eMedicine Specialties > Emergency Medicine > Toxicology

Plant Poisoning, Phytophototoxins

Author: Suzanne Moore Shepherd, MD, MS, DTM&H, FACEP, FAAEM, Associate Professor, Department of Emergency Medicine, Hospital of the University of Pennsylvania; Director of Education and Research, PENN Travel Medicine
Coauthor(s): Thomas Joseph Lydon, MD, PhD, Consulting Staff, Section of Emergency Medicine, Dartmouth-Hitchcock Medical Center; William H Shoff, MD, DTM&H, Director, PENN Travel Medicine, Associate Professor, Department of Emergency Medicine, Hospital of the University of Pennsylvania
Contributor Information and Disclosures

Updated: Sep 23, 2008

Introduction

Background

Phytophotodermatitis (PPD) is a photosensitive dermal reaction induced by exposure to certain plants with subsequent exposure to sunlight. Both components (plant and light) are required; neither agent alone can cause PPD.

Pathophysiology

PPD can occur through ingestion of the plant or, more commonly, through topical contact. Furocoumarins (psoralens) are the major photoreactive essential plant oils involved in PPD reaction. Plants are thought to produce furocoumarins for disease resistance.

Members of plant families Apiaceae, Rutaceae, Moraceae, Rosaceae, Asteraceae, Brassicaceae, Clusiaceae, Convolvulaceae, Anacardiaceae, Fabaceae, and Ranunculaceae are noted to cause PPD 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.

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 PPD reaction; areas of skin reaction correspond to areas exposed to perfume.

Exposure to certain wavelengths of ultraviolet A (UV-A) light enables furocoumarin to absorb the energy, thereby altering reactivity of the molecule and causing the molecule to attain a high-energy state. The activated molecules form photoaddition products with DNA pyrimidine bases and result in epidermal cell nucleic acid damage (type I reaction). Activated furocoumarins can also produce oxygen, superoxide, and hydroxy radicals, which cause cellular membrane damage (type II reaction).

Both mechanisms result in cellular dysfunction and tissue destruction. When acute, the process is phototoxic. Chronic presentation of PPD 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 mechanism of injury.

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.

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 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.

Clinical

History

PPD often occurs in linear and odd patterns, including "handprints."

  • A phototoxic reaction can result from contact with a specific plant via skin exposure, or less commonly, ingestion, followed by exposure to sunlight.
  • Symptoms usually occur within 24-48 hours following sunlight exposure.
  • Symptoms are frequently described as an initial burning pain and erythema, followed by blistering. Blistering may occur within 10 minutes.
  • Pruritus is uncommon, distinguishing PPD from allergic phytodermatitis (eg, toxicodendron dermatitis).

Physical

  • A usually sharp demarcation between normal covered and abnormal exposed skin
  • Initial nonpruritic erythema of exposed areas
  • Development of edema, leading to vesicles and/or bullae
  • Possible desquamation
  • Resultant dense hyperpigmentation from melanocytic response

Causes

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.

More on Plant Poisoning, Phytophototoxins

Overview: Plant Poisoning, Phytophototoxins
Differential Diagnoses & Workup: Plant Poisoning, Phytophototoxins
Treatment & Medication: Plant Poisoning, Phytophototoxins
Follow-up: Plant Poisoning, Phytophototoxins
References
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References

  1. Bansal I, Kerr H, Janiga JJ, Qureshi HS, Chaffins M, Lim HW. Pinpoint papular variant of polymorphous light eruption: clinical and pathological correlation. J Eur Acad Dermatol Venereol. Apr 2006;20(4):406-10. [Medline].

  2. Berkley SF, Hightower AW, Beier RC, et al. Dermatitis in grocery workers associated with high natural concentrations of furanocoumarins in celery. Ann Intern Med. Sep 1986;105(3):351-5. [Medline].

  3. Epstein WL, Epstein JH. Plant induced dermatitis. In: Wilderness Medicine. 3rd ed. 1995:843-61.

  4. Gross TP, Ratner L, de Rodriguez O, et al. An outbreak of phototoxic dermatitis due to limes. Am J Epidemiol. Mar 1987;125(3):509-14. [Medline].

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

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Further Reading

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Keywords

phytophotodermatitis, PPD, photosensitization, phytophotosensitivity, photosensitive reaction, furocoumarins, psoralens, Umbelliferae, Rutaceae, Moraceae, Compositae, Ranunculaceae, perfume-induced berloque dermatitis, ultraviolet light, UV, UVA , UV-A

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Contributor Information and Disclosures

Author

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

Coauthor(s)

Thomas Joseph Lydon, MD, PhD, Consulting Staff, Section of Emergency Medicine, Dartmouth-Hitchcock Medical Center
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
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: Glaxo Smith Kline Consulting fee Consulting; Glaxo Smith Kline Honoraria Speaking and teaching

Medical Editor

Miguel C Fernandez, MD, FAAEM, FACEP, FACMT, Associate Clinical Professor; Medical and Managing Director, South Texas Poison Center, Department of Surgery/Emergency Medicine and Toxicology, University of Texas Health Science Center at San Antonio
Miguel C Fernandez, MD, FAAEM, FACEP, FACMT is a member of the following medical societies: American Academy of Clinical Toxicology, American Academy of Emergency Medicine, American College of Emergency Physicians, American College of Medical Toxicology, Society for Academic Emergency Medicine, and Texas Medical Association
Disclosure: Nothing to disclose.

Pharmacy Editor

John T VanDeVoort, PharmD, ABAT, Director of Pharmacy, Sacred Heart Hospital
John T VanDeVoort, PharmD, ABAT is a member of the following medical societies: American Academy of Clinical Toxicology and American Society of Health-System Pharmacists
Disclosure: Nothing to disclose.

Managing Editor

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.

CME Editor

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Chief Editor

Asim Tarabar, MD, Assistant Professor, Department of Surgery, Section of Emergency Medicine, Yale University School of Medicine; Consulting Staff, Department of Emergency Medicine, Yale-New Haven Hospital
Disclosure: Nothing to disclose.

 
 
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