# 2007 The Authors

Contact Dermatitis 2008: 58: 67–75 Journal compilation # 2007 Blackwell Munksgaard
Printed in Singapore. All rights reserved
CONTACT DERMATITIS

Review Article

Immunological occupational contact urticaria and

contact dermatitis from proteins: a review
CRISTINA AMARO1 AND AN GOOSSENS2
1
Department of Dermatology, Hospital de Curry Cabral, Rua da Beneficência, n° 8, 1069-166 Lisbon, Portugal and
2
Department of Dermatology, University Hospital, Katholieke Universiteit Leuven, B-3000 Leuven, Belgium

Protein contact with the skin can be associated with 2 major clinical conditions: contact urticaria and
protein contact dermatitis. This article reviews the pathogenesis, clinical pictures and the literature on
the proteins having caused immunological occupation-related skin problems, i.e. fruits, vegetables,
spices, plants, and woods; animal proteins; grains and enzymes, all affecting a wide variety of jobs.
This is illustrated with some cases observed in the contact-allergy unit in Leuven.

Key words: contact dermatitis; contact urticarial; delayed; immediate; immunological; occupational;
proteins; protein contact dermatitis. # Blackwell Munksgaard, 2008.
Accepted for publication 1 August 2007

The term contact urticarial (CU) was introduced
by A. A. Fisher in 1973 (1) and refers to a wheal
and flare reaction following external contact with
a substance. If immunologic in nature, it is called
immunologic contact urticaria (ICU). It usually
appears within 30 min, clears completely within
hours and can be caused by a multitude of sub-
stances ranging from simple chemicals to macro-
molecules i.e. proteins (2).
In 1976, Hjorth and Roed-Petersen (3) reported
a particular form of contact dermatitis in Danish
food handlers, which they called ‘protein contact
dermatitis’ (PCD). Most patients suffered from
eczema of the hands and forearms.
The development of an immediate-type, immuno-
globulin (Ig)E-mediated allergy to the proteina-
ceous material is a common feature of these 2
entities (1, 2, 4, 5). Only those agents, for which
such a mechanism was proven, will be discussed
here. Over the years, numerous agents have been
added to an ever-expanding list of causes, most
often occupation-induced.
Clinical Features
Clinical manifestations of ICU reflect the dose
and route of exposure to the allergen (1): they
can be strictly limited to the contact areas, but
sites other than the contact site may be affected,
as for example the face, or even present as gener-
alized urticaria. Also internal organs, i.e. the res-
piratory or gastrointestinal tracts (6) may be
involved, depending upon the allergen or pre-
existing conditions such as atopic eczema (7).
The severity of this possible multi-systemic disease
has been reported as the ‘CU syndrome’ by Von
Krogh and Maibach (8) (Table 1).
The most frequent clinical presentation of
PCD is a chronic or recurrent eczema. It may
be manifested just as a fingertip dermatitis or
extend to wrists and arms. An urticarial or vesicu-
lar exacerbation can be noted a few minutes after
contact with the causal protein on previously
affected skin. Some cases of chronic paronychia
were considered a variety of PCD, with redness
and swelling of the proximal nail fold, for exam-
ple, after handling food (9) and natural rubber
latex (10).
As for ICU, the allergen characteristics influ-
ence the coexistence of extra-cutaneous symp-
toms: if it is volatile, allergic rhino-conjunctivitis
or asthma may accompany the skin manifesta-
tions, as it occurs with bakers who are in continu-
ous contact with flour (11). Abdominal pain,
diarrhoea and the ‘oral allergy syndrome’ may
occasionally develop when the allergen comes in
contact with the oropharyngeal mucosa (4), the
latter particularly in an atopic context.
68 AMARO & GOOSSENS Contact Dermatitis 2008: 58: 67–75

Table 1. The ‘contact urticaria syndrome’ [Von Krogh and Table 2. Proteins having caused immunological contact urticar-
Maibach (8)] ial and/or protein contact dermatitis (4)
Stage 1 Localized urticaria. Non-specific symptoms References
(itching, tingling, and burning)
Stage 2 Generalized urticaria with or without angioedema Fruits, vegetables, spices, plants, (4)
Stage 3 Extracutaneous involvement (rhinoconjunctivitis, and woods
bronchospasm, orolaryngeal or gastrointestinal Almond
symptoms) Asparagus (12, 13)
Stage 4 Anaphylactic shock Banana
Bean
Bishop’s weed (14)
Caraway
Carrot (15–17)
Castor bean
Causes Cauliflower
Classically, the protein sources are divided into Celery
Chicory
4 main groups: group 1: fruits, vegetables, spices, Chives (18)
plants, and woods; group 2: animal proteins; Chrysanthemum (23)
group 3: grains and group 4: enzymes. Taking into Coriander (16)
account the nature of the causal proteins, a wide Cress
Cucumber (15)
variety of jobs can be affected. Cumin (19)
Table 2 gives a list of the proteins having caused Curry (19, 20)
CU and/or PCD of the immunological type. For Dill
Eggplant
references see the report of Janssens et al. (4), to Endive
which more publications have been added (6, 7, Fig
10–93). Garlic (15, 21, 22)
Some of the suspected proteins are still not yet Gerbera (23, 24)
Green pepper (15)
clearly identified; reports of extremely rare, or Hazelnut
even isolated cases (without epidemiologic value) Hedge mustard (18)
may have contributed to this situation. This is in Horseradish
contrast to, for example, natural rubber latex, Kiwi
Lemon
a serious occupational hazard in the past 2 deca- Lettuce (15, 23, 25)
des in health care workers, which has been exten- Melon (15, 26)
sively studied (94–101). 13 different proteins Mushroom (27–29)
derived from Hevea brasiliensis have been charac- Natural rubber latex (6, 10, 22, 30, 31)
Olive (26, 32)
terized (102) and cornstarch powder, added dur- Onion (15)
ing glove manufacturing, identified as a vector to Orange (15)
the latex allergens, facilitating both skin and air- Papaw skin (33)
way contact (5). Although CU is the commonest Paprika (19, 20)
Parsley
reported form of natural rubber latex allergy, Parsnip
there are also a few cases of PCD (10, 30, 31) Peach (26)
and at least 1, as already mentioned above, of Peanuts
Pear (26)
paronychia (10). Pecan nuts (34)
Food handlers, cooks, housewives, caterers are Pineapple
at risk from fruits, vegetables and spices (Table 2). Potato (7, 15, 16, 26, 35)
Typical localizations can be observed as with gar- Ruccola (36)
Sapele wood (37)
lic and onion, affecting only the first, third and Spathe flowers (38–40)
fourth fingers of the non-dominant hand (4). Spinach (18)
Plants (Table 2) are known to cause immediate Tomato (15, 26)
skin and mucosal symptoms among gardeners, Walnut (41)
Watercress (15)
greenhouse workers, florists, plant caretakers, Weeping fig (40, 42)
and researchers (23, 25, 38, 39, 40, 42). Numerous Yucca (40)
families of plants have been implicated (Asteracea, Animal derived proteins (4)
Apiaceae, Agavaceae, Moraceae, and others), Amniotic fluid (43, 44)
Amphibian serum
making the prevalence of ICU fairly high in this Blood
occupational group. An IgE binding protein iden- Pig (35)
tified as profilin in several plant species (trees, Cow
grasses, and weeds) has been suggested to act as Lamb (33)
Horse (35)
a plant panallergen (38, 40). Other allergens are
Contact Dermatitis 2008: 58: 67–75 PROTEIN CONTACT URTICARIA AND DERMATITIS 69

Table 2. Continued Table 2. Continued

References References
Brains Crab (72)
Frog (45) Seminal fluid: Dog (75)
Cockroach (46) Skin
Dairy products Chicken
Milk Cow Turkey
Milk Dog (47) Wool: ewe (76)
Cheese Worms/larvae
Cheddar Nereis diversicolor (77, 78)
Emmental Calliphora vomitoria (79, 80)
Parmesan (48) Midge larvae (81)
Cheese products (49, 50) Lumbrinereis impatiens (82)
Dander/epithelium Grains (4)
Cow (51–54a) Rye (31, 35, 73, 83, 84)
Giraffe (55) Wheat (31, 35, 73, 83–85)
Egg yolk Barley (31)
Gut: pig Oat (31)
Hydrolyzed collagen (56) Cornstarch (86)
Liver Enzymes (4)
Calf/Ox (33) a-amylase (11, 83, 84, 87, 88)
Chicken Glucoamylase (89)
Lamb (33) Cellulase (90, 91)
Locust (57, 58) Xylanase (90)
Meat Protease (92)
Cow (35, 59–61) Papain (93)
Pork (35, 62) a
Chicken Only proved delayed hypersensitivity?
Horse (35)
Lamb (63)
Frog (45)
Mesenteric fat: pig being recognized such as lipid transfer proteins in
Parasites patients suffering from lettuce anaphylaxis (103)
Anisakis simplex (64, 65) and asparagus (13).
Placenta: calf (66)
Saliva: cow A case of PCD from sapele wood was reported
Seafood in a carpenter, adding wood and carpentry to
Codfish (15, 33, 67) the list of causes of occupational immediate
Mackerel dermatitis (37).
Horse mackerel (72)
Plaice (15) Cases of eczematous contact eruptions from
Herring (68) mushroom species, proven to be IgE-mediated,
Perch (33, 69) such as the Lentinus edodes (shiitake mushroom)
Rainbow trout (69)
Salmon (33, 15, 61)
(27, 28) and Boletus edulis (29) have been reported
Baby squid (70) in mushroom growers and in selecting and pack-
White fish (69) ing activities, respectively.
Whitebait (15) Proteins of animal origin constitute the largest
Whiting (15)
Angler fish (71, 67)
group (Table 2): they can cause problems in
Tuna fish (33) slaughterhouse workers (104, 105) and butchers,
Fluke (33) but also veterinarians are at great risk of CU or
Dory (33) PCD from amniotic or seminal fluid, blood, and
Fish mix (22)
Haddock (67) saliva having their origin in obstetric procedures
Red mullet (67) or daily contact with the animals (44, 106, 107).
Sea bream (67) Fig. 1 illustrates a PCD from cow dander in a
Sole (72) slaughter (data on file, Leuven).
Sea eel (72)
Cuttlefish (73) Geographic differences, reflecting countries’
Abalone (72) costumes, have become evident. In statistical data
Clam (67) from Finland, cow dander persists as a major
Mussel (67) cause of occupational disease among farmers
Oyster (67)
Shrimp (67, 74) (108), as previously reported (53, 109, 110). Finn-
Lobster ish farmers’ exposure to cow dander is extremely
Scampi (15) high, as cows are kept inside for most of the year.
Prawn (15, 33)
Shellfish
Animal keepers can be affected in multiple
contexts, though. Recently, a case of CU even to
70 AMARO & GOOSSENS Contact Dermatitis 2008: 58: 67–75

Fig. 2. Protein contact dermatitis from locusts in a labora-

tory worker (Genus Schistocerca and Genus Locust).

Fig. 3 gives an example of PCD from midge

larvae (Chironomus thummi thummi) used as fish-
ing bait (81).
Also protein hydrolysates present in hair-care
products (e.g. Crotein Q1, trimonium hydrolysed
collagen) have induced CU in hairdressers (56).
Fig. 1. Protein contact dermatitis from cow dander in a
slaughter man.

giraffe hair (Giraffa camelopardis rothschild) was

reported in a young girl working as a zookeeper
(55).
Case reports of laboratory workers suffering
from skin and respiratory symptoms following
contact with insects have also been published.
Cockroaches have provoked CU, dermatitis, rhini-
tis, and asthma (46). Contact urticaria to locusts is
an occupational hazard well known to professional
entomologists or breeders (57, 58). In a recent
study (58), 10 workers exposed to the African
migratory locust, Locusta migratoria, were evalu-
ated: 6 of them experienced symptoms ranging from
urticaria, rhinoconjunctivitis to asthma. In addi-
tion to the perithrophic membrane in the midgut,
identified some years ago as the major source of
allergen, the insect wings seem also to have potent
allergenic properties. Fig. 2 shows a PCD from
locusts in a laboratory worker (Genus Schistocerca
and Genus Locust) (data on file, Leuven).
Numerous fish or seafood species, as well as
fishing bait maggots (Nereis diversicolor, Calliphora
vomitoria, Chironomus thummi thummi, and
Lumbrinereis impatiens) have been described in Fig. 3. Protein contact dermatitis from midge larvae
relation to fisherman and fishing for leisure time. (Chironomus thummi thummi) used as fishing bait.
Contact Dermatitis 2008: 58: 67–75
Different grains and enzymes (Table 2) are
known to cause CU and PCD, sometimes accom-
panied by respiratory problems in bakers.
Pathogenesis
The occupations involved may be associated with
pre-existing dermatitis, i.e. atopic dermatitis, for
which associations have been noted in about 50%
of the cases (4), as well as irritant contact derma-
titis, physical damage (burns and wounds), chem-
ical damage (detergents and other penetration
enhancers), increased hydration (excessive hand
washing), and occluded skin (e.g. wearing gloves)
(111, 113). All such causes of reduced stratum
corneum barrier integrity may indeed facilitate
high molecular weight proteins to penetrate into
the skin.
The pathogenesis of ICU and PCD reflects
a type I hypersensitivity reaction, mediated by
allergen-specific IgE in a previously sensitized
individual.
The exact pathophysiological mechanism in
PCD is still unclear. Several authors have reported
a combination of type I and IV allergic skin reac-
tions, the latter supported by positive delayed
patch tests (7, 21, 52, 64, 74), while this association
has been difficult to prove in most cases (16, 37,
73, 76). Negative patch testing on intact skin does
not necessarily mean that a type IV reaction is not
involved though: false-negative results might be
because of insufficient penetration of the proteins.
Since the showing of IgE receptors on the epider-
mal Langerhans cells (112), it has been speculated
that these cells could be responsible for a delayed
IgE-mediated reaction, a similar process to that of
atopic dermatitis (4).
Homologies between proteins are now known to
explain the cross-reactivity described in certain
sources, i.e. natural rubber latex and fruits
(banana, kiwi, and avocado) (6, 114), with similar-
ities between Hev b 6 and endochitinases in avo-
cado and banana; the mugwort-spice syndrome
(16, 19), a form of pollen-related food allergy
because of cross-reactivity of epitopes, and a subset
of perioral syndrome and PCD with cross-reactivity
between profilin in birch pollen, apple, and peach
(26). Alonso et al. reported cross-reactivity between
the clupeiformes herring, sardine and anchovy (68),
and cross-reactivity between cockroaches and
locusts, arthropods of the Insecta class were also
observed (46, 58). Associations between other
invertebrates, with unrelated classes have also been
reported, like the crustacean-dust mite syndrome,
with tropomyosin as the major cross-reacting aller-
gen (74). Interestingly, in several of the reported
clinical cases multiple allergens were implicated
PROTEIN CONTACT URTICARIA AND DERMATITIS 71
(16, 22, 31, 33, 69, 73). Along with structural homo-
logies, this probably also reflects a priming factor
to the subsequent allergic process.
Different antigenicity to raw versus cooked al-
lergens reflects heat-sensitivity (64, 71), although
in some cases symptoms did persist after ingestion
of the cooked allergen (61).
Diagnostic Tests
Tests for immediate IgE-mediated allergy are of
paramount importance when CU or PCD are
investigated and reactions appear within 20 min.
Prick tests with fresh material or commercial
reagents are the gold standard (1, 4, 5, 108).
Open testing (quite similar to the Skin Applica-
tion Food Test or SAFT, which has only been
mentioned in the diagnosis of food allergy in
atopic children, (115) can be helpful, but is gener-
ally negative unless the substance is applied on
damaged or eczematous skin [where it may even
cause a vesicular reaction, (3)]. Sometimes a rub-
bing test (gentle rubbing with the material) on
intact or lesional skin might be indicated, if an
open test is negative. Scratch and scratch-patch
testing carry a higher risk of false-positive reac-
tions and the latter lacks sensitivity compared
with prick testing (1, 116). As mentioned above,
patch tests in PCD are usually negative.
If there is a suspicion of any kind of serious
extra-cutaneous symptoms, tests should be carried
out with the necessary precautions and resuscita-
tion facilities should be adequately available.
Measurement of specify IgE in serum (e.g.
radioallergosorbent-RAST) is useful for some of
the known proteins. Indeed, as mentioned above,
many of the protein allergens have not been iden-
tified yet.
The basophil activation test is a relatively new
procedure: it is based on the showing of a mem-
brane protein marker that appears following
exposure to allergens and can be particularly
interesting when assessing reactions to rare aller-
gens, for which routine diagnostic tests, such as
measurement of specific IgE antibodies, are not
available (117, 118).
Differential Diagnosis
ICU from low-molecular chemicals also exists.
Specific antibodies to e.g. ammonium persulfate
in the serum of hairdressers with skin and respir-
atory symptoms have been shown (119). Sparse
reports of other substances causing similar clinical
pictures have been published, such as an immediate
mezlocillin allergy in a nurse, in which symptoms
cleared following a job change (2).
72 AMARO & GOOSSENS
A variety of low-molecular weight substances
frequently encountered in our environment, such
as preservatives, fragrances and foodstuffs can
induce a distinct form of non-immunological con-
tact urticaria (NICU). These agents may produce
a reaction without any previous sensitization in
most, if not all, exposed persons (1, 2).
Concerning PCD, an allergic contact dermatitis
to low-molecular weight allergens, should be ruled
out as the major cause of the eczematous clinical
picture (4). Both conditions can occur simulta-
neously, however: for example, PCD from pro-
teins in onion and garlic and allergic contact
dermatitis from diallyldisulfide present in them
(21, 22).
It should be kept in mind that the same sub-
stance can originate different clinical pictures by
distinct mechanisms. Recently, curcumin, a poten-
tial cause of immediate and delayed allergic reac-
tions has recently also been reported as a cause of
NICU in a woman exposed to this spice powder
at work (120).
Last but not least, atopic and irritant contact
dermatitis have to be considered in the differential
diagnosis.
Conclusion
Macromolecules can penetrate the skin and cause
immunological urticarial or eczematous clinical
pictures, which seem to share a common patho-
genic mechanism of a type I immediate reaction,
making prick testing the gold standard method for
diagnosis. A large number of causes have been
documented, plant or animal derived, flours or
enzymes, grouped in an ever-expanding list of
occupational sources.
Infrequent clinical features may not be recog-
nized if they are not properly investigated and new
potent protein allergen sources need to be kept in
mind. Indeed, new social habits will probably
open new pathways for other allergens, as for
the growing consumption of raw and smoked fish
because of the influence of Japanese cuisine (64,
121), or for natural remedies such as the wide-
spread use of garlic (21) or alternative and herbal
products (120). Moreover, processed chemical or
enzymatic proteins can also become a hazard,
such as collagen hydrolysates in cosmetics.
Extensive studies on the incidence and follow-
up of latex allergy in health care workers were of
utmost importance and resulted in specific guide-
lines that succeeded in reducing its incidence in
high-risk populations within the medical field
(102, 122). In time, other occupational groups
might need to be targeted as well, proving new
Contact Dermatitis 2008: 58: 67–75
opportunities for starting potential prevention
programmes.
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