Australasian Journal of Dermatology (2008) 49, 1–11
PROFESSIONAL DEVELOPMENT PROGRAM
Irritant contact dermatitis: A review
Dan Slodownik,1 Adriene Lee2 and Rosemary Nixon1,3
1
Occupational Dermatology Research and Education Centre, Skin and Cancer Foundation, Melbourne,
2
Dermatology Unit, Monash Medical Centre, Clayton, and 3Department of Medicine, University of Melbourne,
Melbourne, Victoria, Australia
SUMMARY
Irritant contact dermatitis is the most common form
of contact dermatitis, and yet is often overlooked.
Recent progress in understanding the pathogenesis
has reignited the interest of clinicians in this area of
dermatology. Irritant contact dermatitis is not a
homogenous entity, but rather a number of subtypes
contributing to different clinical presentations. The
diagnosis of irritant contact dermatitis is often clini-
cal, and may only be possible after the exclusion of
allergic contact dermatitis with patch testing. There
is no readily available diagnostic test. There is an
incomplete understanding of the factors which lead to
the development of cumulative irritant contact der-
matitis and persistent postoccupational dermatitis.
We have used the experience from our tertiary re-
ferral occupational dermatology clinic to illustrate
various aspects of irritant contact dermatitis, and to
highlight the difficulty sometimes encountered in
making this diagnosis. We believe that increased
awareness of the often pivotal role of irritant contact
dermatitis, as well as all the other factors contributing
to occupational dermatitis, will lead to improvement
in outcomes for patients.
Key words: allergy, atopy, cumulative, difficulty
in diagnosis, hand, occupational, persistent post-
occupational, work.
Correspondence: Dr Rosemary Nixon, Occupational Dermatology
Research and Education Centre, Skin and Cancer Foundation Inc.,
Carlton South, Vic. 3053, Australia. Email: rnixon@occderm.asn.au
Dan Slodownik, MD. Adriene Lee, FACD. Rosemary Nixon, FACD.
Funding sources: Recipient of the Fred Bauer prize, Annual Sci-
entific Meeting, Australasian College of Dermatologists, May 2006.
Submitted 5 April 2007; accepted 18 October 2007.
© 2008 The Authors
Journal compilation © 2008 The Australasian College of Dermatologists
doi: 10.1111/j.1440-0960.2007.00409.
INTRODUCTION
Irritant contact dermatitis has been defined as a non-
immunological, non-specific reaction of the skin to an irri-
tant. It is now recognized that this definition is too
simplistic. This condition is now considered to involve a
combination of endogenous and exogenous factors,1 which
triggers a pathophysiological cascade of skin barrier disrup-
tion, cellular damage to the keratinocyte membrane and
pro-inflammatory mediator release, resulting in a clinical
presentation which may be divided into 10 subtypes.2,3 This
review will summarize recent progress in the understand-
ing of ICD. Where relevant, we have included illustrative
cases from the Occupational Dermatology Clinic at the Skin
and Cancer Foundation, Victoria, Australia.
EXOGENOUS AND ENDOGENOUS FACTORS
CONTRIBUTING TO THE DEVELOPMENT
OF ICD
The onset of ICD depends on both exogenous and endog-
enous factors.
Exogenous factors
Skin irritants
Almost all chemicals have the potential to cause ICD. Iden-
tifying one cause is often not possible, as ICD is usually
multifactorial. The most common and important skin irri-
tant is wet work.4 Wet work is defined as the exposure of
the skin to liquid for longer than 2 hours per day, the use of
Abbreviations:
ACD allergic contact dermatitis
CLA cutaneous lymphocyte association
ICD irritant contact dermatitis
IgE immunoglobulin E
SLS sodium lauryl sulfate
TEWL transepidermal water loss
TNF tumour necrosis factor
2 D Slodownik et al.
occlusive gloves for longer than 2 hours per day or frequent
hand cleaning.5 Workers in occupations involving wet work
are especially prone to occupational ICD. These include
hairdressers, food handlers and health-care workers.6 Our
experience confirms that wet work is the most common
skin irritant locally, followed by exposures to soaps and
detergents, solvents and oils (Fig. 1).
Inherent nature of irritants
The potential for irritancy of a substance is determined by
its chemical and physical properties. Molecular size, ioniza-
tion state and fat solubility determine skin penetration, and
thus contribute to irritancy. For some aliphatic solvents in
an animal model, skin irritation from low-level repeat expo-
sures was thought to relate to affinity for the stratum
corneum, and also to gradual accumulation in the skin.7
Different chemicals act on different targets in the epider-
mis. The irritant SLS alters the synthesis of new lipids.8
Acetone causes increased basal keratinocyte proliferation.9
At high levels of exposure, many chemicals will act as
irritants.
Exposure to irritants
Concentration, volume, application time and duration of
irritant exposure on the skin will determine the outcome.
The penetration of an irritant through the skin increases
both with exposure volumes and duration of exposure.10
Longer intervals between exposures will generally
decrease the likelihood of irritation. Simultaneous or sub-
sequent exposures may cause an additive effect, although
sometimes irritants may neutralize each other.11 Different
effects of irritants have been reported, depending on
whether they were applied to the skin first or following
another irritant. For example, pretreatment with retinoic
acid appeared to reduce the irritant responses to SLS.12
Pharmacological synergism or antagonism between the
test compounds may explain this phenomenon; alterna-
tively, an agent may change the percutaneous penetration
Most common causes of irritant contact dermatitis
Water
Detergents
Solvents
Oils
Heat and sweating
Dusts and fibres
Acids and alkalis
Other
0 50 100 150
© 2008 The Authors
Journal compilation © 2008 The Australasian College of Dermatologists
of the other. There are several reports in the literature
about the effects of multiple irritants, which are often
complex.13–15
Repeated exposure to irritants induces an initial
increase and a subsequent decrease in TEWL.16 This indi-
cates functional adaptation or hardening. An increased
TEWL indicates worsening function of the skin barrier.
Ceramide 1, a major component of the stratum corneum
lipid, plays a key role in the protection mechanism against
repeated irritation. Its production is upregulated in
repeated exposures.13
Physical irritants and environmental factors
While chemical causes of ICD are well recognized, the con-
tribution of physical, environmental and mechanical factors
to ICD is often neglected.17 Environmental factors include
heat, cold, low humidity and UV irradiation. Mechanical
factors include friction, occlusion, pressure and vibration.
Exposure to heat often leads to sweating, which may pre-
cipitate ICD, especially with occlusion. The retention of
sweat may also contribute to skin irritation, as sweat is
more irritating than water.18 Sweating may also facilitate the
skin penetration of allergens, such as to nickel in jewellery
or chromate in leather.
Use of gloves and clothing may cause an occlusive,
humid, warm environment, and thus enhance irritation
from heat and sweating. Warm temperatures are generally
more damaging than cool temperatures.
Low environmental humidity enhanced irritability by
lowering ceramide levels in the stratum corneum.19 UVB
radiation diminished the non-immunological reactions
caused by SLS, probably as a result of anti-inflammatory
effects.20
Endogenous factors
Endogenous factors influence the susceptibility to ICD.
These include age, sex, anatomic site involved and history
of eczema, including atopic eczema.21 Identifying these
Figure 1 Exogenous causes of irri-
tant contact dermatitis in the Occu-
pational Dermatology Clinic, Skin
and Cancer Foundation, Victoria,
Australia, where the primary diagno-
sis was irritant contact dermatitis
(total 621 patients over the period
200 250 1993–2002).
 Irritant contact dermatitis
factors is important for the prediction and assessment of
ICD and, in particular, for occupational skin disease, which
is predominantly caused by ICD.1 Inter-individual differ-
ences in barrier function may be quantified.22 The first
description of a non-atopic genetic marker for irritant sus-
ceptibility, TNF-a polymorphism in normal individuals, was
reported in 2000.23
Age
Susceptibility to irritation decreases with age. Studies have
reported a higher tendency to skin irritation under the age
of 20 years, and even more so in children less than 8 years.
There is greater reactivity to cumulative exposures and to
low irritant concentrations in young adults.24,25 This is dem-
onstrated by decreased changes in TEWL measurements
after SLS exposure with increasing age.24
Sex
Irritant contact dermatitis is more common in women. It is
not clear if this is due to an increased susceptibility to ICD
in women or greater exposure of women to irritants, in
particular, wet work. One study showed that there were no
differences with respect to 11 different tested irritants,
including SLS, between the sexes,24 whereas another study
reported conflicting results.26 Further studies are needed to
determine if there is indeed any difference in the suscepti-
bility to develop ICD between the sexes.
Anatomic sites
Percutaneous penetration varies with anatomic region, with
the face being the most permeable and three times more
permeable than the back.27 However, there are few data
available on the propensity for skin irritation in different
anatomic sites, although in one study, TEWL was assessed
after exposure of different parts of the face to SLS. Signifi-
cantly higher levels of TEWL were found on the chin and
nasolabial areas of young adults compared with older
people.28
Previous and pre-existing skin diseases,
including atopy
Patients with altered barrier function are more prone to
ICD. Transepidermal water loss of uninvolved sites in
patients with acute ICD was higher than in patients with
healed ICD, who in turn had higher values than controls.29
Existing dermatitis, irrespective of type, enhances reactivity
to various irritants in another location of the body.30 This is
especially so for atopic eczema.31 Barrier function impair-
ment of uninvolved skin sites has been related to the sever-
ity of atopic eczema.32
In a study of subjects with atopic eczema compared with
controls and those with a history of ACD, it was found that
a history of atopic eczema increased the susceptibility to
skin irritants.33 In a German study, there was a significant
Journal compilation © 2008 The Australasian College of Dermatologists
3
impact of an atopic diathesis on the development of occu-
pational hand dermatitis.34 Healthy persons can adapt to
repeated irritation, while those with atopic eczema have
increased TEWL and are more likely to develop occupa-
tional dermatitis. Clearly, people with a history of atopic
eczema, as well as those advising them, need to be aware
of the increased risk of occupational dermatitis in certain
careers,35 and such information is provided on our
website.36
Mucosal atopy, which is a history of hayfever or asthma
but not atopic eczema, does not have such a clear-cut
impact as atopic eczema.37 Individuals with isolated
mucosal atopy were found to have a higher tendency to ICD
in one study,37 while in other studies, patients with mucosal
atopy were found to have similar barrier function as control
subjects.38,39
PATHOGENESIS
In the past, the pathogenesis of ICD was thought to be
non-immunological. However, today, it is generally
accepted that the immune system plays a key role in elic-
iting ICD, via multiple parallel pathways.40 However, irri-
tants share the same pathophysiological changes of skin
barrier disruption, epidermal cellular damage and release
of pro-inflammatory mediators, all of which are inter-
linked. Keratinocytes have a major role in the production
of immunological response to irritants. They release
cytokines on the disruption of the skin barrier, upregulate
their major histocompatability class II antigens and
upregulate cell adhesion molecules.41 The pro-inflam-
matory cytokines interleukin-1a, interleukin-1b and TNF-a
are of special interest, and have been found to be upregu-
lated in the irritant reaction.42,43 The chemokine CCL21,
produced by dermal lymphatic endothelial cells, is
also upregulated in ICD.44 It facilitates the migration of
naive T-lymphocytes, resulting in a skin inflammatory
response.
Several irritants can induce keratinocyte expression of
TNF-a. The importance of irritant-induced TNF-a was high-
lighted by studies where administration of anti-TNF-a anti-
bodies blocked elicitation of ICD.45
T lymphocytes entering the irritated area often express
the CLA antigen.46 This antigen participates directly in
transendothelial migration of T lymphocytes. The ligand for
CLA antigen is E-selectin. Other receptor–ligand pairs, such
as LFA1/ICAM1 and VLA4/VCAM1, are also involved in this
process.47 CLA antigen is important in skin homing for T
lymphocytes recruited to the local inflammatory site. There
seem to be no specific cytokines that clearly distinguish
allergic from irritant reactions.41
The sometimes observed chronicity of ICD has two
possible immunological explanations: first, that ongoing
inflammation exposes the immune system to immunogenic
skin peptides, resulting in persistent recruitment of inflam-
matory mediators; second, that TNF-a is regulated in an
autocrine manner, and thereby involved in the maintenance
of a pro-inflammatory environment.48
© 2008 The Authors
4 D Slodownik et al.
CLINICAL TYPES
Acute irritant contact dermatitis
Acute ICD is caused by exposure to a potent irritant, such as
a strong acid or alkali. The clinical signs include erythema,
oedema and local necrosis, starting soon after exposure to
the irritant. The healing is described as a decrescendo phe-
nomenon, implying that this process starts immediately
after removal of the offending agent, in contrast to ACD, in
which there is a transient increase in the reaction before
healing occurs (crescendo phenomenon).3 Complete healing
may take up to 4 weeks and, generally, the prognosis is
good, although scarring may occur. An example of this is the
exposure to wet cement, causing a ‘cement burn’.
Delayed acute irritant contact dermatitis
Some chemicals, such as dithranol and benzalkonium
chloride, have the potential to cause a delayed inflamma-
tory response, approximately 8–24 hours following the
initial exposure.49 The symptoms are similar to acute ICD,
and the prognosis is good. Both the clinician and patient
could miss the relationship between the exposure and the
dermatitis: the clinician may misinterpret the delayed
nature as ACD.
Irritant reaction
Individuals exposed to wet work, such as hairdressers, may
develop erythema, scaling, vesicles or erosions on the backs
of their hands with repeated exposures. Hardening of the
skin occurs after healing, generally resulting in a good
prognosis, although there is the possibility that cumulative
ICD may develop.2
Subjective or sensorial irritation
These individuals experience sensory discomfort, usually
manifesting as a stinging, burning or itchy sensation, in the
absence of clinical and histological evidence of skin lesions.
The threshold for this reaction varies between subjects, and
is independent of the susceptibility to other types of irrita-
tion. Lactic acid and propylene glycol are common subjec-
tive irritants. Interestingly, SLS, a potent objective irritant,
does not generally induce stinging.50 Subjective irritation
has both neural and vascular components, contributing to
discomfort. The outcome is generally good.
Non-erythematous irritation
This entity refers to irritation which is histologically appar-
ent, but where the skin looks normal.51 The symptoms are
similar to those of subjective irritation. Individuals experi-
ence discomfort with many chemicals. This form is believed
to commonly occur with exposure to consumer products
which have a high content of surfactants, such as cocami-
dopropyl betaine or coconut diethanolamide. The prognosis
is reported to be variable.
© 2008 The Authors
Journal compilation © 2008 The Australasian College of Dermatologists
Cumulative irritant contact dermatitis
This is the most prevalent type of ICD. The causes for this
entity are multiple subthreshold insults induced by weak
irritants. The frequent, repetitive nature of the stimuli does
not allow the skin to recover, leading to persistent derma-
titis.52 This entity is also termed chronic dermatitis.53 The
clinical features include erythema and dryness followed by
hyperkeratosis. The threshold varies between and even
within individuals. The symptoms do not immediately
follow the exposure, leading clinically to the differential
diagnosis of ACD. The prognosis is variable.
One difficulty for the dermatologist is that exposure to
weak irritants often occurs not only at work, but also at
home, adding to the complexity of identifying contributing
factors.
Cumulative ICD is exemplified by Case 1.
Case 1
A 50-year-old maintenance fitter was referred with an
8-month history of hand dermatitis. He had worked in this
occupation for over 30 years with exposure to oils, greases
and solvents. The skin condition improved on holidays and
with oral corticosteroids, but flared rapidly on stopping
them. Patch testing was negative, and he was diagnosed
with cumulative ICD. After 4 months of modified work
duties, without marked improvement, he then had 2 months
off work with appreciable improvement, although it had
taken 4 months to wean him off oral corticosteroids. This
case highlights the cumulative nature of ICD, and that it
takes time to improve, including often requiring time away
from work. However, the duration of time away from work
is often difficult to estimate.
Traumatic irritant contact dermatitis
Traumatic ICD occurs following an acute skin trauma, such
as acute dermatitis or a burn. It is characterized by an
incomplete healing of the original insult followed by num-
mular eczema-like lesions.54 It follows a chronic course, and
is sometimes recalcitrant to therapy.
Case 2
A worker inadvertently applied oven cleaner to his hands,
thinking it was a skincare product. He experienced acute
ICD which improved with time, but did not resolve, and he
was diagnosed with persistent traumatic ICD.
Pustular and acneiform dermatitis
Exposure to metals, tars, oils, chlorinated agents and naph-
thalene may result in a pustular and acneiform dermatitis,
especially in atopic patients. Cosmetic dermatitis may also
assume this morphology. The prognosis is variable.
Case 3
A worker presented with an acneiform eruption over the
right anterior thigh. This was attributed to his tendency to
 Irritant contact dermatitis
carry an oil-soaked rag in his pocket. His rash improved
following cessation of this work practice.
Asteatotic irritant dermatitis
This condition has also been called ‘exsiccation eczema-
toid’, winter eczema and eczema craquelae. This form of
ICD is typical among elderly patients who wash without
adequate use of moisturizing creams, especially in an envi-
ronment of low humidity. The condition is characterized
by icthyosiform scaling. It is thought to be caused by a
decrease in skin surface lipids and the persistence of both
peripheral and non-peripheral corneodesmosomes in the
upper stratum corneum.55 Patients suffer from intense
itching, generally relieved by application of moisturizing
creams.56
Frictional dermatitis
Frictional dermatitis is confined to locations of frictional
trauma to the skin. The causative component is the shearing
force acting horizontally to the surface, rather than pressure,
temperature or ischaemia induced by the mechanical
forces.57 Under-diagnosis is probably the result of lack of
recognition of the potential for physical friction to induce
eczematous changes in the skin.58 In addition, the morphol-
ogy may appear quite psoriasiform, especially in patients
with a background of psoriasis, which may again obscure the
role of ICD. However, cases of ICD usually feature more
pruritus.
Case 4
A 39-year-old non-atopic textiles and home economics
teacher presented with a 6-year history of involvement of
the palmar aspects of the thumb and fingers, more marked
on her non-dominant hand. She described handling fabrics
with this hand while her right hand operated a sewing
machine. Comprehensive patch testing was negative. Over
the next 15 years, she was observed to experience improve-
ment only when she had at least 6 months away from
work. Her symptoms persist, but, with modification of her
duties to reduce handling textiles, are now much more
manageable.
Other clinical aspects
Differing mechanisms of pathogenesis and host responses
to irritants may lead to variable clinical patterns. The spec-
trum of ICD includes vesicles, bullae, papules, scaling,
fissuring and skin necrosis. The clinical picture may be
clinically indistinguishable from ACD, and may vary along
its time course. Irritant contact dermatitis may also result in
non-eczematous rashes, including folliculitis, acne, mil-
iaria, pigmentary alterations, alopecia and granulomatous
reactions. Folliculitis alone has been described as an irritant
reaction.59,60 It was observed that irritant pattern reactions to
Journal compilation © 2008 The Australasian College of Dermatologists
5
cobalt involve the eccrine acrosyringium, suggesting that
the ‘follicular’ pattern described actually represents eccrine
origin pathology.61
Persistent postoccupational dermatitis is poorly under-
stood,62 and this has been defined as an ongoing dermatitis
for which there is no obvious present cause, precipitated by
prior occupational contact dermatitis. Severity of preceding
dermatitis, atopy and cumulative irritation have been sug-
gested to be risk factors.63 Persistent postoccupational der-
matitis poses a particular problem in some Australian
State-based workers’ compensation systems. Approximately
6–12 months after a worker’s compensation claim has been
accepted for work-related skin disease, insurance payments
may be reviewed and then suspended if an independent
examiner believes that on the basis of lack of improvement
off work, the diagnosis is endogenous eczema. As both ICD
and persistent postoccupational dermatitis are subjective
diagnoses with no routine diagnostic tests available, they
can be difficult to substantiate medicolegally.
Finally, ICD may be just one of several contributing
factors to occupational dermatitis.
Our clinic data (unpublished) over 12 years reveal
that nearly half of the patients assessed have at least
two separate diagnoses believed to be contributing to their
condition.
Case 5
A 28-year-old nurse presented with an 8-year history of
facial and hand dermatitis ever since starting nursing. She
washed her hands multiple times during shifts. She had a
positive atopic history, and her total IgE level was 431 kU/L
(normal range 0–120). Radioallergosorbent testing was
positive to latex, weed, grass mix and house dust mite. On
patch testing, she reacted to coconut diethanolamide, a sur-
factant in her hand cleanser. Our diagnoses were multiple:
latex allergy, ACD to her hand cleanser and ICD caused by
wet work in a woman with a background of mucosal atopy.
Each diagnosis required a specific treatment.
DIAGNOSIS
The diagnosis of ICD is based on history, clinical findings
and patch testing, where no relevant allergens are identi-
fied. Histology is generally thought to be unhelpful in estab-
lishing the diagnosis. A comprehensive history, including of
occupational exposures, is essential. Attention should be
given to the intensity, frequency and duration of exposures
and the exposed skin surface area.64 The clinician must also
determine any relationship between fluctuations in the der-
matitis and other factors, for example, time off work and the
performance of certain hobbies.
In a Canadian survey, occupational history taking among
dermatologists was poor, with only 5% enquiring about
exposures and only 3% asking patients to bring their safety
data sheets from work.65
The ability to predict which individuals are prone to irri-
tant skin reactions has practical significance as a pre-
employment screening test. To date, however, there is no
© 2008 The Authors
6 D Slodownik et al.
routine diagnostic test available. Sodium hydroxide has
been used to produce TEWL as a measure of skin damage.66
A TNF-a gene polymorphism offers a novel approach to
detect susceptibility to ICD. In humans, a G to A transition
polymorphism has been identified at position P308 within
the promoter region of the TNF-a gene, with the G form of
the polymorphism being most common. An analysis of dif-
ferent genotypes revealed a correlation between the A allele
and a low threshold to irritants.23
A recent study found reflectance-mode confocal micro-
scopy facilitates the differentiation of acute ACD and ICD.67
Stratum corneum disruption, epidermal necrosis and
hyperproliferation were hallmarks of ICD, whereas ACD
was more typically presented with vesicle formation.
Patch testing has an important role in the evaluation of
eczematous skin diseases. Follow-up studies have shown
beneficial effects in the long-term outcomes for patients,
even when results are negative.68–70 In the absence of patch
testing, morbidity is increased with adverse financial impli-
cations for patients, health services and the state.71
If patch testing is carried out in a dedicated patch-test
clinic, the identification of ACD is further enhanced.72,73 The
increased detection rate is attributable to the increased
number of patch tests being applied, testing patients’ own
products and, most importantly, to the interpretation of
results.74 With some authors proposing a minimum annual
referral rate for patch testing in the order of one per 700 of
the population,75 the need to optimize access to patch testing
services is clear.
Our clinical experience suggests that ICD is under-
diagnosed, as practitioners may be uncertain or reluctant to
diagnose ICD, as there is no routine diagnostic test avail-
able. In addition, the contact dermatitis fraternity contrib-
utes to this problem by less reporting of ICD in the
literature, even though it is more common than ACD.
TREATMENT
Avoiding exposure to irritants, relying on the use of per-
sonal protective equipment and the use of moisturizing
creams are the basis of the treatment of ICD. Understanding
which gloves are appropriate for use with which irritants
may be quite complex.76 In addition, it has been stated that:
‘even if a glove is capable of preventing contact between a
chemical and the skin, it must be worn to accomplish this
preventive effect’.77
Irritant contact dermatitis has been generally treated with
topical corticosteroids,53,78 although there are some recent
reports suggesting that they may compromise barrier func-
tion.79,80 In one report, this was found to relate to inhibition
of epidermal lipid synthesis, which was then corrected by
topical application of lipids.80
There is considerable recent interest in the repair of the
skin barrier with topically applied lipids,81 and evidence has
been accumulating for the treatment of ICD with the use of
moisturizers.82,83 They increase skin hydration, and their
lipid component improves the damaged skin barrier by
influencing the structure of epidermal lipids.84 Moisturizers
may prevent absorption of exogenous substances and accel-
© 2008 The Authors
Journal compilation © 2008 The Australasian College of Dermatologists
erate barrier recovery.82,83 Patients should be advised to
apply moisturizers generously and frequently.
Macrolide antibiotics have been reported to suppress the
immune response.85 Cool compresses may provide a moist
environment, reduce vesiculation,86 increase the capacity
for moisture retention, and decrease inflammation and
surface temperature.87 Washing hands in cool or tepid
rather than hot water may be beneficial.
It has been suggested that sensory irritation may be
treated by applying strontium salts, which selectively block
the activation of cutaneous type C fibers.88 However, this
treatment is currently not available in Australia.
Cumulative ICD has been successfully treated by photo-
therapy.89 Repeated low-level UV exposures may elicit hard-
ening of the skin, suppress cellular proliferation and alter the
local immune system by reducing the number of Langerhans
cells and induction of DNA-dimers.90 Another option is the
use of Grenz-ray therapy, which may induce a long-term
response by suppression of Langerhans cells.91 Our experi-
ence with this modality has been very favourable.
The time course of cumulative or chronic ICD is slow
compared with ACD. Re-exposure to the allergen usually
aggravates the symptoms of ACD within 2 days, while
re-exposure to an irritant gradually aggravates the derma-
titis in 1 to 2 weeks. It has been reported that even after the
skin appears normal, it takes approximately 4 months or
more for barrier function to normalize.92 Germany leads the
world in the rehabilitation of occupational contact derma-
titis. The ‘Osnabruek Model’ includes 2–3 weeks of in-
patient treatment followed by a similar period of outpatient
treatment.93 Interestingly, topical corticosteroids are with-
drawn from their patients.
Our approach to the treatment of ICD is based on deter-
mining all contributing factors to the patient’s dermatitis
and prevention of contact with the causative agents where
possible. In addition, education is provided about appropri-
ate skin care and, in particular, the benefits of regular
moisturizing.94 In the future, we intend to institute an edu-
cational, rehabilitative programme, Skin School, using ele-
ments derived from the German model.
CONCLUSION
There have been a number of advances in the understand-
ing of ICD. While there is still no routine test, and ICD is
often a diagnosis of exclusion, some interesting new areas
of research include the role of TNF-a gene polymorphism
and use of confocal microscopy. However, ICD may present
difficulties to the clinician, especially where there is no
access to patch testing, which is often necessary to exclude
ACD. Despite slight differences in the clinical subtypes of
ICD, the treatment should include avoidance of irritants,
use of appropriate protective gloves where there is hand
involvement, and use of moisturizers. There have been
some recent concerns raised about the use of topical corti-
costeroids in the treatment of ICD as they may impair
barrier function. This has further emphasized the impor-
tance of using moisturizers in the treatment of this
condition.
 Irritant contact dermatitis
ACKNOWLEDGEMENT
The authors would like to acknowledge the support of the
Skin and Cancer Foundation, Victoria.
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Frenk E, Saurat JH, Hauser C. An epidemic outbreak of papular
and follicular contact dermatitis to tocopheryl linoleate in cos-
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Persistent post-occupational dermatitis. Contact Dermatitis
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463–7.
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confocal microscopy. Dermatitis 2006; 17: 182–91.
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of the value of patch testing: the patient’s perspective. Contact
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contact dermatitis evaluation: results of a follow-up study. Am.
J. Contact Dermat. 1995; 6: 63–6.
70. Rajagopalan R, Anderson R. Impact of patch testing on
dermatology-specific quality of life in patients with allergic
contact dermatitis. Am. J. Contact Dermatitis 1997; 8: 215–21.
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dermatitis and the role of patch testing. J. Am. Acad. Dermatol.
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importance of a dedicated patch test clinic. Br. J. Dermatol.
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 Irritant contact dermatitis
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skin treated with a moisturizing cream. Contact Dermatitis
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2006; 47: 97–101.
© 2008 The Authors
10 PDP

PROFESSIONAL DEVELOPMENT PROGRAM

Select the most correct answers – multiple answers possible for questions 1–11

1. Included in the seven most common causes of irritant contact dermatitis are: d. Non-eczematous rashes, i.e. folliculitis, have not been well described as an
a. Detergents. ICD reaction.
b. Heat and sweating. e. Irritant contact dermatitis is less common than ACD.
c. Dust and fibres. 10. When making a diagnosis of contact dermatitis:
d. Oils. a. A comprehensive history including occupational exposures is
e. Water. essential.
2. The potential for irritancy of a substance may relate to: b. Patch testing has a minimal role in the evaluation of eczematous skin
a. Molecular size, ionization site and fat solubility (skin penetration factors). diseases.
b. Ability to alter synthesis of new lipids (e.g. sodium lauryl sulfate). c. The diagnosis of ACD is enhanced by increased numbers of allergens
c. Ability to increase basal keratinocyte proliferation (e.g. acetone). patch tested and testing the patient’s own products.
d. Concentration of chemical exposure. d. Wet work is defined as occurring when individuals have their skin
e. Concurrent application of other chemicals. exposed to liquids for longer than 4 hours per day or use occlusive gloves
3. Concerning the exposure of skin to irritant chemicals: for longer than 4 hours per day or clean their hands often (e.g. 20 times per
a. Shorter intervals between exposures will generally decrease the likeli- day) or fewer times if the cleaning procedure is more aggressive.
hood of irritation. e. Physical, environmental or mechanical factors do not contribute to the
b. Application time of exposure has no effect on chemical skin penetration. pathogenesis of ICD.
c. Functional adaptation of hardening of skin is associated with a decrease in 11. Concerning cumulative ICD:
transepidermal water loss (TEWL). a. Is considered to be a consequence of multiple subthreshold insults to the
d. Ceramide 1, a major component of stratum corneum lipid, plays a key role skin induced by weak irritants with the time between insults being too
as a protective mechanism against repeated irritation. short to allow skin recovery.
e. Simultaneous or subsequent exposures to irritant chemicals results in b. Clinical signs develop when the damage exceeds a threshold, which
predictable additive quantitative impairments of barrier function. seems to be remarkably similar for most individuals.
4. Concerning environmental factors and irritant contact dermatitis (ICD): c. The symptoms do not immediately follow the exposure, leading clinically
a. High environmental humidity enhances irritability by lowering ceramide to a differential diagnosis of ACD.
levels in the stratum corneum. d. Is most commonly caused by weak irritants in the home environment.
b. Warm temperatures are generally more damaging than cool e. This is the most prevalent form of ICD.
temperatures.
c. UVB has not been shown to be involved in ICD. Directions for questions 12–23: For each numbered item, choose the appropriate
d. Use of gloves and protective clothing may enhance irritation from heat lettered item. There is only one correct answer, but the same letter can be chosen
and sweating. more than once in any question.
e. The retention of sweat may also contribute to skin irritation as sweat has
been shown to be more irritating than water. With respect to questions 12–15:
5. Concerning endogenous factors that may influence susceptibility to ICD: a. Allergic contact dermatitis
a. Children below the age of 8 years are generally considered more suscep- b. Acute irritant dermatitis
tible than adults. c. Cumulative irritant dermatitis
b. Existing dermatitis, irrespective of type, may enhance reactivity to various d. Subjective/sensory irritation
irritants only in the same location of the body. 12. Healing is described as decrescendo phenomenon.
c. Barrier function impairment on uninvolved skin sites has been related to 13. The prognosis is variable.
the severity of atopic dermatitis. 14. The prognosis is good.
d. A non-atopic genetic marker (TNF-a polymorphism) has been identified. 15. Healing is described as crescendo phenomenon.
e. Irritant contact dermatitis is most common in males.
6. Concerning anatomical variability for ICD: With respect to questions 16–19:
a. Data is limited concerning different anatomical sites. a. Delayed acute irritant contact dermatitis
b. Percutaneous penetration varies with anatomical region. b. Irritant reaction
c. The face has been shown to be three times less permeable than the c. Non-erythematous irritation
back. d. Subjective/sensory irritation
d. Studies assessing TEWL after exposure to SLS have been used to assess 16. Refers to irritation that is histologically apparent but the skin looks normal.
the propensity for skin irritation at various skin sites. 17. Refers to sensory discomfort, usually manifest as burning, stinging or itch, in the
e. Lower levels of TEWL were found on the chin and nasolabial areas of absence of clinical or histological evidence of skin lesions.
young adults compared to older people. 18. Refers to clinical ICD approximately 0-24 hours following initial chemical
7. Concerning the role of atopy in ICD: exposure.
a. The role of mucosal atopy is not well defined. 19. Refers to clinical ICD subtype that is associated with wet work and may require
b. There is no significant correlation between atopic diathesis and the devel- repeated exposures.
opment of occupational hand eczema.
c. Persons with atopic dermatitis have increased TEWL. With respect to questions 20–23:
d. Career counselling is considered important. a. Asteatotic ICD
e. Atopy is not considered to be a risk factor for ICD. b. Pustular and acneiform dermatitis ICD
8. Concerning irritant contact dermatitis: c. Frictional dermatitis ICD
a. Pathogenesis is entirely non-immunological. d. Traumatic ICD
b. T lymphocytes entering the irritated area do not express cutaneous lym- 20. Characterized by incomplete healing of the original insult followed by nummular
phocyte association (CLA) antigen. eczema-like lesions.
c. Cutaneous lymphocyte association is important in skin homing for T lym- 21. May result from exposure to metals, tars, oils, chlorinated agents, naphthalene
phocytes recruited to the local inflammatory site. and cosmetics.
d. There are specific cytokines that clearly distinguish allergic from irritant 22. Typical pattern of elderly patients who shower without adequate use of moistur-
contact reactions. izing creams, especially with environmental conditions of low humidity.
e. Keratinocytes have a major role in the production of immunological 23. Refers to shearing forces to the skin inducing eczematous change.
response to irritants.
9. Regarding ICD: The answers for the questions published in Vol. 48, No. 4, are as follows:
a. There is a reluctance amongst clinicians to diagnose ICD, for which no 1. a, b, c, d, e 7. a, b, c, d, e 13. a 19. d
routine clinical test exists. 2. a, c, d, e 8. c, d 14. c 20. a
b. The clinical picture may be indistinguishable from allergic contact der- 3. a, b, c 9. a, b 15. b 21. c
matitis (ACD). 4. a, d 10. a, b, c, d, e 16. a 22. d
c. Irritant contact dermatitis may be just one of several contributing factors 5. a, c, e 11. a, b, c, d, e 17. c 23. b
to occupational dermatitis. 6. c, d 12. c 18. b

© 2008 The Australasian College of Dermatologists

 Irritant contact dermatitis 11

The Australasian College of Dermatologists

Professional Development Program

Category B
Australasian Journal of Dermatology
Volume 49, No. 1, 2008

Name: . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . PDP No.: . . . . . . . . . . . . . . . . . . . . .

State:. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Questions 1–11 Questions 12–23

Circle the most appropriate answers — multiple Circle the correct answer.
answers possible. Each question must have all
correct answers circled in order to receive points.

1. A B C D E 12. A B C D

2. A B C D E 13. A B C D

3. A B C D E 14. A B C D

4. A B C D E 15. A B C D

5. A B C D E 16. A B C D

6. A B C D E 17. A B C D

7. A B C D E 18. A B C D

8. A B C D E 19. A B C D

9. A B C D E 20. A B C D

10. A B C D E 21. A B C D

11. A B C D E 22. A B C D

23. A B C D
Pass Mark: 75% (if you obtain this mark or higher you will be granted 1.5 hours Category B PDP credit).

If you feel the need to indicate ambiguity in a question, please do not write comments on the answer sheet.

Please return your answer sheet to College by

1 April 2008. Answer sheets received after
this date will not be accepted.

© 2008 The Australasian College of Dermatologists