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Phytophototoxin Poisoning

  • Author: Toluwumi Jegede, MD; Chief Editor: Asim Tarabar, MD  more...
 
Updated: Apr 20, 2015
 

Background

Phytophotodermatitis (PPD) is a phototoxic inflammatory dermal reaction induced by exposure to certain light-sensitizing plant products followed by exposure to long-wave ultraviolet light (UV-A 320-380 nm). Both components (plant and light) are required; neither agent alone can cause phytophotodermatitis.

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Pathophysiology

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.

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 reaction. Plants are thought to produce furocoumarins for disease resistance.

Members of the plant families Umbelliferae, Leguminosae, Apiaceae, Rutaceae, Moraceae, Rosaceae, Asteraceae, Brassicaceae, Clusiaceae, Convolvulaceae, Anacardiaceae, Fabaceae, and Ranunculaceae 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.[1, 2, 3, 4, 5, 6, 7, 8, 9] Photos of a couple of the common plants are shown below.

Queen Anne's lace, a member of the Umbelliferae fa Queen Anne's lace, a member of the Umbelliferae family of plants, is well known to produce a furocoumarin-induced phototoxic eruption.
Ficus. The common fig contains furocoumarins and s Ficus. The common fig contains furocoumarins and should be considered amidst the list of potential offending agents that cause phytophotodermatitis.

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.

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.[2] 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. 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.[10, 11]

Phytophototoxicity is amplified by humidity and perspiration.

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.

Close-up view of vesicular linear streaks with mor Close-up view of vesicular linear streaks with morphology suggestive of scattered foci of epidermal necrosis.

The acute process may be followed by postinflammatory irregular hyperpigmentation that 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.[2]

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Epidemiology

Frequency

United States

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.

International

No difference exists between US and international occurrence.

Mortality/Morbidity

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

Race

No racial predisposition is demonstrated. Fair-skinned individuals are more frequently reported.

Sex

Both sexes are at risk.

Age

Phytophotodermatitis may be seen in all age groups.

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Contributor Information and Disclosures
Author

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

Disclosure: Nothing to disclose.

Coauthor(s)

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.

Specialty Editor Board

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.

Chief Editor

Asim Tarabar, MD Assistant Professor, Director, Medical Toxicology, Department of Emergency Medicine, Yale University School of Medicine; Consulting Staff, Department of Emergency Medicine, Yale-New Haven Hospital

Disclosure: Nothing to disclose.

Additional Contributors

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.

Acknowledgements

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.

References
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A 37-year-old white woman presented to the clinic complaining of a rash on the medial part of her right thigh and left arm that was acquired after clearing some weeds in her yard. A phototoxic combination of sunlight and a psoralen-containing plant produced this bizarre linear vesicular eruption.
Closer clinical view of bizarre angulated vesicular streaks, which occurred after contact with a plant and ultraviolet light exposure.
A 26-year-old female airline flight attendant exposed to lime while serving drinks en route to the Caribbean. During the Caribbean layover, she had significant sun exposure. The combination of lime juice and sun exposure led to a drip-pattern blister formation on the dorsal forearm consistent with phytophotodermatitis. This picture clearly delineates the potential severity of phytophotodermatitis with extensive blister formation.
The 2-month follow-up photo of the patient above demonstrates the potential postinflammatory pigmentation changes and scarring that may occur with severe blistering of phytophotodermatitis.
Close-up view of vesicular linear streaks with morphology suggestive of scattered foci of epidermal necrosis.
Queen Anne's lace, a member of the Umbelliferae family of plants, is well known to produce a furocoumarin-induced phototoxic eruption.
Ficus. The common fig contains furocoumarins and should be considered amidst the list of potential offending agents that cause phytophotodermatitis.
 
 
 
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