Clinics in Dermatology (2011) 29, 3136

Dry skin, barrier function, and irritant contact dermatitis in

the elderly
Florian Seyfarth, MD , Sibylle Schliemann, MD, Dimitar Antonov, MD, Peter Elsner, MD
Department of Dermatology and Dermatological Allergology, Universittsklinikum Jena, Erfurter Strasse 35,
07743 Jena, Germany

Abstract Dry skin is characterized by a decreased lipid content and a delayed reconstitution of the
epidermal barrier after skin irritation. These are problems of high relevance in the aged population,
especially in the development of irritant contact dermatitis. Asteatotic and perineal irritant dermatitis are
the most important subtypes of irritant contact dermatitis in the elderly. This contribution presents a
compressed survey on these subtypes and elucidates their relation to an impaired barrier function.
Typical irritants affecting aged individuals are explained and compared with irritants that seem to be
more significant in younger people. Results of biophysical investigations, such as measurement of
transepidermal water loss, are discussed regarding their age-dependence. Transepidermal water loss
decreases with age, which was formerly interpreted as an indication of a decreased sensitivity. Today,
we know that reconstitution of the epidermal barrier after irritation is delayed once it has been impaired.
Reasons are decreased activities of enzymes involved in lipid synthesis and processing, a changed
cytokine profile, a reduced acidification of aged skin, and alterations in the function of epidermal stem
cells. Owing to these new insights, a reevaluation of the sensitivity of aged skin has to be initiated,
especially with regard to occupational dermatology.
2011 Elsevier Inc. All rights reserved.

Introduction: dry skin in the focus of irritant

contact dermatitis
Clinical experience has shown that elderly people more
often suffer from dry skin than young, healthy individuals.
This fact is explained by an alteration of the lipid barrier in
older people.1 Electron microscopic analysis revealed a
decreased number of lamellar bodies in the stratum granulosumstratum corneum interface of the elderly, as well as a
reduced lipid content in the mouse model. After irritation of the
epidermal barrier, aged skin needs more time for regenera Corresponding author. Tel.: +49 0 3641 937 398.
E-mail address: florian.seyfarth@med.uni-jena.de (F. Seyfarth).
0738-081X/$ see front matter 2011 Elsevier Inc. All rights reserved.
doi:10.1016/j.clindermatol.2010.07.004

tion,2 which is one important step in the development of

irritant contact dermatitis (ICD) in old individuals.
The classic type of senile ICD is asteatotic irritant
dermatitis (synonyms: exsiccation eczematoid, winter dermatitis, or eczema craquel),3 which is mostly diagnosed
during the winter due to decreased humidity in the air.4
Another contributing factor is inappropriate application of
personal care products, such as extensive usage of soaps and
cleansing products, frequent bathing and showering, especially with water that is too hot, which is assumed to be a
common problem in older people.5 The practice of intensive
washing, learned in the youth, may aggravate this condition
if not adjusted to the special properties of the aged skin,
including decreased stratum corneum hydration and decreased levels of stratum corneum lipids and ceramides.6-8

32

F. Seyfarth et al.

Patients with asteatotic irritant dermatitis show dry skin

with ichthyosiform scaling and fissuring, especially on the
extremities. Transepidermal water loss (TEWL) and pH may
be increased9 and the keratinosomes disturbed.10 The most
disturbing symptom for the patients is intensive itching; thus,
this disease has to be considered as a differential diagnosis in
patients with pruritus senilis (Table 1).11 Xerosis cutis,
induced by 3-hydroxy-3 methyl-glutaryl-coenzyme A (HMG
CoA) reductase inhibitors, mimics asteatotic irritant dermatitis.12 Other forms of ICD are summarized in Table 1, but these
subtypes are not strictly linked to an old age (Table 2).13-28
Important chemical irritants, arranged in order of
frequency, are detergents (eg, soap), solvents, oil, dusts
and fiber, and acids and alkalis. Important physical irritants
are heat, sweat, friction, pressure, vibration, ultraviolet (UV)
irradiation, and occlusion.29 Occlusion increases the signs of
inflammation, pH, TEWL, stratum corneum hydration, skin
surface temperature, and skin permeability.30 In contrast,
lipid organization and metabolism, as well as cellular
function (eg, DNA synthesis, mitosis), are inhibited.30
Other common exogenous factors of irritation are temperature31 and climatic conditions, especially dry air.32,33
The recent investigations on the immune response to
irritants led to a more complex view of ICD.29 Exposure to
irritants causes an unspecific impairment of keratinocytes15,29 and leads to the expression of integrin receptors
and intercellular adhesion molecule 1. 34-36 Enhanced
production of interleukin (IL)-6, IL-8, IL-2, tumor necrosis
factor-, granulocyte macrophage colony-stimulating factor, and IL-1 follows. 37,38 Interestingly, the same
cytokines that are found in allergic contact dermatitis
(ACD) are also detected in ICD. 39-43 Activation of
chemokine (C-C motif) ligand 2, a chemokine of lymphatic
tissues, was also described.44
Recommended measures for the treatment of ICD include
avoidance of irritation, application of topical corticosteroids,
moisturizers, rich oil-based creams, use cold compresses and
cold water for washing, UV radiation, and training programs.15,45 ICD therefore has to be differentiated from ACD,

Table 1

Reasons for pruritus in aged persons11

Pruritus
Xerosis cutis/asteatotic irritant contact dermatitis
Diabetes mellitus
Hepatic and biliary diseases
Nephrologic diseases
Iron deficiency
Drugs
Neoplastic diseases (lymphomas/leukemia, etc.)
Polycythemia
Hypothyreosis, hyperthyreosis
Dermatitis herpetiformis
Psychogenous
Parasite infestation

Table 2 Subtypes of irritant contact dermatitis without

asteatotic irritant contact dermatitis
Subtype

Characteristics

Most common type,13 special relevance in

occupational dermatology (young adults)14
Caused by repetitive irritation of the skin
over years15
Clinical picture: dryness, erythema,
lichenification, hyperkeratosis (xerotic
dermatitis)16
Poor prognosis17
Post-occupational Persistent ICD despite changing the place
dermatitis
of work18,19
Non-erythematous Pathologic skin-physiologic parameters
ICD
without any visible inflammation13,20
Typical irritants: cocamidopropyl betaine,
coconut diethanolamine21
Irritant reaction
Few clinical signs (eg, dryness, scaling,
redness, vesicles, pustules, and erosions)22
Mostly appears after a period of intense
contact with water, especially in young
professionals
Acute ICD
Develops within minutes or hours after
accidental contact to potent irritants
Symptoms: burning, itching, algesia,
formation of erythema, edema, bullae, or
necrosis
Good prognosis
Delayed acute
Symptoms identical to acute ICD
ICD
Delayed clinical course (inflammation
visible not before 8 to 24 hours after
contact with the irritant)23
Typical irritants: anthralin,24
benzalkonium chloride,25 tretinoin,
tetraethylene glycol diacrylate26
Traumatic ICD
Develops after trauma-like burns or
severe acute ICD
Symptoms: erythema, vesicles/
papulovesicles, scaling
Pustular
Causative irritants: metals, tars, oils,
dermatitis
chlorinated agents, naphthalene24
Sensory irritation Symptoms: stinging, burning, tightness,
itching, or painful sensations after contact
with cosmetic products
Mostly diagnosed in middle-aged, white
and Asian women27
Less frequent in aged people (lower
content of nerve fibers in aged skin)28
Cumulative ICD

ICD, irritant contact dermatitis.

which is difficult, because both diseases show a similar

histopathologic and immunohistochemical pattern.46-48
Thus, for the differentiation of ICD from ACD, one has to
rely on the case history and exposure data, patch test results,
and the location of the dermatitis. In the elderly, ICD as well
as ACD are often found on the hands and in the perineal

Dry skin, barrier function, dermatitis

region in older incontinent patients. Perineal or incontinence
dermatitis30 is typical for older individuals and is mostly
related to urinary or fecal incontinence, or both.49 The
clinical picture is characterized by an initially mild and
sometimes pruritic erythema, which becomes complicated
by the development of small vesicles and erosions, with a
tendency to superinfection (Staphylococcus aureus, candidiasis, tinea).30,50 In severe cases, pressure ulcers develop.
Depending on the type of incontinence, the disease begins
in the perianal (fecal incontinence) or vulvar region (urine
incontinence),30 which is more easily irritated and permeable than the skin from other body areas.51 Perineal ICD is
related to typical irritants, primarily to urine or stool as
chemical irritants.
Urine as a cause of a humid environment under occlusive
conditions in the perineal region is an equivalent to wet
work in the younger patient who has to wear gloves
permanently on his or her hands, which may provoke ICD
of the hands. In addition, urine ammonia concentration
increases due to bacterial digestion, which causes a skin pH
increase to 8. Thus, synthesis of lipid barrier components
and keratinization is inhibited, and the repair functions of
the skin are impaired.50 Relevant irritants in feces are
lipases and proteases. Occlusive irritation tests with fecal
enzymes and different bile mixtures on dorsal skin of
individuals aged between 21 and 66 years revealed severe
skin erythema and epidermal barrier disruption after 21 days
of repetitive exposition.52
Specific endogenous factors in the aged people are
important in the pathogenesis of perineal ICD; for example,
lower immune function, inadequate care, impaired cognition,
and decreased mobility.30 Vulvar skin in aged women is
characterized by a decrease of vaginal secretion, 53 a
reduction of lubrication, and a higher susceptibility to
infective agents (eg, enteric organisms).54 Contrary to the
statement that aged vulvar skin is intrinsically less hydrated,
less elastic, more permeable, and more susceptible to
irritation,53 no significant differences accrued from skin
physiologic studies (water barrier function, friction coefficient) of vulvar skin from premenopausal and postmenopausal women.55 Vaginal dryness is present in 47% of
postmenopausal women, 56 which is interpreted as a
manifestation of atrophic vulvovaginitis.57 This disease is
characterized by dryness, itching, and dyspareunia and
depends on and is due to low estrogen levels that cause
vaginal atrophy, an increase of pH, and a higher susceptibility to microbial pathogens.57

Pathophysiology of the epidermal barrier

The drier skin of the aged population is reflected by an
age-dependent decrease of TEWL, which is linked to
damage of the stratum corneum lipid barrier and a
consecutive loss of corneocyte cohesion.2 Because TEWL

33
is used as a marker for irritation and epidermal barrier
disruption, a lower irritability of aged skin was suggested.
The TEWL was shown to decline in aged patients
(median age, 65 years) with dry skin compared with a
younger control group (median age, 29 years), whereas
hydration showed no significant differences between the
groups.9 This was confirmed in another study58 that revealed
a lower TEWL increase and attenuated patch test results
(visual score) after irritation with sodium lauryl sulfate
(SLS) in the elderly.
Comparative patch testing with SLS in an older (50 to 70
years) and a younger (20 to 40 years) age group revealed a
generally lower baseline TEWL level before exposure in the
old age group. After acute irritation, twice as many older
persons showed no erythema compared with the young
group, which presented more intense clinical signs and a
more increased TEWL after irritation.2 When SLS irritation
was stopped, TEWL decreased faster to normal values in
younger persons, suggesting faster barrier recovery in this
age group.
Another study compared the skin reactivity to SLS
irritation on the forearms of premenopausal and postmenopausal women.59 The older group showed a slower and less
intense reaction than the younger women (visual score,
TEWL). Croton oil (but not thymo quinone and crotonaldehyde) was less irritating in aged skin, too.60
An age-dependence of irritation is only be seen if very
young people are compared with very old people. Within the
subgroup of adults younger than 50, there is no correlation
between age and severity of irritation. 61,62 Children,
however, are more susceptible to irritation.58,63 For example,
irritation after exposure to dimethyl sulfoxide and SLS is
more intense in children,22,58 whereas older people show a
milder but persistent skin reaction.64
Most of the studies presented here draw their conclusions
from SLS exposure and determination of the TEWL, which
may be subject to critique. It is unclear to what extent SLS
irritability reflects irritability in general, and some authors
consider that the TEWL decrease in aged skin does not
reflect less irritability.9 This effect is attributed to a generally
decreased hydration of the aged skin,65,66 possibly due to
decreased ceramide levels.2 Other studies could not confirm
decreased water content due to age.55,58,67-69 The decreased
TEWL in the older skin has been interpreted as a result of
reduced sweating rates, decreased microcirculation, and
decreased temperature in old individuals.1 The authors use
the observation of altered drug permeability in aged skin
(water soluble dyes like fluorescin: increased permeability,
lipid soluble drugs like testosterone: decreased permeability)
to explain the alteration of the lipid barrier in old people,1
with a decreased number of lamellar bodies in the stratum
granulosum-stratum corneum interface. In addition, tapestripping experiments resulted in a faster occurring TEWL
increase in old participants than in young participants.
Finally, the time needed for normalization of TEWL after
acetone exposure was longer in older test persons. The

34
authors concluded that the aged epidermal permeability
barrier is both easier to perturb and slower to repair.1
Investigations in recent years have provided some
information about the influence of age on the regulation of
the epidermal barrier after disruption.70 Different biochemical pathways have been elucidated that are enhanced after
barrier disruption and affect its stabilization.
The epidermal barrier is represented mainly by the
hydrophobic stratum corneum lipid structures, comprising
very-long-chain saturated fatty acids, cholesterol and
ceramides in equimolar proportion, and the upper layer of
nucleated keratinocytes. Lipid synthesis and the proliferation of keratinocytes are enhanced after activation of the
IL-1 cascade due to barrier disruption, which is
accompanied by an increase in IL-1 receptor type 2 (IL1R2) and the IL-1 receptor antagonist (IL-1ra).71 Interestingly, the concentrations of IL-1, IL-1R2, and IL-1ra in
old mice show a reduced increase after irritation compared
with young mice. Moreover, aged IL-1 knock-out mice
show a notably impaired barrier reconstitution compared
with wild-type mice.71
Another important molecule more expressed after barrier
disruption is the transcription factor sterol regulatory
element-binding protein 2 (SREBP2), which induces expression of HMG CoA reductase and acetyl CoA carboxylase.
Both enzymes play a key role in the synthesis of long-chain
fatty acids and cholesterol and, thus, in barrier recovery. The
expression of the enzyme serine palmitoyl transferase is
directly enhanced by barrier disruption and facilitates
synthesis of ceramides, which in turn stimulate proliferation
of keratinocytes.
Levels of all three enzymes for lipid synthesis are lower in
the aged skin, supporting the thesis of a reduced barrier
recovery with age. Recovery of the epidermal barrier is also
linked to the acidic-dependent lipid hydrolases -glucocerebrosidase and sphingomyelinase, which are also involved in
lipid processing. When the pH increases, both enzymes
become inactive, compromising permeability barrier homeostasis. High pH activates serine proteases, but on the other
hand, degrades corneodesmosomes. Skin acidity depends on
exogenous factors (eg, detergent abuse) and endogenous
mechanisms (Na+/H+ antiporters, secretory phospholipase
A2 enzymes).72 In addition, there is an age-dependent
increase of pH in humans and mice: reacidification with
lacto bionic acid accelerated barrier recovery in old
individuals and led to increased formation of fully processed
lamellar membranes.72
Another interesting approach for understanding the
increased sensitivity in aged skin is the observation of
altered function of the epidermal stem cells. A recent study
investigated the percentages of stem cells and their cell cycle
kinetics in the skin of young and aged mice.73 The authors
could not detect any significant difference in the numbers of
stem cells in either age class; however, the numbers of socalled transit-amplifying cells were increased in aged skin.
These cells are direct descendants of the stem cells. They do

F. Seyfarth et al.
not show the phenotype of completely differentiated
corneocytes and are thus functionally incomplete.
Furthermore, the authors detected a prolonged cell cycle
and decreased proliferative ability of stem cells and transitamplifying cells from aged individuals. When injected into
the skin of mice, they produced less keratinocyte clusters
with basaloid features compared with transit-amplifying cells
from young individuals. Thus, the high frequency of transitamplifying cells in aged skin was interpreted as a
compensatory mechanism.

Implications for occupational dermatology in

the elderly
Studies in occupational dermatology emphasize wet work
as a crucial factor for the development of ICD. Wet work is
thereby characterized by a repetitive exposure to water and
detergents, especially under occlusive conditions. When
under occlusion, water increases erythema, pH, the cutaneous blood flow, TEWL, and the permeability to lowmolecular-weight irritants.30 The frictional coefficient as a
predictor of skin vulnerability increases as well.
Our knowledge about the influence of age on occupational hand dermatitis is limited because there are generally
few epidemiologic data available concerning occupational
dermatology.74 The influence of age may therefore be
underestimated, which is problematic, especially within the
scope of an aging society and an increasing proportion of
aged workers; however, age-adapted training programs for
secondary and tertiary prevention of occupational ICD are
still missing.
In general, the incidences of hand ICD and atopic hand
dermatitis are assumed to be higher than ACD, whereas
nonoccupational hand dermatitis is more frequent than
occupational ICD.75-77 The estimated point prevalence of
hand dermatitis in Sweden in 1990 was 5.4%, comprising
35% ICD, 19% ACD, and 22% atopic dermatitis. Risk
factors by multiple logistic regression analysis were a history
of childhood dermatitis, female sex, occupational exposure, a
history of asthma or hayfever, and a service occupation.76
The person's age was not considered to have an influence.
The few epidemiologic data concerning age are ambiguous. Some authors detected a decrease in the quality of life,
especially in older patients with occupational hand dermatitis.78 Although previous studies point out a positive
correlation between age and the development of occupational ICD,79,80 recent investigations emphasize that neither sex
nor age are risk factors for the manifestation of this disease.74
Thus, conditions at the workplace together with disposition,
such as atopic skin diathesis, and xerosis cutis are the leading
risk factors.74 Another study dealt with the mean age of
employees at the onset of their occupational skin diseases.14
According to these data, occupational dermatitis is not a
disease of aged employees. Most patients are young when

Dry skin, barrier function, dermatitis

the disease begins; for example, haircutter, 19 years; food
worker, 22 years; medical personal, 24 years; and metal
worker, 33 years,14 In contrast, the mean age of construction
and cement workers with occupational ICD is relatively
high, at about 39 years.81,82

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