The Health Gazette
POISON IVY
Summer is here and it is time to spend some quality time outside. Whether you are hiking or working in your garden, you are always at risk for getting poison ivy. There are three types of plants that cause the same itchy red rash. They are poison ivy, poison oak and poison sumac. Poison ivy is by far the most common cause of the allergic skin reaction. The spring and summer are the most common times of the year for poison ivy and oak. Poison ivy and oak have three leaves on each stem and grow as a vine or bush. Sumac has two rows of leaves opposite each other and one leaf at the end of the stem. It grows as a bush or tree. The leaves of all three plants are shiny and coated with an oily chemical, which causes the allergic reaction. The oils are also in the stems and roots of these plants. Pets can get the oil on their furry coats and spread the oil to humans. A particularly severe case of poison ivy can occurs when you are burning debris that contains poison ivy plants. The fire produces a vapor that can be inhaled or deposited on the exposed parts of the skin. The resulting rash can cause a severe reaction that may need more potent medication like a steroid shot or oral prednisone.
ETIOLOGY
All of these plants contain the same oily chemical that causes the rash. It is an allergic contact dermatitis. The chemical is a resin called urushiol. This chemical is nonvolatile and dries quickly on clothing, shoes, animals and tools. Urushiol remains potent for as long as one year. Therefore, it is important to wash any tools, shoes or clothing after exposure to poison ivy. When your skin comes in contact with any part of the plant, it is only a matter of time before you break-out with a rash, assuming you are allergic to it. Not everyone is sensitive to poison ivy. It has been estimated that 70 percent of the population is susceptible to poison ivy. Dark-skinned individuals seem less susceptible than others. Elderly individuals and infants are not as susceptible to the plant but they can still get it. Children become susceptible by age 3 and are highly susceptible by age 12. If you know you have been exposed to poison ivy, it is important to wash off immediately. The resin is absorbed quickly into the skin. As little as ten minutes of exposure may produce the allergic reaction. The eruption is characterized by redness, papules, vesicles and linear streaking. The eruption usually appears within two days but may occur within eight hours. The eruption rarely is delayed longer than ten days. After washing off with soap and water, all of the damage is done. Contrary to popular belief, the fluid in the vesicles or blisters will not spread the rash. This fluid is totally harmless and in no way can spread the rash or make it worse. It is easy to see how this misconception got started. The rash will frequently break out in stages depending on the length of exposure and the amount of urushiol on the skin. If the face is exposed heavily and for a long period of time, then you may break out within 24 hours. If your arms are exposed for one hour, then you may not break out for 48 hours. If your legs are only exposed for ten minutes, then you may not break out for a week. Obviously, it appears as if the rash is spreading over the body. Another factor to consider is the possibility of re-exposure. As mentioned above, the resin will remain on the exposed objects. If you put on your exposed shoes a week later, you can wipe the resin from your shoes on your face or other areas. One of the most severe reactions that I have seen, occurred when a patient was downwind of a neighbor who was burning poison ivy. The urushiol can be vaporized when exposed to a fire. The unfortunate individual who is downwind, could receive a coat of urushiol on any uncovered areas resulting in a surprise case of poison ivy.
TREATMENT
Treatment will depend on how severe the reaction is. For minor cases it may only be necessary to apply an over the counter hydrocortisone cream and some Calamine lotion. For more severe reactions it may be necessary to take an oral steroid such as prednisone. Occasionally, it is necessary to give a shot of a steroid. Benadryl capsules are over the counter and help control the itching. Atarax and Periactin are also excellent, but they require a prescription. Domeboro solution can be very soothing and decrease the itching. Avoid using topical preparations that contain benzocaine, zirconium, or antihistamines. These substances will frequently cause an allergic skin reaction which may worsen the poison ivy.
PREVENTION
The best prophylaxis for allergic contact dermatitis is complete avoidance of the plants. Individuals should learn to recognize and avoid poison ivy. Unfortunately, barrier creams or other solutions are of no value in preventing poison ivy. Long-sleeved shirts and long pants are advisable when working around poison ivy. Occasionally, people cannot avoid poison ivy because of the nature of their job. Some allergists will attempt to desensitize a patient to poison ivy. Unfortunately, this is not always effective.
REFERENCES
Fisher A. Poison Sumac (Anacardiaceae) Rhus Family. Contact Dermatitis 3rd ed. pp. 405-417.
The information provided above is offered as a community service about health-care issues and is not a substitute for individual consultation. Advice on individual problems should be obtained from your personal physician. This information is based on research by the author and represents his interpretation of the literature.
How Poisoning Occurs
Poison ivy, western poison oak, and poison sumac have the poisonous sap in their roots, stems, leaves and fruit. The sap is released
when the plant is bruised, making it easier to contract Rhus-dermatitis in the spring and early summer when leaves are tender. The sap
may be deposited on the skin by direct contact with the plant or by contact with contaminated objects, such as shoes, clothing, tools and
animals. Severe cases have occurred from sap-coated soot in the smoke of burning plants.
The three plants contain a poisonous sap with four antigenic compounds (catechols). The sap is present in roots, stems, leaves, and
fruit. The only parts without the poison are the anthers, pollen, xylem, and epidermis. The poisonous sap is released only after the
epidermis of plants is ruptured. Although the dermatitic capacity of the sap varies little from plant to plant or at different times of the year,
it is easiest to contract Rhus-dermatitis in the spring and early summer, when leaves are tender and bruise easily. The interval between
contact and the appearance of the dermatitis varies considerably, because of the different susceptibilities of individuals and the amount of
poisonous liquid contacting the skin. Most people develop Rhus-dermatitis 24-48 hours after contact. Healing time varies from a few days
to several weeks, and healed sites often remain supersensitive to any further contact with sap for several months.
Under hot, humid conditions the poisonous sap becomes inert in about a week. However, under dry conditions, the plant can retain
its harmful effect for a long period of time. Clothing can be decontaminated by laundering it in a washing machine with soap or detergent.
Infected skin can never be washed soon enough to prevent some dermatitis in sensitive individuals, but washing is useful because it
minimizes the severity of the rash and also prevents the spread of the sap to uninfected parts of the body.
The sap must penetrate the skin before poisoning results; therefore, the most severe poisoning affects areas with thin skin. Symptoms
are less severe or do not occur at all in areas with thick skin or heavy hair.
Clinical evidence shows that no person is completely immune to the poisonous sap. Some are sensitive to small amounts of the
poison, whereas others react only to large amounts. Severe cases of Rhus-poisoning have occurred after supposedly immune individuals
have purposely rubbed Rhus leaves onto their skin. To date, there is no acceptable method of immunization.
Of the three poisonous Rhus species, usually only poison ivy grows in locations that warrant its eradication.
You can destroy poison ivy by cultivation. A single treatment seldom kills the plant completely, as it consists of a vast interconnected
network of above- and below-ground horizontal rhizomes and above-ground vertical stems. Treat the area again as soon as regrowth
occurs from any living parts. Repeated cultivation will eliminate poison ivy because it does not easily regenerate from plant fragments.
Chemicals are recommended for eradication in areas that do not permit cultivation and where some damage to other vegetation can
be tolerated. You can buy a wide range of suitable chemicals at stores that sell pesticides. You may also obtain the latest
recommendations for chemical control from your local agricultural representative or provincial ministry of agriculture.
CAUTION: Be very careful when eradicating these plants. Your boots, protective clothing and implements may pick up the sap and
transfer it to your skin. Do not burn the plants except under controlled conditions, as the sap-covered soot in the smoke will carry the
poison. Also, dead poison ivy plants can still cause dermatitis and must be handled with care.
Poison Ivy, Sumac, and Oak
What is poison ivy, sumac, or oak?
"Poisoning" from plants such as poison ivy, sumac, and oak is an allergic reaction that results when the skin touches these
plants and their oils. Most people develop a rash, blisters, and itching after contact with them. Cases usually occur in the
spring and summer.
Poison ivy and oak have three leaves on each stem and grow as a vine or bush. Sumac has two rows of leaves opposite each
other and one leaf at the end of the stem. It grows as a bush or tree. The leaves of all three plants are shiny and coated with an
oily chemical, which causes the allergic reaction. The oils are also in the stems and roots of these plants.
How does it occur?
The reaction occurs after touching poison ivy, sumac, or oak. A reaction can also occur after contact with anything else that
may carry the plant's oils, including ashes and smoke from burning plants. It can also be spread by touching oil left on clothes
or tools. The rash often appears on the face first and then on other exposed areas of the body. Typically it is first noticed 24 to
48 hours after contact. How bad the rash will be depends on the thickness of your skin and how much contact you had with
the plant's oils.
Sometimes there is a delayed reaction, and the rash develops on one area of your skin after the others. The rash cannot be
spread by scratching itchy skin or from oozing blisters. However, scratching may lead to infection of the open sores.
What are the symptoms?
The symptoms of an allergic reaction to poison ivy, sumac, or oak include the following, from least serious to most serious:
itching, often intense
red blotches that can be either raised or flat
blisters, which may show up in lines
fever
headache
swelling of your throat and eyes
overall swelling of your body
general feeling of discomfort
stomach cramps, nausea, vomiting, diarrhea.
How is it diagnosed?
Diagnosis is based on your having the symptoms listed above and on a physical exam by your doctor.
How is it treated?
To treat poison ivy, sumac, or oak, follow these steps:
Remove your clothes and shoes and wash them in detergent and hot water.
As soon as possible, wash all exposed skin with strong soap and water (or just water) to remove the plant's oils.
Apply cloths soaked in aluminum acetate solution (Burow's solution), then calamine lotion or ointment to reduce the
redness, ease the itching, and help dry up the blisters. Or take lukewarm baths with cornstarch (1/2 cup) or colloidal
oatmeal added to ease the itching. DO NOT use topical antihistamines.
Cover any oozing blisters with a clean gauze bandage soaked in a baking soda and water solution.
If the rash spreads to your face, mouth, eyes, or genitals, or if you develop a fever, headache, extreme redness, pus, or other
severe symptoms, see your doctor. He or she will recommend one or more of the following:
injecting a corticosteroid (powerful anti-inflammatory drugs, such as cortisone, used in treating allergies)
applying corticosteroid ointment or cream to the affected areas two to three times a day, gradually reducing to once a
day
taking oral corticosteroids such as prednisone
taking oral antibiotics or using an antibiotic cream if an infection develops.
Because these are all potent drugs, ask your doctor about any possible side effects or interactions with other drugs you may
be taking.
How long will the effects last?
In most people, the condition clears up in 2 to 3 weeks.
How can I take care of myself?
Follow the steps outlined above to treat your rash. In addition, keep the affected skin clean and dry. Keep your fingernails
well trimmed and clean. Try not to scratch your skin to avoid an infection.
See your doctor if you develop severe symptoms.
What can be done to help prevent a reaction to poison ivy, sumac, or oak?
Follow these guidelines:
Know what the plants look like and where they grow so you can avoid them.
Wear long-sleeved shirts and long pants if you are going to be in an area where these plants grow.
Within 5 to 10 minutes of contact with the plant, rinse exposed skin thoroughly with soap and water (or just water).
Be sure to clean under your fingernails.
Wash clothes and shoes in hot water and detergent to remove any oil that may be on them.
Give any outdoor pets a bath if you think they have had contact with the plants.
Allergic contact dermatitis may account for as many as 20% of all cases of dermatitis in children. Poison ivy, nickel (jewelry),
rubber (shoe dermatitis), balsam of Peru (hand and face dermatitis), formaldehyde (cosmetics and shampoos), and neomycin
(topical antibiotic ointments) are the most common allergens. [4]
RHUS DERMATITIS
In the United States, poison ivy, poison oak, and poison sumac produce more cases of allergic contact dermatitis than all
other contactants combined. The allergens responsible for poison ivy and poison oak allergic contact dermatitis are contained
within the resinous sap material termed urushiol. Urushiol is composed of a mixture of catechols. All parts of the plant contain
the sap. These plants belong to the Anacardiaceae family and the genus Rhus. Other plants in that family, such as cashew
trees, mango trees, Japanese laquer trees, and ginkgo contain allergens identical or related to those in poison ivy. Thousands
of workers on cashew nut farms in India develop hand dermatitis from direct contact with the irritating resinous oil from
cashew nut shells. [5]
Poison ivy and poison oak are neither ivy nor oak species.
Clinical presentation.
Rhus dermatitis occurs from contact with the leaf or internal parts of the stem or root and can
Figure 4-6 Poison ivy. A classic presentation with vesicles and blisters. A line of vesicles (linear lesions) caused by
dragging the resin over the surface of the skin with the scratching finger is a highly characteristic sign of plant contact
dermatitis.
be acquired from roots or stems in the fall and winter. The clinical presentation varies with the quantity of oleoresin that
contacts the skin, the pattern in which contact was made, individual susceptibility, and regional variations in cutaneous
reactivity. Small quantities of oleoresin produce only erythema, whereas large quantities cause intense vesiculation (Figures 4-6
and 4-7) .
The highly characteristic linear lesions are created when part of the plant is drawn across the skin or from streaking the
oleoresin while scratching. Diffuse or unusual patterns of inflammation occur when the oleoresin is acquired from contaminated
animal hair or clothing or from smoke while burning the plant. The eruption may appear as quickly as 8 hours after contact or
may be delayed for a week or more. The appearance of new lesions a week after contact may be confusing to the patient,
who may attribute new lesions to the spread of the disease by touching active lesions or to contamination with blister fluid.
Blister fluid does not contain the oleoresin and, contrary to popular belief, cannot spread the inflammation.
Treatment of inflammation.
Washing the skin with any type of soap inactivates and removes all surface oleoresin,
Figure 4-7 Poison ivy dermatitis. Diffuse erythema with vesicles over the entire surface.
87
thereby preventing further contamination. Washing is most effective if done within 15 minutes of exposure.
Blisters and intense erythema.
Cold wet compresses are highly effective during the acute blistering stage. They should be used for 15 to 30 minutes several
times a day for 1 to 3 days until blistering and severe itching is controlled. Topical steroids do not penetrate through blisters.
Prednisone, administered in a dosage of 20 mg twice each day for at least 6 days, is used for severe, widespread
inflammation. Patients who may have trouble adhering to a medication schedule may be treated with triamcinolone acetonide
(Kenalog, Aristocort; 40 mg suspension) given intramuscularly. Commercially available steroid dose packs should be avoided;
they provide an inadequate amount of medicine. Patients who do not initially seem to require medication may become much
worse 1 or 2 days after an office visit; they should be advised that prednisone is available if their conditions worsen.
Short, cool tub baths with or without colloidal oatmeal (Aveeno) are very soothing and help to control widespread acute
inflammation. Calamine lotion controls itching but prolonged use causes excessive drying. Hydroxyzine and diphenhydramine
control itching and encourage sleep.
Mild to moderate erythema.
Topical steroid gels or creams (groups III through V) applied 2 to 4 times a day rapidly suppress erythema and itching.
Prophylactic treatment.
Complete desensitization cannot be accomplished. Poison ivy oleoresin in capsules and injectable syringes for
hyposensitization has been removed from the market by the FDA.
Contact Dermatitis.
Contact dermatitis is an inflammatory reaction of the skin to a chemical, physical, or biologic agent. The inducing agent acts as
an irritant or allergic sensitizer. Allergic contact dermatitis is a form of delayed hypersensitivity mediated by lymphocytes
sensitized by the contact of the allergen to the skin. It is less common than irritant contact dermatitis. [70] Caustics, industrial
solvents, and detergents are common causes of irritant dermatitis. Dermatitis may result from a brief contact with a potent
caustic or from repeated or prolonged contact with milder irritants.
Clothing, jewelry, soaps, cosmetics, plants, and medications contain allergens that commonly cause allergic contact dermatitis.
The most common allergens include rubber compounds, plants of the Rhus genus (poison ivy, oak, and sumac), nickel (often
used in jewelry alloys), paraphenyldenediamine (an ingredient in hair dyes and industrial chemicals), and ethylenediamine (a
stabilizer in topical medications). [71] Sensitization to poison ivy results in sensitization to other plants in this family such as
cashew, mango, lacquer, and ginkgo trees. [71]
The primary lesions of contact dermatitis are papules, vesicles, or bullae on an erythematous bed. Of the allergens, Rhus
species are the most likely to cause bullous eruptions. Oozing, crusting, scaling, and fissuring may be found, along with
lichenification in chronic lesions. The distribution of the eruption depends on the specific contactant and may be localized,
asymmetric linear, or unilateral (Figs. 164-12 (Figure Not Available) and 164-13) (Figure Not Available) . Mucous
membranes are usually spared unless directly exposed to the inciting agent. A history of exposure is the most significant factor
favoring the diagnosis. If doubt exists about the diagnosis, the patient should be referred for allergic patch testing.
Figure 164-12 (Figure Not Available) Contact dermatitis secondary to nickel. (Photo by David Effron, MD.)
Figure 164-13 (Figure Not Available) Typical linear lesions of contact dermatitis secondary to poison ivy. (Photo by David Effron, MD.)
The treatment includes avoidance of the irritant or allergen and treatment of secondary bacterial infection. Oozing or
vesiculated lesions should be treated with cool wet compresses of Burow's solution applied for 15 minutes 3 or 4 times daily.
Topical corticosteroid creams or ointments help reduce inflammation and pruritus. A short course of systemic corticosteroids
is necessary. [72] Prednisone in a dosage of 30 to 80 mg/day (depending on the severity of involvement) should be prescribed
initially. This should be tapered over 10 to 14 days with the dosage decreased by 10 mg each day until a dose of 40 mg is
reached. It should then be decreased in daily increments of 5 mg. The treatment may be discontinued without further tapering
when a daily dose of 10 mg is reached. The medication is best taken as a single morning dose. Systemic antihistamines, such
as hydroxyzine or diphenhydramine, may help control pruritus. [71]
Diaper Dermatitis.
Diaper dermatitis is a common disorder. The condition is exacerbated by heat, moisture, friction, and the presence of urine
and fecal material. Occlusive clothing in infants tends to foster all of these. Lesions begin
P2791
Figure 164-14 (Figure Not Available) Erythema multiforme. (Photo by David Effron, MD.)
as erythematous plaques in the genital, perianal, gluteal, and inguinal areas. More severe involvement results in moist, eroded
lesions that may extend beyond the primary areas of appearance.
Infection with C. albicans and fecal bacterial flora is an important contributory factor to the development of diaper dermatitis.
Lesions infected with Candida are moist, red patches with well-demarcated borders. Papular or pustular satellite lesions are
also present.
Diaper dermatitis may reflect the presence of atopic or seborrheic dermatitis in the infant. The presence of lesions elsewhere
on the body, particularly on the face, in cases of atopic dermatitis, or the scalp, in cases of seborrhea, alert the physician to
these possibilities. Ammonia and bacterially produced putrefactive enzymes produce dermatitis as contact irritants. Such
rashes are accompanied by characteristic odors. The existence of diaper dermatitis as a true allergic contact dermatitis is rare.
Treatment consists primarily of altering the physical environment in which diaper dermatitis thrives. Excess clothing should be
removed, and occlusive plastic or rubber diaper covers should not be used. Diapers should be changed frequently and left off
for prolonged periods if possible. Sterilized cloth diapers are preferred.
If exudative lesions are present, treatment with topical cool wet compresses of saline or Burow's solution is indicated for 2 to
3 days. Continuous air exposure of the area should be attempted. [71] Zinc oxide (Desitin) may dry the area. Severe contact or
seborrheic dermatitis may require short-term treatment with topical corticosteroids, such as 1% hydrocortisone in a cream
base. [73] Ointment-based topical medications for treatment of diaper dermatitis should be avoided because their occlusive
nature enhances moisture retention. Nystatin cream or powder should be applied to lesions infected with Candida.
Journal of Allergy and Clinical Immunology
Volume 105 • Number 3 • March 2000
Copyright © 2000 Mosby, Inc.
Current reviews of allergy and clinical
The diagnostic evaluation, treatment, and prevention of allergic contact dermatitis in the new
millennium
Donald V. Belsito MD
Key words
Allergic contact dermatitis
common allergens
clinical manifestations
diagnostic evaluation
immunoregulation
treatment
prevention
From the Division of Dermatology, University of Kansas Medical Center, Kansas City, Kan.
Received for publication Dec 7, 1999.
Accepted for publication Dec 9, 1999.
Reprints not available from the author.
Copyright © 2000 by Mosby, Inc.
0091-6749/2000 $12.00 + 0 1/1/104937
Kansas City, Kan
Identifying the etiology of allergic contact dermatitis is a rewarding yet challenging endeavor. Not all allergic
contact reactions are eczematous in appearance. The most reliable clinical clue to the allergic nature of the
dermatitis is its geographic distribution. Once a list of culprit allergens has been identified by patch testing, the
practitioner must identify the relevant allergen(s) and counsel the patient in avoidance. For most individuals,
allergen avoidance results in resolution of the dermatitis; however, some patients will require continuing
symptomatic therapy despite avoidance. For those patients unable to avoid known allergens, immunosuppressant
therapies (including phototherapy) or barriers can be beneficial. Currently, hyposensitization is not a viable
alternative for the treatment of allergic contact dermatitis. (J Allergy Clin Immunol 2000;105:409-20.)
Abbreviations used
ACD:
Allergic contact dermatitis
DMDM:
Dimethyoldimethyl
GPT:
Guinea pig tests
ICCVAM:
Interagency Coordinating Committee on the Validation of Alternative Methods
LCs:
Langerhans cells
LLNA:
Local lymph node assay
MCI/M:
Methylchloroisothiazolinone/methylisothiazolinone
NACDG:
North American Contact Dermatitis Group
PPD:
para-Phenylenediamine
PUVA:
Psoralens ultraviolet radiation
ROAT:
Repeat open application testing
TAP 2B:
Transporter associated with antigen processing 2B
UVB:
Ultraviolet B radiation
Contact dermatitis can be either allergic or irritant in etiology. The diagnosis is not usually apparent from history or physical
examination alone. Without patch testing, it is impossible to delineate the cause. Thus, although it has been 105 years since
Jadassohn[1] first described the use of patch tests, such testing remains vital to the appropriate diagnosis of contact dermatitis.
Indeed, perhaps the only suspected allergic condition where patch testing is not indicated is that induced by exposure to plants
of the Toxicodendron species, which can usually be recognized by the presence of the intense, often linear, papulovesicular
eruption they induce (Fig 1).
(Figure Not Available) Fig. 1. Acute dermatitis caused by poison ivy. Note linear arrangement of lesions typical of phytodermatitis acquired by
inadvertent contact with the plant. The severe vesiculobullous reaction is typical for urushiol, the pentadecylcatechol of Toxicodendron spp.
(Reproduced with permission of the Ronald O. Perelman Department of Dermatology, New York University School of Medicine.)
For most other suspected allergic reactions, patch testing is indicated and can be quite illuminating.[2] For example, it has been
reported that 46% of patients who are seen with a history of apparent metal-induced dermatitis are patch test negative to
nickel.[3]
Although allergic contact dermatitis (ACD) can occur in any setting, many cases are related to exposures in the workplace.
When all occupationally related illness in the United States was last estimated, ACD accounted for 7%, at an annual cost of
$250 million in lost productivity, medical care, and disability payments.[4] Although the disease has probably plagued humans
for millennia, the term allergy[5] and its clinical recognition by patch testing[1] are barely a century old. With the advent of an
experimental animal model for ACD in 1926,[6] studies concerning its pathophysiologic features became possible. Despite all
the clinical and scientific research since, a thorough understanding of the disease remains elusive.
THE ALLERGENS
Most environmental allergens are haptens, that is, simple chemicals that must link to proteins to form a complete antigen before
they can sensitize. [7] These haptens are primarily small (<500 d) electrophilic molecules that bind to carrier proteins by
covalent bonds [8] (Table I).
Table I. Thirty of the most frequent allergens in the United States, 1996 to 1998*
Allergen
No. of patients tested
Positive reactions (%)
Reactions considered
currently relevant (%)
Nickel sulfate
3429
14.2
49.1
Neomycin sulfate
3436
13.1
46.2
Balsam of Peru (Myroxylon
pereirae)
3439
11.8
82.9
Fragrance mix
4095
11.7
86.9
Thimerosal
4087
10.9
16.8
Sodium gold thiosulfate
4101
9.5
40.6
Formaldehyde
3440
9.3
63.2
Quaternium-15
3436
9.0
88.7
Cobalt chloride
4095
9.0
55.1
Bacitracin
4103
8.7
50.4
Methyldibromo
glutaronitrile/phenoxyethanol
4054
7.6
59.1
Carba mix§
3437
7.3
71.7
Ethyleneurea
melamine-formaldehyde resin
4095
7.2
65.9
Thiuram mix
3435
6.9
79.8
p-Phenylenediamine
3441
6.0
53.1
Propylene glycol
4095
3.8
82.8
Diazolidinyl urea
4096
3.7
91.5
Lanolin
3442
3.3
78.9
Imidazolidinyl urea
4094
3.2
91.7
2-Bromo-2-nitropropane-1,3-diol
4094
3.2
68.5
MCI/MI
4083
2.9
87.2
Cinnamic aldehyde
3443
2.8
83.2
Potassium dichromate
3440
2.8
54.3
Ethylenediamine dihydrochloride
3439
2.6
23.9
DMDM hydantoin
4093
2.6
93.4
Glutaraldehyde
4094
2.6
48.1
Tixocortol-21-pivalate
4100
2.3
91.7
Benzocaine
3444
2.0
34.3
Colophony
3443
2.0
36.2
Epoxy resin
3439
1.9
55.2
Data from Marks et al. [9] MCI/MI, Methylchloroisothiazolinone/methylisothiazolinone; DMDM, dimethyoldimethyl.
*The population studied consisted of patients with suspected ACD referred for patch testing and is therefore not necessarily
representative of the general population.
Although Toxicodendron oleoresin in poison ivy/oak is a frequent cause of ACD, it is not listed because it was not
tested in this study.
Cinnamic alcohol 1%, cinnamic aldehyde 1%, hydroxycitronellal 1%, amylcinnamaldehyde 1%, geraniol 1%, eugenol
1%, isoeugenol 1%, oakmoss absolute 1%.
§1,3-Diphenylguanidine 1%, zinc diethylthiocarbamate 1%, zinc dibutyl-dithiocarbamate 1%.
Tetramethylthiuram disulfide 0.25%, tetramethylthiuram monosulfide 0.25%, tetraethylthiuram disulfide 0.25%,
dipentamethylenethiuram disulfide 0.25%.
The major exception to such covalent bonding occurs among the metallic salts (for example, nickel and cobalt), which are
thought to complex with proteins in a manner analogous to the complexing of cobalt with vitamin B12 . Although there are more
than 2800 known environmental allergens,[10] not all electrophilic, protein-binding substances are haptens.[11] The nature of the
antigenic determinants, the type of binding that the hapten undergoes with the carrier, the final 3-dimensional configuration of
the conjugate, and a variety of unknown factors undoubtedly contribute to the antigenicity of a chemical.[12] However, the
importance of the carrier for the hapten cannot be underestimated because potent contact sensitizers, when complexed to
nonimmunogenic carriers, induce tolerance rather than sensitization.[13] HLA-DR or class II antigens on the surface of the
antigen-presenting Langerhans cells (LCs) act as the binding site (carrier) for contact allergens.[14] Readers interested in
current reviews of the pathophysiologic mechanisms of ACD are referred elsewhere.[15] [16]
IMMUNOREGULATION
Although animal studies have clearly shown genetic restrictions on cell-mediated immunity, the evidence for a genetic influence
in humans has been minimal. Skog[17] found that 5% of a defined population could not be sensitized to dinitrochlorobenzene
and suggested that this was due to inheritance. In another study significant genetic association with the capacity to become
sensitized to para-nitrosodimethylaniline was reported.[18] Nonetheless, attempts to correlate HLA haplotype with nickel
sensitivity[19] or other contact allergies[20] have shown no association. However, recent studies have demonstrated increased
allele and phenotype frequencies of "transporter associated with antigen processing" 2B (TAP 2B) genes in nickel-sensitive
subjects.[21] Thus definitive evidence of genetic influences on ACD in humans has been meager, probably because of our
diverse genetic pool and the current limitations of technology. [22] With continuing advances in molecular biology, any
association(s) should become clearer in the future.
The route of primary sensitization clearly has a regulatory effect on the subsequent immunologic response. Sulzberger[23]
demonstrated that intracardiac injection of neoarsphenamine induced tolerance rather than sensitization. Tolerance induction
has also been reported after primary oral ingestion of allergens[24] and after primary epicutaneous application of allergens to
areas deficient in HLA-DR+ LCs.[25] The exact mechanism by which tolerance ensues is controversial and may depend on the
route of exposure (oral, intravenous, epicutaneous, or intraperitoneal). However, in most instances induction of hapten-specific
suppressor T cells,[25] clonal deletion of the responding CD3-Ti cells,[26] or antibodies directed against the antigen recognition
site of the T-cell receptor (anti-idiotypic antibodies)[27] seem to play a role. Readers interested in a better understanding of the
mechanism(s) of tolerance induction are referred elsewhere.[26] [28]