Version July 2025
INTRODUCTION —
Allergic contact dermatitis (ACD) is a type 4 delayed-type hypersensitivity reaction to a specific substance in contact with the skin. It is the result of sensitization to an allergen and manifests as a pruritic, refractory, eczematous eruption most commonly in the area of direct contact with the implicated allergen. ACD can also be caused by airborne or systemic (oral, intramuscular, or intravenous) exposure to an allergen.
This topic reviews the clinical features and diagnosis of ACD. The pathophysiology and management of ACD, ACD in children, patch testing, and common allergens causing ACD are discussed separately. An overview of eczematous dermatoses is also discussed separately.
●(See "Basic mechanisms and pathophysiology of allergic contact dermatitis".)
●(See "Management of allergic contact dermatitis in adults".)
●(See "Allergic contact dermatitis in children".)
●(See "Common allergens in allergic contact dermatitis".)
●(See "Patch testing".)
●(See "Overview of dermatitis (eczematous dermatoses)".)
EPIDEMIOLOGY
Prevalence — There are relatively few cohort studies examining the prevalence of contact allergy in the general population. In a Danish cohort study from 2010, 20.1 percent had contact allergy [1]. A meta-analysis from 2019 estimated a prevalence of 21.4 percent [2].
The prevalence of ACD may be decreasing in Europe, possibly due to more stringent regulation of several chemicals (including nickel) in the European Union.
●A Danish cohort study from 1990 to 2006 demonstrated a decrease in the prevalence of positive patch test reactions in the general population from 1990 (15.5 percent) to 2006 (10 percent) [3]. However, patches were only read at day 2, likely undercounting positive reactions. Contact allergy was more common in older females and was found to be decreasing in younger individuals.
●In a Finnish nationwide registry-based study from 1998 to 2021, the prevalence of ACD increased from 1998, reached a peak in 2016, and then decreased [4].
ACD occurs in all age groups and affects females more than males, although both are equally susceptible to developing ACD.
Contact allergy is also reported to be more common in females than males, In the North American Contact Dermatitis Group 2019 to 2020 cycle, nearly three-fourths of all patch-tested patients were female, and 64.2 percent were >40 years old [5].
More female patients have been reported to develop contact dermatitis to personal care products compared with male patients [6]. This may reflect different exposure patterns to certain allergens rather than different sex-related sensitivity to specific allergens.
Risk factors
●Age – ACD can occur in all age groups but is most frequently reported in adults. In studies of patch-tested patients, most are females older than 40 [5]. This may be due to referral bias. A larger proportion of children (age 0 to 17) than adults may seek medical care for eczematous dermatitis despite children being referred for patch testing less frequently than adults [7-9].
●Sex – Several studies report a higher prevalence of contact allergy in females. This has been surmised to be due to the higher number of personal care products and cosmetics used by females compared with males [6]. In contrast, male patients are overrepresented in studies of ACD associated with certain occupational exposures [10-12].
In a large European cross-sectional study of over 3000 patch-tested adults, the prevalence of fragrance allergy was twice as high in females as in males, indicating a higher exposure of females to scented personal care products [13]. However, there is an increasing trend in the number of personal care products used by males [6,14].
●Occupational exposure – In a retrospective analysis of 38,614 patients referred for patch testing, 11.6 percent were found to have occupational-related skin disease [12]. Of those patients, 3150 (70.5 percent) were found to have ACD associated with work. The most common occupational-related allergens were rubber chemicals, preservatives, and epoxy. The most common sites involved by occupational contact dermatitis are the hands, arms, and face.
Occupations known to be associated with ACD include service workers and machine operators. However, ACD has been reported in a wide variety of occupations, including food service workers, painters, agricultural workers, metal workers, machinists, nail technicians, health care workers, cosmetologists, and construction workers [12,15-17].
●Atopic dermatitis – Studies are mixed on whether atopic dermatitis increases the likelihood of development of ACD [18]. In a review of 38,482 patients referred for patch testing in North America, patients with or without a past history of atopic dermatitis had an equal likelihood of being diagnosed with ACD [19]. A similar large cohort study of 46,250 patch-tested patients in Europe showed a slight increase in the prevalence of ACD in patients with a history of atopic dermatitis compared with those without atopic dermatitis (74 versus 71 percent, respectively), although the difference was small and not clinically meaningful [20]. Other studies have shown increased prevalence of contact allergy in children with a history of atopic dermatitis [21]. However, lower rates of patch testing in children with a history of atopic dermatitis may be leading to underdiagnosis of ACD in this population.
PATHOGENESIS —
ACD has three distinct stages: sensitization, elicitation, and resolution. (See "Basic mechanisms and pathophysiology of allergic contact dermatitis".)
●Sensitization – The first stage of ACD is sensitization. Haptens (allergens) are absorbed into the skin, bind with dendritic cells, migrate to lymph nodes, and trigger the development of antigen-specific T cells. These cells then differentiate into T effector and T memory cells and recirculate into the blood and skin. This process can take 10 to 15 days, and patients may not develop any active dermatitis during the sensitization phase [13].
●Elicitation – The elicitation phase occurs upon re-exposure of the skin to the allergen. Again, the antigen binds with dendritic cells and is presented to antigen-specific T cells, triggering a rapid inflammatory cascade with release of numerous proinflammatory cytokines and recruitment of inflammatory cells. This process occurs hours to days after exposure and manifests as a pruritic rash at the site of contact. Dermatitis can last for days to weeks after exposure.
●Resolution – In the resolution phase, T effector cells are replaced with a larger population of T memory cells, ensuring that upon subsequent exposure, the immune reaction to the allergen is of increasing intensity [22]. As a result, patients may report worsening severity of reactions with repeated exposure, likely due to the expanding population of memory T cells in the skin.
COMMON ALLERGENS —
In the United States, urushiol present in poison ivy and other Toxicodendron species is the most common allergen causing ACD, affecting between 10 to 15 million people each year [23]. Approximately 50 to 75 percent of the population is sensitized. Patch testing with urushiol is not routinely performed because of the high risk of eliciting an allergic reaction in previously sensitized patients or inducing sensitization through patch testing [23]. (See "Poison ivy (Toxicodendron) dermatitis".)
The most common allergen identified with patch testing in the general population is nickel, followed by fragrances [24-26]. Other common allergens identified in cohort patch test studies include cobalt, colophony, thimerosal, and paraphenylenediamine [1].
The prevalence of positive reactions to specific allergens in studies of patients referred for patch testing as well as the trends in prevalence of positive patch test reactions vary with geographic location.
●In the United States and Canada, the most common allergens are nickel, methylisothiazolinone, fragrance mix 1, hydroperoxides of linalool, and benzisothiazolinone [5].
●In Europe, nickel is most common, followed by fragrances, preservatives (eg, methylisothiazolinone, formaldehyde, and methyldibromo glutaronitrile), and propolis [27].
●In Japan, nickel, gold, urushiol, paraphenylenediamine, and cobalt are most common [28].
CLINICAL MANIFESTATIONS —
ACD most commonly presents in areas of direct contact with the allergen (direct ACD). The clinical manifestations are similar to those of other types of eczematous dermatitis, including atopic dermatitis, nummular dermatitis, and seborrheic dermatitis.
Direct allergic contact dermatitis — Direct ACD is the most common pattern of ACD. It occurs in the areas of direct contact with the implicated allergen (picture 1 and picture 2). The eruption can be acute or chronic. The dermatitis is reproducible with repeated exposure to the allergen. Patients who have a vigorous ACD may develop dermatitis outside the direct area of contact or develop an "id reaction" (autoeczematization) with widespread involvement.
●Acute ACD – Acute ACD presents with erythematous, scaly, thin, eczematous plaques (picture 3). Lesions may be vesicular or bullous, especially in the setting of ACD to plants. Toxicodendron species, such as poison ivy or poison oak, are a frequent cause of acute ACD and can characteristically trigger diffuse and vigorous eruptions (picture 4). Exposure can occur not just through direct contact with the plant but also through contact with plant oils on objects (such as gardening tools), shoes, and clothing. (See "Poison ivy (Toxicodendron) dermatitis".)
●Chronic ACD – In chronic ACD, the lesions are indurated and scaly. Longstanding ACD may be lichenified (picture 5). Pruritus is a key feature of ACD. Other symptoms may include burning, stinging, redness, swelling, crusting, oozing, and flaking. Less common morphologies include lichenoid, purpuric, urticarial, pseudolymphomatous, and erythema multiforme like.
●Specific sites
•Hands – Patients with ACD on the hands tend to have more involvement of the dorsal hands (picture 6A) rather than the palms; the wrists and volar forearms may also be involved. Involvement of the web spaces or under jewelry can sometimes indicate irritant contact dermatitis due to trapping of moisture. Hand dermatitis with a dyshidrotic pattern has been reported to be caused from systemic nickel exposure as well as preservatives [29-31].
Patients with hand dermatitis are more likely to have occupational-related disease compared with other sites of dermatitis [12]. Allergens known to cause allergic hand dermatitis include metals (nickel, cobalt, chromate), preservatives (formaldehyde, quaternium-15, benzalkonium chloride, methylisothiazolinone), fragrances, bacitracin, and rubber chemicals [32-35].
•Feet – ACD on the feet usually involves the dorsal feet (picture 7 and picture 8) rather than the plantar surface. Footwear and medicaments are common causes. Patients can react to chromate and cobalt, both found in leather products, and a careful occupational history should also be taken, particularly if the patient wears protective work boots. Other implicated allergens include para-tertiary butylphenol formaldehyde resin (a common adhesive used in shoes and other textiles), nickel, fragrances, and medicaments [32].
•Face, eyelids, and neck – Face and eyelid dermatitis can be caused by cosmetics, personal care products, hair care products, airborne allergens (eg, aerosolized chemicals), plants, fragrances, or topical medications (picture 6C and picture 3). Because of the thin nature of eyelid skin, this area can develop dermatitis from products that are used on nearby areas (picture 6D) (see "Eyelid dermatitis"). For example, in patients allergic to ingredients in shampoos or hair dyes, the scalp is not typically involved, and the dermatitis appears along the hairline, forehead, eyelids, neck, and face (picture 6B). Importantly, the face can be involved in photoallergic contact dermatitis as well.
•Trunk and under clothing – Textile pattern dermatitis largely involves the trunk and is caused by clothing and textiles. Patients may have symmetric involvement of the axillary folds, flanks, buttock, abdomen, chest, and anterior and posterior upper thighs, which correspond to areas in contact with clothing (picture 9) [36]. Textile ACD tends to be worsened by heat, friction, and sweating. Common allergens causing textile dermatitis include textile dyes and resins; rubber can also be found in certain textiles.
Airborne allergic contact dermatitis — Airborne ACD tends to involve areas of skin that are exposed (ie, not under clothing) such as the head and neck, upper chest, arms, and hands. The most severe involvement tends to be on the face and eyelids.
Common allergens implicated in airborne ACD include plants, fragrances, formaldehyde, acrylates, and epoxy resins [37]. Chemicals that can become aerosolized or off-gas (eg, preservatives like isothiazolinones) are another common cause of airborne ACD [38].
It can be difficult to distinguish airborne ACD from photoallergic contact dermatitis as the distribution can be similar. In photoallergic contact dermatitis, photoprotected areas (eg, the upper eyelids, under the chin and the superior upper lip, and underneath long hair) all tend to be spared.
Systemic contact dermatitis — Systemic ACD can manifest as a symmetric, intertriginous, pruritic eruption after ingestion of an implicated allergen. Areas involved may include the eyelids, neck, axillary vaults, groin and genitalia, and sometimes the flexural arms and legs. Common allergens implicated in systemic contact dermatitis include plants, fragrances, metals, and steroids [39].
Photoallergic contact dermatitis — Photoallergic contact dermatitis is a unique subset of ACD where a photoallergen, in the setting of ultraviolet (UV) light, triggers ACD. Clinically, patients develop rashes in the area of both hapten and UV exposure, and that same allergen does not trigger ACD in the absence of UV light (picture 10).
It can be difficult to differentiate airborne ACD from photoallergic contact dermatitis based on the physical examination because both tend to occur in exposed areas. Allergens implicated in photoallergic contact dermatitis include topical drugs (eg, nonsteroidal anti-inflammatory drugs [NSAIDs], ketoprofen, etofenamate), sunscreens, fragrances, and antimicrobials [40,41]. (See "Photosensitivity disorders (photodermatoses): Clinical manifestations, diagnosis, and treatment", section on 'Photoallergy'.)
PATHOLOGY —
In clinical practice, skin biopsy is not necessary for the diagnosis of ACD as it is a clinical diagnosis. A biopsy of ACD typically shows spongiotic dermatitis (picture 11) and does not distinguish ACD from other spongiotic dermatoses, like irritant contact dermatitis, atopic dermatitis, nummular dermatitis, and seborrheic dermatitis [42]. Importantly, the presence of eosinophils in a skin biopsy does not necessarily indicate ACD as they are not specific for ACD and can be seen in a wide variety of spongiotic dermatoses [43].
DIAGNOSIS
Diagnostic approach — ACD is a clinical diagnosis based on the patient's history, physical examination findings (see 'Clinical manifestations' above), and patch testing (see 'Patch testing' below). It should be noted that positive patch test reactions indicate contact sensitization, and some may not be relevant to the clinical presentation. Thus, all positive reactions must be interpreted in relation to the ongoing clinical picture and exposure history. For example, patients may have a strong positive reaction to gold with no ongoing exposure or known clinical relevance. In this situation, the positive patch to gold does not indicate ACD, only contact allergy. The relevance of positive patch test reactions must be confirmed by clinical improvement of dermatitis with allergen avoidance or by elicitation of ACD with repeated open application test (ROAT).
Patient history — A detailed history, including relevant exposures, is important for the diagnosis of ACD. The timeline of the rash should include exposures five to seven days prior to the onset of the eruption. Travel history, exposure to outdoor plants, and sunlight can also provide important clinical information.
Importantly, new exposures are not necessarily the cause of ACD. Most of the time, patients develop ACD to ongoing exposures because of previous sensitization.
Exposure history includes the following:
●Body site-specific exposures – Patients should be questioned about exposure to potential allergens based on specific sites of dermatitis. For example, patients with hand dermatitis should be asked about hand soaps, personal care products, use of gloves, nail products, and occupational exposures. A patient with facial dermatitis should be asked about hair dye, shampoos, hair styling products, airborne exposures, and exposure to plants or sunlight. Patients with dermatitis involving the flanks, thighs, and buttocks should be questioned about exposure to textiles or uniforms.
●Cosmetics and care products – The patient should be queried regarding the use of personal care products (eg, cosmetics, hair care, dyes, styling products, sunscreen, soaps, essential oils, nail products), including both direct skin and airborne exposure.
●Occupation – A detailed occupational history is critical. Patients should be questioned about workplace exposures including exposure to industrial and work-related chemicals, airborne dust, and personal protective equipment (eg, uniforms, gloves, masks, respirators). To determine if the contact dermatitis is occupational, learning whether the rash clears with workplace avoidance is important. Typically, patients will need several weeks to months away from the workplace exposure to clear ACD.
The Mathias criteria can be used to ascertain whether the contact dermatitis is occupational in nature [44]. Key features are:
•Rash clinically consistent with occupational ACD
•Anatomic distribution consistent with cutaneous exposure in relation to the job task
•Temporal relationship between exposure and onset consistent with ACD
•Exclusion of nonoccupational exposures
•Clearing with workplace avoidance and flaring with re-exposure
•Patch test results supporting an occupational exposure
●Hobbies and home exposures – The patient should be asked about exposures through hobbies and home life. Artistic hobbies may expose the patient to chemicals that off-gas or cure, including acylates or epoxy. Patients should be asked about the use of pools, spas, gyms, and sports or exercise activities. Considerations of home care, including cleaning, yard work, remodeling, and painting, may reveal relevant exposures. For example, a recent remodel that includes painting prior to the onset of the rash could indicate airborne ACD to isothiazolinones. Patients with facial dermatitis could be infusing essential oils around the home or bedroom.
●Children's exposures – Children can also develop ACD. Pertinent history for children includes toys, recreational activities, hobbies, school activities, and caregiver-related exposures (eg, daycare, school). Older children may have exposures related to schooling, recreational activities, sports, or fashion trends. (See "Allergic contact dermatitis in children".)
Physical examination — Although ACD may be clinically indistinguishable from other types of eczematous dermatitis, patients with ACD have an itchy, scaly, erythematous eruption most commonly in the areas of contact with the allergen.
Patch testing — Patch testing is the most important diagnostic test for patients suspected to have ACD. Topical allergens are occluded in place on the patient's upper back for 48 hours. A delayed reading is done five to seven days later to determine if there are any positive reactions. (See "Patch testing".)
Expanded patch testing, or including allergens beyond a standard screening series, increases the diagnostic yield of the test. For example, patch testing with additional textile dyes increases the overall diagnostic yield in cases of suspected textile dermatitis [45]. Photoallergy patch testing must be performed in patients suspected to have photoallergic contact dermatitis.
If patch testing cannot be performed or is inconclusive but there is strong clinical suspicion of ACD to a leave-on personal care product, a ROAT or usage test can be performed. The patient should be instructed to apply the suspected product twice daily to the inner arm just inferior to the antecubital fossa for up to 14 days and see if a skin reaction develops. Of note, ROAT is not appropriate for chemicals of unknown concentration or ingredients (eg, industrial chemicals) and must be recommended with caution for rinse-off products or soaps due to risk of irritation.
DIFFERENTIAL DIAGNOSIS —
ACD can mimic other types of eczematous dermatitis (table 1). Additionally, ACD may coexist with other dermatoses and should be considered in the differential diagnosis when the underlying dermatitis is refractory to standard treatment. Biopsy is generally not helpful in distinguishing among other spongiotic dermatoses as nearly all show similar features on histology.
●Irritant contact dermatitis – Irritant contact dermatitis is a type of contact dermatitis developing after exposure to irritants (picture 12). Unlike ACD, it is not immune related and represents skin barrier breakdown in response to chemical or physical irritants. Clinically, irritant contact dermatitis often presents with more burning and stinging, whereas patients with ACD experience more pruritus. (See "Irritant contact dermatitis in adults".)
●Atopic dermatitis – Atopic dermatitis is a chronic, pruritic, inflammatory skin disorder. There is significant heterogeneity in the presentation of atopic dermatitis depending on the patient's age, race/ethnicity, genetic background, and other clinical features (picture 13A-D). ACD can be superimposed on atopic dermatitis. Patients with atopic dermatitis who developed new areas of involvement or become refractory to standard treatment should trigger an evaluation for concomitant ACD. (See 'Risk factors' above and "Atopic dermatitis (eczema): Pathogenesis, clinical manifestations, and diagnosis".)
●Seborrheic dermatitis – Seborrheic dermatitis is a chronic, waxy eruption that often involves the central face, nasolabial folds, ears, scalp, neck, and intertriginous sites (picture 14A-B). Itch is often a less prominent feature of seborrheic dermatitis as compared with ACD. (See "Seborrheic dermatitis in adolescents and adults".)
●Nummular dermatitis – Nummular dermatitis, also called nummular eczema or discoid dermatitis, is characterized by circular lesions primarily on the trunk and extremities (picture 15A-B). It is more common in males than females and in most cases occurs in the third decade of life or older. It is extremely pruritic and responds to treatments similar to those for atopic dermatitis. In general, patients with nummular dermatitis are less likely to have clinically relevant reactions on patch testing [46]. Patients with nummular dermatitis have been reported to have a higher prevalence of ACD to metals, but studies demonstrating clinical relevance and improvement with allergen avoidance are lacking [47]. (See "Nummular eczema".)
SOCIETY GUIDELINE LINKS —
Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Contact dermatitis".)
SUMMARY
●Definition and pathogenesis – Allergic contact dermatitis (ACD) is T cell-mediated hypersensitivity reaction caused by immune sensitization to a specific substance or ingredient. ACD develops with exposure to specific chemicals and is characterized by three stages: sensitization, elicitation, and resolution. (See 'Common allergens' above and 'Pathogenesis' above.)
●Clinical presentation – ACD affects all ages and may be underrecognized in children. The typical clinical finding is a pruritic dermatitis affecting the area of direct contact with the offending allergen that flares with exposure to and remits with avoidance of specific substances or products (picture 6A-D). (See 'Clinical manifestations' above.)
●Diagnosis – ACD is a clinical diagnosis based on the patient's exposure history, clinical findings, and relevant patch test results. A detailed history should include the use of personal care products, medicaments, occupation, and hobbies or sports. (See 'Diagnosis' above.)
ACKNOWLEDGMENT —
The UpToDate editorial staff acknowledges James Yiannias, MD, who contributed to earlier versions of this topic review.
