Irritant Contact Dermatitis
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Contact dermatitis is an acute or chronic skin inflammation caused by cutaneous interaction with a chemical, biologic, or physical agent. Contact dermatitis after a single exposure or multiple exposures may be irritant or allergenic—clinically it may be difficult to differentiate between these processes. Irritant contact dermatitis (ICD) is caused by direct tissue damage following a single exposure or multiple exposures to a known irritant. By contrast, in allergic contact dermatitis, tissue damage by allergic substances is mediated through immunologic mechanisms. A complete history related to exposures at home, the workplace, and in recreational activities is essential to making the diagnosis and identifying the causative agent. Acutely, eczematous or nonspecific dermatitis is the most common clinical expression of this induced inflammation. The severity of the dermatitis ranges from a mild, short-lived condition to a severe, persistent, job-threatening, and possibly life-threatening disease. Treatment of both irritant contact dermatitis and allergic contact dermatitis begins with removal of the offending substance(s).
The American Academy of Allergy, Asthma & Immunology and the American College of Allergy, Asthma & Immunology published updated clinical practice guidelines on contact dermatitis in 2015. [1] Recommendations pertaining specifically to irritant contact dermatitis are briefly summarized in the Guidelines section.
Irritant contact dermatitis (ICD) is a nonspecific, nonallergic response of the skin to direct chemical damage from a corrosive agent that releases mediators of inflammation predominantly from epidermal cells. Irritant contact dermatitis can be acute or chronic. Irritants can be classified as cumulatively toxic (eg, hand soap causing irritant dermatitis in a hospital employee), subtoxic, degenerative, or toxic (eg, hydrofluoric acid exposure at a chemical plant). [2] Acutely, this inflammation is manifested by redness, erythema, mild edema, and scaling. Chronic irritant contact dermatitis presents with lichenification, hyperkeratotic scale, fissures, or ulcerations. Note the image below.
The hands are the most important sites of irritant contact dermatitis. Irritant contact dermatitis from repeated workplace exposure of the hands to soaps, cleansers, and solvents is the source of most occupational skin disorders.
Although it is much more common, irritant contact dermatitis remains understudied compared with allergic contact dermatitis. Most articles on contact dermatitis concern allergic contact dermatitis. This largely reflects the fact that with history and patch testing, a specific hypersensitivity and a probable cause of dermatitis can be identified in most cases of allergic contact dermatitis.
No reliable diagnostic test exists for irritant contact dermatitis. The diagnosis rests on the exclusion of other cutaneous diseases (especially allergic contact dermatitis) and on the clinical appearance of dermatitis at a site sufficiently exposed to a known cutaneous irritant. Laboratory studies may be of value in eliminating some disorders from the differential diagnosis. (See Workup).
The definitive treatment of irritant contact dermatitis is the identification and removal of any potential causal agents. For hand irritant contact dermatitis, advise individuals to use ceramide-containing creams or bland emollients after washing hands with soap and before sleep. (See Treatment.)
Although the term hypoallergenic is used widely in the marketing of consumer products, no Food and Drug Administration (FDA)–approved definition of “hypoallergenic” exists. Individuals with susceptible skin (eg, atopic dermatitis, facial skin of individuals with rosacea) would benefit greatly from hypoirritating cleansers, cosmetics, moisturizers, and protectants, but there is no standard method for identifying such products.
Go to Allergic Contact Dermatitis, Pediatric Contact Dermatitis, and Protein Contact Dermatitis for complete information on these topics.
Irritant contact dermatitis (ICD) is the clinical result of sufficient inflammation arising from the release of proinflammatory cytokines from skin cells (principally keratinocytes), usually in response to chemical stimuli. Irritant contact dermatitis arises as a result of activated innate immunity without prior sensitization, which differentiates it from allergic contact dermatitis. Different clinical forms may arise. The three main pathophysiological changes are skin barrier disruption, epidermal cellular changes, and cytokine release. [3]
With sufficient concentration or duration of exposures, a wide range of chemicals can act as cutaneous irritants. Common cutaneous irritants include solvents, microtrauma, and mechanical irritants.
Cumulative irritant contact dermatitis from repeated mild skin irritation from soap and water is common. For example, hand-washing frequency of more than 35 times per shift was associated strongly with occupational hand dermatitis in intensive care unit workers (odds ratio = 4.13). Similarly, most cases of “homemaker’s” eczema are irritant contact dermatitis resulting from repeated skin exposure to low-grade cutaneous irritants, particularly soaps, water, and detergents.
Solvents cause cutaneous irritation because they remove essential fats and oils from the skin, which increases transepidermal water loss and renders the skin susceptible to the increased direct toxic effects of other previously well-tolerated cutaneous exposures. The alcohol propanol is less irritating to the skin than the detergent sodium lauryl sulfate.
p Ka, an acid dissociation constant, is a quantitative measure of the strength of an acid in solution. p Ka has been shown to be highly predictive of acute skin irritation for acids and bases: acids with a p Ka of less than 4 and bases with a p Ka of less than 8 are highly irritative. [4]
Microtrauma may produce skin irritation. A common example is fiberglass, which may produce pruritus with minimal visible inflammation in susceptible individuals. Many plant leaves and stems bear small spicules and barbs that produce direct skin trauma.
Physical irritants (eg, friction, abrasive grains, occlusion) and detergents such as sodium lauryl sulfate produce more irritant contact dermatitis in combination than singly. [5] Propanol and sodium lauryl sulfate are not additive irritants, however.
Skin irritation predisposes the skin to develop sensitization to topical agents. Skin irritation by both nonallergenic and allergenic compounds induces Langerhans cell migration and maturation. [6] An exacerbation of irritant contact dermatitis may reflect development of allergic contact dermatitis to topical creams, medications, or rubber gloves.
The pathogenesis of irritant contact dermatitis involves resident epidermal cells, dermal fibroblasts, endothelial cells, and various leukocytes interacting with each other under the control of a network of cytokines and lipid mediators. Keratinocytes play an important role in the initiation and perpetuation of skin inflammatory reactions through the release of and responses to cytokines. Resting keratinocytes produce some cytokines constitutively.
A variety of environmental stimuli (eg, ultraviolet light, chemical agents) can induce epidermal keratinocytes to release the following cytokines [3] :
Inflammatory cytokines (interleukin 1, tumor necrosis factor-alpha)
Chemotactic cytokines (interleukin 8, interleukin 10)
Growth-promoting cytokines (interleukin 6, interleukin 7, interleukin 15, granulocyte-macrophage colony-stimulating factor, transforming growth factor–alpha)
Cytokines regulating humoral versus cellular immunity (interleukin 10, interleukin 12, interleukin 18)
Intercellular adhesion molecule 1 promotes the infiltration of leukocytes into the epidermis in cutaneous inflammatory reactions, including irritant contact dermatitis.
Significantly increased numbers of dividing keratinocytes are present 48 and 96 hours after exposure to the anionic emulsifying agent sodium lauryl sulfate (used in shampoos, skin cleansers, acne treatments, and toothpastes and in laboratories as an experimental irritant). However, Heinemann et al found that repeated occlusive application of 0.5% sodium lauryl sulfate over 3 weeks often resulted in adaptation (the so-called hardening phenomenon), with an increase in ceramide 1 in the lipid composition of the stratum corneum. [7]
All irritants provoke a similar pattern of cellular infiltration in the dermis; the densities of most of the cell types rise in proportion to the intensity of inflammation. Within the epidermis, marked differences exist in the patterns of cellular infiltration among different irritants.
Individuals with a history of atopic dermatitis are prone to develop irritant contact dermatitis of the hands. Polymorphisms in the filaggrin (FLG) gene, which result in loss of filaggrin production, may alter the skin barrier and are a predisposing factor for atopic dermatitis. FLG null alleles are associated with increased susceptibility to chronic irritant contact dermatitis. [8, 9]
Almost any material may be a cutaneous irritant, if the exposure is sufficiently prolonged and/or the concentration of the substance sufficiently high. The likelihood of developing irritant contact dermatitis (ICD) increases with the duration and intensity of exposure to the irritant. [2] Environmental factors may enhance the effect of other irritants. [10, 11, 12]
Dry air renders the skin more susceptible to cutaneous irritants. Sufficiently dry air alone may provoke irritant contact dermatitis. Most cases of winter itch are a result of dry skin from the drier air found during sustained periods of cold weather.
An increase in temperature (up to 43°C from 20°C) increases the cutaneous effect of an irritant. [13]
Continual exposure to water may produce maceration or repeated evaporation of water from the skin may produce cutaneous irritation by desiccation of the skin. Even distilled water experimentally provokes increased CD11c+ cells and neutrophils in the epidermis.
Many individuals are exposed to solvents, particularly at work. Solvents such as alcohol or xylene remove lipids from the skin, producing direct irritant contact dermatitis and rendering the skin more susceptible to other cutaneous irritants, such as soap and water.
Irritant contact dermatitis from alcohol most often is cumulative. Manual workers may wash their hands inappropriately with solvents to remove oil, grease, paints, or other materials; thus, they develop irritant contact dermatitis.
Inappropriate skin cleansing is a primary cause of irritant contact dermatitis in the workplace. Washing facilities and methods must be inspected when investigating the workplace for 1 or more cases of occupational irritant contact dermatitis. The irritating agents include aromatic, aliphatic, and chlorinated solvents, as well as solvents such as turpentine, alcohol, esters, and ketones. Some organic solvents produce an immediate erythematous reaction on the skin and remove lipids from the stratum corneum.
Neat oils most commonly produce folliculitis and acne. They may cause irritant contact dermatitis (as well as allergic dermatitis). Water-based metalworking fluids often cause irritant contact dermatitis in exposed workers; surfactants in these fluids are the main culprit.
This is common in many occupations that often are termed “wet work.” Healthcare workers wash their hands 20-40 times a day, producing cumulative irritant contact dermatitis. Similar exposures occur among individuals who wash hair repeatedly or in cleaners or kitchen workers.
Multiple skin irritants may be additive or synergistic in their effects. Alcohol-based hand-cleansing gels cause less skin irritation than hand washing and therefore are preferred for hand hygiene from the dermatological point of view. An alcohol-based hand-cleansing gel may even decrease, rather than increase, skin irritation after a hand wash, owing to a mechanical partial elimination of the detergent. [14]
Fiberglass produces direct damage to the skin, usually manifested by pruritus that may result in excoriation and secondary skin damage. Cutaneous irritation primarily is caused by fiberglass with diameters exceeding 4.5 µm.
Most workers with irritant contact dermatitis resulting from fiberglass develop hardening, in which they tolerate further cutaneous exposure to fiberglass.
Many plant leaves and stems bear small spicules and barbs that produce direct skin trauma.
Pressure produces callus formation. Pounding produces petechia or ecchymosis. Sudden trauma or friction produces blistering in the epidermis. Repeated rubbing or scratching produces lichenification. Sweating and friction appear to be the main cause of dermatitis that appears under soccer shin guards in children. [15]
Some rubber gloves may provoke direct cutaneous irritation. Many workers complain of irritation from the powder in rubber gloves.
Remember that gloves compromised by a hole may allow an irritant to enter; occlusion dramatically increases skin damage from the irritant. Occlusion accentuates the effects, good or bad, of topical agents. Kerosene may produce skin changes similar to that of toxic epidermal necrolysis following occluded cutaneous exposure. Excessive amounts of ethylene oxide in surgical sheets also may produce similar changes.
This chemical is found in some topical medications, particularly acne medications, as well as a range of soaps and shampoos. It is also a classic experimental cutaneous irritant.
A hydrofluoric acid burn is a medical emergency. Remember that onset of clinical manifestations may be delayed after the acute exposure (this is crucial to diagnosis). Unfortunately, hydrofluoric acid burns are most frequent on the digits, where the pain is most severe and management is most difficult (see Hydrofluoric Acid Burns).
Skin surfaces normally have an acidic pH, and alkalies (eg, many soaps) produce more irritation than many acids. The “acid mantle” of the stratum corneum seems to be important for both permeability barrier formation and cutaneous antimicrobial defense. Use of skin cleansing agents, especially synthetic detergents with a pH of approximately 5.5 rather than alkaline pH, may help prevent skin disease. [16]
Irritant contact dermatitis (ICD) is common in occupations that involve repeated hand washing or repeated exposure of the skin to water, food materials, and other irritants. High-risk occupations include cleaning, hospital care, food preparation, and hairdressing. [17, 18]
The prevalence of occupational hand dermatitis was found to be 55.6% in two intensive care units and was 69.7% in the most highly exposed workers. Hand-washing frequency of more than 35 times per shift was associated strongly with occupational hand dermatitis. [19]
In some European studies among employees in high-risk occupations, such as hairdressing, healthcare, and metal working, the 1-year prevalence was between 20% and 30%. [9] Specifically, in Denmark, cleaners comprise the greatest number of affected workers, but culinary workers have the highest incidence. A higher proportion of prolonged sick leave is seen among those in food-related occupations compared with those in wet occupations. [20] The incidence rates of contact dermatitis in Germany were 4.5 cases per 10,000 workers for irritant contact dermatitis, compared with 4.1 cases per 10,000 workers for allergic contact dermatitis. The highest irritant contact dermatitis annual incidence rates were found in hairdressers (46.9 cases per 10,000 workers per year), bakers (23.5 cases per 10,000 workers per year), and pastry cooks (16.9 cases per 10,000 workers per year. [21]
Irritant contact dermatitis is significantly more common in women than in men. The high frequency of hand eczema in women in comparison with men is caused by environmental factors, not genetic factors.
Occupational irritant contact dermatitis affects women almost twice as often as men, in contrast to other occupational diseases that predominantly affect men. Women are exposed more highly to cutaneous irritants from their disproportionately greater role in housecleaning and the care of small children at home. In addition, women predominantly perform many occupations at high risk for irritant contact dermatitis (eg, hairdressing, nursing).
Irritant contact dermatitis may occur at any age. Many cases of diaper dermatitis are irritant contact dermatitis resulting from direct skin irritants present in urine and, especially, feces. Older persons have drier and thinner skin that does not tolerate soaps and solvents as well as younger individuals. Occupational hand eczema often is associated with persistent dermatitis and prolonged sick leave, with substantially greater severity among those with occupational irritant contact dermatitis and atopic dermatitis and age older than 50 years.
Prognosis is good for nonatopic individuals in whom irritant contact dermatitis (ICD) is diagnosed and managed promptly. Individuals with atopic dermatitis remain highly susceptible to irritant contact dermatitis and may find that the tasks of many common occupations (eg, nursing, hairdressing) produce too much direct skin inflammation to continue with these careers.
Hardening may be specific to the irritant inducing the hardening phenomenon and does not occur in all persons exposed long term to an irritant. [4] Hardened skin may also have a thickened stratum granulosum, with changes in the expression of various inflammatory mediators and markers. [4] An induction of an increase in the stratum corneum lipid ceramide 1 may play a key role as a protection mechanism against irritation by repeated application of sodium lauryl sulfate. [5, 7]
Activities of daily living and work may be reduced by severe irritant contact dermatitis.
Acute irritant contact dermatitis reactions to potent irritants (eg, acids, alkaline solutions) are comparable to a chemical burn and can be graded like thermal burns (ie, first-, second-, or third-degree burns). With appropriate symptomatic management, the prognosis for this type of irritant contact dermatitis is usually good, and, unless the dermis is damaged, no permanent scarring should occur. See Chemical Burns for more information.
Hydrofluoric acid is a potent cutaneous irritant used in low-technology and high-technology industries and at home in rust removal. [22] Death from hypocalcemia may ensue if as little as 1% of the skin’s surface area is exposed sufficiently to this strong inorganic acid and if complications are not managed optimally (see Hydrofluoric Acid Burns).
Remind individuals that they must continue to avoid cutaneous irritants; they will redevelop or aggravate dermatitis if they continue to have the same skin care exposures that resulted in irritant contact dermatitis (ICD). The possibility of secondary or complicating allergic contact dermatitis or impetigo always must be considered as well.
For patient education information, see the Skin, Hair, and Nails Center, as well as Contact Dermatitis.
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Savina Aneja, MD Dermatologist, Bay Area Dermatology Associates
Disclosure: Nothing to disclose.
Michael J Wells, MD, FAAD Dermatologic/Mohs Surgeon, The Surgery Center at Plano Dermatology
Michael J Wells, MD, FAAD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, Texas Medical Association
Disclosure: Nothing to disclose.
Paul Krusinski, MD Director of Dermatology, Fletcher Allen Health Care; Professor, Department of Internal Medicine, University of Vermont College of Medicine
Paul Krusinski, MD is a member of the following medical societies: American Academy of Dermatology, American College of Physicians, Society for Investigative Dermatology
Disclosure: Nothing to disclose.
William D James, MD Paul R Gross Professor of Dermatology, Vice-Chairman, Residency Program Director, Department of Dermatology, University of Pennsylvania School of Medicine
William D James, MD is a member of the following medical societies: American Academy of Dermatology, Society for Investigative Dermatology
Disclosure: Received income in an amount equal to or greater than $250 from: Elsevier; WebMD.
Daniel J Hogan, MD Clinical Professor of Internal Medicine (Dermatology), Nova Southeastern University College of Osteopathic Medicine; Investigator, Hill Top Research, Florida Research Center
Daniel J Hogan, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Contact Dermatitis Society, Canadian Dermatology Association
Disclosure: Nothing to disclose.
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