Substances Included Synonyms

Therapeutic Toxic Class

A)

Specific Substances

A)

1) Butternut
2) Lemon nut
3) Oil nut
4) References: Bailey & Bailey, 1976; Budavari, 1989;
5) Bolyard, 1981; Dirr, 1990

1) Black Walnut
2) References: Bailey & Bailey, 1976; Budavari, 1989;
3) Bolyard, 1981; Dirr, 1990

1) Persian walnut
2) Common Walnut
3) English Walnut
4) Derum
5) Dendasa
6) Corteza de Nogal
7) Maderia nut
8) References: Bailey & Bailey, 1976; Budavari, 1989;
9) Bolyard, 1981; Dirr, 1990

1) Juglans Neotropica
2) References: Bailey & Bailey, 1976; Budavari, 1989;
3) Bolyard, 1981; Dirr, 1990

1) Chinese butternut
2) References: Bailey & Bailey, 1976; Budavari, 1989;
3) Bolyard, 1981; Dirr, 1990

1) 5-hydroxy-1,4-naphthalenedione
2) 5-hydroxy-1,4-naphthoquinone
3) 8-hydroxy-1,4-naphthoquinone
4) CI 75500
5) CI Natural Brown 7
6) Nucin
7) Regianin
8) Juglone is also found in some species
9) of Carya (hickory)
10) Walnuts-plants
11) Reference: Keeler & Tu, 1983

1) Benzoaric acid
2) Produced by acid hydrolysis of tannins
3) form walnuts
4) References: Bailey & Bailey, 1976; Budavari, 1989;
5) Bolyard, 1981; Dirr, 1990

Available Forms Sources

A)

1) Juglone has been identified in the nuts, roots, and bark of the black walnut. One study showed the concentration in the bark is 3.6 micrograms/gram, and in the nut there is 1.9 micrograms/gram (Minnick et al, 1987).
2) Ellagic acid is produced by the acid hydrolysis of tannins from walnuts. It is a hemostatic and a potent antagonist of mutagenicity (Budavari, 1989).
3) Jugalnin is found in the Chinese medicine Hu Tao Ren or He Tao and is used to invigorate the lungs and kidneys (Huang, 1993).

B)

1) Black walnut has been used in folk medicine for a number of purposes, including treatment of fungus infections, for eczema, and as a laxative and purgative. It is said to have astringent, detergent, and antihemorrhagic activity (Duke, 1989; Westfall et al, 1961).
2) Juglans rigia is called Derum in Saudi Arabia and Dendasa in India and Pakistan. Twigs from the bark are used for oral hygiene and to color the lips (Ashri & Gazi, 1990; Gazi, 1986).
3) The hulls are boiled to make a yellow dye, the wood is extensively used in furniture and gun-stock making (Duke, 1989; Mitchell & Rook, 1979).
4) The nuts are edible, and are used in the flavoring of baked goods (Duke, 1989).
5) Butternut has been brewed as a tea for the treatment of pinworms. Crushed green walnut hulls have been used topically as a remedy for ringworm (Bolyard, 1981).
6) A decoction of Juglans insularis is used in Cuba for the treatment of skin diseases, especially in children (Lewis & Elvin-Lewis, 1977).
7) Black walnut extracts, including juglone and ellagic acid, have been investigated for their antitumor activity (Bhargava & Westfall, 1968).
8) Juglone has been used as a pH indicator (Budavari, 1989).
9) The naphthoquinone juglone, from black walnuts, is used in semi-permanent hair dyes and self-tanning products (Bonamonte et al, 2001).

Overview

Life Support

A)

Clinical Effects

0.2.1)

A) Handling black walnuts can cause staining of the skin, and has rarely caused dermatitis.
B) The nuts are edible. Ingestion of the leaves and twigs by humans has not caused toxicity. CNS depression, reported in animals, has not been reported in humans.
C) Horses are particularly sensitive to ingestion of black walnut shavings.

0.2.4)

A) Chronic chewing of the twigs can produce discoloration of the gingiva and lips.

0.2.7)

A) Sedation has occurred in experimental animals.

0.2.13)

A) Juglone and ellagic acid have antihemorrhagic activity.

0.2.14)

A) Black walnuts contain a yellow-brown pigment. Staining of the hands can occur while removing the hulls.
B) Dermatitis from handling black walnuts has been reported but is NOT common.

0.2.19)

A) Contact sensitivity to juglone or its derivatives has been reported in man and in animals, but others claim it is not a sensitizer.
B) Pollen, from Juglans species, may induce hayfever.

0.2.20)

A) At the time of this review, there are no data available regarding the potential teratogenicity or effects during pregnancy/lactation of this agent.

0.2.21)

A) IARC Category Group 1: The agent is carcinogenic in humans.
B) Adenocarcinoma of the nasal cavities and paranasal sinuses is clearly associated with occupational exposure to hardwood dust (WHO, 1995). Exposure to walnut wood dust is included in this assessment.
C) ANIMAL DATA -

1) PAPILLOMA formation was promoted by the topical application of juglone in mice (Monks et al, 1990).

0.2.22)

A) Diets rich in walnuts improve the serum lipoproteins profile.
B) Animals have been intoxicated after eating moldy walnuts contaminated with mycotoxin penitrem A.

Laboratory Monitoring

A)

B)

Treatment Overview

0.4.2)

A) No treatment is necessary.

0.4.4)

A) DECONTAMINATION: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, the patient should be seen in a healthcare facility.

0.4.5)

A) OVERVIEW

1) Handling the nuts and hulls may cause staining and has caused one case of dermatitis. Washing, after handling the nuts, is recommended.
2) DECONTAMINATION: Remove contaminated clothing and jewelry and irrigate exposed areas with copious amounts of water. A physician may need to examine the area if irritation or pain persists.

Range Of Toxicity

A)

B)

Clinical Effects

Dermatologic

3.14.1)

A) Black walnuts contain a yellow-brown pigment. Staining of the hands can occur while removing the hulls.
B) Dermatitis from handling black walnuts has been reported but is NOT common.

3.14.2)

A) DISCOLORATION OF SKIN

1) Black walnuts contain a naphthaquinone that turns the skin brown to brownish-red. Staining of the hands can occur while removing the hulls. This staining usually lasts from 1 to 4 weeks, depending on the extent of the exposure (Bonamonte et al, 2001; Siegel, 1954).

B) CONTACT DERMATITIS

1) CASE REPORT - Burning, itching, blistering, eruptions with bullae in the finger webs were reported in a man who picked black walnuts (J. nigra) for two days. He did not wear protective gloves nor did he wash his hands frequently. The patient was re-exposed later without reaction. The author concluded the contact dermatitis was a primary irritant effect rather than an allergic reaction (Siegel, 1954). Dermatitis from handling black walnuts is NOT common.
2) CASE REPORT - A 65-year-old woman, who shelled 15 kilos of black walnuts over 3 days, developed intense skin hyperpigmentation, blisters on the palms and fingers, and brown stains, erosions, and eczematous lesions on the forearms. Contact allergy patch testing showed a bullous reaction to the hydroalcoholic extract from the walnut husks on the second day. The patient was treated with cool, weak aluminum acetate solution compresses. By the fifth day, the contact dermatitis had healed; the pigmentation cleared up within 3 weeks (Bonamonte et al, 2001).

Immunologic

3.19.1)

A) Contact sensitivity to juglone or its derivatives has been reported in man and in animals, but others claim it is not a sensitizer.
B) Pollen, from Juglans species, may induce hayfever.

3.19.2)

A) ACUTE ALLERGIC REACTION

1) JUGLONE - Contact sensitivity to juglone or its derivatives has been reported (Mitchell & Rook, 1979; Barniske, 1957) in man and in animals (guinea pigs), but others claim it is not a sensitizer. Sensitization in man is rare (Bonamonte et al, 2001; Telegina, 1965).
2) HAYFEVER may be induced in susceptible individuals by the pollen from Juglandacea (Lewis & Elvin-Lewis, 1977).
3) Life-threatening food allergy to english walnuts has been reported (Robotham et al, 2002; Teuber et al, 1999).

a) The english walnut (Juglans regia) is known to contain the 2S albumin seed storage allergen, Jug r1. This is a sulfur-containing food storage protein found in the seed (nut). English walnuts also contain a vicilin allergen, Jug r2 (a globular seed storage protein) (Breiteneder & Ebner, 2001; Breiteneder & Ebner, 2000).
b) Testing in human serum showed little or no cross-reactivity between the English walnut vicilin and the vicilins of cacao, pea, or peanut vicilins (Teuber et al, 1999). However, cross-reactivity to coconut and walnut allergens has been reported in 2 subjects. In these cases, patients who had tree nut allergies also manifested life-threatening reactions to coconut (Teuber & Peterson, 1999).

Reproductive

3.20.1)

A) At the time of this review, there are no data available regarding the potential teratogenicity or effects during pregnancy/lactation of this agent.

3.20.2)

A) LACK OF INFORMATION

1) At the time of this review, no data were available to assess the teratogenic potential of this agent.

3.20.3)

A) LACK OF INFORMATION

1) At the time of this review, no data were available to assess the potential effects of exposure to this agent during pregnancy or lactation.

Carcinogenicity

3.21.2)

A) IARC Category Group 1: The agent is carcinogenic in humans.
B) Adenocarcinoma of the nasal cavities and paranasal sinuses is clearly associated with occupational exposure to hardwood dust (WHO, 1995). Exposure to walnut wood dust is included in this assessment.
C) ANIMAL DATA -

1) PAPILLOMA formation was promoted by the topical application of juglone in mice (Monks et al, 1990).

Summary Of Exposure

A)

B)

C)

Heent

3.4.1)

A) Chronic chewing of the twigs can produce discoloration of the gingiva and lips.

3.4.6)

A) BROWN-ORANGE DISCOLORATION of the gingiva and lips developed after chronic use of Derum (or Dendasa from J. regia), a fibrous chewing stick used as an oral hygiene product (Ashri & Gazi, 1990; Gazi, 1986). The lips were also dry in appearance and crusted.

Neurologic

3.7.1)

A) Sedation has occurred in experimental animals.

3.7.3)

A) ANIMAL STUDIES

1) SOMNOLENCE

a) Sedation has been reported in test animals (rats, rabbits, fish) who have been exposed to juglone or black walnut extract. Sedative effects were seen in rabbits who were injected with 0.07 mg intravenously (Westfall et al, 1961).

Hematologic

3.13.1)

A) Juglone and ellagic acid have antihemorrhagic activity.

3.13.2)

A) UNEXPECTED THERAPEUTIC EFFECT

1) Juglone is said to have antihemorrhagic activity (Duke, 1989).

Laboratory Monitoring

Monitoring Parameters Levels

4.1.1)

A) No abnormal laboratory values are expected in humans.
B) Juglone can be detected on gas chromatography-mass spectrophotometry, but levels are not clinically useful.

4.1.2)

A) OTHER

1) No abnormal laboratory values are expected in humans.

Methods

A)

1) Juglone can be detected on gas chromatography-mass spectrophotometry, but levels are not clinically useful (Minnick et al, 1987).

Treatment

Life Support

A)

Patient Disposition

6.3.1)

6.3.1.2) HOME CRITERIA/ORAL

A) The nuts are edible; treatment is unnecessary. Human toxicity from chewing the leaves or bark has not been reported, therefore patients can be managed at home.

6.3.4)

6.3.4.1) ADMISSION CRITERIA/EYE

A) Walnut juice or sap is not particularly irritating to the eyes. If pain, lacrimation or photophobia persists after 15 minutes of irrigation with tepid water, examination by a physician should be performed.

6.3.5)

6.3.5.1) ADMISSION CRITERIA/DERMAL

A) Walnut juice or sap is not particularly irritating to the skin. If irritation persists after adequate washing with soap and water, consultation with a physician may be necessary.

Monitoring

A)

B)

Oral Exposure

6.5.1)

A) EMESIS -

1) Emesis is not necessary for human exposures to the nuts or foliage.

6.5.2)

A) EMESIS

1) Emesis is not necessary for human exposures to the nuts or foliage.

6.5.3)

A) ASYMPTOMATIC

1) The nuts are edible. No treatment is necessary for human exposures to the nuts or foliage. Humans are not likely to eat sufficient quantities of moldy nuts to result in mycotoxin toxicity.

Eye Exposure

6.8.1)

A) EYE IRRIGATION, ROUTINE: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, an ophthalmologic examination should be performed (Peate, 2007; Naradzay & Barish, 2006).

Dermal Exposure

6.9.1)

A) DECONTAMINATION: Remove contaminated clothing and wash exposed area thoroughly with soap and water for 10 to 15 minutes. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).

6.9.2)

A) SUPPORT

1) Dermatitis is rare. Treatment is symptomatic and supportive.

B) HYPERPIGMENTATION OF SKIN

1) One case of hyperpigmentation and blisters on the hands and forearms was treated with compresses of weak aluminum acetate (Burow's solution). The blisters and contact dermatitis cleared within 5 days, the hyperpigmentation in 3 weeks (Bonamonte et al, 2001).

C) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Enhanced Elimination

A)

1) No studies have addressed the utilization of extracorporeal elimination techniques in poisoning with this agent.

Abstracts

Range Of Toxicity

Summary

A)

B)

Minimum Lethal Exposure

A)

1) There have been NO reports of death after human exposure to walnuts.

Maximum Tolerated Exposure

A)

1) Sedative effects were noted in animals given 0.07 mg of juglone IV (Westfall et al, 1961).
2) Diarrhea developed in mice given intraperitoneal doses of juglone of 10 mg/kg and 100 mg/kg (Bhargava & Westfall, 1968).

Toxicity Information

7.7.1)

A) JUGLONE

1) LD50- (INTRAPERITONEAL)MOUSE:

a) 0.25 mg/100 g (Westfall et al, 1961).

Pharmacology Toxicology

Toxicologic Mechanism

A)

1) Juglone is known to have a sedative effect on fish, rabbits, and rats. The dose used in rabbits was 0.7 mg (Westfall et al, 1961).
2) Juglone cytotoxicity is caused by bioreduction to the semiquinone which produces oxygen radicals (Zhang, 1994).
3) Juglone is known to inhibit seedling growth at concentrations as low as 10(-7) molar and can kill seedlings at 10(-4) molar (p 422).
4) Juglone contains activated ketones (C=O), which interact with keratine aminoacids (NH2), producing C=N chromophore groups that absorb visible colors, especially violet, reflecting yellow and red. This gives the skin the red to deep brown color which is utilized in skin tanning products (Bonamonte et al, 2001).

B)

1) Walnuts may decrease serum cholesterol because they contain a high concentration of n-3 linoleic acids. They also provide a source of dietary fiber and they have a low ratio of lysine to arginine (Sabarte, 1993).

Physicochemical

Physical Characteristics

A)

Molecular Weight

A)

Animal Toxicology

Clinical Effects

11.1.3)

A) JUGLONE - Juglone acts as a depressant and can cause severe pulmonary interstitial and alveolar edema when administered to dogs (Boelkins et al, 1968; Auyong et al, 1963).
B) MYCOTOXINS - Dogs will eat moldy walnuts. The mycotoxin penitrem A is produced by the fungus Penicillium crustosum, which grows on decaying walnuts (both English and black walnuts). Symptoms of intoxication in dogs are generally seen within 5 to 30 minutes and included gastroenteritis, seizures (with opisthotonus possible), panting, mydriasis, increased urination, increased temperature, and defecation (Fuller & McClintock, 1986).

11.1.5)

A) LAMINITIS -

1) Horses stabled on freshly prepared black walnut shavings may develop acute laminitis (Peterson, 1984; (True et al, 1978). An early report attributing an outbreak of laminitis to fresh English walnut shavings (Ralston & Rich, 1983) was subsequently shown to have been due actually to black walnut (Ralston, Pers Comm, 1983). Laminitis is usually associated with systemic and local hypertension, alterations in blood flow to the foot, and lameness as the laminae of the feet become necrotic. Digital blood flow increases while foot perfusion decreases (Galey et al, 1990). Severely affected horses may develop chronic laminitis with separation of the hoof wall from the bone of the foot (Galey et al, 1991).
2) ORAL EXPOSURE - Juglone may produce mild laminitis, but is not the sole cause of this illness in horses exposed to black walnut (Galey et al, 1991; Minnick et al, 1987; True & Lowe, 1980). Aqueous extracts of black walnut caused laminitis when given to horses via nasogastric tube (Galey et al, 1991; Minnick et al, 1987).
3) DERMAL EXPOSURE - Topical administration of juglone to horse hooves produced some local irritation, but not laminitis (True & Lowe, 1980). Packing the feet of ponies in shavings failed to produce laminitis like that seen in a typical outbreak (True et al, 1978).

B) PULMONARY EDEMA occurred in a horse given synthetic juglone orally following a previous exposure (True & Lowe, 1980). The reaction was considered allergic in nature, with juglone possibly acting as a hapten. Respiratory distress may be seen with clinical black walnut toxicosis in some cases (Uhlinger, 1989; Ralston & Rich, 1983).
C) ABDOMINAL PAIN has been infrequently reported in cases of black walnut toxicosis (Uhlinger, 1989).
D) SEDATION - Some horses will become lethargic, quiet, anorexic, and nonresponsive to stimuli after exposure to black walnut shavings (Galey et al, 1991; Uhlinger, 1989; Minnick et al, 1987).
E) LIMB EDEMA - Swelling of the limbs is a frequent report (Galey et al, 1991; Minnick et al, 1987; True et al, 1978).
F) VITAL SIGNS - Horses with black walnut toxicosis will have increased body temperatures, increased heart and respiratory rates, palpable increases in coronary band and hoof temperatures, and pounding digital pulses (Galey et al, 1991; True et al, 1978).
G) HEMATOLOGICAL - Horses with experimental black walnut toxicosis developed a transient, marked neutropenia following nasogastric intubation with an aqueous extract of black walnut (Galey et al, 1991). That study revealed no hematological evidence of shock, which may be present in horses with laminitis due to causes other than black walnut. Plasma cortisol and epinephrine concentrations may be elevated (or have diurnal peaks prolonged) in horses with black walnut toxicosis (Galey et al, 1991).
H) PATHOLOGICAL - Necrosis of hoof laminae occurs in horses with black walnut toxicosis. The severity of that change parallels the severity of the clinical laminitis. Secondary dermal laminae and dermal tips of epidermal laminae were vacuolated and the dermis was congested in hooves from horses with acute black walnut-induced laminitis (24 hours after dosing horses with an aqueous extract of black walnut via nasogastric tube). Few dorsal laminar lesions were seen in horses with mild (Obel grades 1 and 2) laminitis at 84 hours after dosing with black walnut. Horses that had severe (Obel grade 3 or 4) laminitis had severe epidermal laminar necrosis with architectural destruction and evidence of regeneration of epidermal cells (Galey et al, 1991).

11.1.7)

A) CLINICAL EFFECTS - Fresh walnut hulls have been used to immobilize fish (Gries, 1943), a process that is currently illegal. Affected fish gradually lose equilibrium and awareness of their environment (Westfall et al, 1961). Effects were reversible in mildly to moderately depressed fish.

11.1.12)

A) Juglone acts as a depressant when administered to rats, mice, and rabbits (Auyong et al, 1963; Westfall et al, 1961).

Treatment

11.2.1)

A) GENERAL TREATMENT

1) Begin treatment immediately.
2) Remove the patient and other animals from the source of contamination.
3) Treatment should always be done on the advice and with the consultation of a veterinarian. Additional information regarding treatment of animals with black walnut toxicosis may be obtained from a Board Certified (ABVT) Veterinary Toxicologist (check with nearest veterinary school or veterinary diagnostic laboratory) or the National Animal Poison Control Center.
4) ANIMAL POISON CONTROL CENTERS

a) ASPCA Animal Poison Control Center, An Allied Agency of the University of Illinois, 1717 S. Philo Rd, Suite 36, Urbana, IL 61802, website www.aspca.org/apcc
b) It is an emergency telephone service which provides toxicology information to veterinarians, animal owners, universities, extension personnel and poison center staff for a fee. A veterinary toxicologist is available for consultation.
c) The following 24-hour phone number is available: (888) 426-4435. A fee may apply. Please inquire with the poison center. The agency will make follow-up calls as needed in critical cases at no extra charge.

11.2.2)

A) GENERAL

1) MAINTAIN VITAL FUNCTIONS: Secure airway, supply oxygen, and begin supportive fluid therapy if necessary.

11.2.4)

A) GASTRIC DECONTAMINATION

1) HORSE

a) Remove the horses from exposure to the black walnut shavings.
b) INHALATION - Inhalation has not been thoroughly tested as a possible route of exposure for black walnut toxicosis. Therefore, move the patient to fresh air.
c) DERMAL - Despite the lack of evidence for dermal exposure causing black walnut laminitis, such an occurrence is possible. Therefore, wash exposed animals with soap and water. If necessary, shave or clip long hair to facilitate cleaning. Handlers should wear gloves to protect themselves from exposure.
d) EMESIS - Do not attempt to induce emesis in ruminants (cattle) or equids (horses).
e) ACTIVATED CHARCOAL - Definitive evidence of the efficacy of activated charcoal in treating black walnut toxicosis is lacking. Despite that, activated charcoal may be of benefit to horses acutely exposed to black walnut since the toxic effect of juglone to fish is removed from water by activated carbon compounds (Dawson et al, 1976). Adult horses: administer 0.5 to 1 kilogram of activated charcoal in up to 1 gallon warm water via nasogastric tube. Neonates: administer 250 grams (one-half pound) activated charcoal in up to 2 quarts of water.

11.2.5)

A) HORSE

1) LAMINITIS - Prognosis is favorable in cases where rapid reversal of signs (within 24 hours) can be achieved and maintained. Chronic laminitis may require long term phenylbutazone treatment and specialized hoof care.

a) PHENYLBUTAZONE - Horses with uncomplicated laminitis have been treated successfully with phenylbutazone (4.4 milligrams/kilogram intravenously twice daily). Horses with Obel grade 3 or less of laminitis due to black walnut recovered completely within 24 to 48 hours of the initiation of phenylbutazone therapy (Galey et al, 1991). If chronic laminitis develops, phenylbutazone therapy may need to be more prolonged (2 weeks in one report) (Uhlinger, 1989).
b) Other therapies that may be of benefit include provision of soft bedding (without black walnut), treatment with vasodilators (acepromazine, prazosin, and isoxsuprine have been suggested), and regional anesthesia.

Range Of Toxicity

11.3.2)

A) DOG

1) Dogs given juglone at 10 milligrams/kilogram (mg/kg) of body weight via intravenous injection developed severe pulmonary interstitial and alveolar edema, whereas dogs given juglone at 3 mg/kg of body weight by the same route developed no signs or lesions (Boelkins et al, 1968).

B) FISH

1) The 96 hour LC50 for juglone in water for 9 species of fish ranged from 0.027 milligrams/liter (mg/L) in northern pike (Esox lucius) to 0.088 mg/L for carp (Cyprinus carpio) (Marking, 1970). The LC50 for juglone in aquarium water for goldfish was 0.2 mg/L (Westfall et al, 1961). Toxicity was unaffected by changes in temperature but was reduced by making the water more alkaline (Marking, 1970). Activated carbon compounds removed the piscicidal properties of juglone from water (Dawson et al, 1976).

C) HORSE

1) Shavings used as bedding containing as little as 20% (or less) of fresh black walnut may cause laminitis (Pederson, 1984).
2) The aqueous extract made from 1 kilogram of fresh heartwood from black walnut shavings will uniformly cause laminitis in a typical horse (Galey et al, 1991; Minnick et al, 1987).
3) One gram of juglone (roughly equivalent to 6.7 kilogram (kg) of leaves), given to each of 2 ponies (332 to 360 kg body weight) and 6 horses (450 kg body weight) orally caused only mild laminitis in the ponies and no signs in the horses (True & Lowe, 1980).
4) Allergic-type pulmonary edema was caused on the second dose when juglone was given to horses intravenously at doses of up to 250 milligrams (True & Lowe, 1980).

Continuing Care

11.4.1)

11.4.1.2) DECONTAMINATION/TREATMENT

A) GENERAL TREATMENT

1) Begin treatment immediately.
2) Remove the patient and other animals from the source of contamination.
3) Treatment should always be done on the advice and with the consultation of a veterinarian. Additional information regarding treatment of animals with black walnut toxicosis may be obtained from a Board Certified (ABVT) Veterinary Toxicologist (check with nearest veterinary school or veterinary diagnostic laboratory) or the National Animal Poison Control Center.
4) ANIMAL POISON CONTROL CENTERS

a) ASPCA Animal Poison Control Center, An Allied Agency of the University of Illinois, 1717 S. Philo Rd, Suite 36, Urbana, IL 61802, website www.aspca.org/apcc
b) It is an emergency telephone service which provides toxicology information to veterinarians, animal owners, universities, extension personnel and poison center staff for a fee. A veterinary toxicologist is available for consultation.
c) The following 24-hour phone number is available: (888) 426-4435. A fee may apply. Please inquire with the poison center. The agency will make follow-up calls as needed in critical cases at no extra charge.

11.4.2)

11.4.2.2) GASTRIC DECONTAMINATION

A) GASTRIC DECONTAMINATION

1) HORSE

a) Remove the horses from exposure to the black walnut shavings.
b) INHALATION - Inhalation has not been thoroughly tested as a possible route of exposure for black walnut toxicosis. Therefore, move the patient to fresh air.
c) DERMAL - Despite the lack of evidence for dermal exposure causing black walnut laminitis, such an occurrence is possible. Therefore, wash exposed animals with soap and water. If necessary, shave or clip long hair to facilitate cleaning. Handlers should wear gloves to protect themselves from exposure.
d) EMESIS - Do not attempt to induce emesis in ruminants (cattle) or equids (horses).
e) ACTIVATED CHARCOAL - Definitive evidence of the efficacy of activated charcoal in treating black walnut toxicosis is lacking. Despite that, activated charcoal may be of benefit to horses acutely exposed to black walnut since the toxic effect of juglone to fish is removed from water by activated carbon compounds (Dawson et al, 1976). Adult horses: administer 0.5 to 1 kilogram of activated charcoal in up to 1 gallon warm water via nasogastric tube. Neonates: administer 250 grams (one-half pound) activated charcoal in up to 2 quarts of water.

Pharmacology Toxicology

A)

1) Juglone has a sedative effect on fish and mammals.
2) Juglone causes dilation of ear vessels of rabbits when administered systemically and arteries of isolated perfused rabbit hearts (Auyong et al, 1963).
3) The compound also depressed smooth muscle activity of isolated rat gut and uterus in the same study.
4) Juglone also may damage capillary permeability and histologic lesions in dog lung and liver (Boelkins et al, 1968).
5) Juglone administration was also associated with development of pulmonary edema in horses (perhaps allergic in nature) (True & Lowe, 1980).
6) Juglone is known to poison earthworms (pp 114-122).

B)

1) An aqueous extract of black walnut heartwood was tested using isolated equine digital arteries and veins. The extract did not produce direct vasoconstriction, but did reversibly enhance the vasoconstriction caused by epinephrine (Galey et al, 1990).
2) The toxin responsible for laminitis in horses with black walnut toxicosis has not been isolated. Oral juglone administration produced only mild laminitis (True & Lowe, 1980). Juglone is not present in heartwood of black walnut (Minnick et al, 1987), yet aqueous extracts of heartwood uniformly cause up to Obel grade 4 laminitis within 10 to 12 hours of administration via nasogastric tube in horses (Galey et al, 1991; Galey et al, 1990; Minnick et al, 1987).

References

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PLANTS-WALNUTS

Classification | Detailed evidence-based information

Therapeutic Toxic Class

Specific Substances

Available Forms Sources

Life Support

Clinical Effects

Laboratory Monitoring

Treatment Overview

Range Of Toxicity

Dermatologic

Immunologic

Reproductive

Carcinogenicity

Summary Of Exposure

Heent

Neurologic

Hematologic

Monitoring Parameters Levels

Methods

Life Support

Patient Disposition

Monitoring

Oral Exposure

Eye Exposure

Dermal Exposure

Enhanced Elimination

Summary

Minimum Lethal Exposure

Maximum Tolerated Exposure

Toxicity Information

Toxicologic Mechanism

Physical Characteristics

Molecular Weight

Clinical Effects

Treatment

Range Of Toxicity

Continuing Care

Pharmacology Toxicology

General Bibliography