Toxicodendron Toxicity

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Continuing Education Activity

Plants within the Anacardiaceae family cause Toxicodendron toxicity. It includes plants such as poison ivy, poison oak, poison sumac and is the most common cause of allergic dermatitis in North America. This activity outlines the evaluation and treatment of Toxicodendron toxicity and highlights the interprofessional team's role in managing patients with this condition.


  • Identify the etiology of Toxicodendron toxicity.
  • Review the appropriate evaluation of Toxicodendron toxicity.
  • Outline the management options available for Toxicodendron toxicity.
  • Describe the interprofessional team strategies for improving care coordination and communication to advance Toxicodendron toxicity and improve outcomes.


Toxicodendron is a genus of plants, shrubs, vines, and trees within the Anacardiaceae family. Common names of plants within the family include poison oak, poison ivy, poison sumac, and the Chinese lacquer tree. Many of these names come from similar appearances to other leaves that are non-toxic. The genus as a whole is widespread throughout North America except for Hawaii and Alaska and can have regional variations in appearance. Many of these plants prefer lower elevations and are typically found below 1500 meters. An often-repeated adage regarding their identification is “leaves of three, leave it be,” but it should not be the sole method used. Poison ivy is pervasive throughout North America and has been known to hybridize where its geographic distribution overlaps. Eastern poison ivy (Toxicodendron radicans) is commonly found in the eastern half of North America and typically appears as a vine with almond-shaped leaves in groups of three. Leaves change from green to red in the fall. Western or Rydberg’s poison ivy (Toxicodendron rydbergii) is commonly found as a shrub with small yellow berries. It is distributed throughout much of North America, with the general exception of the Southeastern United States.

All parts of both plants contain urushiol, which causes characteristic dermatitis associated with exposure. While the genus and its many subspecies have a strong predilection for North America, they can both be found in China, Mexico, Africa, Australia, and New Zealand, to name a few other places. Poison oak has two common variations. Western poison oak (Toxicodendron diversilobum) is a deciduous shrub with scalloped or lobed leaves, generally appearing in groups of three that resemble true oak leaves. It is found primarily west of the Rocky Mountains, as the name suggests. While Eastern or Atlantic poison oak (Toxicodendron pubescens or quercifolium) is frequently confused with Eastern poison ivy as it has three grouped leaves that are structurally similar in appearance. A unique feature useful in identification is the presence of clustered small green fuzzy berries on the plant. Distribution is more common in the Southeastern United States but can extend as far north as New Jersey. The leaves of both western and Atlantic poison oak change colors in the fall time and drop off in the Western species. Poison sumac (Toxicodendron vernix) is a deciduous tree or tall shrub found in moist, swampy areas of the eastern United States. It has red stems with a pinnate or feather-like leaf arrangement comprised of 7 to 13 oblong or oval-shaped leaves. The plant also produces green clustering flowers and small globular fruit. The leaves and fruit of the plant are the primary sources of urushiol.

The Chinese lacquer tree (Toxicodendron vernicifluum) is a common deciduous tree in many Asian countries and gets its name for the use of its urushiol-containing sap in lacquer production. Leaves are large and grouped in leaflets of 7 to 19 with flowers that bloom in the summer. All parts of Toxicodendron plants contain urushiol, which is found in sap channeled within the plant. When exposed to air, urushiol turns black and hardens to prevent moisture loss and can be useful in identifying plants in the fall. Urushiol is the primary allergenic cause of contact dermatitis and is typically encountered by brushing up against damaged stems or leaves. Skin exposure results in rapid absorption of the urushiol due to its lipophilic nature. Names for the toxicity are variable and include names such as Rhus dermatitis, urushiol-induced contact dermatitis, and Toxicodendron dermatitis.


Toxicodendron dermatitis is the most common cause of allergic contact dermatitis in North America and is caused by skin exposure to urushiol, producing a type IV hypersensitivity reaction.[1] The chemical structure of urushiol is variable and primarily comprised of catechol with a long hydrocarbon chain.[2][3] Evidence suggests longer saturated hydrocarbon side chains, the addition of aliphatic side chains and phenolic groups are associated with increasing clinical severity.[4][5] It is estimated that 50 to 75% of adults are allergic to urushiol.[6] 


A large portion of the population is sensitized to urushiol. Acute allergic dermatitis affects virtually all ages, ethnicities, and skin types, with an estimated 25 to 40 million cases requiring treatment yearly.[7][8] Occupational exposure is common in forest service workers and comprises many of these cases, with exposure to extremities being more common.[8][9][10] 


Acute allergic dermatitis is caused by contact with bruised or broken parts of plants within the Toxicodendron species. Urushiol is the primary inciting compound causing the release of local cytokines and inflammatory mediators that initiate the process of sensitization. The compound is rapidly absorbed due to its lipophilic nature and picked up by Langerhans cells in the epidermis, making additional efforts to wash or remove the compound ineffective after absorption.[4] Initial exposure results in pruritus and erythema, followed by a papulovesicular eruption, edema, and oozing within 10 to 14 days. Symptoms of re-exposure are more acute and appear in 24 to 72 hours.[11] Aerosolized urushiol from forest fires or burning plant debris has been known to cause airway inflammation or generalized dermatitis in severe cases.


Sensitization and reexposure are mediated by a type IV cell-mediated hypersensitivity reaction.[12][13][14] Langerhans cells, or antigen-presenting cells (APCs), and other acute inflammatory mediators are activated, initiating a local response. APCs break down urushiol into antigens, which either combine with major histocompatibility complex II (MHC II) or are exposed on the surface of APCs. Transit of Langerhans cells to lymph nodes results in the presentation of the MHC II/antigen complex or free surface antigens to T cell receptors on CD8+ T cells via MHC II or through MHC I on CD4+ T cells, respectively. Clonal expansion then occurs, and subsequent exposure and recognition of antigens by T cells result in repeat allergic dermatitis. While it is estimated that 50 to 75% of adults are allergic to urushiol, variations can occur where T cells cannot recognize the presenting antigens are present, and no immunologic response occurs.[6] Activation of T cells on initial exposure results in the production of CD4 and CD8 T cells sensitive to urushiol, which then activate a more robust immune response on repeat exposure to the offending agent. Keratinocytes and monocytes also appear to place a role in the release of local cytokines and pro-inflammatory mediators.[14][15][16] Many of these pathways are the target of corticosteroid treatment.

History and Physical

A thorough history should include any potential occupational and environmental exposure within the past 2 to 3 weeks as initial sensitization may be unknown. Clinicians should be aware of local geographic distributions of the Toxicodendron species. Patients often initially present with complaints of intense pruritis and the beginning stages of a papular or vesicular rash in a linear pattern. Distribution may be scattered as patients often do not recognize exposure until they have contacted other body areas. Black spots may be noted on affected skin or clothing and should be avoided, and it is the result of oxidized urushiol exposed to air.[17][18][19][20] Secondary exposure can occur when the skin is exposed to oxidized urushiol or animal fur that came in contact with the Toxicodendron species.


A thorough history and physical primarily determine the diagnosis, and no additional testing is required. Allergy patch testing is widely available and may help identify patients with severe urushiol sensitivity, but it is not necessary. It can also increase the risk of sensitization in unsensitized subjects. Dermoscopy, if available, is another alternative for evaluation of black spot dermatitis caused by Toxicodendron species and would show jagged red-rimmed dark brown lesions.[18]

Treatment / Management

Toxicodendron dermatitis is typically self-limited and resolves within a couple of weeks.[1] Initial management consists of immediate irrigation with soap and decontamination of clothing upon exposure.[4] Specific instruction should be given to clean under fingernails as they are commonly missed.[21] Mild detergents are a reasonable choice when compared to expensive alternatives.[22] Additional anecdotal options include cool, moist compresses, oatmeal baths, calamine lotion, and topical astringents.[7][23] A small study comparing topical commercially available cream containing polyethylene granules, sodium lauroyl sarcosinate, nonoxynol-9, C12-15 pareth-9, disodium EDTA, quaternium-15, carbomer (2%), triethanolamine, and water, to placebo showed improvement in symptoms if applied early. Some literature suggests the use of prophylactic homeopathic oral preparations of poison ivy may be somewhat protective, but randomized controlled trials (RCTs) are lacking.[24] 

Topical and oral antihistamines are commonly taken medications to decrease pruritus and are typically ineffective outside of their sedative effects as the biochemical process is not due to histamine release. Management should be centered on moderate to high dose topical or systemic corticosteroids that are beneficial early in the disease course, particularly before the appearance of papules or vesicles.[25][26][27] A tapered dose of prednisone for severe cases can begin at 1 mg/kg/day (0.5 mg/kg/day in pediatric patients) for a max dose of 60mg/day and tapered weekly over three weeks to prevent rebound dermatitis.[28][29] Alternatives for patients who are not candidates for systemic corticosteroids include applying moderate strength topical corticosteroids with an occlusive dressing for 24 hours that is then repeated 48 hours after initial application.[30] 

Initial studies assessing the use of topical immunosuppressants for atopic dermatitis were mixed.[31][32] Newer evidence shows some benefit with the use of tacrolimus and pimecrolimus compared to topical corticosteroids (TCS); however, a meta-analysis of RCTs showed increased adverse events in comparison to TCS.[33] Both appear to be well tolerated and may play a role in patients who require long-term treatment. While there is considerable interest in developing a vaccine-like compound, current research is ongoing, with the initial phases of clinical trials sound promising.[34] Although patients typically appear relatively late in the clinical course, care should be taken to actively treat any signs of secondary skin infection with appropriate antibiotics. Excoriations and decreased skin integrity are common etiologies of secondary infections, with the most common pathogen being Staphylococcus aureus. Evidence also supports the possibility of polymicrobial infections.[35] Hyperpigmentation is a possible complication of contact dermatitis in patients with darker skin types and typically resolves within a couple of months.[1]

Differential Diagnosis

Several other conditions may be confused with Toxicodendron toxicity, and a careful history and physical examination are necessary to differentiate between them. Herpes zoster often presents as a vesiculopapular rash but follows a dermatomal pattern that doesn’t cross the midline of the body. It is also often preceded by pain in the affected area and would not have a history of environmental exposure. Phytophotodermatitis is another potential mimicker, as it follows a similar timeline. Differentiating factors include plant exposure to sun-exposed areas of the body and the absence of pruritus. Irritant dermatitis is usually sudden in onset and associated with exposure to metals or other irritating compounds with distinct dermal patterns. Other arthropod bites such as bed bugs (Cimex lectularius) or scabies (Sarcoptes scabiei) may present similarly and be pruritic but lack the appropriate timing and are typically non-vesicular. Scabies has a characteristic burrowing pattern, while bed bug bites tend to have a rapid onset in skin findings. 

Pertinent Studies and Ongoing Trials

Ongoing clinical trials are being performed by the University of Mississippi in conjunction with a biochemical company. Several patents have been issued with regards to vaccine development and initial phase 1 safety studies were completed in 2017.


Presenting symptoms vary in their onset depending upon initial or repeat exposure and consist of a linear appearing papulovesicular eruption of the dermis with erythema and pruritus.[12][36] As the rash begins to resolve, it is often followed by continued intense pruritis and excoriations. Repeat exposure can last 14 to 21 days, and care should be taken to treat any signs suggestive of secondary infection due to excoriations.[7] A small subset of the population is hypersensitive to urushiol and presents with rapid onset of widespread symptoms within a few hours. Hyperpigmentation can be a late finding and does not require treatment despite potentially lasting up to several months.

Toxicodendron dermatitis can be mild, moderate, or severe. Mild cases present mainly with localized or linear erythema and/or edema with minimal symptoms. Moderate to severe cases will have more diffuse involvement associated with severe pain, burning, and/or pruritus.


Prognosis is largely dependent upon the extent and duration of exposure. Outcomes are typically excellent as management is directed primarily at decreasing innate and adaptive responses. In rare cases of complications or severe exposure, management may be prolonged and require hospital admission.


Uncommon complications include secondary bacterial infection and skin hyperpigmentation. Secondary infections are most commonly due to Staphylococcus aureus or streptococci and should be treated appropriately with additional consideration of concurrent polymicrobial infection.[7] Hyperpigmentation of darker skin types is often self-limited with resolution within months. More severe symptoms are often associated with hypersensitive individuals or cases of aerosolized urushiol exposure. These cases should begin with airway assessment and management of any potential signs of anaphylaxis followed by systemic high-dose corticosteroids. In rare circumstances, nephropathy has been reported with Toxicodendron dermatitis.[37]

Deterrence and Patient Education

Patients should be counseled regarding the identification of local Toxicodendron species and avoidance. If occupational exposure is encountered, proper protective equipment should be outlined with specific instructions to use vinyl gloves as urushiol can penetrate rubber or latex gloves.[8] As part of decontamination, all clothing and objects with potential exposure should be cleaned with warm water and detergents. There is evidence to alternatively support the use of bentonite, and other commercially available organoclay barrier creams, prior to exposure.[38][39] Current evidence does not support the use of desensitization programs.[40][41][42]

Pearls and Other Issues

The best prevention of Toxicodendron dermatitis is avoidance, followed by appropriate barriers and decontamination. Regional variations in plant structure often make identification challenging, making misidentification the most common pitfall. Poison ivy comprises a large percentage of exposures throughout North America and is the most commonly misidentified species.[43] Key points in the identification of poison ivy include leaves that are found in groups of three without the presence of thorns or jagged/scalloped edges. Management of exposure should begin by immediately washing affected skin with soap and water and early application of topical corticosteroids. In severe cases or where there is respiratory system involvement, hospital admission may be necessary. Of special note, several other species within the cashew/sumac family or Anacardiaceae have cross-reactivity with urushiol sensitized patients. Some of the more commonly known causes include exposure to the fruit or trees of mangos, cashew nuts, and ginkgo biloba.[44][45]

Enhancing Healthcare Team Outcomes

Communication between physicians and other professionals, acting as an interprofessional team, is essential in managing these patients as they may present in a variety of clinical settings. This healthcare team will consist of clinicians, mid-level practitioners, nurses, and pharmacists, working collaboratively to achieve optimal patient outcomes. [Level 5]

Management should be followed primarily by a primary care provider or dermatologist as the mainstay of treatment is corticosteroids, which have many potential side effects. Evidence supporting the use of corticosteroids or other topical immunosuppressives is well documented and supported by a meta-analysis of randomized controlled trials (RCT). [Level 1] Knowledge and understanding of management by nurses and pharmacists is also critical as they tend to be more readily accessible to patients and should be knowledgeable regarding potential complications and management. Outcomes are typically excellent with or without treatment, and patients should be given specific instructions regarding prevention, decontamination, and when to return if symptoms spread or worsen. [Level 4]

If there is a concern for systemic or respiratory exposure, patients should be admitted to the hospital for further observation and management.



5/16/2023 11:06:34 PM



Fisher AA. Poison ivy/oak/sumac. Part II: Specific features. Cutis. 1996 Jul:58(1):22-4     [PubMed PMID: 8823544]


DAWSON CR. The chemistry of poison ivy. Transactions of the New York Academy of Sciences. 1956 Mar:18(5):427-43     [PubMed PMID: 13312069]


SYMES WF, DAWSON CR. Separation and structural determination of the olefinic components of poison ivy urushiol, cardanol and cardol. Nature. 1953 May 9:171(4358):841-2     [PubMed PMID: 13054743]


McGovern TW, Barkley TM. Botanical dermatology. International journal of dermatology. 1998 May:37(5):321-34     [PubMed PMID: 9620476]


Stoner JG, Rasmussen JE. Plant dermatitis. Journal of the American Academy of Dermatology. 1983 Jul:9(1):1-15     [PubMed PMID: 6886091]


Kim Y, Flamm A, ElSohly MA, Kaplan DH, Hage RJ Jr, Hamann CP, Marks JG Jr. Poison Ivy, Oak, and Sumac Dermatitis: What Is Known and What Is New? Dermatitis : contact, atopic, occupational, drug. 2019 May/Jun:30(3):183-190. doi: 10.1097/DER.0000000000000472. Epub     [PubMed PMID: 31045932]


Baer RL. Poison ivy dermatitis. Cutis. 1990 Jul:46(1):34-6     [PubMed PMID: 2143465]


Epstein WL. Occupational poison ivy and oak dermatitis. Dermatologic clinics. 1994 Jul:12(3):511-6     [PubMed PMID: 7923948]


Oltman J, Hensler R. Poison oak/ivy and forestry workers. Clinics in dermatology. 1986 Apr-Jun:4(2):213-6     [PubMed PMID: 2941133]


Rademaker M, Duffill MB. Allergic contact dermatitis to Toxicodendron succedaneum (rhus tree): an autumn epidemic. The New Zealand medical journal. 1995 Apr 12:108(997):121-3     [PubMed PMID: 7739818]


Williams JV,Light J,Marks JG Jr, Individual variations in allergic contact dermatitis from urushiol. Archives of dermatology. 1999 Aug;     [PubMed PMID: 10456367]


Gladman AC. Toxicodendron dermatitis: poison ivy, oak, and sumac. Wilderness & environmental medicine. 2006 Summer:17(2):120-8     [PubMed PMID: 16805148]


Andersen KE, Benezra C, Burrows D, Camarasa J, Dooms-Goossens A, Ducombs G, Frosch P, Lachapelle JM, Lahti A, Menné T. Contact dermatitis. A review. Contact dermatitis. 1987 Feb:16(2):55-78     [PubMed PMID: 3552400]


Kalish RS. Recent developments in the pathogenesis of allergic contact dermatitis. Archives of dermatology. 1991 Oct:127(10):1558-63     [PubMed PMID: 1929465]


Barker JN. Role of keratinocytes in allergic contact dermatitis. Contact dermatitis. 1992 Mar:26(3):145-8     [PubMed PMID: 1505178]


Kupper TS. Production of cytokines by epithelial tissues. A new model for cutaneous inflammation. The American Journal of dermatopathology. 1989 Feb:11(1):69-73     [PubMed PMID: 2644870]


Kurlan JG, Lucky AW. Black spot poison ivy: A report of 5 cases and a review of the literature. Journal of the American Academy of Dermatology. 2001 Aug:45(2):246-9     [PubMed PMID: 11464186]

Level 3 (low-level) evidence


Rader RK, Mu R, Shi H, Stoecker WV, Hinton KA. Dermoscopy of black-spot poison ivy. Dermatology online journal. 2012 Oct 15:18(10):8     [PubMed PMID: 23122015]


Haitz K, Mikailov A, Carter J. Black linear streaks on the face with pruritic plaques on the trunk and arms. Cutis. 2017 May:99(5):E5-E6     [PubMed PMID: 28632804]


Pittman MA, Lane DR. Black spot poison ivy: under the cover of darkness. The Journal of emergency medicine. 2013 Apr:44(4):e331-2. doi: 10.1016/j.jemermed.2012.11.062. Epub 2013 Feb 16     [PubMed PMID: 23419214]


Tanner TL. Rhus (Toxicodendron) dermatitis. Primary care. 2000 Jun:27(2):493-502     [PubMed PMID: 10815057]


Stibich AS, Yagan M, Sharma V, Herndon B, Montgomery C. Cost-effective post-exposure prevention of poison ivy dermatitis. International journal of dermatology. 2000 Jul:39(7):515-8     [PubMed PMID: 10940115]


Williford PM, Sheretz EF. Poison ivy dermatitis. Nuances in treatment. Archives of family medicine. 1994 Feb:3(2):184-8     [PubMed PMID: 7994440]


Cury Martins J, Martins C, Aoki V, Gois AF, Ishii HA, da Silva EM. Topical tacrolimus for atopic dermatitis. The Cochrane database of systematic reviews. 2015 Jul 1:2015(7):CD009864. doi: 10.1002/14651858.CD009864.pub2. Epub 2015 Jul 1     [PubMed PMID: 26132597]

Level 1 (high-level) evidence


Vernon HJ, Olsen EA. A controlled trial of clobetasol propionate ointment 0.05% in the treatment of experimentally induced Rhus dermatitis. Journal of the American Academy of Dermatology. 1990 Nov:23(5 Pt 1):829-32     [PubMed PMID: 2147698]


Goodall J. Oral corticosteroids for poison ivy dermatitis. CMAJ : Canadian Medical Association journal = journal de l'Association medicale canadienne. 2002 Feb 5:166(3):300-1     [PubMed PMID: 11868634]


Moe JF. How much steroid for poison ivy? Postgraduate medicine. 1999 Oct 1:106(4):21, 24     [PubMed PMID: 10533503]


Brodell RT, Williams L. Taking the itch out of poison ivy. Are you prescribing the right medication? Postgraduate medicine. 1999 Jul:106(1):69-70     [PubMed PMID: 10418575]


Wooldridge WE. Acute allergic contact dermatitis. How to manage severe cases. Postgraduate medicine. 1990 Mar:87(4):221-4     [PubMed PMID: 2138290]

Level 3 (low-level) evidence


Guin JD. Treatment of toxicodendron dermatitis (poison ivy and poison oak). Skin therapy letter. 2001 Apr:6(7):3-5     [PubMed PMID: 11376396]

Level 3 (low-level) evidence


Ashcroft DM, Dimmock P, Garside R, Stein K, Williams HC. Efficacy and tolerability of topical pimecrolimus and tacrolimus in the treatment of atopic dermatitis: meta-analysis of randomised controlled trials. BMJ (Clinical research ed.). 2005 Mar 5:330(7490):516     [PubMed PMID: 15731121]

Level 1 (high-level) evidence


Amrol D, Keitel D, Hagaman D, Murray J. Topical pimecrolimus in the treatment of human allergic contact dermatitis. Annals of allergy, asthma & immunology : official publication of the American College of Allergy, Asthma, & Immunology. 2003 Dec:91(6):563-6     [PubMed PMID: 14700441]


Abędź N, Pawliczak R. Efficacy and safety of topical calcineurin inhibitors for the treatment of atopic dermatitis: meta-analysis of randomized clinical trials. Postepy dermatologii i alergologii. 2019 Dec:36(6):752-759. doi: 10.5114/ada.2019.91425. Epub 2019 Dec 30     [PubMed PMID: 31998006]

Level 1 (high-level) evidence


Baldwin RW, Clegg JA, Curran AC, Austin EB, Khan T, Ma Y, Gunn B, Hudecz F, Byers VS, Lepoittevin JP, Price MR. Regulation of the contact sensitivity response to urushiol with anti-urushiol monoclonal antibody ALG 991. Archives of dermatological research. 1999 Dec:291(12):652-8     [PubMed PMID: 10651166]


Brook I, Frazier EH, Yeager JK. Microbiology of infected poison ivy dermatitis. The British journal of dermatology. 2000 May:142(5):943-6     [PubMed PMID: 10809852]


Lee NP, Arriola ER. Poison ivy, oak, and sumac dermatitis. The Western journal of medicine. 1999 Nov-Dec:171(5-6):354-5     [PubMed PMID: 10639874]


Devich KB, Lee JC, Epstein WL, Spitler LE, Hopper J Jr. Renal lesions accompanying poison oak dermatitis. Clinical nephrology. 1975:3(3):106-13     [PubMed PMID: 124640]


Marks JG Jr, Fowler JF Jr, Sheretz EF, Rietschel RL. Prevention of poison ivy and poison oak allergic contact dermatitis by quaternium-18 bentonite. Journal of the American Academy of Dermatology. 1995 Aug:33(2 Pt 1):212-6     [PubMed PMID: 7622647]


Grevelink SA, Murrell DF, Olsen EA. Effectiveness of various barrier preparations in preventing and/or ameliorating experimentally produced Toxicodendron dermatitis. Journal of the American Academy of Dermatology. 1992 Aug:27(2 Pt 1):182-8     [PubMed PMID: 1430354]


Marks JG Jr, Trautlein JJ, Epstein WL, Laws DM, Sicard GR. Oral hyposensitization to poison ivy and poison oak. Archives of dermatology. 1987 Apr:123(4):476-8     [PubMed PMID: 2950827]


Epstein WL, Byers VS, Frankart W. Induction of antigen specific hyposensitization to poison oak in sensitized adults. Archives of dermatology. 1982 Sep:118(9):630-3     [PubMed PMID: 6180687]


Fisher AA. Poison ivy/oak dermatitis. Part I: Prevention--soap and water, topical barriers, hyposensitization. Cutis. 1996 Jun:57(6):384-6     [PubMed PMID: 8804839]


McGovern TW, LaWarre SR, Brunette C. Is it, or isn't it? Poison ivy look-a-likes. American journal of contact dermatitis : official journal of the American Contact Dermatitis Society. 2000 Jun:11(2):104-10     [PubMed PMID: 10908180]


Hershko K, Weinberg I, Ingber A. Exploring the mango-poison ivy connection: the riddle of discriminative plant dermatitis. Contact dermatitis. 2005 Jan:52(1):3-5     [PubMed PMID: 15701120]


Yoo MJ, Carius BM. Mango Dermatitis After Urushiol Sensitization. Clinical practice and cases in emergency medicine. 2019 Nov:3(4):361-363. doi: 10.5811/cpcem.2019.6.43196. Epub 2019 Sep 30     [PubMed PMID: 31763588]

Level 3 (low-level) evidence