Fig. 6.1
Irritant contact dermatitis in the web spaces, the dorsal surfaces of the fingers and back of the hand
6.3 Main Groups of Irritants
ICD is induced by direct contact of the skin with liquids, pastes and solids, including contact between aerosols, gases and vapors and the skin. Exposures to irritants that give rise to hand eczema are listed in Table 6.1.
Table 6.1
Main groups of irritants
Chemical irritants | Physical irritants | Other |
---|---|---|
Acids (also from fruit) | Mechanical | Water |
Alkaline substances | Friction | Climate: cold |
Cement/lime | Pressure | Environmental condition: low relative humidity |
Cooling lubricants | Heat | |
Oil products, including cutting oils | Dusts | |
Organic solvents (benzene, acetone) | Occlusion (gloves) | |
Detergents | Mineral and glass fibers | |
Sand | ||
UV radiation | ||
Ionizing radiation | ||
Wool |
Wet work is an important stressor for the skin and plays a prominent role in the majority of ICD cases. Activities during which workers spend a considerable portion of their working time in a wet work environment or wear liquid-tight gloves or wash their hands frequently or intensively count as wet work. Although gloves protect the skin from contact with allergens and irritants, the occlusion of the skin caused by the glove itself is a risk factor for hand eczema [3, 4]. The liquid-tight effect of protective gloves prevents the dissipation of perspiration to the outside; subsequently, the skin swells up as the time the gloves are worn increases, which reduces the barrier effect. Fartasch et al. investigated the differences between water exposure and occlusion by gloves in an experimental setting on forearm skin [3]. They demonstrated that short occlusion seems to harm the skin less than water exposure for the same time. However, their experiments were performed on forearm skin which indicates that the results may have been different when performed on the hands, in which occlusion of gloves may cause more perspiration due to abundant eccrine sweat glands on the palmar surfaces.
When the skin is pre-damaged by irritants or liquid-tight gloves, it becomes easier for irritants, potentially allergenic substances or infectious agents to penetrate [5]. In the case of combinations of irritative conditions, the damage to the skin is more than the separate effects, e.g., the harmful effect of soap is increased if it is followed by the use of liquid-tight gloves. Fartasch et al. demonstrated that previous occlusion and water exposure were capable of inducing higher susceptibility to sodium lauryl sulfate (SLS) irritation [3].
6.4 Risk Factors and Skin Barrier Dysfunction
The cause of hand eczema is often multifactorial. In addition to exogenous risk factors, there are endogenous risk factors that influence the development of ICD. A current or previous history of atopic dermatitis (AD) increases the risk for ICD [6, 7]. However, among individuals with atopic dermatitis who are exposed to irritants, it is difficult to distinguish between atopic hand eczema and hand eczema as a manifestation of ICD. Patients with AD have an impaired skin barrier, also in uninvolved skin, which was demonstrated by a higher penetration of SLS [8]. However, individuals without a history of atopic dermatitis may also have an increased susceptibility to irritants. Tupker et al. [9] investigated the susceptibility of the skin to various irritants, among other SLS, in individuals with a history of AD, individuals with a dry skin, and in individuals with clinically normal skin. In those with a previous history of AD, the transepidermal water loss values were both preexposure and throughout the entire period of exposure, higher than in the other groups. Though also individuals with clinically dry skin, without a history of AD, appeared to be more susceptible to irritants than those with normal skin, there was no difference noted in the preexposure barrier function.
The uppermost layer of the skin, the stratum corneum, acts as a barrier that prevents the entry of external irritants, microbes and allergens and controls the transcutaneous movement of water. An impaired skin barrier function in AD can partly be explained by a reduction or absence of the protein filaggrin in the skin. The filaggrin gene (FLG) encodes the protein profilaggrine, a major component of the keratohyalin granules in the stratum granulosum of the epidermis. During the later stages of epidermal differentiation, profilaggrine is dephosphorylated and cleaved to form filaggrin monomers, which contribute to the cornified cell envelope [10]. The filaggrin monomers are further proteolyzed, contributing to the natural moisturizing factor of the stratum corneum, and playing a central role in the hydration of the stratum corneum. Loss-of-function mutations in the FLG result in either a reduction or complete absence of epidermal filaggrin and its degradation products [11]. These mutations are predisposing factors for AD and are carried by 15–55 % of the patients with AD in European populations [12–14]. However, epidermal filaggrin and its degradation products are influenced not only by the filaggrin genotype but also by inflammation and exogenous stressors [11]. Filaggrin deficiency is observed in patients with AD regardless of filaggrin mutation status [11].
De Jongh et al. [7] demonstrated an increased risk for the development of ICD in individuals with FLG mutations. However, this association appeared to be dependent on the presence of a history of AD. In one study, a small, but significant association between ICD and FLG mutations persisted after adjustment for the history AD [11]. Both a history of AD and FLG mutations contribute to the development of ICD. More research into the skin barrier function in patients with AD and patients with FLG mutations is warranted to investigate the role of the different predisposing stimuli in the development of ICD.
6.5 How to Make the Diagnosis
The morphology and distribution of eczema are of limited help in making the diagnosis, and specific tests for ICD are not available. Allergic contact dermatitis and contact urticaria/protein contact dermatitis should be excluded as contributory causes, since combinations of irritant and allergic cases are common. Therefore, diagnostic patch testing should be performed in all patients with hand eczema with duration of more than 3 months and/or relapse, to identify the role of contact allergens [1]. Hand eczema patients reporting immediate skin reactions may have protein contact dermatitis. This is a distinct form of allergic or irritant hand eczema in which IgE-mediated mechanisms or nonimmunological mechanisms give rise to clinical manifestations characterized by an initial urticarial phase followed by eczema [1]. Triggers are natural rubber latex, food allergens or certain animal proteins. Skin prick testing or serum radioallergosorbent (RAST) testing should be performed to assess these reactions. However, nonimmunological types also exist [1]. See also Chap. 8 on protein contact dermatitis.
A history of hand eczema or AD provides important information on risk factors to develop ICD. Determination of allergen-specific IgE levels can help to establish the atopy status, though is not routinely recommended.
The diagnosis of ICD is based on a documented exposure to an irritant that is quantitatively likely to cause contact dermatitis [1]. A careful history about occupational and nonoccupational exposure to irritants is necessary. Occupational information should be obtained about accidents, new products or defective machinery. Environmental conditions such as changes in season, temperature and humidity and the influence on the contact dermatitis should be obtained. Questioning about the conditions of exposure is crucial to find the offending agents. Information about preceding or concomitant exposure is important if more than one product is involved. Detailed information on chemicals, products and materials should be traced. In case there are suspected materials or products from patient’s work environment, material data safety sheets and lists of ingredients should be examined carefully for information about the product, the ingredients, concentrations, etc. [15].
It is important to estimate the duration of the exposures to irritants at the workplace, at home and during leisure activities. In addition, it is important to have insight into the frequency of exposure, whether it is a single exposure or a repeated exposure. Working procedures should be reviewed in order to quantify exposure to irritants. A well-defined exposure to irritants likely to cause ICD is wet work. TRGS 401 is the only existing guideline to regulate exposure to wet work [5]. Criteria for wet work include wet hands or wearing of liquid-proof gloves for 2 h or more per day or more than 20 handwashes daily. This limit of 2 h should be included in the quantification of exposure to irritants to make the diagnosis of ICD. The only correct method to measure wet work seems to be observation since questionnaires appeared not reliable in a study [16]. In Table 6.2, a work-up for a consultation of a patient with ICD is presented. Actually, the work-up is suitable for hand eczema in general. However, some parts such as the extensive, detailed history regarding exposure are important if ICD is suspected.
Table 6.2
Work-up consultation of a patient with hand eczema in general, with specific focus on exposure to irritants and recommendation on various gloves