Poison Ivy

 

Common Name: Poison Ivy, tsuta urushi (Japan, climbing lacquer vine), tan chi (China, climbing vine), herbe de la puce  (Quebec, herb of the flea).

Scientific Name: Toxicodendron radicans – The generic name Toxidendron is from Greek toxicon, poison and dendrites, of a tree; also the genus of Poison Oak and Poison Sumac; radicans means rooting and refers to the aerial roots of Poison Ivy; formerly of Genus Rhus

Potpourri:  Poison ivy isn’t poisonous. Poisons are substances that cause illness or death when consumed or absorbed; poison ivy contains an oil that activates the body’s own immune system to produce an allergic reaction; basically a rash. The common name is widely attributed to Captain John Smith of the English Colony at Jamestown, who came with about one hundred cohorts to expropriate the riches of what was considered a latter-day Garden of Eden in 1607. The stark realty was far from Edenic, the swampy encampment was rife with biting insects, unwelcoming natives and strange plants with the thorns and thistles that God had promised in Genesis. Smith soldiered on with remarkable fortitude and provided written accounts to the Virginia Company in London who had financed the venture. Of particular note was a plant that “being touched, the poysoned weed causeth rednesse, itchynge, and lastly blisters.” Since it grew along the ground like English ivy, what could be more mnemonic than poison ivy? [1] The privation of the men of the Jamestown colony is one of history’s more poignant tales of survival. One chronicler bemoaned that “There were never Englishmen left in a foreign country in such miserie (sic) as we were in this new discovered Virginia.” Diseases such as dysentery and malaria took their toll, “bodies being trailed out of their cabins like dogs to be buried.” At the end of the first year, only thirty-eight remained alive. Had it not been for Smith’s connivance with the local natives for food, the fate of the Lost Colony at Roanoke Island would have been repeated. Jamestown was finally sustained only by the tobacco entrepreneur John Rolfe in 1614, he married Pocahontas later that year. [2] Tobacco only grew according to the vicissitudes of human habit and health; poison ivy has endured according to nature.

Poison ivy isn’t ivy either. It is taxonomically assigned to the sumac genus (Rhus) of the mostly tropical Cashew Family (Anacardiceae) that includes mango, pistachio, and its namesake cashew trees. In addition to fruits and nuts, the family is also noted for a number of North American and East Asian plants that produce a milky juice that probably has something to do with keeping insects away or retaining water or both; only nature knows. One of the ingredients of “sumac sap” is an oil that causes contact dermatitis that is so culturally relevant and prevalent that it is synonymous with poison ivy, which is just one of the plants that produce it. As most other animals are unaffected – deer eat the leaves and birds eat the berries (and therefore spread the seeds) – the real culprit is the sensitivity of human skin and its eternal vigilance as the immune gatekeeper against marauding invaders. To accentuate the inimitable hazards of handling the oleaginous sumacs, a special genus was created: Toxicodendron means ‘poison tree’ in Latin. Ergo, poison ivy is T. radicans (rooting) for the aerial roots by which it climbs trees ivy-like, poison oak is T. pubescens (hairy) for the hairiness of its leaves, and poison sumac is T. vernix (resin) to distinguish it from the other sumacs which lack resinous secretions. There is a second poison oak (T. diversilobum) that is indigenous to the Pacific coast that can also be either a shrub or a vine; the name is more

apt as the leaves are usually lobed like those of the oak trees. [3]

The so-called poison plants all produce a substance called urushiol oil, which could also be called hiker’s bane. The name derives from an Asian species of sumac (Toxidendron vernicifluum – flowing resin) mostly widely known as the Japanese lacquer tree, which is urushi in Japanese; the oil was and is used as a glossy decorative finish. [4] The use of an oil that causes severe rash in most people for its esthetic appeal as a work of art speaks to the nobler side of human creativity, akin to the sericulture using larval cocoons for silk fabric. The coarser side of that same ingenuity invented gunpowder and chlorine gas; the arts and sciences are often at odds. The use of plant resins (lacquer derives from lacre, French for resin – etymologically ‘plant milk’ from the Latin lac) for artistic purpose probably originated in China as a reflection of the dualism of its culture’s foundational individualism in wisdom and art. Wisdom was centered on personal development in the social order. Art was of the artisan, a personal affair of hand crafting small objects. Unlike the West, where mass production in energy intensive industries produced consumer conveniences, the Chinese culture demanded bespoke objects of beauty to be appreciated as an esthetic of everyday life. [5] The intricate characters of the Chinese written language that number in the tens of thousands were hand-scribed with meticulous detail of symbolic simplicity. They have been retained over the alphabetized phonemes of modernity in spite of the communist principle of utilitarian simplicity; Chen Duxiu, one of the party’s founders advocated a “literary revolution” to get rid of the “ornate, sycophantic literature of the aristocracy.” But they remain to this day, as it is the characters of artistic language that hold China together. [6]

The application of lacquer from the lacquer tree was an essential part of Chinese local handicraft. Arising in the Zhou Dynasty (1046-256 BCE), the urushiol oil was collected from trees, strained and heated to concentrate the lipid content and then applied to a variety of objects, including wood, metal and porcelain. With meticulous attention to detail, each of up to thirty layers was applied, dried and polished in different colors and thicknesses. On completion, a sharp scribe was used to apply a design by removing layers to the color selected for the artistic effect intended; the slightest slip destroying days of labor. Initially applied to bamboo strips as a form of writing, the process spread through succeeding centuries to include everything from musical instruments to serving vessels. At its zenith in the feudal Qing Dynasty, the emperor Kangxi presented Leopold I, the Holy Roman Emperor, with a lacquered screen of exquisite detail. The influx of European merchants in the nineteenth century and its attendant demand for exports of inferior quality overwhelmed the cottage centers of excellence. The art of lacquering passed from the Middle Kingdom across the East China Sea to Japan, where it reached perfection. [7] The origins of lacquerware are by no means settled, however, as black and red earthenware pots dating from 4500 BCE have been found in Japan. After the establishment of cultivated lacquer trees (the same Toxidendron vernicifluum) and refined techniques of specially trained artisans (due to the toxic effects of the sap) in the 17th century, what became known as Japanning flourished. That the many names of layers and techniques of Japanese lacquerware use the Chinese-based kanji characters rather than the Japanese phonetic kana suggests that China may be the fons et origio of the process as well. [8] In the United States, fast-drying polyurethane varnish suffices for bowling alleys and bars; the lacquered art of urushiol oil survives only as an irritating rash.

“Leaves of three, let it be” rolls of the tongue with poetic alliteration to warn against the three-leaf plants that poison; however, it is not that easy to distinguish Toxicodendron in the tangle of the understory. For one thing, there are several common plants that have the same three leaflet pinnately-compounded arrangement that trigger the poison warning signal such as box elder and raspberry. The poison ivy leaflet is broadly characterized as shiny with an entire (smooth) leaf margin and an acuminate (pointed) leaf tip. The reality is a broad spectrum from shiny to matte, smooth to toothed or notched, and pointed to rounded. There is even some credence to the notion that poison oak and poison ivy are the same species that vary in morphology due of habitat. Cuttings of poison ivy left in dry, sunny spots grow into shrubby poison oaks and poison oak cuttings left in moist areas become climbing poison ivy; there are some reported instances of poison ivy with five leaves. Poison sumac is none of the above, having multiple leaflets that are practically indistinguishable from native staghorn and smooth sumacs. [9] Poison ivy is in the woods, in parks, and in your garden; the berries are effective in their use of avian vectors for seed dispersal everywhere that birds go (literally). Toxidendron species are cryptic due to their variability and therefore innocuous absent careful scrutiny – until several days later. Unless one is ever vigilant (and who is?), finding a rash spreading across the forearm or calf is the first indication of an encounter that calls for the introspective how did it get there? It is only at this point that attribution is considered; it must have been when sitting down beside the trail to have lunch, when looking for the golf ball in the rough, or weeding the back corner of the garden. Avoiding the dysphoric rashes of poison ivy and its cousins requires habitat sensitivity, an ounce of prevention or a pound of cure.

There is an old adage for those afflicted with urushiol rash: If you use the best remedies it will go away in two weeks; If you do nothing it will last for fourteen days. The tenacity and unpredictability of an autoimmune disease elicits the frustration of futility that the adage conveys. Not only is there a broad spectrum of reactivity to urushiol among individual victims, but there is an equally broad spectrum to the effects of treatment. A definitive study was conducted in 1935 on over one hundred city dwelling adults (presumably having had little to no exposure to poison ivy) using swabs infused with various concentrations of urushiol oil on their forearms and left for seven days to observe the result. At the lowest level of concentration, 24 percent were affected while at the highest level 75 percent were affected. With the unblinking exactitude of science, they concluded that “the proportion of the population affected increases arithmetically as the concentration of the irritant is increased geometrically, which is similar to the action of physiological stimuli in general as expressed by the Weber-Fechner law.” Who could argue with that? [10] Over the last half-century, improvements in scientific knowledge, methods and tools have slowly but inexorably yielded a better understanding. The basic mechanism is that urushiol oil constituent molecules bind to cell proteins of epidermal keratinocytes and Langerhans cells so that they appear to the immune system to be antigens, foreign agents that must be destroyed. White blood cells (called T-lymphocytes) mobilize to alert the lymph nodes of the immune system to produce specific anti-bodies (like histamine) to rush to the scene to repel boarders, the itchy red splotches and blisters are the battlefield that results. [11] The immune system is very clever, maybe too clever. The T-cells have a memory of every antigen that they ever met and are in constant vigilance at the ramparts should the invader return. A second exposure results in a heightened counterattack that raises the DEFCON to further escalate mobilization. [12] The more you are exposed to poison ivy, the worse it gets and the more you hike in the woods, the more likely you are to get exposed; unless you are one of the fortunate 25 percent who have no sensitivity, you eventually will be victimized by the rash of nature’s wrath.

Treatments for the “poison tree” encounters have been around ever since Adam and Eve were evicted from Eden; add Toxicodendron to thorns and thistles. There are a priori and a posteriori versions of palliative. Since preventing exposure is in essence a chemistry problem, albeit with biological implications, there are ways to get the oil to bond to an introduced agent to which it is more attracted than skin and washing the compound off later. One example from 1929: “A preventive recommended by Dr. James B. McNair, of the Field Museum of Natural History, Chicago, is a five per cent. solution of ferric chloride in water, or in a mixture of water, alcohol and glycerin. This is to be washed on all exposed skin surfaces before going into the woods and allowed to dry without wiping. The thin deposit of iron salt neutralizes the ivy poison immediately upon contact. This remedy has been in use by the botany classes of the University of Chicago for several years, with very good results.” [13] There are a number of commercial products on the market that probably do about the same thing as Dr. McNair’s if used properly and religiously for every potential field excursion; how likely is that? Homeopathy is one surprising alternative that has been demonstrated in a controlled trial. Twenty one adults who were highly sensitive to poison ivy were given up to 300 mg of urushiol over a six month period while twelve others were given a placebo as a control group; a double blind protocol was followed to minimize the placebo effect. Fifteen of those receiving urushiol became hyposensitized compared to only two of the control group. [14] So one can a priori avoid the onslaught of urushiol by slathering all exposed skin with a chemical cocktail barrier or gradually desensitizing the immune system using a vaccination-like approach. Or, like most people, you can go out into the woods and hope for the best.

So what’s a hiker to do? The ABC caveats of poison ivy are Avoid, Block and Clean. Avoidance is not that easy; it is difficult to distinguish the signature tripartite leaves. However, characteristic moist habitats are recognizable; Toxidendron plants lurk wherever leafy greenery is persistent along the ground or in the shrubby undergrowth. Alerted by habitat, a careful inspection is feasible and indispensable; experience helps but scrutiny is key. Blocking poison ivy need not involve the chemistry of coated arms and legs; long sleeved shirts and more importantly long pants are barriers against direct dermal contact. While feet are mostly protected by stout hiking shoes or boots with full enclosure, hands are mostly not; gloves should be worn in any circumstance where direct contact with vegetation is intended. Urushiol oil is insidious, insinuating itself onto any surface including protective clothing; with a persistence that measures in months if not years; the protective layers must then be carefully removed without any skin contact and washed, leading to the third and most important caveat. [15] Cleaning is the sine qua non of poison ivy prevention. Because urushiol is an oil, it must be removed with soap and water; soap is a salt of fatty acids. Salts are chemically defined as any compound formed from an acid by removing the hydrogen atom and replacing it with a metal ion. Thus table salt is sodium chloride (NaCl) from hydrochloric acid (HCl) with the sodium ion (Na) as hydrogen (H) replacement. Fatty acids are a group of lipids from plants and animals; long chain polymers comprised of carbon, hydrogen and oxygen. Historically soap was made by mixing wood ashes with animal tallow, a discovery no doubt having something to do with cooking meat over a fire; pot ashes with metal ions were collected giving rise to the element name potassium. Oils cannot be removed with water because they are hydrophobic; soap makes them soluble. The soap molecule has the lipid long chain fatty acid on one end that attaches to the oil and the salt metal ion on the other that attaches to the water. The encapsulated oil is rendered hydrophilic and the soap-surrounded oil globule can be rinsed away. [16] As elementary as ABC. Not quite.

Urushiol oil penetrates the outer epidermal layers in about ten minutes, setting off the hue and cry of repel boarders to the immune dragoon T-cells. Rash is irreversible once the event horizon has passed; the clock starts ticking at first touch. Avoidance and blockade having failed, the only recourse is clean and the only agent is soap. A small vial of liquid dish soap is an excellent addition to the standard hiking first aid kit that most hiker’s carry (and all should). This is useful in at least three scenarios: 1) Stumbling into poison ivy inadvertently by falling or grasping; 2) Resting at a quiet spot in the woods and realizing that you are in a patch of poison ivy; and 3) An alert provided by an observant third party informant. It takes less than a minute to break out the soap, lather it on liberally and thoroughly, and rinse it off; doing this twice is advisable. If the a priori ounce of prevention doesn’t work, there is always a posteriori pound of cure. Due to the ubiquity of poison ivy rashes and the imaginative marketing of the pharmaceutical industry, there are any number of products that claim miraculous cures costing up to $60 an ounce. However, as urushiol oil skin rash is an autoimmune condition, the only thing that these topical ointments and lotions can do is alleviate the itch and perhaps reduce some of the redness and blistering; treating the symptoms but not the cause. Benadryl is an over the counter antihistamine that might mitigate the immune response to some extent. There are an equal number of folk remedies that range from oatmeal baths to calamine lotion that at least make you feel like you’re doing something – with the potential for a placebo effect if you really believe it. For medically severe rashes, dermatologists prescribe a 14 day treatment with oral corticosteroids [17] A poison ivy panacea may be on the horizon; recent genetic research demonstrated that blocking the immune system protein interleukin-33 mitigated urushiol oil rash symptoms by isolating the discomfiture at its source. [18] For the present, however, you can use every treatment known or do nothing; it will all be over in a fortnight.

Notes

1. Sanchez, A. In Praise of Poison Ivy, Taylor Trade Publishing, 2016, Introduction.
2. Harlow, R. The United States: From Wilderness to World Power, Henry Holt and Company, New York, 1949, pp 10-12.
3. Brown, R. and Brown, M. Woody Plants of Maryland, University of Maryland, Port City Press, Baltimore, Maryland, 1972, pp 195-200.
4. https://npgsweb.ars-grin.gov/gringlobal/taxonomydetail.aspx?101869  Website of the U.S. National Plant Germplasm System
5. Durant, W. The Story of Civilization. Volume I Our Oriental Heritage, Simon and Schuster, New York, 1935 pp 735-737.
6. Mullaney, T. The Chinese Typewriter, a history, MIT Press, Cambridge, Massachusetts, 2017. pp 12-23.
7. Durant, W. Op. cit.
8. http://www.aisf.or.jp/~jaanus/deta/u/urushinuri.htm – Website of the Japanese Art and Architecture Net Users System (JAANUS)
9. Harris, M. Botanica North America, Harper Collins, New York, 2003, pp 75-77, 429.
10. Spain, W., Newell, J., and Meeker, M. “Susceptibility to Poison Ivy and Poison Oak” Science, 1935, Volume 80, Number 2065. p 104.
11. Griffiths, C. and Nickoloff, B. “Keratinocyte Intercellular Adhesion Molecule-1 (ICAM-1) Expression Precedes Dermal T Lymphocytic Infiltration in Allergic Contact Dermatitis (Rhus dermatitis)” American Journal of Pathology, 1989, Volume 135, pp 1045-1053.
12. DEFCON is a military acronym for Defense Condition and is used to formally ramp up from peace to war in a series of steps from 5 to 1. It is the code of mobilization.
13. “Poison Ivy” Science, 24 May 1929, Volume 69 Number 1795, p xii.
14. Epstein, W., Byers, V., and Frankart W. “Induction of antigen specific hyposensitization to poison oak in sensitized adults” Archives of Dermatology 1982, Volume 118, Number 9, pp 630-633.
15. Ginsburg, E. “In Search of a More Perfect Remedy for Poison Ivy” Washington Post, August 31, 2004.
16. Petrucci, R. H. General Chemistry, Principles and Modern Applications, 4th ed. Macmillan, New York, 1985. pp 684-685, 703, 842.
17. Stehlin, I. “Outsmarting Poison Ivy and Its Cousins” U.S. Food and Drug Administration Consumer Updates at https://www.fda.gov/consumers/consumer-updates
18. Cross, R. “Poison Ivy’s Itch Can Be Calmed by a Protein” Chemical & Engineering News, November 10, 2016.