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Appendix THE LOGISTICS OF WORKING WITH POISON OAK This appendix is part of my dissertation, which I wrote before I changed my name to Barbara Lachenbruch. Gartner, Barbara L. 1992. Consequences of the vine vs. shrub growth forms for biomechanics, growth, and hydraulic architecture of western poison oak, Toxicodendron diversilobum. Ph.D. Dissertation, Stanford University.

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Appendix

THE LOGISTICS OF WORKING WITH POISON OAK

This appendix is part of my dissertation, which I wrote before I changed my name to Barbara Lachenbruch.

Gartner, Barbara L. 1992. Consequences of the vine vs. shrub growth forms for biomechanics, growth, and hydraulic architecture of western poison oak, Toxicodendron diversilobum. Ph.D. Dissertation, Stanford University.

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"The poisonous weed, being in shape but little different from our

English ivie; but being touched causeth reddness, itchings, and lastly

blysters, the which howsoever, after a while they pass away of

themselves without further harme; yet because for the time they are

somewhat painefull, and in aspect dangerous, it hath gotten itselfe an

ill name, although questionless of noe very ill nature."

Smith 1609, as quoted in Kligman 1958)

(Captain John

In choosing to study the ecology of western poison oak

(Toxicodendron diyersilobum (T. & G.) Greene, Anacardiaceae, also known

as~ diyersiloba), I was aware that I was at risk of contracting

dermatitis and of causing other people to contract dermatitis. 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 employed to minimize exposure to the

allergen and to decrease the severity of my reaction after exposure. I

would like to caution that these methods worked well for me, a person of

low to moderate sensitivity, but that because of the complexity of the

immune system's reaction, these methods may not be successful for other

people.

THE DERMATITIS CAN CAUSE SERIOUS DISCOMFORT

More cases of allergic contact dermatitis are caused in the United

States by plants of the genus Toxicodendron than all other

"provocatives" combined (Fisher 1986) . At any one time, about half of

the U. S. population is sensitive to poison oak (reviewed in Epstein

1987), and more people would become sensitive if exposed over a period

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of time (Fisher 1986) . Almost a quarter of the workers who are flown to

California, Oregon, and Washington to fight fires have to leave the

fireline because of poison oak dermatitis (Oltman and Hensler 1986).

Poison oak and poison ivy dermatitis is the biggest single cause of

injuries for USDA Forest Service employees, and accounts for more than

10% of all lost-time injuries for their forestry workers (Oltman and

Hensler 1986). In California about 0.3% of the occupational injury

reports in agricultural workers are due to poison oak dermatitis

(Gellin, Wolf, and Milby 1971), and this costs about 0.1% of the state's

Workman Compensation budget (Epstein 1974) . Because Toxicodendron is

distributed over most of the contiguous United States (Gillis 1971),

people involved in recreational activities such·as hiking and mountain

biking frequently encounter poison oak or ivy and suffer the

consequences.

RELATIONSHIP OF EXPOSURE TO SENSITIVITY

The type of allergic contact dermatitis caused by Toxicodendron is

termed type IV delayed hypersensitivity. The basic mechanism of

sensitization is believed to work as follows (Breathnach 1986, Epstein

1989). The allergens, called urushiols, are a class of ortho catechols

with side chains of 15-17 carbons and various numbers of double bonds.

In the presence of oxygen, urushiols become quinones and bind to

proteins on certain cells of the skin surface. These cells are believed

to present signals related to the urushiol on their outer membrane

inside the body. Also presented are certain proteins that flag the cell

as an active part of the immune system. Helper T-cells react to these

signals by initiating production of at least four classes of cells or

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factors: effector T-cells (also called killer T-cells) which circulate

in the body and kill the flagged skin cells, memory T-cells which enable

the body to have a reaction to the flags should they be presented some

time in the future, suppressor cells, and circulating suppressor

factors, both of which inactivate the effector T-cells. One's

sensitivity to urushiol, then, depends upon the relative population

levels of these immune system fa c tors. The first time one is exposed to

poison oak there are no killer cells, and so one will not react (unless

one has memory cells resulting from previous sensitization through

cross-reactive allergens. All members of the genus Toxicodendron are

cross-reactive, as are several other members of the Anacardiaceae, such

as mango, cashew, and probably Schinus; Fisher 1986) . With time, the

relative populations of effector T-cells and suppressor T-cells will

probably change, resulting in different sensitivity of the individual as

a function of quantity and frequency of his or her exposure to

urushiols.

At present, the best way to predict one's reaction to poison oak

with time is to gauge from an one's previous experience. Some

individuals will become less sensitive the more they are exposed to

urushiols and others will become more sensitive (Epstein 1974) . About

15% of individuals are truly tolerant : they can not be sensitized even

with very high doses of urushiol (Kligman 1958, Epstein 1959) .

Epidemiological studies can predict the proportion of the population

that is sensitized to poison oak or ivy at any time, but these studies

do not control for amount of exposure or a patient's history of exposure

(Epstein 1974) .

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Over the course of my study of poison oak, Dr . William Epstein

(UCSF Medical Center) monitored my sensitivity to urushiol in order to

give me an objective indication of my status . Had tests shown that I

was becoming increasingly sensitive, I would have needed to find ways to

decrease my exposure, and had my sensitivity decreased, I could have

dispensed with some of the time-consuming precautions I was taking . The

tests consisted of placing four known quantities of urushiol on my inner

forearm, then monitoring reactions two days later (method described in

Epstein 1989). Dr. Epstein applied 2 . 50, 1.25 , 0.50, and 0.25 ~g of

urushiol in acetone to an area 1 . 2 em in diameter, where pure sap

generally corresponds to a dosage of 2-2.5 ~g of urushiol (Epstein

1990) . For the first trial, he used a larger range of quantities in

order to bracket my sensitivity.

I am relatively insensitive to poison oak ; some peop l e react to

urushiol at less than 0 . 004 % the dosage necessary to cause a reaction in

me (Epstein 1984) . My sensitivity to urushiol remained relatively

constant throughout the study, although it was higher at the outset,

before I had had any but recreational exposure for the previous several

years (Fig. 1). It also rose towards the middle of 1989, when my

exposure to poison oak had been steady and high . Since ceasing to

handle poison oak , my sensitivity has remained constant , but lower than

at the outset of the study . Note that the vertical a x is in Fig . 1a

shows only the bottom quarter of Dr . Epstein's grading system, which

spans from no reaction (0) to 4+ , and my strongest reactions were 1+ .

For a person with my level of sensitivity , desensitization is not

feasible. The oral preparations sold over-the-counter until the late

1970s have been shown to be ineffective , for the quantities o f urushio l

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2.50 1+

0.50 +1- .. -- .... - ---.. ------

Q) ... :I

high

en moderate 0 Q. >< Q)

low

none

1987

r--1 i I

I

I I I I

' I

' I I I

' I

' I

' I

' I

' I

' I

' I I

1988

r--1 i l I ' I ' r ' ' ' ' ' ' ' ' , L

I I

'

137

\ .. ----A)

1989 1990

I I

I : I

' ' I ' ' ' ' I

' I

' I I I I I I I B) I

Figure 1a) . My sensitivity to poison oak throughout this study at four

levels of urushiol, 2.50 ~g, 1.50 ~g, 1.25 ~g, and 0.50 ~g applied on

1.2 em diameter spots on my forearm. Severity of reaction increases

with numerical value. b). My exposure to poison oak throughout this

study, (subjectively determined) .

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were much too low to cause any real effect (Epstein 1974). Oral

urushiol preparations are used successfully, however, to induce some

level of desensitization in extremely sensitive individuals (Epstein

1984, Watson 1986). Unfortunately, the procedure is quite inconvenient:

desensitization only decreases a person's sensitivity to the level of a

moderately sensitive person, it takes two to four months to become

desensitized, a person must continue on the medication to remain

desensitized, and the treatment itself often causes uncomfortable side-

effects.

HOW I LESSENED MY CHANCES OF CONTRACTING AND CAUSING OTHERS TO CONTRACT

DERMATITIS

Urushiol is readily transferred from one item to another, and i t

remains stable (in the absence of high humidity) for long periods of

time. One individual is reported to have contracted dermatitis from

handling 100-year old herbarium specimens (Gillis 1975). Therefore, it

was essential that I learned not only how to avoid contracting

dermatitis, but how to keep equipment and other objects free from

urushiols . I highly recommend the pamphlet "Preventing and treating

poison oak and poison ivy" (USDA 1981) . My recommendations for other

people of similar sensitivity are summarized in Table 1 . I used the

following methods .

Avoidance

The best way to avoid dermatitis is to avoid contact with the

plant. However, almost all of my work required contacting the plant, so

the next best alternative was to handle the plant gently .

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Table 1 . Recommendations to minimize reactions to poison oak in a

person of low to moderate sensitivity. Urushiols are the class of

substances that cause allergic reactions.

Avoidance :

Cl othing :

Chemical barriers :

Solvents :

Learn to recognize the plant in all seasons , and

avoid it .

If you touch the plant, do not break its surface :

move through it slowly and carefully .

Decontaminate all objects that have contacted

poison oak to avoid re-exposing yourself o r

e xposing other people.

Cover parts of your body that are likely to contact

the plant .

Wrists are particularly sensitive areas, and if you

will be handling the plant , wear long socks on

your arms (provide cut - outs for your finge r s).

Apply spray antiperspirant to your skin before

e xposure.

Soaps and detergents are effective emulsifiers but

do not use them within the six hours before

you are e xposed to urushiol , and use only mild

soap .

Organic solvents (alcohol , acetone , methanol , etc . )

are effective solvents of unoxidized urushiol .

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Inactivators:

Medication:

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Once the urushiol oxidizes, use these solvents to

wipe off any free molecules of urushiol, then

consider the black-stained object safe.

Rinse objects, skin, and hair with water as soon as

is practical after exposure to poison oak.

For relief from itching, nothing seems very

effective.

To decrease the severity of reaction, apply

fluocinonide gel to affected areas as soon as

the reaction starts. Note: this is a

prescription drug, and must be used with care,

especially on the face.

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The uninjured plant is innocuous. If one can avoid breaking the

plant's surface, one will avoid contact with urushiols (unless there is

a urushiol seep on the surface, that can result from a previous injury

to the plant. These seeps can usually be seen if one takes the time.)

Urushiol is located in ducts in the roots, stems, leaves, and seeds . If

one nicks a stem or leaf, or pulls a leaf off, the urushiols (mixed with

other substances) are easily seen as a milky white fluid that flows out

like a heavy syrup . After exposure to the air the fluid will dry and

blacken, forming a shiny black plaque. (Urushiols are closely related

to the chemicals used to produce Japanese lacquer.) When the plaque is

truly dry, it is no longer allergenic.

My methods of avoidance started with the decision not to study

roots because they bear urushiols , and because it would be ha r d to d i g

with intact latex gloves. To avoid breaking aboveground surfaces I

handled the plant very gently, and when I moved through stands of it I

moved slowly and carefully. It was preferable to have uninjured stems

resting on my neck and face than to force the stems into other

positions, risking their breakage.

I could, however, isolate my work from that of others, to lessen

the chances of their becoming affected. I conducted field work at an

off-campus biological preserve. When possible, I used only my personal

vehicle for transport of samples, equipment, and notes, and which,

during field season, I discouraged others from driving or sitting in. I

conducted the indoor work in a building near the study site, which few

other people used. I tried to restrict contamination to one half of the

building. The first half of the building I considered contaminated: I

worked there, and left equipment, supplies, samples, and notes there.

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The other half of the building I considered clean. One or two other

graduate students used this area off and on, mainly for storage of

equipment. I used that area for clean activities, and I kept equipment

and clothes there which I did not want contaminated. Before taking

notes to the computer, I photocopied them. I taped paper towels over

much of the photocopy machine, and after making copies, I cleaned the

area and the photocopy machine with water. The original notes are in

clean file folders with other field notes.

ClothinQ

I wore protective clothing in the field and lab. These consisted

of heavy coveralls and long cotton socks on my legs and on my arms (with

holes cut for my fingers), and latex gloves. Initially I also wore a

hat, but I found 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 trees or crawled through dense shrubby areas. 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.

Fisher (1986) said that urushiol goes through rubber gloves. This

concerned me because much of my workday was spent with gloves entirely

wet with urushiol; also, my fingers developed itchy blisters. At one

session Dr. Epstein administered sensitivity tests over three separate

panels of latex glove taped to my forearm. He administered the highest

dosage that he uses on me. 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

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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 my hands

wet inside gloves all day.

Chemical barriers

I tried using spray antiperspirant as a barrier to poison oak.

This has been found effective in tests, both due to the organophilic

bentonite clays used as filler ("inert ingredients") and due to the

aluminum chlorohydrate (Oltman and Hensler 1986, Epstein 1989). This

may become available commercially under the name Ivy-Block (pending

testing, United Catalysts, Inc., Louisville, KY). I found it more work

than it was worth, especially because my neck and face were the main

parts that were directly exposed, it was difficult to wash off, and the

spray hole clogged easily when I left the can in a hot vehicle. Another

barrier being used by outdoor workers in northern California and whose

testing is just now starting is a linoleic acid dimer marketed as Stoko­

Gard Outdoor Cream (Stockhausen), available through industrial supply

houses. I have not yet used it.

Solvents

Urushiols can be emulsified by soaps and detergents and dissolved

by organic solvents (such as alcohol, methanol, acetone, gasoline, and

paint thinner) . Soaps and detergents can break up and remove micelles,

but they also remove what protective oils the skin has, allowing any

urushiol remaining on the skin (or steering wheel, shoes, camera case,

etc. that will later transfer urushiol back to the skin) to more easily

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cause a reaction. Kligman (1958) showed that a mildly sensitive

individual may benefit from washing the skin with Ivory soap and water

30 minutes after exposure but not 60 minutes (a highly sensitive person

will benefit from washing 1 or 5 minutes after exposure, but not 10

minutes; however, after 1 or 5 minutes he or she will still develop

dermatitis) . These protective skin oils require three to six hours to

replenish after having been stripped. Therefore, as recommended (USDA

1981), I used soap only in circumstances when I would not be exposed for

the next six hours, usually at the end of the day . I did not shower or

swim within the six hours before I would be exposed to poison oak. The

use of mild soap (such as a glycerine-based soap) is recommended over a

harsh one (Fels-Naptha, for example), in order to leave a little more

protection on the skin in case one misses a few molecules or encounters

them later on some object (such as the clothes one carries to the

washing machine) .

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. I do not know of

a case of anyone's contracting poison oak from using equipment I had

previously used.

On my skin, the solvents were not always so successful. At the

end of the day, I used soap or detergent on my wrists, hands , face, and

neck. Even if I had been careful, at some point I would have pulled off

a glove to get a spider-web off my face or frass out of my eye, etc .,

and inevitably I would have transferred a little urushiol from place to

place. Also, my hands got much urushiol on them when I was studying

hydraulic conductivity because my hands were under water in basins with

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pools of urushiol floating on top. Those pools entered my gloves at the

wrist and remained there until the end of the day. When pure urushiol

would get on my skin, it made an oily spot that I could not always

remove with soap, detergent, ethanol, or acetone. These spots turn

black after they oxidize--a daily occurrence on my hands in 1989--and

the skin would often produce a severe reaction that could not be stopped

by the fluocinonide gel (see Medication, below) .

I tried to remove black spots from skin with acetone. These were

primarily on my hands, but occasionally elsewhere. Within a few hours

of exposure I could usually remove about half of the black; afterwards,

less. However, near the end of the last (1989) field season, the skin

on my hands seldom reacted except occasionally as if I had experienced a

chemical burn (which is a secondary effect of urushiol) . This left some

scars, mainly on my wrists. During a two-day period in 1989 I measured

water potentials in plants. I was unable to remove the bark and then

seal the stem into the pressure chamber with gloves on, so I worked

bare-handed. At the end of each day 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 finger

nails (with which I had peeled away bark), where the nails temporarily

separated a bit from my skin.

Inactiyators

Urushiols are easily degraded in the presence of water unless the

urushiols are clustered into micelles (Epstein 1974). Degradation will

be hastened by the addition of an oxidizing agent to the water; both

hydrogen peroxide and photographer's hypo are readily available and

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effective (W. L. Epstein, pers. communication). I washed my coveralls

and arm-protecting socks with cold water at the end of the 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 it on the affected region.

Medication

Even with my low sensitivity and the precautions I took, during

most of the period of this study I had some dermatitis somewhere. I

tried treating it in several ways. For topical relief I occasionally

applied a substance with phenol, which seemed to nwub my skin for a half

hour or so. Scalding or chilling my skin did not seem worth my effort.

There are many home remedies (Baker, 1979, lists over 100), but for my

sensitivity, I felt the best remedy was to scratch it when it itched,

and let time take the itch away.

There is one topical medicine that I used frequently that was

highly effective for me: fluocinonide gel 0.05% (Lidex gel, Syntex, but

also marketed as a generic drug; available by prescription only).

Fluocinonide gel may to alter the skin cells that are part of the immune

system, perhaps by rendering their immune-system signals unreadable to

the immune system, although this is not well-understood at the molecular

level (W. L. Epstein, pers. communication). I applied the gel to areas

as the first signs of reaction occurred (a pink blush or a raised pale

welt), and repeated the application several times a day. It reversed

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the reaction if the exposure was small, and decreased it substantially

if the exposure was moderate. If the rash would have been severe (if

the skin had black, oxidized urushiol on it) I still had a bad but

localized reaction. There is a danger to prolonged use of fluocinonide,

and Dr. Epstein cautioned me not to use it on my face or neck (where the

skin is thin and visible): it can cause necrosis. Also, it contains

steroids, which enter the body to a small extent, and for this reason

one should not use it over a large proportion (say, one-sixth) of the

body. I never had a bad enough case to warrant the use of systemic

corticosteroid therapy (prednisone taken orally or Medrol

intramuscularly), but Dr. Epstein reminded me that if I ever thought I

had had an extreme exposure (such as drops of urushiol directly in my

eye, or dermatitis on much of my body) I should rush to the health

center for such oral or intra-muscular treatment.

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LITERATURE CITED

These references are for the entire thesis, but they include the ones cited in the appendix.

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Adamson, R. S . 1939 . The classification of life-forms of plants.

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Baker, S . J. 1979 . Poison Oak and Poison Ivy: Why it itches/what to

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Bamber, R. K. 1984 . Wood anatomy of some Australian rainforest vines.

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properties in individual growth rings of plantation-grown eastern

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Blackman, G. E. and G. L. Wilson . 1951. Physiological and ecological

studies in the analysis of plant environment. VII. An analysis

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supporting plants in a tropical deciduous forest . Biotropica

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Cannell, M. G. R . and J. Morgan. 1987 . Young's modulus of sections of

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Cannell, M. G. R., J. Morgan, and M. B . Murray . 1988. Diameters and

dry weights of tree shoots: effects of Young's modulus, taper,

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woody southern Californian flora. IAWA Bull ns 6 : 319-347.

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Carter, G. A. and A. H. Teramura. 1988 . Vine photosynthesis and

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Appendix

THE LOGISTICS OF WORKING WITH POISON OAK

Citation: Gartner, Barbara Lachenbruch. 1990. Appendix, The logistics of working with poison oak. Pages

132-162, in Consequences of the vine vs. shrub growth forms for biomechanics, growth, and hydraulic architecture of western poison oak, Toxicodendron diversilobum. PhD Dissertation, Dept. ofBiological Sciences, Stanford University. 162 pp.

Other articles related to the dissertation: Gartner, B. L., C. Wasser, E. Rodriguez, and W. L Epstein. 1993. Seasonal variation of urushiol

content in poison oak. American Journal of Contact Dermatitis 4:33-36. Gartner, B. L. 1991. Structural stability and architecture of vines vs. shrubs of poison oak,

Toxicodendron diversilobum. Ecology 72 :2005-2015. Gartner, B. L. 1991. Relative growth rates ofvines and shrubs ofwestern poison oak,

Toxicodendron diversilobum (Anacardiaceae). American Journal of Botany 10:1345-1353. Gartner, B. L. 1991. Is the climbing habit of poison oak ecotypic? Functional Ecology 5:696-704. Gartner, B. L. 1991. Stem hydraulic properties of vines vs. shrubs of western poison oak,

Toxicodendron diversilobum. Oecologia 87:180-189.