produce toxins and/or cause irritation on contact are referred to as poisonous plants.^[1] The toxins in poisonous plants affect herbivores, and deter them from consuming the plants. Plants cannot move to escape their predators, so they must have other means of protecting themselves from herbivorous animals. Some plants have physical defenses such as thorns, spines and prickles, but by far the most common type of protection is chemical.^[2]

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Over millennia, through the process of natural selection, plants have evolved the means to produce a vast and complicated array of chemical compounds to deter herbivores. Tannin, for example, is a defensive compound that emerged relatively early in the evolutionary history of plants, while more complex molecules such as polyacetylenes are found in younger groups of plants such as the Asterales. Many of the known plant defense compounds primarily defend against consumption by insects, though other animals, including humans, that consume such plants may also experience negative effects, ranging from mild discomfort to death.

Many of these poisonous compounds also have important medicinal benefits.^[3] The varieties of phytochemical defenses in plants are so numerous that many questions about them remain unanswered, including:

1. Which plants have which types of defense?
2. Which herbivores, specifically, are the plants defended against?
3. What chemical structures and mechanisms of toxicity are involved in the compounds that provide defense?
4. What are the potential medical uses of these compounds?

These questions and others constitute an active area of research in modern botany, with important implications for understanding plant evolution and medical science.

Below is an extensive, if incomplete, list of plants containing one or more poisonous parts that pose a serious risk of illness, injury, or death to humans or domestic animals. There is significant overlap between plants considered poisonous and those with psychotropic properties, some of which are toxic enough to present serious health risks at recreational doses. There is a distinction between plants that are poisonous because they naturally produce dangerous phytochemicals, and those that may become dangerous for other reasons, including but not limited to infection by bacterial, viral, or fungal parasites; the uptake of toxic compounds through contaminated soil or groundwater; and/or the ordinary processes of decay after the plant has died; this list deals exclusively with plants that produce phytochemicals. Many plants, such as peanuts, produce compounds that are only dangerous to people who have developed an allergic reaction to them, and with a few exceptions, those plants are not included here (see list of allergens instead). Despite the wide variety of plants considered poisonous, human fatalities caused by poisonous plants – especially resulting from accidental ingestion – are rare in the developed world.^[4]

Many plants commonly used as food possess toxic parts, are toxic unless processed, or are toxic at certain stages of their lives. Some only pose a serious threat to certain animals (such as cats, dogs, or livestock) or certain types of people (such as infants, the elderly, or the immunocompromised). Most of these food plants are safe for the average adult to eat in modest quantities. Notable examples include:

More information Scientific name, Common name(s) ...

Scientific name	Common name(s)	Family	Description	Picture
Allium spp.	onion, garlic, leek, and chive	Amaryllidaceae	Many members of the genus Allium contain thiosulphate, which in high doses is toxic to dogs, cats, and some types of livestock. Cats are more sensitive.[5]
Asparagus spp.	asparagus	Asparagaceae	Several species including Asparagus officinalis and Asparagus densiflorus. Though asparagus plants cultivated for food are typically harvested before they reach reproductive maturity, the berries of the mature plant are poisonous, containing furostanol and spirostanol saponins. Rapid ingestion of more than five to seven ripe berries can induce abdominal pain and vomiting. Sulfur compounds in the young shoots are also considered at least partially responsible for mild skin reactions in some people who handle the plant.[6]
Blighia sapida	ackee	Sapindaceae	The seeds, unripened arils, and inedible portions of the ackee fruit contain the toxins hypoglycin A and hypoglycin B, which inhibit enzymes involved in fatty acid metabolism and thereby cause a depletion of stored glucose in order to meet the body's energy needs, leading to hypoglycemia.[7]
Citrus spp.	lemon, lime, grapefruit, orange, etc.	Rutaceae	Most citrus fruits, including lemon (Citrus limon), lime, and orange (Citrus × sinensis), among others, are known to contain aromatic oils, the terpenes limonene and linalool, and the furanocoumarin psoralen, which are toxic to dogs, cats, and other animals.[8][9][10] The concentration and distribution of these compounds can vary widely by species, but they are often concentrated in the fleshy rinds.[9] Symptoms include vomiting, diarrhea, depression, and photosensitivity. Citrus essential oils do not appear to be toxic to humans.[11][12]
Lathyrus sativus	Indian pea, grass pea, chickling pea, white pea	Fabaceae	A legume grown in Asia and East Africa as an insurance crop for use during famines. Like other grain legumes, L. sativus produces a high-protein seed. The seeds contain variable amounts of β-N-Oxalyl-L-α,β-diaminopropionic acid (ODAP), a neurotoxic amino acid.[13] ODAP causes wasting and paralysis if eaten over a long period, and is considered the cause of the disease neurolathyrism, a neurodegenerative disease that causes paralysis of the lower body and emaciation of gluteal muscle (buttocks). The disease has been seen to occur after famines in Europe (France, Spain, Germany), North Africa, and South Asia, and is still prevalent in Eritrea, Ethiopia, and parts of Afghanistan when Lathyrus seed is the exclusive or main source of nutrients for extended periods.
Malus domestica	apple	Rosaceae	The seeds are mildly poisonous, containing a small amount of amygdalin, a cyanogenic glycoside.[citation needed] The quantity contained in the seeds of a single apple is usually not enough to be dangerous to humans, but it is possible to ingest enough seeds to provide a fatal dose.[citation needed]
Mangifera indica	mango	Anacardiaceae	Mango leaves, stems, peels, and sap contain urushiol, an allergen also present in poison ivy, poison oak, and poison sumac that can cause urushiol-induced contact dermatitis in susceptible people.[citation needed] Cross-reactions between mango contact allergens and urushiol have been observed. Those with a history of poison ivy or poison oak contact dermatitis may be most at risk for such an allergic reaction. During mango's primary ripening season, it is the most common source of plant dermatitis in Hawaii.
Manihot esculenta	cassava	Euphorbiaceae	Roots and leaves contain two cyanogenic glycosides, linamarin and lotaustralin. These are decomposed by linamarase, a naturally occurring enzyme in cassava, liberating hydrogen cyanide.[14] Cassava varieties are often categorized as either sweet or bitter, respectively signifying the absence or presence of toxic levels of cyanogenic glycosides. The 'sweet' cultivars can produce as little as 20 milligrams of cyanide per kilogram of fresh roots, whereas bitter ones may produce more than 50 times as much (1 g/kg). Cassavas grown during drought are especially high in these toxins.[15][16] A dose of 40 mg of pure cassava cyanogenic glycoside is sufficient to kill a cow. It can also cause severe calcific pancreatitis in humans, leading to chronic pancreatitis. Processing (soaking, cooking, fermentation, etc.) of cassava root is necessary to remove the toxins and avoid getting sick. In the tropics, where cassava farming is a major industry, "Chronic, low-level cyanide exposure is associated with the development of goiter and with tropical ataxic neuropathy, a nerve-damaging disorder that renders a person unsteady and uncoordinated. Severe cyanide poisoning, particularly during famines, is associated with outbreaks of a debilitating, irreversible paralytic disorder called konzo and, in some cases, death. The incidence of konzo and tropical ataxic neuropathy can be as high as 3 percent in some areas."[17] For some smaller-rooted sweet varieties, cooking is sufficient to eliminate all toxicity. The cyanide is carried away in the processing water and the amounts produced in domestic consumption are too small to have an environmental impact.[14] The larger-rooted, bitter varieties used for the production of flour or starch must be processed to remove the cyanogenic glycosides.[18] Industrial production of cassava flour, even at the cottage level, may generate enough cyanide and cyanogenic glycosides in the effluvia to have a severe environmental impact.[14]
Myristica fragrans	nutmeg	Myristicaceae	Contains myristicin, a naturally occurring insecticide and acaricide with possible neurotoxic effects on neuroblastoma cells.[19] It has psychoactive properties at doses much higher than used in cooking. Raw nutmeg produces anticholinergic-like symptoms, attributed to myristicin and elemicin.[20] The intoxicating effects of myristicin can lead to a physical state somewhere between waking and dreaming; euphoria is reported and nausea is often experienced. Users also report bloodshot eyes and memory disturbances.[21] Myristicin is also known to induce hallucinogenic effects, such as visual distortions. Nutmeg intoxication has an extremely long delay before peak is reached, sometimes taking up to seven hours, and effects can be felt for 24 hours, with lingering effects lasting up to 72 hours.[22][23]
Phaseolus lunatus	Lima bean, butter bean, sieva bean, double bean, Madagascar bean	Fabaceae	Raw beans contain dangerous amounts of linamarin, a cyanogenic glycoside.[citation needed]
Phaseolus vulgaris	kidney bean, common bean	Fabaceae	Phytohaemagglutinin, a toxic lectin, is present in many varieties of common bean but is especially concentrated in red kidney beans. The lectin has several effects on cell metabolism; it induces mitosis and affects the cell membrane regarding transport and permeability to proteins. It agglutinates most mammalian red blood cell types. Consumption of as few as four or five raw kidney beans may be sufficient to trigger symptoms, which include nausea, vomiting, and diarrhea. Onset is from one to three hours after consumption of improperly prepared beans, and symptoms typically resolve within a few hours.[24] Phytohaemagglutinin can be deactivated by cooking beans at 100 °C (212 °F) for ten minutes, which is required to degrade the toxin and is much shorter than the hours required to fully cook the beans themselves. For dry beans, the U.S. Food and Drug Administration (FDA) also recommends an initial soak of at least five hours in water, after which the soaking water should be discarded.[24] However, lower cooking temperatures may have the paradoxical effect of potentiating the toxic effect of haemagglutinin. Beans cooked at 80 °C (176 °F) are reported to be up to five times as toxic as raw beans.[24] Outbreaks of poisoning have been associated with the use of slow cookers, the low cooking temperatures of which may be unable to degrade the toxin.
Prunus spp.	cherry, peach, plum, apricot, almond, etc.	Rosaceae	Leaves and seeds contain amygdalin, a cyanogenic glycoside. Many other Prunus species, such as peach (Prunus persica), plum (Prunus domestica), almond (Prunus dulcis), and apricot (Prunus armeniaca), also possess poisonous parts.[citation needed]
Rheum rhaponticum	rhubarb	Polygonaceae	The leaf stalks (petioles) are edible, but the leaves themselves contain notable quantities of oxalic acid, which is a nephrotoxic and corrosive acid present in many plants. Symptoms of poisoning include kidney disorders, convulsions, and coma, though it is rarely fatal. The LD50 (median lethal dose) for pure oxalic acid in rats is about 375 mg/kg body weight,[25] or about 25 grams for a 65-kilogram (143 lb) human. Although the oxalic acid content of rhubarb leaves can vary, a typical value is about 0.5%,[26] so almost 5 kg of the extremely sour leaves would have to be consumed to reach the LD50. Cooking the leaves with soda can make them more poisonous by producing soluble oxalates.[27] However, the leaves are believed to also contain an additional, unidentified toxin,[28] which might be an anthraquinone glycoside (also known as senna glycosides).[29] In the edible leaf stalks, the concentration of oxalic acid is much lower, contributing only about 2–2.5% of the total acidity, which is dominated by malic acid.[30] This means that even the raw stalks may not be hazardous (though they are generally thought to be in the US). However, the tart taste of the raw stalks is so strong as to be unpalatable to most consumers.
Solanum lycopersicum	tomato	Solanaceae	Like many other members of the nightshade family Solanaceae, tomato leaves and stems contain solanine, a glycoalkaloid which is toxic if ingested, causing digestive upset and nervous excitement. Use of tomato leaves as an herbal tea (infusion) has been responsible for at least one death.[31] Leaves, stems, and green unripe fruit of the tomato plant also contain small amounts of the poisonous alkaloid tomatine,[32] although levels are generally too small to be dangerous.[32][33] Ripe tomatoes do not contain any detectable tomatine.[32] Tomato plants can be toxic to dogs if they eat large amounts of the fruit or chew the plant material.[34]
Solanum tuberosum	potato	Solanaceae	Potatoes contain toxic glycoalkaloids, of which the most prevalent are solanine and chaconine. Solanine is also found in other members of the Solanaceae plant family, which includes Solanum lycopersicum (tomato), Atropa belladonna (deadly nightshade), and Hyoscyamus niger (henbane) (see entries below). The concentration of glycoalkaloids in wild potatoes is sufficient to produce toxic effects in humans. The toxin affects the nervous system, causing headaches, diarrhea and intense digestive disturbances, cramps, weakness and confusion, and in severe cases coma and death. Poisoning from cultivated potatoes occurs very rarely, however, as toxic compounds in the potato plant are generally concentrated in the green portions of the plant and in the fruits, and cultivated varieties contain smaller concentrations than wild plants.[35][36] Cooking at high temperatures (over 170 °C or 340 °F) also partly destroys the toxin. However, exposure to light, physical damage, and age can increase glycoalkaloid content within the tuber,[37] with the highest concentrations occurring just underneath the skin. Tubers that are exposed to light turn green from chlorophyll synthesis, thus giving a visual clue as to areas of the tuber that may have become more toxic; however, this does not provide a definitive guide, as greening and glycoalkaloid accumulation can occur independently of each other. Some varieties of potato contain greater glycoalkaloid concentrations than others; breeders developing new cultivars try to keep solanine levels below 200 mg/kg (200 ppmw). However, when these commercial varieties turn green, even they can approach solanine concentrations of 1000 mg/kg (1000 ppmw). The U.S. National Toxicology Program suggests that the average American consume no more than 12.5 mg/day of solanine from potatoes (the toxic dose is several times this, depending on body weight).
Vitis spp.	grape	Vitaceae	Potentially toxic to dogs, although the precise mechanism is not fully understood.[citation needed] See grape and raisin toxicity in dogs.

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Countless other plants not commonly used in food or drink are also poisonous, and care should be taken to avoid accidentally contacting or ingesting them. Some of these are popular ornamental plants or are cultivated for purposes other than consumption.

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• List of psychoactive plants
• List of poisonous fungus species
• List of venomous animals
• Biopesticide
• Mushroom poisoning
• Secondary metabolite
• Toxin
• Weed