Effects of diet on skin sensitization by nickel, poison ivy, and sesquiterpene lactones.

Skin contact or exposure to sensitizers often occurs as a consequence of occupational exposures (e.g. poison ivy in forestry), wearing jewelry (e.g. nickel), or use of cosmetics (e.g. fragrances). However, many of the known skin sensitizers or their chemical variants are also consumed orally through foods or other sources. Since oral exposure to antigenic substances can lead to tolerance, consumption of sensitizers may impact the development and potency of skin sensitization, especially if the sensitizer is consumed early in life, prior to the first skin contact. To address this issue, we have reviewed human clinical and epidemiological literature relevant to this subject and evaluated whether early oral exposures to relevant sensitizers, or their chemical variants, are associated with reduced prevalence of skin sensitization to three main allergic sensitizers - nickel, urushiols of poison ivy, and sesquiterpene lactones of chrysanthemum and other plants.

Airborne contact dermatitis: common causes in the USA.

Airborne contact dermatitis (ABCD) is an inflammatory reaction involving the skin upon exposure to allergenic agents or irritants suspended in air. In allergic ABCD, the hypersensitivity is classified as a type IV reaction. Substances responsible for such reactions can be of plant or non-plant origin. Commonly reported plants include those of the Compositae family, which includes ragweed, goldenrod, and sunflowers. Establishing an accurate diagnosis is critical for preventing exposure and improving symptoms in patients. Obtaining a detailed history and performing a physical examination to determine the sites of involvement, as well as patch testing to establish the causative allergen, are the main methods of arriving at the correct diagnosis. Treatment often involves avoidance of the allergens or irritants when possible and may also include the application of topical barrier creams or systemic therapy in more severe cases. This article reviews the topic of ABCD and highlights its most common etiologies in the USA.

Urushiol detection using a profluorescent nitroxide.

A method to visually detect minute amounts of urushiol, the toxic catechol from poison oak, poison ivy, and poison sumac, has been developed utilizing the reaction of a profluorescent nitroxide with the B-n-butylcatecholboronate ester formed in situ from urushiol and B-n-butylboronic acid. The resulting N-alkoxyamine is strongly fluorescent upon illumination with a fluorescent lamp, allowing the location of the toxic urushiol contamination to be visualized. This methodology constitutes the groundwork for the future development of a spray to detect urushiol to avoid contact dermatitis, as well as to detect catecholamines for biomedical applications.

Biomass and toxicity responses of poison ivy (Toxicodendron radicans) to elevated atmospheric CO2.

Contact with poison ivy (Toxicodendron radicans) is one of the most widely reported ailments at poison centers in the United States, and this plant has been introduced throughout the world, where it occurs with other allergenic members of the cashew family (Anacardiaceae). Approximately 80% of humans develop dermatitis upon exposure to the carbon-based active compound, urushiol. It is not known how poison ivy might respond to increasing concentrations of atmospheric carbon dioxide (CO(2)), but previous work done in controlled growth chambers shows that other vines exhibit large growth enhancement from elevated CO(2). Rising CO(2) is potentially responsible for the increased vine abundance that is inhibiting forest regeneration and increasing tree mortality around the world. In this 6-year study at the Duke University Free-Air CO(2) Enrichment experiment, we show that elevated atmospheric CO(2) in an intact forest ecosystem increases photosynthesis, water use efficiency, growth, and population biomass of poison ivy. The CO(2) growth stimulation exceeds that of most other woody species. Furthermore, high-CO(2) plants produce a more allergenic form of urushiol. Our results indicate that Toxicodendron taxa will become more abundant and more "toxic" in the future, potentially affecting global forest dynamics and human health.

Extract of Toxicodendron quercifolium caused genotoxicity and antigenotoxicity in bone marrow cells of CD1 mice.

As has been shown in numerous studies, naturally occurring compounds can have protective effects towards mutagens and carcinogens. In the present study, the genotoxic/antigenotoxic effect of Toxicodendron quercifolium (poison ivy) extract, which has been identified as antigenotoxic in human HepG2 cells in former studies, was examined in the in vivo micronucleus assay using polychromatic erythrocytes (PCE) of bone marrow of CD1-mice. For this, D0 (1:10), D0 (1:25), D0 (1:50), D1 (1:50), D2 (1:50), and D4 (1:50) dilutions of ethanolic plant extract prepared on the basis of the "Hömoopathisches Arzneimittelbuch (HAB 2000)" were administered orally to CD1 mice over a period of two days. A significant increase (p < 0.05) in micronucleus frequencies was found after administration of D0 (1:10), the highest tolerated dose. Additionally, antigenotoxic effects of T. quercifolium towards benzo(a)pyrene-induced micronucleus formation were studied. For that, four dilutions of the plant extract [D0, D2, D4, D6, each 1:50] were administered orally to CD1 mice for five days prior to the administration of benzo(a)pyrene (250 mg/kg b.w.) for another two days. It was found that the administration of the dilutions D0 (1:50) and D2 (1:50) of T. quercifolium extract significantly inhibited benzo(a)pyrene-induced micronucleus formation (p < 0.0001). The results of this study indicated that T. quercifolium extract has the character of a so-called "Janus"-genotoxin: High doses led to a weak but significant increase of micronucleus frequencies whereas low doses showed chemopreventive effects towards benzo(a)pyrene-induced DNA damage. The constituents of T. quercifolium responsible for the genotoxic and antigenotoxic effects may be flavonoids, which are known to have prooxidative and scavenging effects and identified by HPLC-MS/MS.

Regulation of the contact sensitivity response to urushiol with anti-urushiol monoclonal antibody ALG 991.

The objective of the studies was to demonstrate that the contact sensitivity (CS) response to poison ivy/oak could be downregulated following treatment with a monoclonal antibody (mAb) reacting with the allergen urushiol. Conjugation of urushiol and its synthetic analogue 3-n-pentadecylcatechol (PDC) to N-acetylcysteine yielded hydrosoluble derivatives which induced humoral immune responses in BALB/c mice. Hybridomas secreting monoclonal antibodies (mAbs) reacting with urushiol and PDC were generated by fusion of B lymphocytes from immunized mice with mouse myeloma P3NS0 cells. The specificity of mAb ALG 991 (IgM isotype) was defined by inhibition of antibody binding by PDC analogues. This demonstrated that mAb ALG 991 reacted with the catechol moiety of urushiol, the region of the allergen being critically important in the induction of contact dermatitis. The CS response to urushiol in BALB/c mice was suppressed by stimulation with mAb ALG 991 and the role of sensitized T cells, including suppressor T cells, has been considered. Suppression of CS was most effective with low doses (1 microg) of mAb incorporated into a vaccine with Freund's adjuvant. This treatment suppressed CS responses in BALB/c mice already sensitized to urushiol.