Lacquer is a natural polymer collected from lacquer trees; it has durability and beauty and has been used in Asia for a thousand years.1-5 Lacquer was first used as an adhesive for fixing gold foil, chipped porcelain, or attaching arrowheads to the wooden shaft. Then, with the accumulation of experience and awareness, lacquer was applied to bamboo, wood, and other furniture. It is still used in daily life in crafts and industrial equipment. Collecting lacquer sap is like collecting gum from a rubber tree. The bark of the lacquer tree is tapped and the milky-white saps exude collected. The sap of lacquer is collected from the 5- to 10-year-old lacquer trees between June and October. The sap obtained is an emulsion of water in oil, which is called raw lacquer. After being stirred to homogenize it and heated to evaporate the water, fine lacquer, also called kurome lacquer in Japanese, is produced.
In Asian countries, lacquer sap is obtained mainly from the lacquer trees of Rhus vernicifera in China, Japan, and Korea, Rhus succedanea in Vietnam and Taiwan, and Melanorrhoea usitata in Myanmar and Thailand. The constituents and properties of the lacquers differ not only with the species but also with the age of trees, place grown, and season of collection. The constituents are lipid components (60-70%), water (20-30%), plant gum (4-10%), the enzyme laccase (1.5-2%), and water-insoluble glycoprotein (3-5%).6
Early in 1922, a Japanese researcher, Majima, sketched the skeleton of urushiol, a dihydric phenol with a side chain of 15 carbon atoms and suggested that at least three similar compounds were also present, with one, two, or three double bonds in the side chain.7 Further studies revealed that some of the side chains can contain up to 17 carbon atoms, and that the double bonds may occur in a variety of positions. The nucleus may also differ, both in the position and the number of side groups with at least two forms of a monohydric phenol having been detected.8
Lacquer has been studied in our laboratory for over thirty years. Fast drying,9 hybrid,10, 11 nano,12 and synthetic lacquers13 have been examined in detail. The deterioration and restoration of lacquer film,14 structural analysis of lipid components of lacquers,15 and enzymatic dehydrogenative polymerization16 have also been reported. The comprehensive results of lacquer research performed so far on the structures of lipid compositions of oriental lacquer saps are summarized in Table 1.
Because the main component of lacquer has a catechol ring structure, it caused dermatitis in lacquer workers.17-19 Therefore, studies of the external manifestations, results, allergic mechanism, medical treatment, and prevention have been ongoing. This review is to reveal the recent advances in the research of lacquer allergy including urushiol haptens, allergic mechanism analysis, immunological explanation, allergic medication, and the prevention.
Lacquer allergy usually refers to the allergic contact dermatitis that caused by the lipid components contained in lacquer sap. The lacquer lipid component is a hapten from the viewpoint of immunology.20 It is generally believed that the O-quinones derived from the oxidation of urushiols are susceptible to nucleophilic attack at the catechol ring in positions 4, 5, and 6 by proteins to form a complete antigen.21 The mechanism of allergic contact dermatitis has been evolved considerably by Polak22 and Benezra et al.,23 respectively.
The cellular events of lacquer allergy can be divided into induction and elicitation phases. In the induction phase, the hapten penetrates the skin and becomes a protein-hapten complex as a complete antigen, which can be incorporated into Langerhans cells (internalization) and present antigen information to T lymphocytes. These T lymphocytes then migrate to the lymph nodes where they differentiate and proliferate into effector cells and memory cells. At this point, the individual is hypersensitive and has immunologically prepared T lymphocytes that can react to a later attack by the same hapten.
In the elicitation phase, the hapten once again comes into contact with the skin and the previously formed protein-hapten complex. The effecter cells that were formed during the first contact and circulate in the blood now come into contact with the complex. These effector cells release chemical mediators called cytokines whose properties have been studied extensively.24 Cytokines are aimed at different targets: macrophages, lymphocytes, and other cell types (cytotoxic for T cells particular). These cytokines are responsible for the pathologic manifestations of allergic contact dermatitis, erythema, papules, vesicles, and/or swelling.25, 26
In the case of lacquer, the lipid components of lacquer urushiol, laccol, and thitsiol, are not electrophiles and can not react with electrophilic proteins to form an antigen.21 When these lipid molecules penetrate the skin, an enzyme catalyzes oxidation reaction and converts the lipids into O-quinones, which are authentic electrophiles, and react to keratin or protein in the cellular membrane to form a complete antigen, as shown in Figure 1. This urushiol antigen is captured by Langerhans cells, presents antigen information to T lymphocytes, and induces sensitization of T cells. In the initial sensitization process, while interleukin-1β (IL-1β) is produced by Langerhans cells, major histocompatibility complex (MHC) class II is expressed on the cell surface of Langerhans cells and recognized by T cells via T cells receptor (TCR) together with antigen fragments.27 The keratinocytes produce urushiol-generated cytokines such as tumor necrosis factor α (TNF-α), IL-1α, and granulocyte/macrophage colony-stimulating factor (GM-CSF), which further activates the Langerhans cells.28 After establishment of sensitization to urushiol, contact dermatitis occurs with the re-invasion of urushiol antigen, as shown in Figure 2. On the other hand, sometimes when the MHC class II presents antigen information to T lymphocytes, T cells does not react to the same antigen as they should, which is called "anergy", and this phenomenon is considered to be desensitization or hyposensitization. Watanabe et al.29 have showed that, in mice, inflammasome-signaling level can be modulated to turn dinitrothiocyanobenzene into a sensitizer and dinitrofluorobenzene into a tolerizer, and this is correlated with Th1, Th17, and regulatory T cells. The feature of lacquer allergy is that with the increased exposure experience to lacquer sap, the symptoms gradually relieved. The reason may be considered due to the regulatory T cells, and affecting the balance of Th1 and Th2.
Kidder EJ. Ancient Peoples and Places: Japan. London: Thames & Hudson, 1959.
KurakuY. Urushi. In: Brommelle NSSmith P (eds). Los Angeles, CA: Getty Conservation Institute, 1988; 45.
DuYM. Urushi. In: Brommelle NSSmith P (eds). Los Angeles, CA: Getty Conservation Institute, 1988; 194.
Hu J. Conservation and Restoration of Cultural Property: Conservation of Far Eastern Objects. Tokyo: Tokyo National Research Institute of Cultural Property, 1980; 89-112.
Miyakoshi T, Nagase K, Yoshida T. Progress of Lacquer Chemistry. Tokyo: IPC Publisher, 1999.
Kumanotani J. Urushi (oriental lacquer)—a natural aesthetic durable and future-promising coating. Prog Org Coat 1995; 26: 163-95.
Majima R. Berichte der deutschen chemischen Gesell-schaft. 1922; 55B: 172-91 (in German).
Du YM, Oshima R, Kumanotani J. Reversed-phase liquid chromatographic separation and identification of constituents of urushiol in the sap of the lac tree, Rhus vernicifera. J Chromatog 1984; 284: 463-73.
Lu R, Harigaya S, Ishimura T, Nagase K, Miyakoshi T. Development of a fast drying lacquer based on raw lacquer sap. Prog Org Coat 2004; 51: 238-43.
Lu R, Ishimura T, Tsutida K, Honda T, Miyakoshi T. Development of a fast drying hybrid lacquer in a low relative humidity environment based on kurome lacquer sap. J Appl Polym Sci 2005; 98: 1055-61.
Lu R, Honda T, Ishimura T, Miyakoshi T. Study of a naturally drying lacquer hybridized with organic silane. Polym J 2005; 37: 309-15.
Lu R, Ono M, Suzuki S, Miyakoshi T. Studies on a newly designed natural lacquer. Mater Chem Phys 2006; 100: 158-61.
Kamiya Y, Miyakoshi T. Synthesis of urushiol components and analysis of urushi sap from Rhus vernicifera. J Oleo Sci 2001; 50: 865-73.
Kamiya Y, Lu R, Kumamoto T, Honda T, Miyakoshi T. Deterioration of surface structure of lacquer films due to ultraviolet irradiation. Surf Interf Anal 2006; 38: 1311-5.
Lu R, Kamiya Y, Miyakoshi T. Characterization of lipid components of Melanorrhoea usitata lacquer sap. Talanta 2007; 71: 1536-40.
Harigaya S, Honda T, Lu R, Miyakoshi T, Chen LC. Enzymatic dehydrogenative polymerization of urushiols in fresh exudates from the lacquer tree, Rhus vernicifera DC. J Agric Food Chem 2007; 55: 2201-8.
Kawai K, Nakagawa M, Kawai K et al. Hyposensitization to urushiol among Japanese lacquer craftsmen. Contact Dermatitis 1991; 24: 146-7.
Kawai K, Nakagawa M, Kawai K, Konishi K, Liew FM, Yasuno H. Hyposensitization to urushiol among Japanese lacquer craftsmen: results of patch tests on students learning the art of lacquerware. Contact Dermatitis 1991; 25: 290-5.
Kawai K, Nakagawa M, Kawai K, Miyakoshi T, Miyashita K, Asami T. Heat treatment of Japanese lacquerware renders it hypoallergenic. Contact Dermatitis 1992; 27: 244-9.
Kawai K, Nakagawa M, Kawai K, Miyakoshi T, Miyashita K, Asami T. Hypoallergenic lacquerware. Environ Dermatol 1996; 3(Suppl 1): 119-25.
Kawai K, Nakagawa M, Zhang XM et al. Evaluation of structure-activity relationships for the allergenicities of urushiol analogs by using patch tests and lymphocyte stimulation tests in humans. Environ Dermatol 1996; 3(Suppl 1): 73-81.
Polak L. Immunological Aspects of Contact Sensitivity (Monographs in Allergy, Volume 15). Basel: S Karger, 1980.
Benezra C, Ducombs G, Sell Y, Foussereau J. Immunologic and molecular aspects of plant contact dermatitis: Plant Contact Dermatitis. Philadelphia: Decker, 1985; 21-8.
Kligman AM. Hyposensitization against Rhus dermatitis. Arch Dermatol 1958; 78: 47-72.
Ikeda Y, Yasuno H, Miyakoshi T, Sato A, Kawai K. Induction of tolerance to pentadecylcatechol in the guinea pig by intravenous injection of 1-O-α-D-glucopyranosyl-3-pentadecylcatechol. Enviro Dermatol 1995; 2: 27-31.
Ikeda Y, Yasuno H, Sato A, Kawai K. Oral and epicutaneous desensitization in urushiol contact dermatitis in guinea pigs sensitized by two methods of different sensitizing potency. Contact Dermatitis 1998; 39: 286-92.
Schornic LP, Togni PD, Mariathasan S et al. Mice deficient in IL-1β manifest impaired contact hypersensitivity to trinitrochlorobenzone. J Experimental Med 1996; 183: 1427-36.
Enk AH, Katz SI. Early molecular events in the induction phase of contact sensitivity. Proc Nat Acad Sci (PNAS) 1992; 89: 1398-402.
Watanabe H, Gehrke S, Contassot E et al. Danger signaling through the inflammasome acts as a mastre switch between tolerance and sensitization. J Immunol 2008; 180: 5826-32.
Ptak W, Herzog WR, Askenase PW. Delayed-type hypersensitivity initiation by early-acting cells that are antigen mismatched or MHC incompatible with late-acting, delayed-type hypersensitivity effector T cells. J Immunol 1991; 146: 469-75.
Waldorf HA, Walsh LJ, Schechter NM, Murphy GF. Early cellular events in evolving cutaneous delayed hypersensitivity in humans. Am J Pathol 1991; 138: 477-86.
Gocinski BL, Tigelaar RE. Roles of CD4+ and CD8+ T cells in murine contact sensitivity revealed by in vivo monoclonal antibody depletion. J Immunol 1990; 144: 4121-8.
Bour H, Peyron E, Gaucherand M et al. Major histocompatibility complex class I-restricted CD8+ T cells and class II-restricted CD4+ T cells, respectively, mediate and regulate contact sensitivity to dinitrofluorobenzene. Europ J Immunol 1995; 25: 3006-10.
Kalish RS, Wood JA, Laporte A. Processing of urushiol (poison ivy) hapten by both endogenous and exogenous pathways for presentation to T cells in vitro. J Clin Invest 1994; 93: 2039-47.
Kalergis AM, López CB, Becker MI et al. Modulation of fatty acid oxidation alters contact hypersensitivity to urushiols: Role of aliphatic chain β-oxidation in processing and activation of urushiols. J Invest Dermatol 1997; 108: 57-61.
López CB, Kalergis AM, Becker MI, Garbarino JA, Ioannes AE. CD8+ T cells are the effectors of the contact dermatitis induced by urushiol in mice and are regulated by CD4+ T cells. Inter Arch Allergy Immunol 1998; 117: 194-201.
Oka K, Saito F, Yasuhara T, Sugimoto A. A study of cross-reactions between mango contact allergents and urushiol. Contact Dermatitis 2004; 51: 292-6.
Xia ZY, Miyakoshi T, Yoshida T. Lipoxygenase-catalyzed polymerization of phenolic lipids suggests a new mechanism for allergic contact dermatitis induced by urushiol and its analogs. Biochem Biophy Res Comm 2004; 315: 704-9.
Kalish RS, Johnson KL. Enrichment and function of urushiol (poison ivy)-specific T lymphocytes in lesions of allergic contact dermatitis to urushiol. J Immunol 1990; 145: 3706-13.
Kalish RS, Wood JA. Induction of hapten-specific tolerance of human CD8+ urushiol (poison ivy)-reactive T lymphocytes. J Invest Dermatol 1997; 108: 253-7.
Wakabayashi T, Hu DL, Tagawa Y et al. IFN-γ and TNF-a are involved in urushiol-induced contact hypersensitivity in mice. Immunol Cell Biol 2005; 83: 18-24.
Roberts DL. An outbreak of contact dermatitis from Japanese lacquer tree. Contact Dermatitis 1997; 37: 237.
Oh SH, Haw CR, Lee MH. Clinical and immunologic features of systemic contact dermatitis from ingestion of Rhus (Toxicodendron). Contact Dermatitis 2003; 48: 251-4.
Myers W, Newman M, Katz B, Gottlieb AB. Ability to develop Rhus allergic contact dermatitis in a patient with psoriasis receiving etanercept. J Am Academy Dermatol 2006; 55: S127-8.
Epstein WL. Topical prevention of poison ivy/oak dermatitis. Arch Dermatol 1989; 125: 499-501.
Williford PM, Sherertz EF. Poison ivy dermatitis. Arch Family Med 1994; 3: 184-8.
Marks JG, Fowler JF, Sherertz EF, Rietschel RL. Prevention of poison ivy and poison oak allergic contact dermatitis by quaternium-18 bentonite. J Am Academy Dermatol 1995; 33: 212-6.
Paulsen E, Christensen LP, Andersen KE. Dermatitis from common ivy (Hedera helix L. subsp. helix) in Europe: past, present, and future. Contact Dermatitis 2010; 62: 201-9.
Guin JD. Treatment of toxicodendron dermatitis (poison ivy and poison oak). Skin Therapy Letter 2001; 6: 3-5.
Li SZ. Compendium of Materia Medica (Bencao Gangmu). Beijing: Foreign Language Press, 2003; 1991-4.
Santucci B, Picardo M. Occupational contact dermatitis to plants. Clin Dermatol 1992; 10: 157-65.
Kullavanijaya P, Ophaswongsi S. A study of dermatitis in the lacquerware industry. Contact Dermatitis 1997; 36: 244-6.
Baldwin RW, Clegg JA, Curran AC et al. Regulation of the contact sensitivity response to urushiol with anti-urushiol monoclonal antibody ALG 991. Arch Dermatol Res 1999; 291: 652-8.
Yarbrough WM, Schroeter C. Urushiol induced contact dermatitis and method of use. United States Patent, US 6423746 B1, 2002.
Park SD, Lee SW, Chun JH, Cha SH. Clinical features of 31 patients with systemic contact dermatitis due to the ingestion of Rhus (lacquer). Br J Dermatol 2000; 142: 937-42.
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