Irritant Contact Dermatitis from Plants

Gunjan M. Modi; Christy B. Doherty; Rajani Katta; Ida F. Orengo


Dermatitis. 2009;20(2):63-78. 

In This Article

Clinical Considerations

Risk Factors and High-Risk Populations

It is generally accepted that because of the nature of chemical and mechanical irritants, the primary factors determining the level of irritation to a particular irritant are the length of exposure, the concentration or amount of irritant in contact, and the integrity of the normal skin barrier function. Modjtahedi and Maibach found that ethnicity does not appear to play a role in risk stratification for ICD.[53] Similarly, while it was previously thought that females have a higher risk of developing ICD in the occupational setting, this assertion has since been disputed.[54,55]

Individuals at risk tend to be those who may come into frequent contact with plant irritants. Therefore, many cases of ICD from plants can be viewed as occupational dermatoses.[33] ICD is the most common presentation of occupational skin disease and is extremely common among florists, farmers, grocers, and outdoor workers.[7,55] For example, hand dermatitis from plants can affect up to 30% of all florists in a given year.[9]

Other documented occupational risk factors for ICD from plants include humid or wet working conditions, perspiration, the relative expertise of the florist or worker, and the technique used to cut and handle the plants.[2,4,8,23]

Clinical Presentation

As discussed, the clinical appearance of ICD from plants is quite polymorphous. The general rule is that any part of the body in direct contact with the plant irritant can be affected. Typical examples are the fingers, hands, wrists, forearms, and face. Irritants can be transferred from fomites and already exposed skin areas to those parts normally protected by clothing or not in direct contact with plants. Such secondarily affected regions commonly include the axilla, eyes, buttocks, and genitalia. The presentation of individuals with dermatitis on these secondarily affected areas makes the diagnosis of ICD particularly challenging.

Acute forms of ICD can occur within a few hours of contact and include erythema, edema, papules, and vesicles. Chronic ICD from plants following repeated exposure to the irritant presents commonly with xerosis, hyperkeratosis, and fissures.[8] While already varied in presentation, ICD may be particularly difficult to diagnose when patients present with more striking manifestations such as superficial necrosis, hemorrhagic bullae, and ulcerations.[5,8,39] The clinical picture of ICD may be further complicated by the presence of systemic findings, such as when the plant or plant product is consumed or inhaled.[4,32]

Histologically, ICD lesions vary from mild keratinocyte degeneration with spongiosis to epidermal necrosis with ulceration. Typically, there are superficial changes that involve disruption of the corneal layer as well as some intraepidermal necrosis. Plant irritants may also result in exocytosis of lymphocytes or neutrophils. Even the histologic patterns of karyorrhexis and perivascular neutrophilic infiltrate with leukocytoclastic vasculitis have been noted in the lesions of patients with ICD from plants.[3]

In contrast to allergic contact dermatitis (ACD), the exocytosis and spongiosis seen in ICD is accompanied by prominent epidermal hyperproliferation.[56] Generally, structural changes in the stratum corneum, karyorrhexis, pyknosis, and the presence of superficial vesicles with neutrophilic infiltrate are all more characteristic of an ICD reaction than an ACD reaction.[57] However, there are no histologic features that absolutely distinguish between ICD and ACD.

Diagnosis Of ICD

In spite of its ubiquity, ICD may be a difficult diagnosis to make. Distinguishing it from other plant dermatoses (ACD in particular) can be challenging. ICD is quite frequently a diagnosis of exclusion.[55]

A good history is essential in evaluating ICD from an irritant plant. Lovell states that, in addition to ascertaining the patient's occupation, it is necessary to acquire a "mental picture" of how the patient works with plants, which parts of the plant come into contact with the skin, and the extent to which such contact occurs.[6] Other important information includes the onset of first symptoms, the initial site of onset, sites of subsequent spread, improvement or worsening when the patient returns to work, and whether others have experienced similar symptoms in the workplace.[2]

Patch testing, while crucial in ruling out an allergic reaction, may often be misleading in cases of irritant plant reactions.[2] Irritant plants often cause false-positive patch-test results.[21] A major caution for dermatologists is that patch testing must never be performed with an unidentified plant. As our review highlights, a number of plants have mechanical or chemical irritant potential, which would only be intensified in a closed patch test. Negative patch-test results are mainly of value in ruling out an ACD reaction and keeping open the possibility of ICD.[58]

Tissue histology may be helpful in distinguishing ACD from ICD, but there is frequent histologic overlap in features.[57] Benezra and colleagues described the presence of trichome remnants seen under polarized light from a biopsy specimen, which can aid in the diagnosis of MICD from a plant.[8] Furthermore, Mascarenhas and colleagues reported that, if the suspected culprit plant sap or tissue is available, mechanical irritants such as calcium oxalate raphides may be visible under magnification.[25]

By clinical appearance alone, ICD and ACD may be very similar and difficult to distinguish. Like ICD, ACD can present in many different forms; the most common and easily identifiable form is an erythematous edematous eruption at sites of allergen contact. ICD tends to develop on the day of contact with the irritant. ACD generally intensifies between 24 and 48 hours after exposure, but persons who have been previously sensitized to an allergen may develop symptoms more rapidly.[58] Pruritus is also not a distinguishing feature as both types of reactions have been documented to be extremely pruritic[6,59] (see Table 1 ).

New techniques that may have the potential to aid in distinguishing between ACD and ICD include reflectance confocal microscopy, transepidermal water loss measurements, fluorescence excitation spectroscopy in vivo, and a novel "behind-the-knee" irritant test.[56,60]

Determining the Culprit Plant and Irritant

Once the diagnosis of ICD has been made, further investigation into the culprit plant and its constituent chemicals responsible for the irritation is challenging. Often the plant is not available for evaluation or identification. For situations in which the plant is available, Avalos and Maibach documented a systematic methodology for preserving the plant and its flowering parts for botanical identification and subsequent literature search.[1] Of note, a Web-based botanical dermatology database is available, along with numerous books documenting irritant plants.[1,34,61]

In many cases, the structure or name of the individual plant irritant is unknown. This is partly due to the complexity of the identification process, which includes preparation of the plant extract, isolation and purification of the active molecules, and identification of the structure of the compound. These steps involve liquid, gas, or high-performance chromatography and the combination of identification techniques such as mass spectrometry, infrared spectrometry, and nuclear magnetic resonance. Additionally, many plant irritants (including those discussed above) are short-lived and volatile, making isolation extremely difficult.[1]

Immunologic Response in ICD

Although it does not elicit an antigen-specific immune response, ICD is nonetheless the result of inflammation arising from the release of proinflammatory cytokines.[62] Cytokine release studies show that irritants are heterogeneous in both the individual cytokines released and the quantity of cytokines released. However, there is believed to be underlying commonality among all ICD reactions with regard to the mediators involved; these mediators include interleukin (IL)-1a, IL-1ß, and tumor necrosis factor-a.[58,63] Smith and colleagues reported that ICD may promote or enhance ACD because some of these mediators play a role in both ICD and ACD.[64]