The leaves and seeds of all members of this genus are more or less edible. As a result this genus has a long history of human use both as a food source and medicinal herb. The Native American people of northwestern Mexico would steep Chenopodium leaves into a super concentrated decoction for the treatment of fevers and to remove intestinal worms. Whereas the Navajo would use members of the genus as part of a poultice to treat bruises and skin irritation. Native Americans also learned that the long taproot of Chenopodium californicum could be dried, stored and grated for use as soap. Even today many species are still gathered from the wild and cooked as potherbs, some species are also cultivated for their seeds, which have low gluten content and can be cooked similarly to rice and yet others have found use as culinary herbs.

These plants, however, can be toxic and in fact quite deadly to humans and livestock alike under the right circumstances. The potential toxic ability these plants is not so much the result of the inherently lethal chemicals that they produce naturally, as it is the result of the environmental factors present during their growth. It is true that many species in this genus contain oxalates, saponins and cyanogenic glycosides; substances that in other species of plant can naturally occur in potentially lethal amounts. In this genus, however, under healthy growing conditions, the amounts are usually in quantities too small to do any harm and to be of significance toxicologically. It is the ability of plants in this genus to uptake and hold excess nutrients (specifically nitrate) in response to adverse growing conditions or environmental stress that can make them toxic to the point of being lethal.

A quick primer on the nitrogen cycle as it relates to plant growth. Plants take nitrogen from the soil, by absorption through their roots in the form of either nitrate ions or ammonium ions. All nitrogen obtained by animals can be traced back to the eating of plants at some stage of the food chain. If nitrate is absorbed, it is first reduced to nitrite ions and then ammonium ions for incorporation into amino acids, nucleic acids, and chlorophyll; all of which are essential for plant growth. Under normal conditions the conversion of nitrate takes place at about the same rate that it is absorbed by the root system so its concentration in plant tissues will remain low. When plants are stressed, however, excess nitrate accumulation can be triggered; especially in times of drought where plant growth is restricted but absorption of nitrate from soil continues. Under normal conditions it can be expected that plants will have safe nitrate levels of under 4400 ppm, whereas plants that have suffered severe environmental stress can achieve nitrate levels as high as 70,000 ppm. Amounts over 15,000 ppm are considered to have serious potential for toxicity (University of Wisconsin), although cattle have become intoxicated when fed well-fertilized hay with nitrate concentrations as low as 8250 ppm nitrate (Ozmen et. al 2003). Other factors that can contribute to the accumulation of excess nitrate include extended periods of reduced sunlight from cloudiness or shading, injury from temperatures below 32°F which causes ice crystals form on plant leaves, extended periods of low growing temperature, acidic soils, deficiencies of essential nutrients (phosphorus, sulfur, molybdenum), and certain herbicides including 2,4-D and 2,4,5-T. It is also possible for plants to accumulate nitrate in the absence of environmental stress when more soil nitrogen is present than needed for maximum growth as would be the case in excessively fertilized soil.

Ruminants (cattle, goats, sheep) are the most likely to be affected by plants containing high levels of nitrates. When a ruminant ingests nitrates, the bacteria in the rumen convert the nitrate, to nitrite (which is 10 times more toxic than nitrate), and finally to ammonia. The ammonia is then converted to urea and either recycled to the digestive tract to form bacterial protein allowing the cycle to repeat as many times as necessary to continually convert incoming nitrate or voided in the urine. In the rumen, the reduction of nitrate to nitrite is a rapid process, whereas the detoxification of nitrite and subsequent conversion to ammonia is a much slower one. If overwhelmed, however, the rumen, unable to convert the excess nitrate at a level commensurate with its intake will allow both nitrate and nitrite to be absorbed directly through the rumen wall and into the bloodstream causing the toxicity.

Once in the bloodstream the excess nitrite will combine with hemoglobin in the red blood cells oxidizing its ferrous iron into the ferric state forming methemoglobin, which is incapable of transporting oxygen. A normal non intoxicated animal will have methemoglobin values in the range of 1 to 3 percent of hemoglobin content, but severely intoxicated animals can have levels upwards of 70 percent. Thus, when an animal dies from nitrate poisoning, it is due to multiple organ failure as a result of oxygen deprivation. The excess nitrate in the bloodstream does not, in and of itself, create toxicity problems, but can contribute to the overall syndrome when it is recycled back into the rumen via saliva or gastro-intestinal secretions where it will be converted to more toxic nitrite and reabsorbed into the bloodstream.

Nitrate reduction (and nitrite production) also occurs in the cecum (hindgut) of equids (horses, donkeys etc.), but not to the same extent as in ruminants. As a result horses are generally much more tolerant of high concentrations of nitrate. In fact nitrate poisoning is horses is considered to be very rare and is more often associated with exposure to fertilizer spills than it is with grazing on plants containing high nitrate levels.

Nitrate poisoning in ruminants can be either an acute or subacute condition and in many cases the first indication of a problem will be the discovery of a dead animal in the field. This is due to the fact that affected animals may die suddenly without appearing ill within an hour of ingesting high nitrate forage. In other cases clinical signs may persist a few hours to a few days preceding death; most often culminating in terminal anoxic convulsions due to lack of oxygen to the brain.

In most cases the symptoms of nitrate poisoning will appear suddenly as a result of tissue hypoxia and low blood pressure due to vasodilation. In the early stages of intoxication, when methemoglobin levels begin to exceed 20%, vaginal and other mucous membranes may turn from pink to a gray-brown as a result of tissue hypoxia. As the nitrite continues to be released into the blood, the levels will continue to rise. At 30 to 40 percent animals may exhibit a rapid, weak heartbeat with subnormal body temperature, muscular tremors, weakness, and ataxia (lack of voluntary coordination of muscle movements). The freshly drawn blood from an animal afflicted with nitrate poisoning will often be a dark chocolate-brown color. Once the total methemoglobin content exceeds 50%; dyspnea (air hunger/gasping), tachypnea (rapid breathing), anxiety, and frequent urination are common; seizures and death are also a likely possibility. Monogastric animals (with a single-chamber stomach such as humans, dogs, cats, horses rabbits etc.) which usually suffer intoxication from nonplant sources such as fertilizers or contaminated water may exhibit depression, inappetance, hypersalivation, moderate to severe gastrointestinal upset (vomiting, diarrhea, abdominal pain) gastric hemorrhage and possibly death.

Some animals may not exhibit adverse effects until after they have eaten high nitrate forages for days to weeks at which point the progression from clinical signs to death may be rapid. Severely intoxicated animals that develop marked dyspnea may recover only to then develop interstitial pulmonary emphysema and continued respiratory distress; many of these will recover fully within 1 to 2 weeks.

Unfortunately, the symptoms of cyanide poisoning are very similar to those of nitrate toxicity. In cases where livestock may have had access to pasture containing plants known to be a source of cyanogenic glycosides like Triglochin maritima (arrow grass), Hoecus lunatus (velvet grass), Sorghum spp (Johnson grass, Sudan grass, common sorghum), Prunus spp (apricot, peach, chokecherry, pincherry, wild black cherry), Sambucus canadensis (elderberry), Pyrus malus (apple), Zea mays (corn), and Linum spp (flax), one must determine whether nitrate or cyanide is the culprit. In the field the simplest test is to draw fresh blood, cyanide contaminated blood will generally turn a brilliant cherry red upon exposure to air, whereas methemoglobin contaminated blood will be dark brown or chocolate in color.

Nitrate accumulation also has an effect on a plants accumulation of oxalate. A number of studies have shown that nitrate can efficiently induce the accumulation of high levels of oxalates in plants. Although, how it does this is not well understood. Typically the concentrations of oxalates are 1-2%, however, nitrate accumulation can result in oxalate accumulation in excess of 20%. As a plant matures oxalate levels in the leaves will increase while the levels in the stems will decrease. Signs of oxalate intoxication may occur abruptly a few hours following the consumption of contaminated plants, and animals may die within 12 hours. There is typically a progression of symptoms from depression, weakness, tremors, weak pulse, and labored respiration to prostration, coma, and death in a few hours.

Prevention is the best medicine, if you are unsure of a plants nitrate content have it tested. If plants have been subjected to drought condition or other unusual stresses, have forage samples tested before allowing animals to graze the area.

Ozmen O, Mor F, and Ayhan U (2003) Nitrate poisoning in cattle fed Chenopodium album hay. Veterinary and Human Toxicology 45:83-84.

University of Wisconsin “Nitrate Poisoning In Cattle, Sheep and Goats”; Dan Undersander, Dave Combs, Randy Shaver, and Dave Thomas

Nitrate Toxicity: Diagnosis and Treatment; Robert Smith, DVM and Glenn Selk

The leaves and seeds of all members of this genus are more or less edible. As a result this genus has a long history of human use both as a food source and medicinal herb. The Native American people of northwestern Mexico would steep Chenopodium leaves into a super concentrated decoction for the treatment of fevers and to remove intestinal worms. Whereas the Navajo would use members of the genus as part of a poultice to treat bruises and skin irritation. Native Americans also learned that the long taproot of Chenopodium californicum could be dried, stored and grated for use as soap. Even today many species are still gathered from the wild and cooked as potherbs, some species are also cultivated for their seeds, which have low gluten content and can be cooked similarly to rice and yet others have found use as culinary herbs.

These plants, however, can be toxic and in fact quite deadly to humans and livestock alike under the right circumstances. The potential toxic ability these plants is not so much the result of the inherently lethal chemicals that they produce naturally, as it is the result of the environmental factors present during their growth. It is true that many species in this genus contain oxalates, saponins and cyanogenic glycosides; substances that in other species of plant can naturally occur in potentially lethal amounts. In this genus, however, under healthy growing conditions, the amounts are usually in quantities too small to do any harm and to be of significance toxicologically. It is the ability of plants in this genus to uptake and hold excess nutrients (specifically nitrate) in response to adverse growing conditions or environmental stress that can make them toxic to the point of being lethal.

A quick primer on the nitrogen cycle as it relates to plant growth. Plants take nitrogen from the soil, by absorption through their roots in the form of either nitrate ions or ammonium ions. All nitrogen obtained by animals can be traced back to the eating of plants at some stage of the food chain. If nitrate is absorbed, it is first reduced to nitrite ions and then ammonium ions for incorporation into amino acids, nucleic acids, and chlorophyll; all of which are essential for plant growth. Under normal conditions the conversion of nitrate takes place at about the same rate that it is absorbed by the root system so its concentration in plant tissues will remain low. When plants are stressed, however, excess nitrate accumulation can be triggered; especially in times of drought where plant growth is restricted but absorption of nitrate from soil continues. Under normal conditions it can be expected that plants will have safe nitrate levels of under 4400 ppm, whereas plants that have suffered severe environmental stress can achieve nitrate levels as high as 70,000 ppm. Amounts over 15,000 ppm are considered to have serious potential for toxicity (University of Wisconsin), although cattle have become intoxicated when fed well-fertilized hay with nitrate concentrations as low as 8250 ppm nitrate (Ozmen et. al 2003). Other factors that can contribute to the accumulation of excess nitrate include extended periods of reduced sunlight from cloudiness or shading, injury from temperatures below 32°F which causes ice crystals form on plant leaves, extended periods of low growing temperature, acidic soils, deficiencies of essential nutrients (phosphorus, sulfur, molybdenum), and certain herbicides including 2,4-D and 2,4,5-T. It is also possible for plants to accumulate nitrate in the absence of environmental stress when more soil nitrogen is present than needed for maximum growth as would be the case in excessively fertilized soil.

Ruminants (cattle, goats, sheep) are the most likely to be affected by plants containing high levels of nitrates. When a ruminant ingests nitrates, the bacteria in the rumen convert the nitrate, to nitrite (which is 10 times more toxic than nitrate), and finally to ammonia. The ammonia is then converted to urea and either recycled to the digestive tract to form bacterial protein allowing the cycle to repeat as many times as necessary to continually convert incoming nitrate or voided in the urine. In the rumen, the reduction of nitrate to nitrite is a rapid process, whereas the detoxification of nitrite and subsequent conversion to ammonia is a much slower one. If overwhelmed, however, the rumen, unable to convert the excess nitrate at a level commensurate with its intake will allow both nitrate and nitrite to be absorbed directly through the rumen wall and into the bloodstream causing the toxicity.

Once in the bloodstream the excess nitrite will combine with hemoglobin in the red blood cells oxidizing its ferrous iron into the ferric state forming methemoglobin, which is incapable of transporting oxygen. A normal non intoxicated animal will have methemoglobin values in the range of 1 to 3 percent of hemoglobin content, but severely intoxicated animals can have levels upwards of 70 percent. Thus, when an animal dies from nitrate poisoning, it is due to multiple organ failure as a result of oxygen deprivation. The excess nitrate in the bloodstream does not, in and of itself, create toxicity problems, but can contribute to the overall syndrome when it is recycled back into the rumen via saliva or gastro-intestinal secretions where it will be converted to more toxic nitrite and reabsorbed into the bloodstream.

Nitrate reduction (and nitrite production) also occurs in the cecum (hindgut) of equids (horses, donkeys etc.), but not to the same extent as in ruminants. As a result horses are generally much more tolerant of high concentrations of nitrate. In fact nitrate poisoning is horses is considered to be very rare and is more often associated with exposure to fertilizer spills than it is with grazing on plants containing high nitrate levels.

Nitrate poisoning in ruminants can be either an acute or subacute condition and in many cases the first indication of a problem will be the discovery of a dead animal in the field. This is due to the fact that affected animals may die suddenly without appearing ill within an hour of ingesting high nitrate forage. In other cases clinical signs may persist a few hours to a few days preceding death; most often culminating in terminal anoxic convulsions due to lack of oxygen to the brain.

In most cases the symptoms of nitrate poisoning will appear suddenly as a result of tissue hypoxia and low blood pressure due to vasodilation. In the early stages of intoxication, when methemoglobin levels begin to exceed 20%, vaginal and other mucous membranes may turn from pink to a gray-brown as a result of tissue hypoxia. As the nitrite continues to be released into the blood, the levels will continue to rise. At 30 to 40 percent animals may exhibit a rapid, weak heartbeat with subnormal body temperature, muscular tremors, weakness, and ataxia (lack of voluntary coordination of muscle movements). The freshly drawn blood from an animal afflicted with nitrate poisoning will often be a dark chocolate-brown color. Once the total methemoglobin content exceeds 50%; dyspnea (air hunger/gasping), tachypnea (rapid breathing), anxiety, and frequent urination are common; seizures and death are also a likely possibility. Monogastric animals (with a single-chamber stomach such as humans, dogs, cats, horses rabbits etc.) which usually suffer intoxication from nonplant sources such as fertilizers or contaminated water may exhibit depression, inappetance, hypersalivation, moderate to severe gastrointestinal upset (vomiting, diarrhea, abdominal pain) gastric hemorrhage and possibly death.

Some animals may not exhibit adverse effects until after they have eaten high nitrate forages for days to weeks at which point the progression from clinical signs to death may be rapid. Severely intoxicated animals that develop marked dyspnea may recover only to then develop interstitial pulmonary emphysema and continued respiratory distress; many of these will recover fully within 1 to 2 weeks.

Unfortunately, the symptoms of cyanide poisoning are very similar to those of nitrate toxicity. In cases where livestock may have had access to pasture containing plants known to be a source of cyanogenic glycosides like Triglochin maritima (arrow grass), Hoecus lunatus (velvet grass), Sorghum spp (Johnson grass, Sudan grass, common sorghum), Prunus spp (apricot, peach, chokecherry, pincherry, wild black cherry), Sambucus canadensis (elderberry), Pyrus malus (apple), Zea mays (corn), and Linum spp (flax), one must determine whether nitrate or cyanide is the culprit. In the field the simplest test is to draw fresh blood, cyanide contaminated blood will generally turn a brilliant cherry red upon exposure to air, whereas methemoglobin contaminated blood will be dark brown or chocolate in color.

Nitrate accumulation also has an effect on a plants accumulation of oxalate. A number of studies have shown that nitrate can efficiently induce the accumulation of high levels of oxalates in plants. Although, how it does this is not well understood. Typically the concentrations of oxalates are 1-2%, however, nitrate accumulation can result in oxalate accumulation in excess of 20%. As a plant matures oxalate levels in the leaves will increase while the levels in the stems will decrease. Signs of oxalate intoxication may occur abruptly a few hours following the consumption of contaminated plants, and animals may die within 12 hours. There is typically a progression of symptoms from depression, weakness, tremors, weak pulse, and labored respiration to prostration, coma, and death in a few hours.

Prevention is the best medicine, if you are unsure of a plants nitrate content have it tested. If plants have been subjected to drought condition or other unusual stresses, have forage samples tested before allowing animals to graze the area.

Ozmen O, Mor F, and Ayhan U (2003) Nitrate poisoning in cattle fed Chenopodium album hay. Veterinary and Human Toxicology 45:83-84.

University of Wisconsin “Nitrate Poisoning In Cattle, Sheep and Goats”; Dan Undersander, Dave Combs, Randy Shaver, and Dave Thomas

Nitrate Toxicity: Diagnosis and Treatment; Robert Smith, DVM and Glenn Selk

Celastrus scandens, commonly called American Bittersweet or Bittersweet is a species of Celastrus that prefers rich, well-drained woodland soils. This plant is a sturdy perennial vine that may have twining, woody stems 30 feet or longer and an inch or more thick at the base. The stems are yellowish-green to brown and often wind around and strangle out other vegetation and small trees. In June the tiny, scentless flowers at the tips of the branches will typically bloom. Once pollinated the flowers produce colorful, orange fruits the size of a pea.

It is at this point that the relative toxicity of the plant comes into question. Some sources state that “all parts of the American Bittersweet are toxic with the highest toxicity being found in the berries”. Other sources discount the overall toxicity of the plant and consider it relatively harmless. According to the US Department of Agriculture the American Bittersweet (Celastrus scandens) plant has a toxicity level of “None”. Most sources, however, agree that the plant found use by Native Americans for a wide variety of medicinal purposes. The leaves, bark, and roots were used as aids for rheumatism, childbirth pains, gastrointestinal discomfort, skin ulcers, coughs, tuberculosis, toothaches, and even cancer. Whereas the inner bark was sometimes cooked into a thick soup in times of starvation and the fruits were reportedly used to make poisons. This would at the very least tend to substantiate the possibility that the plant has shown the capacity to have an effect upon the body. These uses, however, probably involved a poultice wherein the plant would have been mixed with other items and applied, or the plants constituents were boiled down concentrating the desired chemical components into a decoction.

Further decreasing the risk of serious intoxication by a pet is the fact that the plant contains saponins that exhibit the irritant effect of burning the mouth and throat upon ingestion. As a result only in rare cases would an animal be able to tolerate the consumption of enough plant material to cause a potentially serious poisoning situation; if it is indeed possible. There may also be a species specific component in regards to consumption of this plant. The fruit and seeds have a somewhat confirmed history of being mildly toxic for humans, while rabbits, squirrels and birds can eat them with impunity. What this means for dogs, cats or other domesticated animals such as horses, cows, sheep or goats is unknown.

Additionally there has been little research done to determine the toxicity potential of genus as a whole. Some studies have stated that Celastrus scandens contains cardenolides, although specific information on the type, amount or toxicity is lacking. To err on the side of caution this plant should be considered capable of at least causing mild to severe gastrointestinal disturbances, especially with consumption of the fruits and seeds.

Plants of the Euonymus genus in general are attractive as border shrubs, hedgerows, espaliers, screens, foundation plantings and as single subjects. Named “Wahoo” by American Indians, this plant was once widely used in folk medicine and native American Indian medicine as a stimulant, laxative, emetic, purgative and physic drug. It was also used topically as a poultice for facial sores. The Euonymus genus take its name from the Greek goddess Eurynome, the mother of the Furies ("the Angry Ones"). Known as the Furies in Roman, they were the feared avenging goddesses in Greek and Roman mythology whose job it was to pursue and torment evildoers and sinners. The connection between the plant and the goddess being that the shrub apparently has very irritating and painful properties.

All parts of the plant are toxic and all are dangerously purgative (strongly laxative in effect) and emetic (induces vomiting). Additionally several cardiac glycosides have been found in the seeds of this plant, including evomonoside, a cytotoxic (toxic to cells) cardiac glycoside, whose aglycone is digitoxigenin. Alkaloids make up about 0.1% of the seeds, including evonine. Although the toxicity of the alkaloidal fraction has not been studied it is said that the consumption of as little as four berries can prove fatal for a small child. Currently the plant appears on the Food and Drug Administration's unsafe herb list and is emphatically not recommended for home medicinal use.