Phytophototoxin Poisoning

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

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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