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Phytophototoxin Poisoning

Phytophototoxin Poisoning

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Phytophotodermatitis (PPD) is a phototoxic inflammatory dermal reaction mimicking a burn injury. It is induced by exposure to certain light-sensitizing plant products, most often furocoumarins, followed by exposure to long-wave ultraviolet light (UV-A 320-380 nm). [1] Both components (plant and light) are required; neither agent alone can cause phytophotodermatitis.

The phototoxic inflammatory eruption usually appears 24 hours after exposure and peaks within 48-72 hours. Initial burning erythema is followed by blistering, epidermal necrosis (shown in the photo below), and desquamation. The acute process may be followed by postinflammatory irregular hyperpigmentation that can last weeks to months.

Phototoxic dermatitis is 1 of the 4 mechanisms of cutaneous inflammation produced by plant exposure. Plants may also cause irritant contact dermatitis, urticarial dermatitis, or allergic contact dermatitis. [2]

Phytophotodermatitis (PPD) can occur through ingestion of the plant or, more commonly, through topical contact. Furocoumarins (bergaptol, xanthotal, 5-methoxypsoralens, 8 methoxypsoralens, angelican) are the major photoreactive essential plant oils involved in PPD. Plants are thought to produce furocoumarins for disease resistance.

Melough and collegues measured the total furocoumarin concentration in various foods and beverages and showed that grapefruit juice (95341 ng/g), fresh parsley (23215 ng/g), grapefruits (21858 ng/g), lime juice (14580 ng/g), limes (9151 ng/g), and lemon juice (1561 ng/g) had the greatest concentration of furocoumarins. Additional foods with high furocoumarin concentration included celeriac (also known as turnip-rooted celery, celery root, or knob celery) (396 ng/g), parsnips (335 ng/g), and carrots (68 ng/g). [3]

Exposure to certain wavelengths of ultraviolet A (UV-A 320-380 nm) light enable furocoumarins to absorb energy, thereby altering reactivity of the molecular structure and causing it to attain a high-energy state. [4] In the presence of oxygen, activated molecules form photoaddition products with DNA pyrimidine bases via DNA interstrand crosslinking at cytosine and thymidine with the furan ring of the psoralen and result in epidermal cell nucleic acid damage (type I reaction). In the absence of oxygen, activated furocoumarins can also produce oxygen, superoxide, and hydroxy radicals, which cause cellular membrane damage (type II reaction).

Both mechanisms result in arachidonic acid pathway activation, cellular dysfunction, and tissue destruction. When acute, the process is phototoxic.

The chronic presentation of phytophotodermatitis involves a photoallergic response; light-activated plant products act as haptens and produce a cell-mediated hypersensitivity response. Psoralens may not be primarily involved in this chronic mechanism of injury. [5, 6]

Phytophototoxicity is amplified by humidity and perspiration.

Postinflammatory irregular hyperpigmentation may develop and can last weeks to months. Affected areas may remain hypersensitive to ultraviolet light for many years. In some individuals, these pigmentary changes may be the only portion of the process that is noticed, as the initial inflammatory reaction may be minimal. Irregular hyperpigmentation occurs via 2 mechanisms. Melanin is displaced from the epidermis into the dermis and ingested by melanophages. A larger number of melanocytes and melanosomes are distributed in the epidermis. Hyperpigmentation may be a protective mechanism to avoid additional solar injury. [4]

Phytophotodermatitis (PPD) is induced by exposure to certain plants with subsequent exposure to sunlight. PPD can occur through ingestion of the plant or, more commonly, through topical contact.

Members of the following plant families are noted to cause a phytophotodermatitis reaction:

Common plants implicated in these families include celery, giant hogweed, angelica, parsnip, fennel, dill, anise, parsley, lime, lemon, rue, fig, mustard, scurf pea, and chrysanthemums. [7, 4, 8, 9, 10, 11, 12, 13, 14, 15]  Photos of a couple of the common plants are shown below.

Oil of bergamot, extracted from the rind of fresh bergamot oranges (Citrus bergamia), is commonly used to scent commercial perfumes and colognes. Perfume-induced berloque dermatitis is a specific form of a phytophotodermatitis reaction; areas of skin reaction correspond to areas exposed to perfume.

A case of phytophotodermatitis caused by carrot extract-containing sunscreen has been reported. [16]

Incidence varies per population and exposure. Individuals who handle produce or receive significant sunlight exposure (eg, field workers, farmers, gardeners, grocery workers, bartenders, vegetarians, persons who use tanning salons) are at an increased risk. Cases of phytophotodermatitis (PPD) more commonly occur in late spring and summer, when furocoumarins are found in increased concentration in plants and when individuals experience increased UV exposure. [17]

No difference exists between United States and international occurrence. 

No racial predisposition is demonstrated. Cases are more frequently reported in fair-skinned individuals. Both sexes are at risk. PPD may be seen in all age groups. [17]

Significant long-term skin changes (hyperpigmentation, scarring) can occur with chronic exposure. Secondary wound infection may occur.

Patients should be educated regarding plants that produce phytophototoxicity in order to avoid skin exposure. Patients may be counseled to wear gloves and skin coverings when their work necessitates ongoing exposure to these plant oils and to the sun. Patients should be educated regarding use of appropriate sunscreens when sun-exposed.

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Pragya Nair. Dermatitis, Contact. Amber Atwater. StatPearls. Treasure Island (FL): StatPearls Publishing LLC; 2018 Jan. [Full Text].

Melough MM, Lee SG, Cho E, Kim K, Provatas AA, Perkins C, et al. Identification and Quantitation of Furocoumarins in Popularly Consumed Foods in the U.S. Using QuEChERS Extraction Coupled with UPLC-MS/MS Analysis. J Agric Food Chem. 2017 Jun 21. 65 (24):5049-5055. [Medline].

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Ivie GW, Holt DL, Ivey MC, et al. Natural toxicants in human foods: psoralens in raw and cooked parsnip root. Science. 1981 Aug 21. 213(4510):909-10. [Medline].

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Toluwumi Jegede, MD Resident Physician, Department of Emergency Medicine, State University of New York Downstate Medical Center

Disclosure: Nothing to disclose.

Antonia Quinn, DO Assistant Professor, Department of Emergency Medicine, State University of New York Downstate Medical Center; Assistant Residency Director, Attending Physician, Department of Emergency Medicine, Kings County Hospital Center, SUNY Downstate Medical Center

Antonia Quinn, DO is a member of the following medical societies: American College of Emergency Physicians, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

John T VanDeVoort, PharmD Regional Director of Pharmacy, Sacred Heart and St Joseph’s Hospitals

John T VanDeVoort, PharmD is a member of the following medical societies: American Society of Health-System Pharmacists

Disclosure: Nothing to disclose.

Sage W Wiener, MD Assistant Professor, Department of Emergency Medicine, State University of New York Downstate Medical Center; Director of Medical Toxicology, Department of Emergency Medicine, Kings County Hospital Center

Sage W Wiener, MD is a member of the following medical societies: American Academy of Clinical Toxicology, American Academy of Emergency Medicine, American College of Medical Toxicology, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Miguel C Fernandez, MD, FAAEM, FACEP, FACMT, FACCT Associate Clinical Professor, Department of Surgery/Emergency Medicine and Toxicology, University of Texas School of Medicine at San Antonio; Medical and Managing Director, South Texas Poison Center

Miguel C Fernandez, MD, FAAEM, FACEP, FACMT, FACCT is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American College of Medical Toxicology, Society for Academic Emergency Medicine, Texas Medical Association, American College of Occupational and Environmental Medicine

Disclosure: Nothing to disclose.

Michael Hodgman, MD Assistant Clinical Professor of Medicine, Department of Emergency Medicine, Bassett Healthcare

Michael Hodgman, MD is a member of the following medical societies: American College of Medical Toxicology, American College of Physicians, Medical Society of the State of New York, and Wilderness Medical Society

Disclosure: Nothing to disclose.

Thomas Joseph Lydon, MD, PhD Consulting Staff, Section of Emergency Medicine, Dartmouth-Hitchcock Medical Center

Disclosure: Nothing to disclose.

Suzanne Moore Shepherd, MD, MS, DTM&H, FACEP, FAAEM Professor of Emergency Medicine, Education Officer, Department of Emergency Medicine, Hospital of the University of Pennsylvania; Director of Education and Research, PENN Travel Medicine; Medical Director, Fast Track, Department of Emergency Medicine

Suzanne Moore Shepherd, MD, MS, DTM&H, FACEP, FAAEM is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American Society of Tropical Medicine and Hygiene, International Society of Travel Medicine, Society for Academic Emergency Medicine, and Wilderness Medical Society

Disclosure: Nothing to disclose.

William H Shoff, MD, DTM&H Director, PENN Travel Medicine; Associate Professor, Department of Emergency Medicine, Hospital of the University of Pennsylvania, University of Pennsylvania School of Medicine

William H Shoff, MD, DTM&H is a member of the following medical societies: American College of Physicians, American Society of Tropical Medicine and Hygiene, International Society of Travel Medicine, Society for Academic Emergency Medicine, and Wilderness Medical Society

Disclosure: Nothing to disclose.

Phytophototoxin Poisoning

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