Poison oak (Toxicodendron diversilobum) and its eastern counterpart poison ivy (T. radicans) are two of the most notoriously painful plants in North America. [Note: These species were formerly placed in the genus Rhus.] Although hundreds of scholarly articles have been written, there are probably more myths about these plants than any other native species. Poison oak and poison ivy do not spare age, sex, race or economic status. Each year thousands of people are afflicted with moderate to severe dermatitis from touching the foliage of these plants. Poison oak and poison ivy account for an estimated ten percent of lost work time in the U. S. Forest Service. In fact, hundreds of fire fighters who battle summer and fall blazes in California's coastal ranges are so severely affected that they are unable to work. People who breathe in the smoke and soot may develop serious inflammation of respiratory mucous membranes. Because of the serious economic impact due to lost employment time, poison oak "injuries" are covered by Workers' Compensation Insurance in California. The monetary cost of this affliction is approximately one percent of the state's workers' compensation budget (Epstein, 1994).

The first published records of poison ivy in North America date back to the early 1600s in the writings of Captain John Smith. In fact, Captain Smith included an illustration of the plant and originated the common name because of its superficial resemblance to English ivy (Hedera helix) or Boston ivy (Parthenocissus tricuspidata). The name ivy or "hiedra" was also used by early Mexican settlers in California who mistakenly thought poison oak was a kind of ivy. A little-known subspecies of poison ivy, T. radicans ssp. divaricatum, is native to southern Baja California and Sonora, Mexico. Our California poison oak was noted by another British explorer of the 19th century, Captain Frederick Beechey, who took samples back to England. Much to the chagrin of unwary gardeners, both poison oak and poison ivy were planted in English gardens for their graceful climbing habit and beautiful autumnal coloration.

North Americans and English gardeners are not the only ones exposed to Toxicodendron dermatitis. In his monograph of poison oak and poison ivy, Gillis (1971) lists four native species of Toxicodendron in North America, including seven subspecies of poison ivy. He also lists three species in Malaysia and China, including two subspecies of poison ivy, one in China and one in Japan.

Poison oak is a widespread deciduous shrub throughout mountains and valleys of California, generally below 5,000 feet elevation. In shady canyons and riparian habitats it commonly grows as a climbing vine with aerial (adventitious) roots that adhere to the trunks of oaks and sycamores. Poison oak also forms dense thickets in chaparral and coastal sage scrub, particularly in central and northern California. It regenerates readily after disturbances such as fire and the clearing of land. Rocky Mountain poison oak (Toxicodendron rydbergii) occurs in canyons throughout the western United States and Canada. Because the two species of western poison oak often exhibit a viny growth form, they are listed as subspecies of eastern poison ivy by some authors.

The pinnately trifoliate leaves typically have three leaflets (sometimes five), the terminal one on a slender rachis (also called a stalk or petiolule). Eastern poison ivy often has a longer rachis and the leaflet margins tend to be less lobed and serrated (less "oak-like"). In the similar-appearing squaw bush (Rhus trilobata) the terminal leaflet is sessile (without a stalk). Like many members of the sumac family (Anacardiaceae) new foliage and autumn leaves often turn brilliant shades of pink and red due to anthocyanin pigments. In the eastern states poison ivy is often mistaken for another common native called Virginia creeper (Parthenocissus quinquefolia). Virginia creeper has a similar growth habit and beautiful autumn foliage, but typically has five leaflets rather than three. It belongs to the Grape Family (Vitaceae) along with the common wild grape (Vitis girdiana).

During late spring loose clusters (panicles) of small greenish-white flowers are produced in the leaf axils. Functional male and female flowers are typically produced on separate plants (dioecious), or occasionally, unisexual and bisexual flowers may occur on the same plant (polygamous). Male flowers contain five stamens and a rudimentary pistil surrounded by five cream-colored petals and five sepals. Female flowers have a fertile pistil (gynoecium) and reduced, sterile stamens. During summer and fall, female plants produce small clusters of ivory-white fruits, each with a papery outer exocarp, a soft waxy mesocarp and a hard stony endocarp surrounding the seed. The fruits of related shrubs such as squaw bush, lemonadeberry (Rhus integrifolia) and sugar bush (Rhus ovata) are reddish with a sticky-pubescent exocarp. The old adage about poison oak and poison ivy is quite accurate: "Leaves of three, let it be; berries white, poisonous sight."

Freshly cut stems exude a sticky, terpene oleoresin that oxidizes and polymerizes into a shiny black lacquer resembling pruning sealer. The resinous sap is produced in resin canals of the stems, roots, leaves and flowers. J.H. Langenheim (2003) discusses resins of the sumac family (Anacardiaceae) in her book entitled Plant Resins: Chemistry, Evolution, Ecology, and Ethnobotany. Cross sections of poison oak stems show distinct concentric annual rings (ring-porous wood). Numerous resin canals appear as tiny black dots and are confined to the phloem layer just inside the bark. [Caution: Cutting and sanding poison oak wood is extremely unwise and hazardous--even if you think you are immune to its dermatitis. This is how one of the authors (WPA) was rudely initiated into the ranks of poison oak sufferers, after tramping through it for decades with impunity.] Dark resin canals (appearing as black striations) also occur in the waxy mesocarp of the fruits just beneath the papery skin. Abundant resin canals is one of the reasons poison oak and poison ivy are now placed in the genus Toxicodendron rather than the older genus Rhus. Toxicodendron is also the updated generic name for poison sumac (T. vernix) and the Japanese lacquer tree (T. vernicifluum), the commercial source of natural lacquer. In fact, Pomo Indians of California used the natural lacquer of poison oak to dye their baskets. The resin canals also contain urushiol, the insidious allergen that gives poison oak its bad reputation. The name is derived from "urushi," Japanese name for lacquer made from the sap of the Japanese lacquer tree ("kiurushi" or "urushi ki").

Urushiol is a general term applied to the toxic substance in the sap causing allergic contact dermatitis in people. It is actually a mixture of phenolic compounds called catechols, potent benzene ring compounds with a long side-chain of 15 or 17 carbon atoms (Figure 1). The side chain may be saturated or unsaturated with one, two, or three double bonds (Dawson, 1954, 1956). The remarkable immune reaction and specificity of the catechol molecule is determined by the long side-chain (Baer et al, 1967, 1968). Poison oak urushiol contains mostly catechols with 17 carbon side-chains (heptadecylcatechols), while poison ivy and poison sumac contain mostly 15 carbon side-chains (pentadecylcatechols). See Figure 1 below.

Urushiol is found in resin canals only--it is on plant surfaces only if leaves and stems are bruised or attacked by chewing/sucking insects. In does not occur in pollen or honey made from poison oak flowers. Although nonvolatile, it may be carried in ash and dust particles and as minute droplets in smoke from burning foliage.

Some people are so sensitive that it only takes a molecular trace of urushiol (two micrograms or less than one millionth of an ounce) on the skin to initiate an allergic reaction (Epstein et al, 1974). Even the amount on a pinhead is sufficient to cause rashes in 500 sensitive people. The following paragraph and illustration was included to satisfy a skeptical colleague who questioned the amount of urushiol that could fit on the head of an ordinary straight pin.

Arrangement of 17 uniform grains of table salt (NaCl) on the head of an ordinary straight pin with a diameter of 1.5 mm and area of 1.767 mm². Each grain is 0.3 mm on a side, so that 4.5 grains fit across the diameter of the pinhead (three grains are exactly one mm). Because of their square shape, some of the grains overlap the edge of the round pinhead. Grains of table salt out of a shaker vary slightly in size; we are using salt grains exactly 0.3 mm on a side in this illustration. Fewer salt grains would fit on the head of a pin if larger grains were used.

Approximately 80-90 percent of adult Americans will get a rash if they are exposed to 50 micrograms of purified urushiol (Epstein et al, 1974). This is indeed a minute amount when you consider that one grain of table salt weighs about 60 micrograms. An urushiol residue on the skin is difficult to wash off and may be spread by scratching. Contrary to popular belief, it is not spread through blister fluids. It is a relatively stable compound and can retain its potency for years in the absence of oxidation. Herbarium specimens 100 years old have been known to cause dermatitis. It is readily transferred from contaminated clothing, objects and fur of animals. To make matters worse it readily penetrates the epidermal layer of the skin where it binds to proteins of deeper skin cell membranes. Before the protein bond can occur the catechol is oxidized to a more reactive quinone in which the two OH groups are replaced by double-bonded oxygens. See Figure 2 below.

In the conjugated state (bound to cell membranes) urushiol is virtually impossible to wash off. By itself the urushiol molecule (also called a hapten) probably would not initiate a full-blown immune response, but when attached to the cell membrane it becomes a "warning flag" that attracts patrolling T-cells.

In addition to poison oak, poison ivy and poison sumac, a number of other species in the sumac family contain urushiol mixtures (Figure 3). In Japan, dermatitis reactions have been reported from contact with lacquered objects (from Japanese lacquer tree) such as bar tops, rifle stocks and toilet seats. Dermatitis has also been reported in people handling mangoes (Mangifera indica), shells of cashew "nuts" (Anacardium occidentale), the Rengas tree (Gluta renghas), Burmese lacquer tree (Melanorrhoea usitata) and two attractive Caribbean shrubs, Metopium toxiferum and Comocladia dodonaea. The name Rengas actually refers to several genera of large Malaysian trees with resinous sap that blackens when exposed to the air. The heartwood is dark red-brown with a beautiful grain, but it is dangerous to work. Were it not for this drawback, Rengas timber would be one of the finest decorative hardwoods. Imported Haitian voodoo dolls and swizzle sticks made from cashew "nuts" have produced dermatitis reactions similar to poison oak. Laundry markings made from the India marking nut tree (Semecarpus anacardium) have caused neck irritation and rashes, even after the clothing was repeatedly washed. Urushiols also occur in the seeds of Ginkgo biloba (Ginkgoaceae) and in several genera of the Proteaceae. See Figure 3 below.

The stem anatomy of the Japananese lacquer tree is similar to poison oak. The left image is a magnified view of a poison oak stem cross section taken through a compound microscope at 400x magnification. It shows circular resin ducts (rd) in the outer phloem layer (green) just beneath the bark. The resin ducts also contain urushiol, the insidious allergen that causes the painful, itching rash. Image copyright © 2008 by W.P. Armstrong.

Japanese lacquer (urushi) is obtained from the sap of the Japanese lacquer tree (Toxicodendron vernicifluum). Cuts are made in the bark where the resin ducts are located. The sap flows out and is scraped into a small bucket. It oxidizes into a dark resin when exposed to the air.

Japanese lacquer is a high quality, beautiful finish that requires several coats of black or transparent lacquer, often enhanced with various pigments. The art of using this exquisite natural finish is a complicated process that dates back thousands of years.

Poison oak urushiol causes a complicated delayed allergic reaction with the body's immune system. It is technically classified as a cell-mediated immune response and the "peak misery" may not appear until days or weeks later. It is quite different from the primary irritants of nettle and euphorbias, the effects of which are immediate. The following hypothetical "two-phase" scenario for poison oak dermatitis is summarized from Epstein (1984). PHASE I (Induction): Initial contact with poison oak may result in urushiol penetrating the stratified squamous epithelial cells of the skin and binding to large dendritic (branched) white blood cells in the epidermis called Langerhan's cells. See Figure 4 below.

The Langerhan's cell (with urushiol allergen and MHC protein on its membrane) migrates to a nearby lymph node where clones of special white blood cells, called effector T-cells, are programmed to recognize urushiol. [Note: Some immunology textbooks refer to these clones of T-cells, with urushiol receptor sites on their membranes, as "helper T-cells." There are literally millions of effector T-cells (helper T-cells) roaming throughout the blood and lymphatic system, each with special receptor molecules on their membranes for a particular allergenic chemical, such as the urushiol of poison oak. T-cells patrol our circulatory system looking for invading cells and viruses, inspecting surface membranes like security guards checking I.D. cards.

PHASE II (Elicitation): If you get urushiol absorbed into the skin during a subsequent encounter with poison oak, an effector T-cell may encounter it bound to a Langerhan's cell and attach to it by a complicated and specific recognition system. The effector T-cell then produces more clones of itself and releases special proteins called lymphokines (cytokines) which attract a legion of different white blood cells, including "cell engulfing" macrophages and cytotoxic ("killer") T-cells. The killer T-cells are also produced in regional lymph nodes during the Elicitation phase, and according to some textbooks, they also have urushiol receptors on their membranes. The new army of white blood cells releases lytic enzymes and protein toxins (perforins) which destroy everything in the vicinity including membrane-bound urushiol and other skin cells, thus producing a blistering rash. Fluid oozes from the blood vessels and lymphatics (edema) and cell death and necrosis (breakdown) of skin tissue occurs. Milder effects range from redness (vasodilation) and itching (nerve injury) to small blisters (vesicles and bullae).

According to James L. Wilmer (Personal Communication, 2005), epidermal keratinocytes can also be induced by urushiols to synthesize and secrete proinflammatory cytokines that can activate Langerhan's cells as well as attract macrophages and T-lymphocytes to the skin. This additional involvement from keratinocytes undoubtedly ramps up the immune response and cell killing phases. [Dr. James L. Wilmer, Director of Scientific Affairs, Market America, Inc.]

Another cell-mediated immune response is induced by the topical cream Aldara® (5% imiquimod). The mechanism is similar to poison oak because it causes the body's immune system to destroy cancerous skin cells at the site where the cream is absorbed into the epidermis. Since it involves the body's own immune system to attack the cancer cells, it is classified as an immunotherapy treatment. The mechanism is complex, but involves some of the same cells as the poison oak reaction, including the release of cytokines that attract T-lymphocytes (killer T-cells). Cytokines are a group of proteins secreted by cells of the immune system that act as chemical messengers. Cytokines released from one cell affect the actions of other cells by binding to receptors on their surface. Through this process, cytokines help regulate the immune response. In fact, one type of cytokine called interferon has been shown to be effective in certain cancer chemotherapies. Depending on the number of applications, the area may become red with an intensely stinging, itching rash and oozing lymphatic fluids. The positive side of this blistering rash is that a potential carcinoma is destroyed without surgery. Another product called Zyclara™ contains a reduced concentration of imiquimod (3.75%). It is applied to larger areas of the face to eliminate widespread precancerous tissue.

Upper: Author's forehead after 5 applications of Aldara®. Depending on the number of applications, the area may become red with an intensely stinging, itching rash and oozing lymphatic fluids. Lower: Author's forehead after 9 applications of Zyclara™. Untreated, basal cell carcinomas must be removed surgically. The following images show some of the basal cell carcinoma surgeries experienced by this author.

Skin Cancer #1 Removed From Left Nostril & Ala Skin Cancer #2 Microscopic Images Of Ala Tissue   Skin Cancer #3 Basal Cell Carcinoma On Forehead

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8. Natural Immunity To Urushiol

Explanations for natural immunity to poison oak are complicated by myths, conflicting reports and ongoing controversies among authorities. Sensitization depends on the chance meeting of a special effector T-cell (with correct receptor site) and the poison oak allergen--a painful biochemical rendezvous. You may not have effector T-cells with the special receptor for urushiol--or perhaps your relatively few effector T-cells with precise poison oak receptor may never encounter the urushiol allergen. The allergen may be absorbed and degraded before the T-cells find it. If the truth is known, most people will probably experience some degree of dermatitis if a sufficient quantity of urushiol is thoroughly rubbed into their skin. You may even be sensitized by a white blood cell transfusion from a sensitized person. Immunity to poison oak with age, exposure and homeopathic remedies may involve suppressor T-cells which inhibit or block the action and reproduction of other T-cells. Circulating IgG immunoglobulin antibodies that block the T-cell receptor for urushiol may also be involved (Stampf et al, 1990).

Since the HIV virus attacks helper T-cells, persons afflicted with the deadly disease AIDS have a serious deficiency in cellular (T-cell) immunity. AIDS patients may not have problems with poison oak dermatitis and this likely reflects their decreased cellular immunity. In fact, one treatment for AIDS patients is to try to sensitize them to another allergenic chemical (dinitrochlorobenzene) in order to stimulate T-cell production (Striker et al, 1994).

During the last century scientists have tried all sorts of homeopathic remedies made from extracts of poison oak. Some products, such as poison oak tablets and droplets, have been withdrawn from the market because of severe allergic reactions in hypersensitive people. In fact, the side effects in some people, such as severe anal itching, is often unacceptable. One promising area of desensitization research involves oral pills and intramuscular injections of related or modified urushiol: A molecule similar enough to urushiol to have the same immunological effect, but different enough to avert its excruciating side effects. Several compounds have been used successfully with laboratory animals (Stampf et al, 1986). Future research currently underway may lead to a vaccine that blocks the specific urushiol T-cell receptor and immunizes "high risk" people against urushiol for periods of time (Stampf et al, 1990). In fact, Allergene, a biotech company in San Mateo, California has successfully produced a hybridoma (fused lymphocyte and carcinoma cell) that makes urushiol-binding monoclonal antibodies. These antibodies prevented sensitized mice from reacting with urushiol and may eventually be available in a serum for people.

According to Albert M. Kligman's classic paper on poison oak (1958), there is no evidence of racial immunity to poison oak urushiol, not even among full-blooded Indians; however, black skin is slightly less susceptible. Native Americans were much more "in tune" with nature and probably learned to recognize, respect and avoid the plant at an early age. There is some evidence suggesting that native-born Hawaiians and Asians may be less susceptible to poison oak possibly due to early exposure to mangoes and Japanese lacquer (Epstein and Claiborne, 1957). Eskimos also are thought to be relatively immune, but the genetics of poison oak/ivy susceptibility are very poorly understood on a population basis. On an individual basis, children of very sensitive parents are highly likely to become poison oak sufferers (Walker et al., 1989).

It is difficult to explain how California Indians utilized poison oak so extensively without suffering the ill-effects of urushiol. Perhaps some may have acquired an immunity from early exposure to the plant, or perhaps they handled the plant very cautiously. In addition to using poison oak lacquer as a black dye, Pomo Indians reportedly used it to cure warts (Saunders, 1933). The wart was incised and then fresh resin was applied to the incision. Fresh resin was also used as a cure for ringworm and was applied to rattlesnake bites. Several tribes used the young flexible stems to weave baskets, although squaw bush (Rhus trilobata) branches were more commonly used. According to Balls (1970), Karok Indians of northwestern California covered the bulbs of soap lilies (Chlorogalum pomeridianum) with poison oak leaves and then baked them in earth ovens for food. Other northern California tribes wrapped acorn meal with poison oak leaves during baking.

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9. Treatments For Poison Oak Rash

The list of "treatments" for poison oak is bewildering and in some cases preposterous. Just about every conceivable substance has been tried for topical therapy, from morphine and kerosine to buttermilk and gunpowder. Most authorities agree that lotions, creams and sprays containing anti-inflammatory corticosteroids (hydrocortisones) are the most effective agents to relieve painful, itching rashes. Serious outbreaks may require medical attention and hospitalization. Ideally the best therapy when exposed to poison oak is to wash the contaminated areas thoroughly. The problem is that most ordinary bath soaps have little effect on removing the resinous sap. Have you ever tried removing pine pitch from your arm with facial soap? In fact, added moisturizers and oils in the soap together with brisk rubbing may even spread the urushiol, increasing the area of allergic response. Strong laundry soaps, such as Fels Naptha, may also spread the allergen and be harsh on sensitive skin. Some books still recommend antipruritic (anti-itch) agents such as calamine lotion for mild cases.

Another remedy for the discomfort of itching poison oak lesions was recently reported to Wayne's Word. It is a "pore minimizer" acne treatment with 2% salicylic acid and skin soothers to prevent irritation and overdrying. This product is available from several manufacturers, including Neutrogena® and Johnson & Johnson. According to several e-mail messages, the pore cleaner "really stops the itching of poison oak much better than any cortisone or calamine type product, and also stops the weeping and proliferation of the lesions." Although we have not tested this treatment on the Wayne's Word staff, it might be worth trying. You might also apply an ice pack or ice cube directly to the afflicted area to temporarily numb the itching.

A poultice made from the resinous flowers and leaves of gum plant (Grindelia robusta) was commonly used by Indians and early settlers in California to relieve inflammation and itching.

San Diego gum plant (Grindelia camporum var. bracteosum), a resinous California wildflower used to relieve poison oak dermatitis by native Americans and early immigrants. The unopened flower buds are covered with a white, sticky, aromatic resin that was applied to afflicted areas of the body. This species is listed in older references as G. robusta var. robusta.

Native Americans also made concentrated poultices from boiled leaves of the common shrubs yerba santa and manzanita (Eriodictyon and Arctostaphylos spp.), and from the thick roots of mule ears (Wyethia longicaulis), a resinous, balsam-scented sunflower with large basal leaves (Balls, 1970; Bean and Saubel, 1972). Other reported naturopathic remedies to relieve the inflammation and itching of poison oak rashes include salves made from the crushed leaves of Aloe vera and narrow-leaf plantain (Plantago lanceolata). A poultice made from juicy stems of the North American jewelweeds (Impatiens capensis and I. pallida), succulent wildflowers that grow with poison ivy in the eastern states, is also listed in herbal manuals (Schwartz, 1986); although its value as an effective therapy has been amply disproved (Zink et al, 1991).

A recent editorial in Mushroom The Journal (Winter 1994-95) discussed a mycological cure for poison oak rash by rubbing fungi such as Boletus and Polyporus on the affected skin. This treatment is based on the fact that freshly cut pieces of mushrooms, apples and potatoes turn dark when exposed to the air. The actual mechanism for this blackening process involves the oxidation of phenolic compounds in the tissues of these pieces by the enzyme tyrosinase. The resulting quinones rapidly polymerize into a brown residue. Placing the pieces under water prevents this "unsightly" oxidation. In fact, chefs add lemon juice, which contains the strong reducing agent ascorbic acid; this keeps the phenolics reduced. Since urushiol is a phenolic compound, tyrosinase would probably also detoxify it. The enzymes might also reduce the spreading of urushiol to other parts of the body by deactivating it at the initial site of exposure.

One of the authors (WLE) has studied an even more specific and potent oxidase for urushiol called catechol 2,3 oxidase. This enzyme actually oxidizes the ring structure between carbon atoms # 2 and # 3 and basically destroys the molecule. A bacterial gene was cloned and expressed to produce this recombinant enzyme. In vitro (in a test tube), it oxidized urushiol within seconds. When applied to skin it sometimes prevented a rash, but only if the urushiol was inactivated before penetrating the epidermis. The efficacy of patented creams containing oxidase enzymes depends on the oxidation of urushiol at the initial site of contact before it has penetrated the skin. Once urushiol binds to the protein of skin cell membranes, these creams would have little effect on the subsequent immune response.

A product called Tecnu Oak-n-Ivy® Cleanser is now marketed through forestry supply catalogs. It contains a mixture of organic solvents and wood pulp by-products which remove terpene resins and urushiol from the skin. Thorough rinsing with water is recommended. Other organic solvents, such as rubbing alcohol, would probably also remove the urushiol residue. Of course, if the allergen has already penetrated the epidermal layer and bonded to deeper skin cells it is too late. Interestingly enough, the original Tecnu product was developed to remove radioactive fallout dust from the skin without water (Mermon, 1987). It was supposed to be stocked in fallout shelters across the United States. Later it was found to be highly effective in removing paint resins and, quite by accident, urushiol. [Tecnu is a crude distillate of gasoline and is quite expensive compared to other solvents such as gasoline, paint thinner and acetone.] Another product that claims to remove urushiol from the skin, even after a rash has developed, is called Zanfel™. Check the Zanfel web site for more information.

Another product developed for the U.S. Forest Service is called Ivy Block®. It is an aerosol spray or lotion containing activated bentonite clay used in antiperspirants. Ivy Block® forms a barrier that both prevents urushiol from touching the skin and chemically binds with it so it becomes inactive. Ivy Block® is very effective, but is not a panacea for extremely sensitive people. Another effective blocking agent called StokoGard Outdoor Cream®, a fatty acid ester, is available through industrial supply houses and by asking your pharmacist to order it from Stockhausen, Inc. of Greensboro, North Carolina.

Ivy Block® is a protective lotion containing activated bentonite clay. Ivy Block® forms a barrier that both prevents urushiol from touching the skin and chemically binds with it so it becomes inactive. The cream is applied to exposed areas of the body before going out into poison oak country.

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10. Significance of Poison Oak Resin

The evolutionary significance of poison oak resin containing urushiol is difficult to explain. The resinous sap probably helps to seal wounds and may retard the growth of infectious fungal and bacterial spores. A chemical defense strategy against "predatory pressure" seems unlikely since the foliage and fruits are eaten by deer, goats, horses, cattle and a variety of birds. In fact, wood rats even use the branches to construct their nests. Only humans appear to have painful encounters with the plant, although laboratory studies indicate sensitivity on exposed skin of guinea pigs, rabbits, mice, sheep, dogs and rhesus monkeys.

In the case of humans, our well-developed immune system may be overreacting to a relatively innocuous plant resin on the skin. But there is a positive side to all of this--research on poison oak may lead to a better understanding of the human immune system and the treatment of renegade viruses and tumor cells. In the final analysis, poison oak may be a blessing in disguise.

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11. Literature Cited Armstrong, W.P. and W.L. Epstein. 1995. "Poison Oak: More Than Just Scratching The Surface." Herbalgram 34: 36-42. Baer, H., Watkins, R.C., Kurtz, A.P., Byck, J.S. and C.R. Dawson. 1967. "Delayed Contact Sensitivity to Catechols." Journal of Immunology 99: 370-375. Baer, H., Dawson, C.R., and A.P. Kurtz. 1968. "Delayed Contact Sensitivity to Catechols." Journal of Immunology 101: 1243-1247. Balls, E.K. 1970. Early Uses of California Plants. University of California Press, Berkeley. Barker, J.N. 1992. "Role of Keratinocytes in Allergic Contact Dermatitis." Contact Dermatitis 26 (3): 145-148. Barker, J.N., Mitra, R.S., Griffiths, C.E., Dixit, V.M., and B.J. Nickoloff. 1991. "Keratinocytes as Initiators of Inflammation." Lancet 337 (8735): 211-214. Bean, J.L. and K.S. Saubel. 1972. Temalpakh: Cahuilla Indian Knowledge and Usage of Plants. Malki Museum, Inc., Banning, California. Dawson, C.R. 1954. "The Toxic Principle of Poison Ivy and Related Plants." Recent Chemical Progress 15: 39-53. Dawson, C.R. 1956. "The Chemistry of Poison Ivy." Transactions of the New York Academy of Sciences 18: 427-443. Epstein, W. L. 1984. "Allergic Contact Dermatitis." In: Current Perspectives in Immunodermatology pp. 253-263. Churchill Livingstone. Epstein, W.L. 1994. "Occupational Poison Ivy and Oak Dermatitis." Dermatologic Clinics 12 (3): 511-516. Epstein, W.L., Baer, H., Dawson, C.R. and R.G. Khurana. 1974. "Poison Oak Hyposensitization: Evaluation of Purified Urushiol." Archives of Dermatology 109: 356-360. Gillis, W. T. 1971. "The Systematics and Ecology of Poison-Ivy and the Poison-Oaks." Rhodora 73: 72-159, 161-237, 370-443, 465-540. Kligman, A. M. 1958. "Poison Ivy (Rhus) Dermatitis." Archives of Dermatology 77: 149-180. Langenheim, J.H. 2003. Plant Resins: Chemistry, Evolution, Ecology & Ethnobotany. Timber Press, Portland Oregon. Mermon, D. 1987. "Life's an Itch." Outdoor Life October: 76- 77, 119-120. Reynolds, G. 1978. "Why Some Plants Make You Itch." Fremontia 6: 19-23. Saunders, C. F. 1933. Western Wildflowers and Their Stories. Doubleday Doran and Company, New York. Schwartz, D.M. 1986. "Leaflets Three: The Sense and Nonsense of Poison Ivy and its Itchsome Kin." Blair & Ketchum's Country Journal 13: 42-50. Spjut, R.W. 1994. "A Systematic Treatment of Fruit Types." Memoirs of the New York Botanical Garden 70: 1-182. Stampf, J-L., et al. 1986. "Induction of Tolerance to Poison Ivy Urushiol in the Guinea Pig by Epicutaneous Application of the Structural Analog 5-Methyl-3-n-Pentadecylcatechol." Journal of Investigative Dermatology 86: 535-538. Stampf, J-L., Castagnoli, N., Epstein, W., et al. 1990. "Suppression of Urushiol-Induced Delayed-Type Hypersensitivity Responses in Mice with Serum IgG Immunoglobulin from Human Hyposensitized Donors." Journal of Investigative Dermatology 95: 363-365. Striker, R.B., et al. 1994. "Clinical and Immunologic Evaluation of HIV-Infected Patients Treated with Dinitroclorobenzene." Journal of American Academy of Dermatology 31: 462-466. Young, J.D-E. and Z.A. Cohn. 1988. "How Killer Cells Kill." Scientific American 258: 38-44. Zink, B.J., et al. 1991. "The Effect of Jewel Weed in Preventing Poison Ivy Dermatitis." Journal of Wilderness Medicine 2: 178- 182.

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