Indian J Dermatol

Indian J Dermatol. 2011 Nov-Dec; 56(6): 707710.
doi: 10.4103/0019-5154.91833
PMCID: PMC3276901
PLANT DERMATITIS: ASIAN PERSPECTIVE

Anthony Teik Jin Goon and Chee Leok Goh
Author information Article notes Copyright and License information
Abstract
Occupational and recreational plant exposure on the skin is fairly common. Plant products
and extracts are commonly used and found extensively in the environment. Adverse reactions
to plants and their products are also fairly common. However, making the diagnosis of
contact dermatitis from plants and plant extracts is not always simple and straightforward.
Phytodermatitis refers to inflammation of the skin caused by a plant. The clinical patterns
may be allergic phytodermatitis, photophytodermatitis, irritant contact dermatitis,
pharmacological injury, and mechanical injury. In this article, we will focus mainly on allergy
contact dermatitis from plants or allergic phytodermatitis occurring in Asia.
Keywords: Phytodermatitis, phytophotodermatitis, plant dermatitis
Introduction
Clinical features
Once an individual is sensitized to a plant allergen, subsequent contact will elicit acute
cutaneous lesions within 12-48 hours. The reaction is an acute eczema with severe pruritus,
oedema, erythematous papules and urticarial-looking plaques that rapidly become studded
with vesicles and tense bullae. Skin lesions appear where the plant has brushed against the
skin, typically on the legs, thighs, hands and upper limbs. They classically display a linear
morphology of crisscrossing streaks. The sticky sap can be transferred from the fingers to
more distant sites, such as the face, trunk, and genitals. New lesions tend to continue to erupt
for 1-2 weeks and may last for 4-8 weeks, or to flare up after stopping short courses of
systemic corticosteroids. In subsequent episodes, the skin eruptions tend to become more
severe, and they tend to appear after a shorter interval following exposure to the plant.
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Plants that Cause Allergic Phytodermatitis in Asia
Allergic phytodermatitis
Several families in the plant kingdom are notorious causes of allergic phytodermatitis. Of
particular importance are the Anacardiaceae (i.e., the cashew or sumac family) and
Compositae (also known as the Asteraceae, including the aster, daisy or sunflower family).
Different types of allergic phytodermatitis exist in different regions of the world.
The Anacardiaceae family
Plants such as the poison ivy, poison oak and poison sumac is a common cause of allergic
phytodermatitis in North America. When damaged, all parts of the plant exude a sticky,
strongly allergenic oleoresin, called urushiol. The allergens are pentadecylcatechols or
heptadecylcatechols which possess benzene rings that bear hydroxyl groups at position 1 and
2, and aliphatic side chains at position 3. The length of the side chain and the number of its
double bonds determine the allergenicity of the molecule.
In Asia, the Anacardeaceae family includes the mangoes fruit tree (Mangifera indica), lacquer
tree (Toxicodendron vernicifluum) and hardwood (Gluta renghas) are the commonest causes
of allergic phytodermatitis. The mango fruits contain urushiol in their exocarp (outer skin).
Facial and perioral dermatitis occurs when a sensitized individual bites into an unpeeled
mango. Approximately 80% of Japanese cabinetmakers exposed to the varnish extracted from
the lacquer tree develop hand and forearm dermatitis. The cashew nut tree, Anacardium
occidentale, bears reddish fruits that contain the kidney-shaped nut within a three-layered
pericarp. The middle layer is filled with brownish oil rich in cardol and anacardic acid,
chemically similar to urushiol. These catechols are destroyed when the nut is properly roasted
and processed, but harvesters can develop allergic phytodermatitis from exposure to the oil.
Although unrelated to the Anacardiaceae, the Ginkgo biloba tree, which is found in temperate
Asian countries, is also a source of urushiol-like catechols. The allergenic ginkgolic acid is
present exclusively in the flesh of the drupe-like ovule.
The compositae family
Causes ragweed dermatitis in North America and chrysanthemum allergy worldwide. In

India, airborne allergic contact dermatitis caused by Parthenium hysterophorus, from this
family of plants is well known. The allergens are sesquiterpene lactones, 15-carbon
molecules made of a sesquiterpene linked to a lactone ring. The allergenicity of sesquiterpene
lactones is increased by the presence of an -methylene group attached to the lactone ring.
Sesquiterpene lactones are present in fresh plants, pollen, and in particles from dried plants of
the Compositae family. Classically, sesquiterpene lactone-induced dermatitis affects men
more than women. Outdoor workers e.g., farmers and gardeners, have a higher risk for
sensitization, but florists and nursery workers may be affected. Sensitization occurs through
direct and airborne skin contact. Subacute eczematous lesions initially involve the face, neck,
and the exposed areas of the upper limbs. On the face, massive lichenification may give rise
to a leonine facies mimicking cutaneous lymphoma and actinic reticuloid.
Phytophotodermatitis
Phytophotodermatitis often mimics allergic phytodermatitis. Some families of plants contain

psoralens or furocoumarins that trigger a phototoxic eruption when activated by exposure to
ultraviolet-A light after contact with the skin. This reaction is not immunologically mediated,
and it affects anyone under appropriate circumstances. The plant chemicals loosely bind to
DNA but, when photoexcited, become covalently bound to pyrimidine bases on DNA strands,
leading to cell death.
Phytophotodermatitis is most often caused by contact with plants of the Apiaceae, or
Umbelliferae family. They include weeds and edible plants, such as carrot, parsnip, dill,
fennel, celery and anise.
Lesions will appear within 8-24 hours of exposure to the sap of a psoralen-containing plant
followed by sun exposure. Accompanied by a burning sensation, erythematous, irregular
patches and streaks appear on areas that were exposed to both plant and light. Vesicles and
large blisters may be present, but pruritus is not a major feature of the eruption, as opposed to
allergic phytodermatitis. As the lesions heal, they are replaced by deeply pigmented macules
that slowly fade in a few weeks to months. The juice of lime or other citrus fruits may flow
around the mouth, spill over the hands from squeezing the fruits, or drip on the body followed
by sun exposure during beach and poolside activities, producing bizarre blotches, spotty and
trickle-shaped streaks of pigmentation. Contact with the cut ends of psoralen-containing
celery has been reported to caused an epidemic of phytophotodermatitis affecting the
forearms of grocery store workers.
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Reports of Phytodermatitis in Asia
India
Plant contact dermatitis is one of the commonest causes of contact dermatitis in India. Of
these, parthenium contact dermatitis is the most common cause of plant contact dermatitis.
This is may be due to direct contact or airborne contact to the plant allergen. Parthenium
hysterophorus[110] is a weed that grows profusely the whole year round, especially during
the wet season. It is found in wasteland, along roads and railway tracks, water channels and
in fields. The allergen is a sesquiterpene lactone called, parthenin. Parthenin is present in all
parts of the plant, especially in the trichomes under the leaves. Airborne contact dermatitis
affects the chest. The hands, forearms, feet, legs, other exposed parts are usually affected and
the dermatitis may become generalized when severe.
Xanthium strumarium,[1013] is another weed in the Compositae family reported to cause
allergic contact dermatitis in India. Patients with airborne contact dermatitis from
Parthenium hysterophorus often have concomitant positive patch tests to this weed, although
there have also been patients with allergy this weed alone without conconmittant allergy to
parthenium.
Allergies to other plants have also been reported in India. They include the
chrysanthemums[10,1419] viz., Helianthus annuus (sunflower),[10] Dahlia pinnata
(pinnate dahlia),[17] Mikenia scandens[18] and Holigarna ferruginea.[19]
Laundrymen in India, called dhobis, mark their customers clothes with an urushiolcontaining black oleoresin extracted from the nut of Semecarpus anacardium. The ink is
unaffected by boiling and has caused numerous cases of dhobi itch, an allergic contact
dermatitis at the site of contact, usually the nape of the neck.[20]
Florists making garlands with the white flowers of Walidda antidysenterica[21] has been
reported to develop occupational allergic contact dermatitis from the flowers.
Indonesia
Similar to Malaysia, rengas (Gluta rengas) hardwood has been reported to cause allergic
contact dermatitis in Indonesian woodworkers. Such contact dermatitis is seen in carpenters
handling the rengas woods and foresters and hickers coming into contact the the resin exuded
by the plant.
Japan
The Japanese lacquer tree (Toxicodendron vernicifluum) of the Anacardiaceae family has
been reported to cause occupational allergic contact dermatitis in carpenters and furniture
makers and polishers. Allergic contact dermatitis to the plant resin has also been reported in
consumers[22] who comes into contact with freshly varnished furniture where uncured resins
remains. The causative allergen is urushiol.
Cases of occupational allergic contact dermatitis to tobacco leaves,[23] mitsuba
(Cryptotaemia japonica Makino) vegetable leaves and its stalks[24] and okra (or lady's
fingers, Hibiscus esculentus) leaves[25] have been reported in Japanese farm workers.
Airborne contact dermatitis due to Japanese cedar pollen has recently been reported.[26]
Korea
Rhus dermatitis, especially from Toxicodendron vernicifluum (lacquer tree or varnish tree), is
still a cause of allergic phytodermatitis in Korea. Plants of the Rhus genus are related to
poison ivy, poison oak and poison sumac. They belong to the Anacardiaceae family. Rhus
sensitization is high in the general Korean population. In several Korean reports of patients
with suspected contact dermatitis, the incidence of urushiol-positive patch tests was 18%,[27]
while that of commercial Japanese Rhus allergen-positive patch tests was 13.9%.[28]
Ingestion of chicken with Rhus may also cause systemic contact dermatitis.[29]
Erythema multiforme-like contact dermatitis from contact with a lacquer tree, also from the
Anacardiaceae family, has also been reported. Other cases of plant dermatitis from Korea
include allergic contact dermatitis from chrysanthemum;[30] irritant contact dermatitis from
Ranunculus (buttercup)[31,32] and Pulsatilla koreana (Korean pasque flower);[33] contact
urticaria from Castanea crenata (Japanese chestnut),[34] apple, plum and peach; and
photocontact dermatitis from Ficus carica (common fig)[35] and Angelica gigas[36] have
also been reported.
Malaysia
There have been reports of allergic contact dermatitis to a member of the Anacardiaceae
family, Gluta renghas (rengas), a hardwood which resulted in dermatitis in woodworkers.
Photocontact dermatitis from lime used in traditional medicine has been seen in several
patients and may present in bizarre patterns. The cause of the photocontact dermatitis was
reported to be psoralen the lime juice.
Philippines
Anacardiaceae such as the cashew nut tree (Anacardium occidentale) has been reported cause
allergic contact dermatitis in the Philippines.[37] The fumes from roasting cashews may also
cause skin irritation. Another member of the Anacardiaceae, the mango fruit (Mangifera
caesia), may also cause allergic contact dermatitis on the lips, face and/or neck. Contact with
the fruit or sap of red pepper (Capsicum annum) has been reported to cause erythematous or
bullous dermatitis.
Irritation reactions from several plants have been reported in the Philippines. These include
Dieffenbachia (an ornamental house plant), Hierba mala (which has a caustic sap), Fleurya
interrupta (lipang-aso, a herbal plant), Calotropis gigantea (crown flower). Some plants
irritate chemically via calcium oxalate crystals, silicates, glycosides or alkaloids, while others
irritate mechanically via hairs (trichomes) or spines (glochids).
Singapore
Allergic phytodermatitis has been reported from mango fruits as described above. Allergic
contact dermatitis from rengas (similar to those seen in Indonesia and Malaysia) have been
reported among carpenters and woodworkers handling the rengas group of wood. Some cases
were reported to cause erythema multiforme-like eruption.
Sri Lanka
Contact urticaria from cinnamon (Cinnamomum zeylanicum) has been observed[38] in Sri
Lanka. Plants belonging to the Anacardiaceae family such as mango (Mangifera indica) and
cashew nut (Anacardium occidentale) are common causes allergic phytodermatitis in Sri
Lanka. Another genus from the same family, Semecarpus, causes streaky laundry mark
dermatitis, as the nut is used to mark laundry. This is similar to marking nut dermatitis in
India, where it is known as dhobi-mark dermatitis.
Sri Lanka also sees its share of Compositae allergic contact dermatitis. The plants
incriminated include the Tithonia diversifolia (a shrub found on roadsides and in wasteland).
Their presentation is similar to that of the parthenium dermatitis in India, where airbornecontact dermatitis may be a presenting feature.
Taiwan
Nettles of the genus Urtica and Asian poison ivy have been reported to cause allergic contact
dermatitis in Taiwan. Betel sellers were reported to develop finger dermatitis, most of which
are irritant contact dermatitis although allergic contact dermatitis to the betel has been
reported. Mango contact dermatitis is common during the mango season in Taiwan.[39]
Thailand
Like the Japanese lacquer tree, the Thai lacquer tree (Melanorrhoea usitata) which belongs to
the Anacardiaceae family is a common cause of allergic phytodermatitis.[40] The allergen in
this case is thitsiol.
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Footnotes
Source of support: Nil

Conflict of Interest: Nil.
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References
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preliminary report. Indian J Dermatol Venereol Leprol. 1968;34:1946.
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6. Bajaj AK, Covil DC, Bhargava SN. Contact dermatitis due to plants. Indian J
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7. Singh KK, Singh C. Air-borne contact dermatitis in Varanasi. Indian J Dermatol
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8. Sharma VK, Kaur S. Contact dermatitis due to plants in Chandigarh. Indian J
9. Sharma SC, Kaur S. Contact dermatitis from compositae plants. Indian J
10. Nandakishore TH, Pasricha JS. Pattern of cross-sensitivity between four
compositae plants Parthenium hysterophorus, Xanthium strumarium, Helianthus
annuus and Chrysanthemum coronarium in Indian patients. Contact Dermatitis.
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11. Pasricha JS. A high rate of cross-sensitivity between Parthenium

hysterophorus and Xanthium strumarium in Indian patients with contact
dermatitis. J Europ Acad Dermatol Venereol Leprol. 1994;3:3643.
12. Pasricha JS, Bhaumik P, Agarwal A. Contact dermatitis due to Xanthium
strumarium. Indian J Dermatol Venereol Leprol. 1990;56:31921.
13. Pasricha JS, Verma KK, DSouza P. Air-borne contact dematitis caused
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14. Sharma SC, Tanwar RC, Kaur S. Contact dermatitis from Chrysanthemum in
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15. Tanwar RC, Sharma SC, Kaur S. Chrysanthemum contact dermatitis: Clinical
patterns and patch testing with ethanolic extracts. Indian J Dermatol Venereol
Leprol. 1990;56:1124.
16. Pasricha JS, Nandakishore TH. Air-borne contact dermatitis due to
Chrysanthemum with true cross-sensitivity to Parthenium hysterophorus and
Xanthium strumarium. Indian J Dermatol Venereol Leprol. 1992;58:26871.
17. Sharma SC, Kaur S. Contact dermatitis from Dahlia pinnata. Contact
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18. Pasricha JS, Barua KN. Contact hypersensitivity to Mikenia scandens - a
recently introduced wild creeper of Assam and Meghalaya. Indian J Dermatol
Venereol Leprol. 1987;53:1123.
19. Srinivas CR, Kulkarni SB, Menon SK, Krupashankar DS, Iyengar MA, Singh KK,
et al. Allergenic agent in contact dermatitis from Holigarna ferruginea. Contact
20. Livingood CS, Rogers AM, Fitz-Hugh T. Dhobie mark dermatitis. JAMA.
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21. Perera WD. Plant dermatitis. Sri Lanka J Dermatol. 1995;1:23.
22. Kawai K, Nakagawa M, Kawai K, Konishi K, Liew ML, Yasuno H, et al.
Hyposensitization to urushiol among Japanese lacquer craftsmen. Contact
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tobacco leaves. Nihon Hifuka Gakkai Zasshi. 1986;96:167780. [PubMed]
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Occupational dermatoses in farmers growing okra (Hibiscus esculentus L.)
Contact Dermatitis. 1989;21:3215. [PubMed]
26. Yokozeki H, Satoh T, Katayama I, Nishioka K. Airborne contact dermatitis due to

Japanese cedar pollen. Contact Dermatitis. 2007;56:2248. [PubMed]
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28. Park KB, Eun HC, Lee YS. A study of the prevalence of contact sensitizationto Rhus and
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30. Kim SW, Lee JD, Kim TY. Two cases of contact dermatitis due to Chrysanthemum
moniliform. Allergy. 1992;12:3205.
31. Jeon BK, KolL MO, Park SD. Three cases of primary irritant dermatitis due to Buttercup
(Rannunculus sceleratus) Korean J Dermatol. 1992;30:88691.
32. Kim JW, Cho YH, Hong CK. A case of irritant dermatitis due to Rannuculus. Allergy.
1994;14:747.
33. Kim JS, Cha SH, Park SD. A case of irritant dermatitis due to Pulsatilla Koreana. Korean
J Dermatol. 1997;35:33943.
34. Lee AY, Lee SH, Lee YS. A case of contact urticaria due to apple, plum andpeach. Korean
J Dermatol. 1989;27:5436.
35. Lee CB, Han EN, Kim NI, Haw CR. Phytophotodermatitis. Korean J Dermatol.
1986;24:27882.
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Photodermatol Photoimmunol Photomed. 1991;8:845. [PubMed]
37. Benezra C, Ducombs G, Sell Y, Foussereau J. Plant Contact Dermatitis. Toronto: B. C.
Decker Incorporated; 1985. p. 68.
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editors. The principles and practice of contact and occupational dermatology in the AsiaPacific Region. Singapore: World Scientific; 2001. pp. 2048.
39. Sun CC. 8th Int Symp Contact Dermatitis. Cambridge, England: 1986. Patch testing with
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40. Kullavanijaya P, Ophaswongse S. A study of dermatitis in the lacquerware industry.

doi: 10.4103/0019-5154.91834
PMCID: PMC3276902
AIRBORNE-CONTACT DERMATITIS OF NON-PLANT ORIGIN:

AN OVERVIEW
Sanjay Ghosh
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AIRBORNE-CONTACT DERMATITIS OF NON-PLANT ORIGIN:

AN OVERVIEW
Sanjay Ghosh
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Abstract
Airborne-contact dermatitis (ABCD) represents a unique type of contact dermatitis

originating from dust, sprays, pollens or volatile chemicals by airborne fumes or particles
without directly touching the allergen. ABCD in Indian patients has been attributed
exclusively by pollens of the plants like Parthenium hysterophorus, etc., but in recent years
the above scenario has been changing rapidly in urban and semiurban perspective especially
in developing countries. ABCD has been reported worldwide due to various type of nonplant
allergens and their clinical feature are sometimes distinctive. Preventive aspect has been
attempted by introduction of different chemicals of less allergic potential.
Keywords: Airborne-contact dermatitis, cement dermatitis, contact dermatitis,
occupational contact dermatitis, phytodermatitis
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Introduction
Airborne-contact dermatitis (ABCD) denotes an unique type of contact dermatitis originating

from dust, sprays, pollens or volatile chemicals by airborne fumes or particles without
directly handling this allergen.[1] This form of dermatitis commonly involves face, neck, varea of chest and eyelids. Exposed as well as nonexposed skin can be affected. Axillae and
waist lines can also be the target of this disease. This form of dermatitis can sometimes also
be generalized.[2,3]
Airborne dermatoses often cause diagnostic problems and create a puzzle not only to the
patient but also to the doctor.[4] The incidence of airborne dermatoses has increased
considerably in recent years.[5]
As per previous reports[6,7] ABCD in Indian patients has been attributed exclusively by
pollens of the plants like Parthenium hysterophorus, Xanthium strumarium, Chrysanthemum
coronarium, Helianthus annus (sunflower) and Dahlia pimrata.
In recent years the above scenario has been changing rapidly in urban and semi\urban
perspective especially in developing countries.[8] Organic compounds that are used or
generated anthropogenically in large quantities in the cities can be the source of human
contact allergens.[9]
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Nonplant etiology
ABCD[10] may be caused by: a) cement and wood dust, causing irritant as well as
sensitization reactions b) fibrous materials like grain dust, glass fiber and rock wool causing
mechanical dermatitis c) aerosols of mineral oils inducing irritant reaction d) pollens or dust
containing particles from plants such as Parthenium hysterophorus, ragweed or certain types
of woods or medicaments by the process of delayed hypersensitivity.
In a study by Ghosh[8] among 64 patients(36 M, 28 F) age ranging from 10 to 67 years
suffering from ABCD in urban perspective 64.1% (n=41) had urban residency whereas 35.9%
(n= 23) had semiurban. Pattern of allergens contributory to ABCD detected in the study were
as follows: potassium dichromate 39.7% (n=25), fragrance mix 28.1% (n=18), epoxy resin
26.6% (n=17), colophony 17.8% (n=12), formaldehyde 13.2% (n=7) and parthenium 9.4%
(n=6). Cement, perfumes or deodorants, volatile paints and synthetic glues have become
commonest allergens contributing to ABCD in urban and semiurban areas.[8]
In urban and semiurban area of India incidence of ABCD due to parthenium has been
gradually become lowered as compared to previous reports[6,7] due to rapid urbanization and
reduction in open land required for the growth of these plants.[8]
ABCD to cement (chromate) has been already published by different workers.[1114]
Extensive housing development projects and construction works in recent years in developing
country like India have caused very high allergic sensitivity rate to potassium dichromate
contained in the cement. Even by non-occupational contact housewives are also commonly
involved.[8,15] In China a high proportion (19%) of patch test positive reaction to chromate
has been reported possibly reflecting the exposure to cement due to China's very active
construction programs.[13]
Fragrance allergy leading to ABCD has been reported by many authors.[1618] In the recent
years increased self-image and beauty consciousness due to media and film influence has
contributed to the increased use of perfume, deodorants, room fresheners among urban and
semiurban people.[8]
Increased incidence of epoxy resins and colophony allergy has been caused by increased
household decoration, newer occupations and various newer personal hobbies. ABCD
originated by paints, epoxy resin, colophony and formaldehyde has been reported by some
previous workers.[1922] Epoxy resin systems are important sensitizers and often
responsible for occupational airborne dermatitis. Vitiligo, both to epoxy resins and reactive
diluents have been reported.[23]
Airborne dermatitis resulted from exposure to metaproterenol (Alupent) used by respiratory
therapist to treat patients.[24]
Airborne dermatitis and asthma reported in a psyllium factory worker. Psyllium, primarily
used as a stool softener, comes from the seed of the genus Plantago.[25]
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Clinical Aspects
ABCD appears on areas of the skin where the dust or fibers can be trapped, e.g., on the
eyelids, neck (under a shirt collar), forearms (under cuffs) or lower legs (inside trouser legs).
[26]
Contact dermatitis from prolonged, repeated exposure to relatively small quantities of
airborne allergens, such as pollens, dusts and vapors, produces diffuse, dry and lichenified
eruptions with vesiculations. The exposed portions of the body as well as wrinkles and folds
are most markedly involved.[27]
Household sprays, insecticides, animal hairs and occupational volatile chemicals can produce
eyelid dermatitis.[27]
Benzoyl peroxide has been used to bleach candles white. Intense exposure to burning candles
in a church has caused facial dermatitis.[28]
Chronic ABCD occasionally may simulate photocontact dermatitis. Even sometimes a
combination of these two forms of dermatitis may also be seen.[29]
The handling of large amounts of carbonless copy paper and laser printed paper can cause
irritation of the mucous membrane of the nose and eyes and pruritus on exposed skin.[10]
Various cutaneous symptoms, including pruritus and paresthesia, have been described after
long-term exposure to computer screens, but few patients exhibit diagnostic skin lesions.[30]
A chronic eczema on exposed areas is usually not due to photosensitivity but is the result of
ABCD. ABCD characteristically involves the upper eyelids and extends below the chin and
behind the ears, but does not always do so. A further source of diagnostic confusion is that
ACD can be photoexacerbated.[31]
Airborne and photoallergic contact dermatitis have a similar clinical expression acute or
subacute dermatitis on exposed areas. They differ from toxic dermatitis because they have a
more polymorphic clinical picture, not precisely limited to exposed areas. However, as stated
with irritant type, there are some locations spared in photodermatitis, which may be affected
in airborne type, such as upper eyelids, under the chin, behind the ears, the back of neck, or
even the scalp.[32]
Airborne irritant contact dermatitis predominates in exposed areas, but, as opposed to
photosensitive dermatitis it does not spare areas such as the upper eyelids, retroauricular folds
or submental area.[32]
ABCD may result from exposure to sawdusteven associated with leukoderma,[33] cutting
oils[34] and even jewellery[35]
The airborne MCI/MI (Chloromethyl- and Methylisothiazolinone) dermatitis may appear in
the face of sensitized individuals who stay in newly painted rooms, and the diagnosis is easily
missed unless specifically considered.[36]
Dental practitioners and their associates may develop dermatitis on face, eyelids and other
exposed skin areas by airborne contact.[37]
Airborne contact urticaria can be associated with rhinitis, conjunctivitis or asthma. These
have been largely reported as an occupational problem in health workers with
hypersensitivity to latex proteins from rubber gloves made with natural latex (usually derived
from Hevea brasiliensis Muell. Arg., family Euphorbiaceae). Airborne transmission of latex
allergens is enhanced by their adsorption onto the cornstarch (derived from Zea mays L.,
family Gramineae) used as glove powder.[38]
Airborne contact urticaria reported in a warehouseman resulted from exposure to dust derived
from cinchona bark (Cinchona spp., family Rubiaceae).[39]
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Preventive Management
The allergic capacity of chromium salts is really intriguing and deserves special mention. The
sensitizing potential of trivalent chromium salts remains high as they form complexes with
proteins in the upper layers of the skin. The trivalent salts are, however, not common
sensitizers due to their low penetration into the skin. In contrast hexavalent chromium salts, a
nonsensitizer by nature, can penetrate the skin and could be reduced to trivalent salts
subsequently and the latter may lead to sensitization by acting as hapten. In some countries
ferrous sulphate is added to cement to transform hexavalent chromates into trivalent ones to
reduce the incidence of sensitization. Otherwise a special type of cement namely Portland
blast furnace slag cement (PBFSC) of low hexavalent chromate content may be used to
reduce cement sensitivity.[40]
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Footnotes

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References
1. Handa F, Handa S, Handa R. Environmental factors and the skin. In: Valia RG,
editor. IADVL Text book and Atlas of Dermatology. 2nd ed. Vol. 1. Mumbai:
Bhalani; 2001. pp. 8191.
2. Gordon LA. Compositae dermatits. Australas J Dermatol. 1999;40:12330.
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doi: 10.4103/0019-5154.91832
PMCID: PMC3276900
AIRBORNE CONTACT DERMATITIS CURRENT

PERSPECTIVES IN ETIOPATHOGENESIS AND
MANAGEMENT
Sanjeev Handa, Dipankar De, and Rahul Mahajan
This article has been cited by other articles in PMC.
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Abstract
The increasing recognition of occupational origin of airborne contact dermatitis has brought
the focus on the variety of irritants, which can present with this typical morphological picture.
At the same time, airborne allergic contact dermatitis secondary to plant antigens, especially
to Compositae family, continues to be rampant in many parts of the world, especially in the
Indian subcontinent. The recognition of the contactant may be difficult to ascertain and the
treatment may be even more difficult. The present review focuses on the epidemiological,
clinical and therapeutic issues in airborne contact dermatitis.
Keywords: Airborne contact dermatitis, occupational airborne contact

dermatitis, Parthenium hysterophorus
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Introduction
Airborne contact dermatitis (ABCD) is a morphological diagnosis that encompasses all acute
or chronic dermatoses predominantly of exposed parts of body, which are caused by
substances which when released into the air, settle on the exposed skin. Although the
diagnosis of ABCD is not difficult for the trained eye, finding the causative contactant and
the treatment of the resultant clinical condition may prove to be a challenge for the treating
dermatologist. Contact dermatitis is designated as airborne on the basis of the history of the
patient and the follow-up, existence of dust or of volatile causative agents, the morphology
and distribution of the lesions and the results of epicutaneous tests.[1] Over the years, there
has been an increasing recognition on the part of dermatologists regarding the occupational as
well as the non-occupational airborne allergens and irritants. The present review is aimed at
discussing the various epidemiological aspects of ABCD, the newly observed occupational
and non-occupational airborne contactants, the protean clinical manifestations and the
therapeutic modalities available in ABCD.
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Epidemiology of Airborne Contact Dermatitis
The prevalence of ABCD is difficult to estimate. This is primarily because of the fact that it
can be very difficult and cumbersome to prove an ABCD, especially of irritant type, and
secondly because the term airborne has been less often used in literature. Epidemiologically,
ABCD can be classified into occupational and non-occupational ABCD. It is generally
believed that occupational airborne irritant contact dermatitis is grossly underreported and is
much more common compared to airborne allergic contact dermatitis. Although ABCD has
been reported to be caused by a number of agents, most of which have been published as case
reports or small case series, majority of the data from India and outside focus largely on plant
antigens as being an important cause of ABCD.
Cabanillas et al., reported a 3% prevalence of allergic dermatitis to plant antigens among
patients presenting with contact dermatitis in the allergy unit, mostly in ABCD pattern.[2]
Many authors have reported a significantly lower incidence and severity of sesquiterpene
lactone (SL) sensitivity in East Asian population (1.4%) compared to European population
(0.95.9%).[35] Mak et al., postulated that consumption of chrysanthemum since childhood
in East Asia may result in induction of oral tolerance.[6] Among the patients with SL
sensitivity, one third acquire it occupationally. In India, parthenium dermatitis, caused by
Parthenium hysterophorus, is an important cause of ABCD.[7] It belongs to the family
Compositae, subfamily Asteroide (tribe heliantheae), which itself is a large, diverse group of
the plant kingdom. P. hysterophorus was accidentally introduced to India in a wheat
shipment. It is a wind pollinated plant and produces an enormous quantity of pollen (up to
624 million per plant) that can be carried away in clusters of 600800 grains. Lonkar and Jog
were the first to report the epidemic of parthenium dermatitis in agriculturists and field
workers at Pune, Maharashtra, in 1968.[8] Presently, it is the commonest cause of plant
dermatitis in India and is responsible for 40% of patients attending contact dermatitis clinics.
Today, there is increased use of herbal ingredients in culinary, cosmetic and medicinal
products. Other members of the Compositae family which are in wide use are the ornamental
annuals like sunflowers, cosmos, marigold, asters; herbaceous perennials like dahlia,
chrysanthemum, marguerites; vegetables like lettuce, chicory, artichokes; herbal medicines
like feverfew (Tanacetrim parthenium), pot marigold (Calendula); natural insecticides like
pyrethrum and weeds like bindii (Soliva pterosperma), ragweed, fleabane, stinkwort and
capeweed.
In a study by Agarwal et al., from South India, 50 patients with a clinical picture and history
consistent with parthenium dermatitis due to exposure to P. hysterophorus were studied.[9]
Ninety percent of the patients were farmers and 74.5% had exacerbations during summer. The
most common type of dermatitis was the classic ABCD pattern (46%) followed by the mixed
pattern (30%), erythroderma (14%) and chronic actinic dermatitis (CAD) (10%). Of the 40
patients patch tested, 90% had patch-test results positive for parthenium. In another study
from Delhi, 75 patients with clinically suspected contact dermatitis were patch tested with the
Indian Standard Series and indigenous antigens.[10] Parthenium was the most common
contact sensitizer (20%), followed by potassium dichromate (16%), xanthium (13.3%), nickel
sulfate (12%), chrysanthemum (8%), mercaptobenzothiazole and garlic (6.7% each). A study
targeting regional Danish floristry gardeners and greenhouse workers determined a lifetime
prevalence of almost 20% of occupational dermatitis and identified working with Compositae
plants, having occupational mucosal symptoms or having a history of previous occupational
eczema as the risk factors for developing occupational ABCD.[11]
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Immunology of Airborne Contact Dermatitis
In airborne allergic dermatitis, initially there is a refractory phase where there is a periodic or
continuous contact with allergen but no response. This is followed by an induction phase
where the hapten penetrates skin, conjugates with epidermal protein, comes in contact with
antigen presenting cells, migrates to draining lymph nodes followed by stimulation of naive T
cells. This leads to proliferation of activated T cells to produce effector and memory cells
which then enter the circulation. Re-exposure to the specific hapten leads to the release of
mediators producing skin inflammation. A persistent inflammation is produced due to
continued presence of effector cells. The inflammation may resolve with cellular and
enzymatic degradation of antigen, inhibition of antigen presenting cells and stimulation of
suppressor T cells. Akhtar et al., studied the cytokine profile in 50 patients with parthenium
dermatitis, with all of them showing increased levels of pro-inflammatory cytokines like
interleukin (IL)-6, IL-8, IL-17 and tumor necrosis factor (TNF)-, and decreased levels of
anti-inflammatory cytokines like IL-4 and IL-10.[12] A study investigating the relationship
between polymorphisms of TNF and contact allergy found that the distribution of TNF-308
genotypes was significantly different between cases with contact allergy and healthy controls,
with carriers of the A allele being more frequent among polysensitized patients.[13] Mahajan
et al. experimentally proved that dermatitis can be caused by inhalation of allergen with
interplay of type 1 and 3 hypersensitivity. Their patient showed a positive patch test to
parthenium, positive delayed reaction to prick test on day 1 and histopathology showing
vasculitis.[14] In contrast, Lakshmi et al. incriminated type 1 and 4 hypersensitivity in
causation of ABCD due to presence of positive prick test and raised serum IgE levels in
patients with patch test positive parthenium dermatitis.[15] ABCD to cedar pollen is a
recently identified disease that generally affects individuals with nasal and/or ocular
symptoms, as well as some patients with atopic dermatitis. It was suggested that in cedar
pollinosis, PGD2-CRTH2 signaling contributes to inflammation, with the lesional skin
showing IL-13, IL-18, eotaxin/chemokine (C-C motif) ligand (CCL) 11, RANTES/CCL5,
macrophage-derived chemokine/CCL22 and thymus and activation-regulated
chemokine/CCL17.[16]
Fillagrin mutation, as in atopic dermatitis, has been linked to causation in contact dermatitis.
However, studies so far have shown conflicting results.[17] Recently, Poltromeri et al. gave
the concept of occupational allergic march to describe the rapid evolution of contact
dermatitis to ammonium persulfate into ABCD with rhinitis and asthma in a hairdresser.[18]
The role of aeroallergens as a cause of allergic contact dermatitis or allergic contact
dermatitis like atopic dermatitis is controversial. Inhalation of pollens, dusts, and animal hair
causes either flare-up of atopic dermatitis or an apparent superimposed contact dermatitis; in
some instances, the airborne allergens may produce positive patch-test reactions (i.e. with
dermatophagoides).[19]
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Causes of Airborne Contact Dermatitis
The common allergens and irritants which have been demonstrated to produce an airborne
dermatitis like picture are listed in Table 1.[1,2032] These include various acids and alkalis,
metals and powders of metallic salts, cement, industrial solvents, glass fibers, sewage sludge,
ammonia, vegetable and wood allergens, plastics, rubbers and glues, insecticides, pesticides,
animal feed additives and many others. The airborne contactants can also be classified on the
basis of their physical state as volatile airborne contactants like acids, alkalis, ammonia and
pesticides; droplets like insecticides, perfumes and hair sprays; powders which include
aluminum, anhydrous calcium silicate, and metallic oxides; and particles like tree sawing
particles, wool and plastics.
Table 1
Common and newer antigens which can cause airborne contact dermatitis
(modified from Santos et al.[1] and Huygens et al.[20])
The most important allergens in P. hysterophorus responsible for allergic contact dermatitis
are SLs, consisting of a lactone ring combined with a sesquiterpene. They are lipophilic and
are present mainly in the oleoresin fraction of the plant. Parthenin, which belongs to the
pseudoguinolide class of SLs, is the major allergen. It has an alpha methylene group
exocyclic to gamma lactone, which is probably essential for the induction of allergy. The
other allergens that have similar group are coronopilin and tetraneurin A. The other
components, namely, thiopenes, monoterpenes and acetylenes, are known to cause
phytophotodermatitis. SLs are also found in other genera, namely, liverwort (Frullania), tulip
tree (Liriodendron, Magnoliacea) and sweetbay (Lauraceae, Laurus nobilis). Cross reaction
may occur among these genera.
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Clinical Presentation
A person can be sensitised to airborne contactants by direct and indirect contact, ingestion of
allergens in herbal teas or exposure to herbal cosmetics. Dooms-Goossens classified airborne
dermatitis into five different types, namely, airborne irritant contact dermatitis, airborne
allergic contact dermatitis, airborne phototoxic reactions, airborne photoallergic reactions and
airborne contact urticaria.[33] Rare presentations include acne like, lichenoid eruptions, fixed
drug eruptions, exfoliative dermatitis, telengiectases, paresthesias, purpura, erythema
multiforme like eruption, pellagra like dermatitis and lymphomatoid CD. Some agents cause
more than one type of reaction. P. hysterophorus can produce allergic CD, photocontact
dermatitis and a lichenoid eruption. Similarly, formaldehyde and phosphorus sesquisulfide
can lead to an airborne irritant or allergic CD and contact urticaria.[34]
In the classical airborne allergic contact dermatitis, there is involvement of exposed areas of
face, V of neck, hands and forearms, Wilkinson's triangle, both eyelids, nasolabial folds
and under the chin. The involvement of both light-exposed and protected areas helps to
differentiate ABCD from a photo-related dermatitis. Another close differential is atopic
eczema as both ABCD and atopic eczema have predominant flexural and skin crease
involvement. Initially, there is an acute flare of the dermatitis during the plant growing season
but, with repeated exposure, the flare becomes prolonged and produces a chronic lichenified
eczema associated with secondary infection, fissuring and hypo or hyperpigmentation. In
patients wearing glasses, dermatitis occurs at the edge of nose due to occlusion. Some
patients present with facial swelling before manifesting classical eczematous lesions. Severe
cases show dissemination to non-exposed areas and may become erythrodermic. Verma et al.,
put forward a clinical severity score (CSS) to assess the severity of ABCD [Table 2].[35] It
takes into consideration both the subjective features like pruritus experienced by the patient
as well as the objective features like the morphology of lesions and the area involved.
Airborne agents like fibrous materials (such as glass fibers, rock wool, and grain dust) give
rise to mechanical dermatitis by friction due to their abrasive physical properties. Dust that
contains glass fibers can produce cuts from sharp glass fragments, and asbestos corns may
be seen on palmer aspect of fingers on exposure to spicules of asbestos. A lichenified
dermatitis may be produced by wood and cement dust collecting around the collar, belt line,
or sleeve end and other points of contact. Dust may also cause irritant dermatitis with clinical
appearance of folliculitis.[36]
Table 2
Clinical severity score to assess severity of ABCD (adapted from Verma et al.[35])
Alternatively, ABCD can be subclassified into that of plant origin and non-plant origin. Wood
and plants are a rich source of airborne allergens and irritants, the causative agent often being
the dried botanical material. The most commonly seen parthenium dermatitis classically
presents as ABCD but may occasionally present with photosensitive lichenoid eruption in
morphology and distribution. Rarely, the disease may present as photocontact dermatitis or
actinic reticuloid syndrome.[37] Few case reports of prurigo nodularis like lesions have been
reported.[38] Occupational type I Compositae allergy is rarely reported because few people
are tested. ABCD sparing vitiliginous skin has been reported from India.[39] A study
observing the evolution of parthenium dermatitis recruited 74 patients who were classified
into ABCD, CAD pattern or mixed pattern dermatitis. Sixty patients had ABCD, five had
mixed pattern and nine had CAD pattern at the onset. Of the 60 patients with ABCD, 27
changed to CAD pattern and 11 to mixed pattern after an average period of 4.2 years.
Additionally, sawdust from teak, redwood, mahogany, and rosewood may contain sensitizers
that produce a dry dermatitis, particularly on the face, penis, and scrotum in carpenters and
woodworkers.[40] Dermatitis of woodworkers may be caused also by liverworts (SLs) and
lichens (usnic acid or atranorin) found on the bark of trees.[41,42] The allergy can also be
derived from the smoke of burning plants.
Cement dust usually presents as a dry, lichenified dermatitis due to its alkaline and
hygroscopic properties. The eruption tends be dry rather than oozy even in cases of allergic
contact dermatitis to the chromium or cobalt content in cement. Genital dermatitis due to
indirect hand contact and accumulation of sawdust on the clothes is often seen in cabinet
makers. Dermatitis from vapors is usually of occupational origin. In these cases, amines used
as epoxy hardeners and resins are the most common culprits.[43] Turpentine used to be the
most frequent cause of airborne dermatitis, but is seen rarely now. Polyolefins, when heated,
degrade and form aldehydes, ketones, and acids and very rarely induce airborne dermatitis.
[44] Additionally, plastic, rubber, glues, metals, insecticides, pesticides, solvents, and other
industrial and pharmaceutical chemicals have been described as causing airborne dermatitis.
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Diagnosis of ABCD
While managing ABCD, care must be taken to distinguish between occupational and nonoccupational disease and between irritant and allergic occupational ABCD, as management
will differ. A temporal correlation with work only raises the suspicion which needs to be
confirmed with patch test or prick test. In suspected cases of occupational irritant dermatitis,
the responsible agent may be isolated by means of chemical analysis or direct microscopic
study of the air or material in the air. The patch test is used to find out causative allergens.
Photopatch tests can be useful for excluding light as a factor in the pathogenesis of the
lesions. During patch testing, volatile allergens sometimes also cause irritant dermatitis;
therefore, high dilutions should be used. Sometimes special glass cups which permit exposure
to the vapor of allergen have to be used. For testing wood dust, it should not be moistened as
it increases irritancy.
SL mix 0.1% petrolatum is commercially available and consists of equimolar quantities of
three pure SLs (alantolactone, dehydrocostus lactone and costunolide). In a study, only 35%
of cases of Compositae allergy were detected by using only SL mix and it was concluded that
SL mix was not an adequate screening test. The SL mix failed to detect 38% of Compositaesensitive patients.[45] These patients can be identified by using additional Compositae
extracts like dandelion or feverfew extracts when there is a clinical suspicion of Compositae
allergy. Another study comparing Compositae mix with SL mix was done in which
Compositae mix led to few irritant reactions and less false-negative test results as compared
to SL mix.[46] It was concluded that Compositae dermatitis is being underdiagnosed and that
the Compositae mix is significantly more sensitive in detecting Compositae allergy than the
SL mix.
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Treatment of ABCD
Treatment of ABCD is difficult, with great emphasis on individualization. Severity of contact

dermatitis depends upon degree of contact hypersensitivity and quantity of antigen to which
the patient is exposed. For effective control of dermatitis, these two factors should be
reduced. As the hypersensitivity is difficult to be reduced, the only option is to reduce

quantity of antigen to which patient is exposed. Substitution reduces the incidence of
occupational dermatitis and urticaria. In cases of ABCD due to parthenium, one should avoid
going outdoors on days when pollen are present in high concentrations in air, especially in
summers and in the months from September to November following the north-east monsoon
showers. Air conditioning decreases indoor pollen counts. Simple routines like taking a bath
after coming indoors; wearing fresh clothes and eliminating weeds and grasses in the house
garden can offer great help. Use of a barrier cream on the exposed areas after every wash is
important to slow down penetration of antigen into skin. Other measures which can be used
are photoprotection, sunscreens, change of job, change of residence, antihistamines, drying
agents in cases of weeping eruptions, aluminum sulfate and calcium acetate and emollients
for lichenified areas, etc.[47]
Topical steroids are the mainstay of therapy as in other eczemas. They decrease the number
of HLA DR+ Langerhans cells and inhibit the production and function of IL-1, IL-2 and
interferon (IFN)-. Systemic steroids decrease T cell proliferation and are indicated when
there is more than 25% body surface area involvement and when dermatitis is suspected to be
caused by allergens which persist in the skin for weeks after exposure (Toxicodendron
oleoresins). Psoralens and UVA (PUVA) decreases HLA DR+ Langerhans cells [LC],
whereas UVB induces epidermal hyperplasia and PGE. Immunosuppressives are indicated
for severe, recalcitrant and photosensitive dermatitisactinic reticuloid patient. The most
commonly used immunosuppressive agent is azathioprine. It blocks DNA replication by
incorporating 6-thioguanine into DNA and prevents lymphocytic proliferation after antigenic
stimulation.[48] Both the number and antigen presenting capacity of LC are affected. In a
study, azathioprine weekly pulses were given to patients with chronic lichenified eczema.[35]
The response was excellent (80100% clearance of disease) in 58.3% patients and good (60%
clearance) in 41.7% patients. There were no significant side effects of the therapy. The cost of
therapy with this regimen was reduced by 60%.[49] In another therapeutic study on patients
of parthenium dermatitis, three therapeutic regimens with azathioprine were used.[50] A total
of 22 patients (group I) were given 50 mg azathioprine twice a day, 11 patients (group II)
received 50 mg azathioprine per day and 300 mg azathioprine every 28 days, and 10 patients
(group III) were given 50 mg azathioprine twice a day along with 300 mg azathioprine every
28 days. The duration of treatment varied from 6 months to 3 years. Twenty out of 22 in
group I and 9/11 patients in group II and 9/10 patients in group III had complete remission.
Nine out of 22, 7/11 and 6/10 patients in the respective groups needed additional oral
betamethasone 12 mg per day for brief periods only during the peak season in order to
maintain complete remission. Sharma et al., treated 16 patients with parthenium dermatitis,
unresponsive to topical treatment, with oral methotrexate (15 mg/week). Clinical response
was monitored using a dermatitis area and severity index. Seven patients completed 6 months
or more of follow-up, and their mean DASI fell to 5, 2.7 and 2.1 at the end of 1, 3 and 6
months, respectively, from a baseline score of 10. Only 3/7 patients required oral
prednisolone in the initial 24 weeks.
Hyposensitization refers to introduction of an antigen into the body by a route different from
the natural one, to induce such a change in the immune system that the body does not develop
clinical manifestations when the antigen is introduced into the body through normal route.
[51] Oral hyposensitization, although demonstrated to be effective for ragweed dermatitis,
has not been widely accepted because it carries considerable risk of provoking and worsening
eczema. In some cases, patients are co-sensitized with several unrelated pollen allergens.
Based on frequent co-sensitization patterns, some of the hybrid proteins have been developed
with the polymerase chain reaction. These hybrids contain all the epitopes from the different
allergen in a single protein. These have been used for vaccination against pollen allergy.
Antibodies induced with the hybrids in mice inhibited the binding of grass pollen-allergic
patients immunoglobulin E to each of the individual allergens and grass pollen extract, and
may thus represent protective antibodies. Handa et al., evaluated the effect of oral
hyposensitization as an alternative therapeutic modality and observed a gradual improvement
in the clinical status of 70% of those patients who completed the study, as evident from a fall
in their clinical severity score for eczema. The treatment had to be stopped in 30% of patients
as they experienced an exacerbation during the course of the study. Overall, patients tolerated
the therapy well and no significant side effects were seen, except for abdominal pain,
heartburn and cheilitis.[52]
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Conclusions
Evidence indicates that up to 50% of patients with ABCD, whether occupational or nonoccupational, experience adverse effects on quality of life, daily function and personal
relationship, and take time off work on sick leave and may lose or change job because of their
skin disease.[46] A significant proportion of patients still tend to have active symptoms many
years after diagnosis, despite treatment and change of job. However, it should be emphasized
to all that avoidance of further exposure can lead to recovery from dermatitis in many cases.
With respect to ABCD occurring secondary to parthenium dermatitis, there are continuing
attempts to control the spread of the weed through biological measures like introduction of
exotic arthropods and opportunistic pathogens, use of antagonistic plants and bioherbicides as
well as use of selective chemical herbicides.
Go to:
Footnotes

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References
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Indian J Dermatol. 2011 Nov-Dec; 56(6): 707710.

PLANT DERMATITIS: ASIAN PERSPECTIVE

The Anacardiaceae family

Causes ragweed dermatitis in North America and chrysanthemum allergy worldwide. In

Phytophotodermatitis often mimics allergic phytodermatitis. Some families of plants contain

Source of support: Nil

11. Pasricha JS. A high rate of cross-sensitivity between Parthenium

26. Yokozeki H, Satoh T, Katayama I, Nishioka K. Airborne contact dermatitis due to