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Plant Poisoning, Phytophototoxins
Updated: Jan 7, 2010
Introduction
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.
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 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.
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 morphology suggestive of scattered foci of epidermal necrosis.
The acute process may be followed by postinflammatory irregular hyperpigmentation that can last weeks to months. 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
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.
Clinical
History
The history is essential in making the diagnosis of phytophotodermatitis. A patient's employment history; eating and drinking habits; recreational activities; tanning habits, including the use of herbal tanning lotions and citrus hair lighteners; prescription and over-the-counter medications; and travel experience may all provide essential information to the health care provider.1,12,13,14,15,16,17,18,19,20,9 Phytophotodermatitis (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. The photos below show a reaction after exposure to a plant and sunlight. The second image is a close-up view of the rash.
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.
- 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).
- The irregular "burns" and handmark patterns produced, often without a clear-cut history, have been mistaken for child abuse. A good history is essential in differentiating the two in children.21,22,23,24
Physical
- A usually sharp demarcation between normal covered skin and abnormal exposed skin is observed. The color of lesions may vary depending on the individual's underlying skin tone and the degree of exposure.
- Initial nonpruritic erythema of exposed areas. A "burst" of skin lesions may been seen after contact with squirted lime juice or with sprayed plant materials onto an individual's uncovered arms or legs while utilizing a "weed whacker". Photos below show a rash caused by lime juice and subsequent sunlight exposure. The second photo was taken at follow-up visit.
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.
- Development of edema, leading to vesicles, bullae, or both (usually within 24-72 h)
- Possible desquamation
- Resultant dense hyperpigmentation from melanocytic response
Causes
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.
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Further Reading
Keywords
phytophotodermatitis, PPD, photosensitization, phototoxicity, phytophotosensitivity, photosensitive reaction, furocoumarins, psoralens, Umbelliferae, Rutaceae, Moraceae, Compositae, Ranunculaceae, perfume-induced berloque dermatitis, ultraviolet light, UV, UVA , UV-A
