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
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.
2. Taxonomy of Toxicodendron
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
Left: basket bush (Rhus trilobata), also referred to by the politically incorrect name of squaw bush; center: poison oak (Toxicodendron diversilobum); right: Baja California poison ivy (T. radicans ssp. divaricatum).
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."
Male flower cluster of poison oak (Toxicodendron diversilobum). The unisexual flowers have 5 fertile stamens and a rudimentary pistil. [Seed-bearing female flowers with sterile stamens typically occur on separate plants.]
Close-up view of poison oak fruits (Toxicodendron diversilobum). Lower right fruits have papery exocarp removed, exposing the inner mesocarp layer striated with black resin canals.
3. Urushiol in Resin Canals
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. 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").
Freshly cut stem of poison oak (Toxicodendron diversilobum) showing adventitious roots and black lacquer oozing from resin canals in the inner bark. Contrary to some Internet articles, the resin canals are located in the phloem region, not in the actual xylem (wood).
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.
Figure 1. Chemical structure of urushiols found in resin canals of poison oak and poison ivy. Poison ivy mostly contains a mixture of four pentadecylcatechols (with 15-carbon side chain), while poison oak contains a mixture of four heptadecylcatechols (with 17-carbon side chain). Note: The above compound without the R group is called catechol or pyrocatechol (1,2-dihydoxybenzene). [Illustration by Mark Hopkins, Palomar College]
Chemical structure of saturated pentadecylcatechol, one of the urushiol catechols found in poison ivy resin canals.
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
If 2 micrograms of urushiol is sufficient to initiate a reaction in one hypersensitive person, then 1000 micrograms of urushiol (2 X 500) could initiate reactions in 500 hypersensitive people. Using 60 micrograms for a size comparison with an average grain of table salt, 1000 micrograms of urushiol would be roughly equivalent to 1000/60 or 17 grains of salt. An average cuboidal grain of table salt (NaCl) is about 0.3 mm on a side with an area of 0.09 mm2. The average pin head is 1.5 to 2.0 mm in diameter. A pin head with a diameter of 1.5 mm (0.75 mm radius) has an area of 1.767 mm2. Dividing the area of an average pin head (1.767 mm2) by the area of a single grain of salt (0.09 mm2) gives a value of 19.63 grains of salt. Therefore, 17 grains of table salt would fit on the head of an ordinary straight pin. [Of course, even more grains would fit on the head of a pin if they were moistened and clumped together.]
4. Urushiol & Its Oxidized Quinone
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.
Figure 2. Chemical structure of poison oak urushiol (heptadecylcatechol) and its oxidized "reactive" quinone. The reactive quinone bonds to white blood cell membranes deep in the skin. [Illustration by Mark Hopkins, Palomar College.]
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.
Figure 3. Plants from around the world that contain the urushiol allergen.
[Illustration by Elaine M. Collins]
5. Urushi Lacquer From Japanese Lacquer Tree
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.
A tube of refined urushi lacquer available from Watanabi-Shoten
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.
A soup bowl with a fine finish of Japanese lacquer.
A beautiful Japanese tray finished with black Japanese lacquer.
6. Cell Mediated Immune Response
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.
Figure 4. Illustration showing a hypothetical mechanism for the poison oak scenario: a delayed action, cell-mediated immune response.
[Note: Some immunology textbooks state that the urushiol allergen is
engulfed by the Langerhan's cells. The allergen and a small protein
fragment called "major histocompatibility complex" (MHC) is then displayed
on its membrane and presented to the effector T-cells.]
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).
Inner forearm of student who walked through patch of poison oak.
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.]
7. 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.
8. 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.
9. 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
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.
10. Literature Cited
(Chemistry, Evolution, Ecology & Ethnobotany). Timber Press, Portland Oregon.
- 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
- 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,
- 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
- 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
Mermon, D. 1987. "Life's an Itch." Outdoor Life October: 76-
Reynolds, G. 1978. "Why Some Plants Make You Itch." Fremontia
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
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-