When I chose to study the ecology of western poison oak (Toxicodendron diversilobum, also known as Rhus diversiloba), I knew I would have to learn how to minimize the risk of “getting poison oak” and of causing other people to get it (11, 12, 13, 14). Here I describe the nature and seriousness of the dermatitis, and discuss my personal experiences with the allergen: my changing sensitivity over time, and practical methods I used to minimize my exposure to the allergen, to minimize my spreading it to other people, and to decrease the severity of my reaction. To learn more about the amazing plant, please see my post, “Poison Oak: A Beautiful Plant ‘of Noe Very Ill Nature.’ ”
Caution! I have a low-to-moderate sensitivity, and so my advice and experience is best aimed at people like me. Also, I’m not “that kind of doctor.” And although I don’t read medical journals, my occasional online searches haven’t turned up anything new since this essay that I first wrote in 1990. Some of what I write about here came from conversations in the late 1980s with Dr. William Epstein (Dept. of Dermatology, UC San Francisco School of Medicine), who at that time was the world expert in rhus dermititis (the dermatitis caused by plants in the genus Toxicodendron, which used to be called Rhus).
The Dermatitis Can Cause Serious Discomfort
Rhus dermatitis is caused by an allergen in plants of the genus Toxicodendron, which include the poison oaks and ivies. Getting rhus dermitis can be miserable: it interferes with sleep and exercise, and can lead to dangerous swelling, and worse, in some people. Because Toxicodendron is distributed over most of the lower 48 states (map at right from 15, 19), it can interfere with recreation and land management for a large proportion of the US population. In the 1980s when I was reading about its impact, I learned that Toxicodendron caused more cases of allergic contact dermatitis in the US than all other “provocatives” combined (9). At any one time, about half of the US population is sensitive to poison oak (6), but a higher proportion would become sensitive if they were exposed to it. Almost a quarter of the workers who were flown to California, Oregon, and Washington to fight wildfires in the 1980s had to leave the fire line because of poison oak dermatitis (23). Rhus dermatitis was the biggest single cause of injuries for USDA Forest Service employees, accounting for more than 10% of all lost-time injuries for their forestry workers (23).
Exposure and Skin Reactions
Rhus dermatitis is an allergic contact dermatitis, and specifically, a type IV delayed hypersensitive reaction. The allergen is an oily substance called urushiol. Urushiols are a class of catechols. They are benzene rings with two OH groups and a side chain of 15-17 carbons. A species of Toxicodendron has a mixture of urushiols that differ by the length and amount of double-bonding in that side chain. That mixture varies by species, but if a person has gone through the induction phase with one species, her or she will be sensitive to another species—they are called “cross-reactive allergens.” All members of the Toxicodendron are cross-reactive, as are several other members of the Anacardiaceae, such as mango, cashews (when not roasted), and probably Schinus (9).
This type of allergic reaction has two phases.
1) In the induction phase, the allergen is recognized by the immune system, and then killer-T-cells and suppressor-T-cells are made. Because of the need for induction, a person cannot get the dermatitis the first time he or she is exposed (2, 7).
Specifically, the urushiols bind to proteins on the skin surface. If the skin cell happens to be a Langerhans cell (which according to Dr. Epstein, make up perhaps 1/20th of the cells), it recognizes the that the “conjugate” of the urushiol and protein is foreign. The Langerhans cells internalize the conjugate, presents fragments in a new form on its surface, and then migrates to the lymph nodes to induce the production of at least four elements: killer T-cells, suppressors (suppressor T-cells and suppressor factors), and memory T-cells. These elements circulate through the body.
2) In the elicitation phase, when a urushiol-specific killer T-cells detects a skin cells onto which urushiol has bound, it will produce cytokines. Cytokines attract monocytes (a type of white blood cell) that combine with the cytokines and then attack all the cells in their vicinity. As our skin become damaged or die, we itch.
Suppressors inactivate the killer T-cells.
The absolute and relative sizes of your populations of killer-T-cells and suppressors will determine how fast you react to poison oak, and how long and intense the reaction is. These population sizes vary from person to person, and depend on how much recent exposure you’ve had.
The first time you are exposed to poison oak, there are no killer T-cells, and so you do not react. After that, the more frequently you are exposed, the more of both types of cells you will have. A typical pattern of dermatitis is to have a very slow and muted reaction after the first exposure of the year. It may take as long as three weeks to start, and when it does, it is not very intense. During that time you have a relatively small population of killer T-cells and few of them induce attacks on your skin at the same time. You have an even smaller population of suppressors. In contrast, at the end of the season, your reaction occurs quickly, perhaps in only one or two hours after exposure, and it is extremely intense. At that time, you have many killer T-cells (their population having built up by your prior exposure). They are shut down quickly by the large population of suppressors that has also built up.
Your skin maintains some record of prior bad rhus dermitits, which what are called “memory T-cells.” I’m unclear on where their production is induced and how they get to the skin, but I know the upshot. I got a bad case of poison oak on my neck early on. Thereafter, if I got poison oak anywhere in my body, my neck flared up with poison oak in exactly the same spot as before. Dr. Epstein told me that this memory is very common. After a few years that particular patch went away.
People sometimes think (incorrectly) that they will spread the rash by spreading the fluid in their blisters. The fluid in the blisters does not contain the allergen. A reaction can develops over time because of differences in how different parts of the skin may react, or because the person may have been exposed at different times. For example, you could be exposed at 9:00 a.m., and then be exposed again at 5:00 pm from your backpack strap, shoelace, steering wheel, or your pet.
I’ve described a cell-mediated allergic reaction, not one that is mediated by antibodies (a functional class of proteins). Antibodies recognize a unique part of the allergen and then induce a reaction to destroy it. However, in 1989 or 1990, Dr. Epstein told me that, in fact, we do also have antibodies to urushiol in our bodies, although they are not much discussed. (I found a recent reference to their induction by a Toxicodendron species, in the journal Homeopathy.) Dr. Epstein said there are antibodies to many substances, and that if there are antibodies, then there could be vaccines for prevention. He said that pharmaceutical companies run such risk in developing and administering vaccines, however, that no company would ever make one for rhus dermatitis. With the advances in so many areas, I don’t know if his statements would be supported by active researchers today.
Urushiol itself causes chemical burns to your skin. In my experience, they look like burns–a pit with the skin missing. They don’t itch but they hurt, and they can scar. Also be aware that people’s sensitivity can change over the years for unknown reasons and with unknown trajectories.
Sensitivity at the Population Level
Some individuals become less sensitive and others become more sensitive the more they are exposed to urushiols (4). About 15% of US population is truly tolerant: they cannot be sensitized even with very high doses of urushiol (3, 21). It is possible that the value is higher in regions where people have been exposed to mangos and other Anacardiaceae since childhood, but information on this is anecdotal. Still, Dr. Epstein suggested to me that if I were to develop an increased sensitivity during my PhD, I may do well to find a student assistant who had grown up eating mangos.
Epidemiological studies do not control for amount of exposure or a patient’s history of exposure (4), but they show that rhus dermatitis was least common in middle-aged people. That result may have been because middle-aged people had the least exposure by spending less time in the Toxicodendron patches. Cases increase around retirement age, perhaps because retirees were out in the woods again. But a researchers who did much of the seminal work on rhus dermatitis, abruptly went from zero sensitivity to extremely sensitivity, showing that change can occur.
How My Sensitivity Changed During My Exposure
At my request, over the course of my study, Dr. Epstein (UCSF Medical Center) monitored my sensitivity to urushiol to give me an objective indication of my sensitivity. If I was becoming increasingly sensitive, I would have needed to decrease my exposure. If my sensitivity was decreasing, I could have dispensed with some of the time-consuming precautions I took.
In each test, he placed four concentrations of urushiol on my inner forearm. Two days later, he scored my reaction (method described reference 7), on a scale of 0 to 4. He applied 2.50, 1.25, 0.50, and 0.25 µg of urushiol in acetone to an area 1.2 cm in diameter. Pure sap corresponds to a dosage of 2-2.5 µg of urushiol (Epstein 1990). For the first trial, he used a larger range of concentrations to bracket my sensitivity.
He found that I am relatively insensitive to poison oak, in the lower 10% of the population; some people react to less than 0.004% the dosage necessary to cause a reaction in me (5). Even so, I was covered with all stages of sores for three years, and had almost constant dermatitis on my neck and wrists. It was often rather miserable, and I feel for people who have stronger reactions.
I plotted the results. The lower panel shows that I reported high exposure to urushiol from February or April until October for three years, and then no exposure during the fourth year. The top panel shows my reaction, using Dr. Epstein’s scores.
First, notice that my highest reaction on the scale of 0 to 4 was 1+, which was not very extreme. You can also see that in the photo of my arm (the patch nearest my wrist).
Second, notice how my sensitivity to the highest level of urushiol changed over four years (the red line, with urushiol concentration similar to pure sap). I had a relatively low sensitivity before my exposure started (1+). That sensitivity dropped (to 1.5) and stayed low for a year, increased again (to 1+), and declined to my non-field-season level again (1.5), which was lower than when I started. It stayed there during the year I had little exposure. His interpretation was that I quickly developed many killer T-cells, but then I developed suppressor T-cells that disabled the killer T-cells throughout the rest of the first year and all of the second year. In the third year, my suppressors had declined, and I had quick, strong reactions. The suppressor T-calls continued to give me some protection over the year that I had little exposure.
Desensitization (circa 1990)
Dr. Epstein showed that the oral preparations for desensitizing people that were sold over-the-counter until the late 1970s were ineffective—they had too little urushiol in them (4). But oral urushiol preparations are successful in giving some level of desensitization in extremely sensitive people (5,24). At best, though, they will decrease sensitivity to that of a moderately sensitive person. For a person with my level of sensitivity, desensitization is not feasible.
Desensitization takes 2-4 months, a person has to stay on the medication to remain desensitized, and the treatment can cause uncomfortable side-effects (one of which is “pruritus ani,” an allergic reaction in the rectum). Many patients decide that the cure is worse than the disease. Dr. Epstein told me the story of a very sensitive patient who was undergoing desensitization. She spilled her bottle of the urushiol preparation in the bathroom of her rental apartment, and ultimately had to move out because she couldn’t get it cleaned enough. He said she left it for the next renter.
I once asked him about the folk remedy for not getting poison oak, of keeping a poison oak plant nearby and exposing oneself every week by eating a leaf or rubbing it on the skin. He smiled and said, basically, “Might work. You would have to get the right exposure and the right frequency, and you’d have to be in the right range of sensitivities for that to work” He went on to tell me that there were stories that some Native Americans in earlier times were insensitive to Toxicodendron. The interpretation was that with the individuals had maintained sufficient periodic exposure.
I was pregnant with both of my children during the period when I studied poison oak. I asked him if my dermatitis could affect them. His answer was, “Yeah, probably, but only because the rash isn’t letting you get enough sleep.”
I asked about the fact that itching seems to occur in bouts, even when I wasn’t thinking about, like at 3:00 am. He confirmed that there is a circadian rhythm to the dermatitis, but that it has not been well-studied.
~ ~ ~
How I Lowered My Chances of Getting Dermatitis and Giving it to Others
Urushiol is stable in low-humidity environments and it is readily transferrable from object to object, so I had to learn how to work with it for my own protection, and how to avoid spreading it to other people. The following mechanisms are ones that worked for me, with my relatively low level of sensitivity. This information is summarized in the table at the end.
The best way to avoid dermatitis is to avoid contact with the plant.
The uninjured plant is harmless: the urushiol is contained in ducts inside the plant. Handle the plant gently, and move gently when you are walking in it (I consider the action “swimming”) to avoid breaking it. Stay away from old injuries on the plants. They show as black seeps on the stems or black bumps, often pin-head sized, on the foliage.
Note—my husband joked that he doesn’t believe this. But husband, it is true: the urushiol is inside the unharmed plant at all times and all seasons. I have wagged young shoots (gently) under my neck to prove it to myself, and I know it from the anatomy. Yes, the leaves are shiny and tender in the spring, but no, the urushiol is not sitting on the surface or in little breakable hairs.
In stems and roots, the urushiol is in ducts within the phloem (just under the outer bark, exterior to the wood). In leaves, it is in ducts that are under the surface. It never sits on top of the plant the way people fear. It never volatilizes, although it does move as droplets on small flakes of ash. One of my avoidance choices was to not study roots, because it would have been too hard to harvest roots while wearing latex gloves.
Urushiol has the same strength at all seasons, but the leaves break more easily in the spring, so it is easier to contract the dermatitis then. In a small study in which I was involved, there was an indication that leaves in the sun had higher urushiol concentration. Not long after leaves fell, they no longer contained potent urushiol (15).
I tried to not to cut or saw stems directly above me, but because I was harvesting on ladders or while climbing trees, sometimes I wanted the sample enough to take a risk. I got sawdust in my eye once, and went down to flush my eyes with water. Then I then washed my face with soap, and went out of the poison oak for the day. It stung at first, but I had no problems. Eye protection would have been prudent, but like a hat, it wouldn’t have stayed on very well in those conditions.
I worked in an off-campus shack in the nature preserve where I did much of the study, to lessen the chances of spreading urushiol to other people. I divided the building in half, putting masking tape on the floor. The first half of the building I considered contaminated: I worked there, and left equipment, supplies, samples, and notes there. The other half of the building I considered clean. One or two other graduate students used this area off and on, mainly for storage. I used that area for clean activities, and I kept equipment and clothes there which I did not want contaminated. I had to walk through the contaminated area to get to the clean area, but I thought the reverse (dragging dripping logs and shoots through the clean area to get to the contaminated area) would have been worse.
Not only do I recommend you avoid the plant, but I recommend you avoid talking about it when you have been in it. A person in the lab accused me of spreading it to her. She got a rash on her ear and said I must have contaminated the telephone that she then used. (She was a mountain biker, and I expect that is where she got it.) For that reason, I did my photocopy regime in the evening behind a closed door (see below). And when I gave professional presentations, at first I would avoid mentioning the plant’s name until late in the talk, because I was frustrated to lose the audience at the beginning, as their hands started rubbing their faces. In the end, I learned to mentioned the plant was poison oak, and to quickly explain that yes, I’m somewhat sensitive, but that I found ways to work with it. Then I could get on with the science talk.
Physical barriers (including clothing)
I wore protective clothing in the field and lab. This consisted of heavy coveralls and long cotton socks on my legs and arms (with holes cut for my fingers), and latex gloves. Initially I also wore a hat, it caused more problems than it solved because it would rotate over my face or the string around my neck would strangle me as I climbed or crawled through branchy materials. Experiments with mammals have shown their hair protects them from dermatitis, so I dispensed with the hat and washed my hair, at least with cold water, after exposure. When I removed my protective clothing, I left it inside out for washing.
One source wrote that urushiol goes through rubber gloves (9). This concerned me because much of my workday was spent with gloves slick with urushiol; also, my fingers developed itchy blisters inside the gloves. At one session, Dr. Epstein administered sensitivity tests over one, two, and three latex sheets cut from gloves that we’d taped to my forearm. I removed latex panels after two, five, and seven hours. I had no reactions. I concluded that if urushiols pass through latex gloves, it is in lower concentrations than those needed to elicit a reaction in me, but I still changed gloves about every two hours because their outer surface became sticky and tarry after that. The itchy blisters I developed probably resulted from having wet hands inside gloves all day; I do not have a latex sensitivity.
I kept many heavy-duty plastic bags in the clean zone, so I had a place to put dirty clothes, equipment, or other items I wanted to transport.
I used only my personal vehicle for transport of samples, equipment, and notes. No one else drove the vehicle during the months spanned by my fieldwork. If I had to have a passenger, which I strongly discouraged, he or she sat on plastic bags that I covered the seat with.
I set up the photocopy machine to copy my notes at a time when I was clean. I taped paper towels on the entire cover of the photocopier as well as under the cover and on the table to its side. I taped plastic wrap over the control buttons. I laid out two pairs of latex gloves, a plastic bag for trash, a squeeze bottle of ethanol, and a stack of paper towels. I put on the gloves, withdrew the notes from double plastic bags (one that may have been dirty, and an outer one certain to be clean), and copied. When I was done, I closed all the plastic wrap, gloves, and towels into a plastic bag and disposed of them. When a field notebook was filled, I wrapped it in plastic wrap and could then store it without risk of contaminating other items.
I tried using spray antiperspirant as a barrier to poison oak. This has been found effective in tests, the effectiveness deriving both from the organophilic bentonite clays used as filler (“inert ingredients”) and the aluminum chlorohydrate (7, 23). However, for me the antiperspirant was more work than it was worth: my neck and face were the main parts that were directly exposed, it was uncomfortable to administer antiperspirant there, it was hard to wash off, and the spray hole clogged when I’d leave the spray can where I needed it, in a hot vehicle.
Another barrier that had been used by outdoor workers in northern California was is a linoleic acid dimer marketed as Stoko Gard Outdoor Cream (Stockhausen), and that was available through industrial supply houses. I disliked the feel of the heavy, caulking-like material. Dr. Epstein tested many products, and he said lots of materials would work as a partial barrier.
I see there are other products on the market, but I haven’t tried them.
Dr. Epstein suggested trying mud.
Urushiols can be emulsified (broken up) by soaps and detergents, and then washed away with water. They can also be dissolved by organic solvents (such as alcohol, methanol, acetone, gasoline, and paint thinner). There are products on the market that people swear by, but Dr. Epstein impressed on me that they were no better than soap and water, or organic solvents. Their packaging is convenient, however.
Unfortunately, soaps, detergents, and organic solvents also remove the natural protective oils from the skin. That allows any errant urushiol molecules to more easily cause a reaction. These protective skin oils require three to six hours to replenish after having been stripped.
How long do you have after exposure to wash yourself up? One study showed that for mildly sensitive people, washing up 60 minutes after exposure was too late to avoid the full reaction, but 30 minutes gave some protection. For a highly sensitive person, washing up 10 minutes after exposure was too late, but even at 5 and 1 minute, the person still got dermatitis, but with a reduction in severity (21). In practice, though, it was too hard to wash up every hour.
I used soap only in circumstances in which I would not be exposed again for the next six hours. That usually meant I’d use soap only at the end of the day. I did not shower or swim within the six hours before I was going out into the poison oak. Experts recommended the use of mild soap (such as a glycerine-based soap like Neutrogena) but not a harsh one (e.g., laundry soap or Fels-Naptha), to leave a little more protection on the skin for the chance molecules you missed while cleaning.
Before returning equipment to a place where others would use it, I usually washed the equipment with detergent, then water, then alcohol, and if the surface could handle it, then with acetone. Similarly, at the end of field season, I cleaned my vehicle with a succession of soaps and solvents.
On my skin, the solvents were not always so successful. Even if I had been careful, it was inevitable that I would have pulled off a glove to get a spider-web off my face or frass out of my eye, inevitably transferring a little urushiol from place to place. If this had been a more dangerous substance for me, I probably would not have even attempted the project. My hands got much urushiol on them when I was studying hydraulic conductivity because my hands were under water in basins with pools of urushiol floating on top. Those pools entered my gloves at the wrist and remained there until the end of the day. The pure urushiol would get on my skin, and make an oily spot that I could not always remove with soap, detergent, ethanol, or acetone. These spots turned black after they oxidized–a daily occurrence on my hands in 1989—and the skin produced a severe reaction that fluocinonide gel (see Medication, below) could not stop.
I tried to remove black spots (called plaques) from my skin with acetone. These were primarily on my hands, but occasionally elsewhere. (I got a large one when I mistakenly balanced the end of a stem on my coverall leg before going down a ladder.) Within a few hours of exposure I could usually remove about half of the black; afterwards, less. Near the end of the third field season, the skin on my hands was no longer sensitive to the allergen, just to the chemical burn. This left some scars, mainly on my wrists. During a two-day period in 1989, I measured water potentials in plants. I had to remove the bark bare handed. At the end of both days my fingers and most of my hand area were stained pure black as if they had been dipped in ink. I removed much of this with acetone, and the only reaction was under my fingernails, where the nails temporarily separated from my skin.
Because urushiol molecules have a hydrophilic and a hydrophobic end, they can form micelles (balls) in water, with the hydrophobic ends facing inward. Emulsifiers and solvents, as well as a cloth or brush, are important for getting them off. There are stories of urushiol remaining potent on rubber boots, and of people getting poison oak from exposure to flood water, explainable by the micelles that remained intact.
Inactivators render the allergen harmless. Urushiols are easily degraded in the presence of water unless the urushiols are clustered into micelles. There’s one report that a person got dermatitis from handling an herbarium sheet (a paper with a dried, pressed piece of Toxicodendron glued to it) that had been stored in a dry location (an herbarium) for 100 years (18). In contrast, urushiol on garden tools often degrades if the tools are left in a humid area.
Degradation will be hastened by the addition of an oxidizing agent to the water. Both hydrogen peroxide and photographer’s hypo are effective, but I never used them.
I washed my coveralls and arm-protecting socks in a bucket with only cold water at the end of every day. I washed my hands, wrists, face, and hair with cold water as often as feasible after exposures throughout each day. If I was not going to be near water for a few minutes and I knew that concentrated urushiol was on me (e.g., if I had cut a branch and its cut surface then brushed against my face) I immediately removed a glove, put saliva on my hand, and spread the saliva on the affected region.
One topical medicine was highly effective for me for prevention was fluocinonide gel 0.05% (Lidex or generic). You can ask your doctor for a prescription so you have it on hand if you get into poison oak. Dr. Epstein emphasized that the gel, not the liquid, was the effective formulation. He surmised that the fluocinonide gel rendered the skin cells with urushiol on them unreadable to the immune system, although this was not well-understood at the molecular level. I applied the gel to areas at the first signs of reaction (a pink blush or a pale raised welt), and repeated the application several times a day. It reversed the reaction if the exposure was small, and decreased it substantially if the exposure was moderate. If the rash would have been severe (e.g., if the skin had black plaques on it), I still had a bad reaction, but with the medication, it was localized.
There is a danger to prolonged use of fluocinonide: we are cautioned to use it sparingly on not at all where the skin is thin because it can cause necrosis. Because it contains steroids that enter the body to a small extent, one should not use it over a large proportion (say, one-sixth) of the body.
During the project, I never had a case bad enough to warrant the use of systemic corticosteroid therapy (prednisone taken orally or Medrol intramuscularly), but it is good to remember that if you ever have an extreme exposure, you should rush to a health center for oral or intra-muscular treatment. For me, Dr. Epstein used the example of getting a drop of urushiol (not just sawdust) in my eye, or having dermatitis over much of my body.
For topical relief of the dermatitis, I occasionally applied a substance with phenol in it, which numbed my skin for a half hour or so. Scalding or icing the rash was not usually worth the effort, although those treatments could delay an itching bout if I had to be somewhere. Dr. Epstein told me that calamine lotion would just dry the skin out and make it itch, which was more than I ever felt calamine lotion did. There are many home remedies (reference 1 lists over 100), but for my sensitivity, I felt the best remedy was to scratch. Once I had scratched the area raw, the itching abated. Regardless of what people tell you, I don’t think you can avoid scratching it if it itches, and none of the products made it itch less. Don’t let it get infected.
The last words come from Thomas Horsfield, from his 1798 dissertation (20). Luckily, we have learned a lot since he and those other brave souls experimented with urushiol and rashes in colonial days. “The remedies are naturally divided into 1. such as act generally on the whole system, and such as 2. are applied locally to the parts affected. Of the former I shall recommend Bloodletting, Purging, cold in the form of ice, cold water or cold air, and Mercury given with the view of exciting a salivation.” His three most effective topical remedies were “a solution of Corrosive sublimate in water…[to produce an] inflammation of greater force than that produced by the Rhus, which it counteracts and destroys;” an ointment of “one dram saccharum saturni with one ounce Unguentum simplex;” and “the Unguentum simplex of the dispensatories, sweet oil, and emollient cataplasms,” followed mercury administered internally if “tedious and ill-conditioned ulcers remain.”
Table: Recommendations to Minimize Poison Oak Reactions
|Avoidance||Learn to recognize the plant in all seasons, and then avoid it.
If you touch the plant, do not break its surface: move through it slowly and carefully.
Do not dig bare-handed in soil that has poison oak roots in it.
Use a solvent to decontaminate objects that contacted poison oak.
|Physical barriers (including clothing)||Cover parts of your body that are likely to contact the plant.
Protect wrists, which are particularly sensitive, with long socks from which you’ve cut holes for our fingers.
Protect hands with latex gloves.
Consider wearing a hat, coveralls, eye protection, shoes, and socks that you can remove and wet after exposure.
Remove clothing inside out for washing; dispose of gloves.
Use plastic wrap to cover items that have been exposed (tools, notebooks, car seats).
|Chemical barriers||Apply spray antiperspirant to your skin before exposure.
Your body’s oils offer some protection, so do not use soap or detergent on your skin, and do not swim in the 6 hours before exposure.
|Solvents||Wipe with soaps and detergents to emulsifiers (break up, lift) urushiol.
Wipe with organic solvents (alcohol, acetone, methanol, etc.) to remove urushiol from surfaces with fresh exposure, or from the surface of oxidized (black-stained) surfaces. The black stain is then safe to touch.
After exposure when you shower, use only mild soap, to leave some protection in case you encounter low-concentration urushiol on objects.
|Inactivators||Rinse objects, skin, and hair with water as soon as practical after exposure.
If water is not available, use almost any other moist material, such as spit, urine, sap of other plants, mud, diesel, food, or juice.
|Medication||For relief from itching, nothing is very effective. You may get some relief from scalding with hot water or numbing with ice.
Just as a reaction starts, to decrease its severity, apply fluocinonide gel to affected areas (prescription, used with care especially on the face).
After a serious reactions starts, take oral steroids like Prednisone (prescription).
- Baker, S. J. 1979. Poison Oak and Poison Ivy: Why it itches/what to do. Sandra J. Baker, Box 513, Soquel, California 95073.
- Breathnach, S. M. 1986. Immunologic aspects of contact dermatitis. Clinics in Dermatology 4:5-17.
- Epstein, W. 1959. Rhus dermatitis. Pediatric Clinics of North America 6:843-852.
- Epstein, W. L. 1974. Poison oak and poison ivy dermatitis as an occupational problem. Cutis 13:544-548.
- Epstein, W. 1984. Allergic contact dermatitis to poison oak and ivy: feasibility of hyposensitization. Dermatologic Clinics 2:613-617.
- Epstein, W. 1987. The poison ivy picker of Pennypack Park: the continuing saga of poison ivy. The Journal of Investigative Dermatology 88 supplement: 7-11.
- Epstein, W. 1989. Topical prevention of poison ivy/oak dermatitis. Archives of Dermatology 125:499-501.
- Epstein, W. 1990. Poison oak and poison ivy dermatitis. Pages 536-542 in R. M. Adams, ed., Occupational Skin Disease, 2nd ed. W. B. Saunders Co., Philadelphia.
- Fisher, A. A. 1986. Poison Sumac (Anacardiaceae) Rhus Family. Pages 405-417, in Contact Dermatitis, 3rd edition. Lea & Febiger, Philadelphia.
- Gartner, B. L. and D. E. Thomas. 1988. Vegetative propagation of poison oak (California). Restoration and Management Notes 6:48- 49.
- Gartner BL. 1991. Relative growth rates of vines and shrubs of western poison oak, Toxicodendron diversilobum(Anacardiaceae). American Journal of Botany 78: 1345-1353.
- Gartner BL. 1991. Structural stability and architecture of vines vs. shrubs of poison oak, Toxicodendron diversilobum. Ecology 72: 2005-2015.
- Gartner BL. 1991. Stem hydraulic properties of vines vs. shrubs of western poison oak, Toxicodendron diversilobum. Oecologia 97: 180-189.
- Gartner BL. 1991. Is the climbing habit of poison oak ecotypic? Functional Ecology 5: 696-704.
- Gartner BL, Wasser C, Rodriguez E, Epstein WL. 1993. Seasonal variation of urushiol content in poison oak leaves. American Journal of Contact Dermitis 4: 33-36.
- Gellin, G. A., C.R. Wolf, and T. H. Milby. 1971. Poison ivy, poison oak, and poison sumac. Archives of Environmental Health 22:280- 286.
- Gillis, W. 1971. The systematics and ecology of poison-ivy and the poison-oaks (Toxicodendron, Anacardiaceae). Rhodora 73:72-160, 161-237, 370-443, and 465-540.
- Gillis, W. 1975. Poison-ivy and its kin. Arnoldia 35:93-123.
- Gillis, W. T. 1971. The systematics and ecology of poison-ivy and the poison-oaks (Toxicodendron, Anacardiaceae). Rhodora 73:72-160, 161-237, 370-443, 465-540).
- Horsfield, T. 1798. An experimental dissertation on the Rhus vernix, Rhus radicans, and Rhus glabrum: commonly known in Pennsylvania by the names of poison-ash, poison-vine, and common sumac. Unpublished dissertation. University of Pennsylvania.
- Kligman, A. M. 1958. Poison ivy (Rhus) dermatitis: an experimental study. Archives of Dermatology 77:149-180.
- Marks, J. G., J. J. Trautlein, W. L. Epstein, D. M. Laws, and G. R. Sicard. 1987. Oral hyposensitization to poison ivy and poison oak. Archives of Dermatology 123:476-478.
- Oltman, J. and R. Hensler. 1986. Poison oak/ivy and forestry workers. Clinics in Dermatology 4:213-216.
- Watson, E. S. 1986. Toxicodendron hyposensitization programs. Clinics in Dermatology 4: 160-170.