Contact dermatitis

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Contact dermatitis
Contact dermatitis around wound.jpg
Rash resulting from skin reactions.

Contact dermatitis is a type of inflammation of the skin. Some symptoms of contact dermatitis can include itchy or dry skin, a red rash, bumps, blisters, and swelling. The rash isn't contagious or life-threatening, but it can be very uncomfortable.

Contact dermatitis results from either exposure to allergens (allergic contact dermatitis) or irritants (irritant contact dermatitis). Phototoxic dermatitis occurs when the allergen or irritant is activated by sunlight. Diagnosis of allergic contact dermatitis can often be supported by patch testing.[1]

Signs and symptoms

Contact dermatitis is a localized rash or irritation of the skin caused by contact with a foreign substance. Only the superficial regions of the skin are affected in contact dermatitis. Inflammation of the affected tissue is present in the epidermis (the outermost layer of skin) and the outer dermis (the layer beneath the epidermis).[2]

Contact dermatitis results in large, burning, and itchy rashes. These can take anywhere from several days to weeks to heal. This differentiates it from contact urticaria (hives), in which a rash appears within minutes of exposure and then fades away within minutes to hours. Even after days, contact dermatitis fades only if the skin no longer comes in contact with the allergen or irritant.[3] Chronic contact dermatitis can develop when the removal of the offending agent no longer provides expected relief.

Irritant dermatitis is usually confined to the area where the trigger actually touched the skin, whereas allergic dermatitis may be more widespread on the skin. Symptoms of both forms include the following:

  • Red rash. This is the usual reaction. The rash appears immediately in irritant contact dermatitis; in allergic contact dermatitis, the rash sometimes does not appear until 24–72 hours after exposure to the allergen.
  • Blisters or wheals. Blisters, wheals (welts), and urticaria (hives) often form in a pattern where skin was directly exposed to the allergen or irritant.
  • Itchy, burning skin. Irritant contact dermatitis tends to be more painful than itchy, while allergic contact dermatitis often itches.

While either form of contact dermatitis can affect any part of the body, irritant contact dermatitis often affects the hands, which have been exposed by resting in or dipping into a container (sink, pail, tub, swimming pools with high chlorine) containing the irritant.


Common causes of allergic contact dermatitis include: nickel allergy, 14K or 18K gold, Balsam of Peru (Myroxylon pereirae), and chromium. In the Americas they include the oily coating from plants of the genus Toxicodendron: poison ivy, poison oak, and poison sumac. Millions of cases occur each year in North America alone.[4] The alkyl resorcinols in Grevillea banksii and Grevillea 'Robyn Gordon' are responsible for contact dermatitis.[5] Bilobol, another alkyl resorcinol found in Ginkgo biloba fruits, is also a strong skin irritant.[6]

Common causes of irritant contact dermatitis include solvents, metalworking fluids, latex, kerosene, ethylene oxide, paper, especially papers coated with chemicals and printing inks, certain foods and drink,[7] food flavorings and spices,[8] perfume,[7] surfactants in topical medications and cosmetics, alkalis, low humidity from air conditioning, and many plants. Other common causes of irritant contact dermatitis are harsh, alkaline soaps, detergents, and cleaning products.[9]

There are three types of contact dermatitis: irritant contact dermatitis; allergic contact dermatitis; and photocontact dermatitis. Photocontact dermatitis is divided into two categories: phototoxic and photoallergic.

Irritant contact dermatitis

Contact dermatitis caused by unprotected handling of damp, impregnated wooden construction debris.

Irritant contact dermatitis (ICD) can be divided into forms caused by chemical irritants, and those caused by physical irritants. Common chemical irritants implicated include: solvents (alcohol, xylene, turpentine, esters, acetone, ketones, and others); metalworking fluids (neat oils, water-based metalworking fluids with surfactants); latex; kerosene; ethylene oxide; surfactants in topical medications and cosmetics (sodium lauryl sulfate); and alkalis (drain cleaners, strong soap with lye residues).

Physical irritant contact dermatitis may most commonly be caused by low humidity from air conditioning.[10] Also, many plants directly irritate the skin.

Allergic contact dermatitis

3-year-old girl with contact dermatitis, one day after contact with poison ivy

Allergic contact dermatitis (ACD) is accepted to be the most prevalent form of immunotoxicity found in humans, and is a common occupational and environmental health problem.[11] By its allergic nature, this form of contact dermatitis is a hypersensitive reaction that is atypical within the population. The mechanisms by which this reaction occurs are complex, with many levels of fine control. Their immunology centres on the interaction of immunoregulatory cytokines and discrete subpopulations of T lymphocytes.

Allergens include nickel, gold, Balsam of Peru (Myroxylon pereirae), chromium, and the oily coating from plants of the genus Toxicodendron, such as poison ivy, poison oak, and poison sumac.

Photocontact dermatitis

Sometimes termed "photoaggravated",[12] and divided into two categories, phototoxic and photoallergic, PCD is the eczematous condition which is triggered by an interaction between an otherwise unharmful or less harmful substance on the skin and ultraviolet light (320–400 nm UVA) (ESCD 2006), therefore manifesting itself only in regions where the sufferer has been exposed to such rays.

Without the presence of these rays, the photosensitiser is not harmful. For this reason, this form of contact dermatitis is usually associated only with areas of skin that are left uncovered by clothing, and it can be soundly defeated by avoiding exposure to sunlight.[13] The mechanism of action varies from toxin to toxin, but is usually due to the production of a photoproduct. Toxins which are associated with PCD include the psoralens. Psoralens are in fact used therapeutically for the treatment of psoriasis, eczema, and vitiligo.

Photocontact dermatitis is another condition in which the distinction between forms of contact dermatitis is not clear-cut. Immunological mechanisms can also play a part, causing a response similar to ACD.


Since contact dermatitis relies on an irritant or an allergen to initiate the reaction, it is important for the patient to identify the responsible agent and avoid it. This can be accomplished by having patch tests, one of various methods commonly known as allergy testing.[14] The top three allergens found in patch tests from 2005–06 were: nickel sulfate (19.0%), Myroxylon pereirae (Balsam of Peru, 11.9%), and fragrance mix I (11.5%).[15]

The patient must know where the irritant or allergen is found to be able to avoid it. It is important to also note that chemicals sometimes have several different names, and do not always appear on labels.[16]

The distinction between the various types of contact dermatitis is based on a number of factors. The morphology of the tissues, the histology, and immunologic findings are all used in diagnosis of the form of the condition. However, as suggested previously, there is some confusion in the distinction of the different forms of contact dermatitis.[17] Using histology on its own is insufficient, as these findings have been acknowledged not to distinguish,[17] and even positive patch testing does not rule out the existence of an irritant form of dermatitis as well as an immunological one.


In an industrial setting the employer has a duty of care to its worker to provide the correct level of safety equipment to mitigate exposure to harmful irritants. This can take the form of protective clothing, gloves, or barrier cream, depending on the working environment.

Topical antibiotics should not be used to prevent infection in wounds after surgery.[18][19] When they are used, it is inappropriate, and the person recovering from surgery is at significantly increased risk of developing contact dermatitis.[18]



  • If blistering develops, cold moist compresses[20] applied for 30 minutes, 3 times a day can offer relief.
  • Calamine lotion may relieve itching.[20]
  • Oral antihistamines such as diphenhydramine (Benadryl, Ben-Allergin) can relieve itching.[20]
  • Avoid scratching.[20]
  • Immediately after exposure to a known allergen or irritant, wash with soap and cool water to remove or inactivate most of the offending substance.
  • For mild cases that cover a relatively small area, hydrocortisone cream in nonprescription strength may be sufficient.
  • Weak acid solutions (lemon juice, vinegar) can be used to counteract the effects of dermatitis contracted by exposure to basic irritants.
  • A barrier cream, such as those containing zinc oxide (e.g., Desitin, etc.), may help protect the skin and retain moisture.

Medical care

If the rash does not improve or continues to spread after 2–3 of days of self-care, or if the itching and/or pain is severe, the patient should contact a dermatologist or other physician. Medical treatment usually consists of lotions, creams, or oral medications.

  • Corticosteroids. A corticosteroid medication like hydrocortisone may be prescribed to combat inflammation in a localized area. It may be applied to the skin as a cream or ointment. If the reaction covers a relatively large portion of the skin or is severe, a corticosteroid in pill or injection form may be prescribed.

In severe cases, a stronger medicine like halobetasol may be prescribed by a dermatologist.

  • Antihistamines. Prescription antihistamines may be given if non-prescription strengths are inadequate.

See also


  1. Mowad, CM (July 2016). "Contact Dermatitis: Practice Gaps and Challenges". Dermatologic Clinics. 34 (3): 263–7. doi:10.1016/j.det.2016.02.010. PMID 27363882.
  2. European Society of Contact Dermatitis. "What is contact dermatitis". Archived from the original on 2018-12-29. Retrieved 2021-02-14.
  3. "DermNet NZ: Contact Dermatitis". Archived from the original on 2006-08-11. Retrieved 2006-08-14.
  4. Gladman A. C. (2006). "Toxicodendron dermatitis: poison ivy, oak, and sumac". Wilderness & Environmental Medicine. 17 (2): 120–8. doi:10.1580/pr31-05.1. PMID 16805148.
  5. Menz, J.; Rossi, ER; Taylor, WC; Wall, L; et al. (1986). "Contact dermatitis from Grevillea 'Robyn Gordon'". Contact Dermatitis. 15 (3): 126–31. doi:10.1111/j.1600-0536.1986.tb01311.x. PMID 2946534. S2CID 2846186.
  6. Matsumoto, K.; Fujimoto, Masao; Ito, Kazuo; Tanaka, Hitoshi; Hirono, Iwao; et al. (1990). "Comparison of the effects of bilobol and 12-O-tetradecanoylphorbol-13-acetate on skin, and test of tumor promoting potential of bilobol in CD-1 mice". The Journal of Toxicological Sciences. 15 (1): 39–46. doi:10.2131/jts.15.39. PMID 2110595.
  7. 7.0 7.1 "Balsam of Peru contact allergy". DermNet NZ. 2013-12-28. Archived from the original on 2014-04-17. Retrieved 2014-04-17.
  8. "Contact Dermatitis and Related Conditions". Archived from the original on 2014-04-17. Retrieved 2014-04-17.
  9. Irritant Contact Dermatitis. Archived 2016-07-15 at the Wayback Machine
  10. Morris-Jones R, Robertson SJ, Ross JS, White IR, McFadden JP, Rycroft RJ (2002). "Dermatitis caused by physical irritants". Br. J. Dermatol. 147 (2): 270–5. doi:10.1046/j.1365-2133.2002.04852.x. PMID 12174098. S2CID 8444176.
  11. Kimber I, Basketter DA, Gerberick GF, Dearman RJ (2002). "Allergic contact dermatitis". Int. Immunopharmacol. 2 (2–3): 201–11. doi:10.1016/S1567-5769(01)00173-4. PMID 11811925.
  12. Bourke J, Coulson I, English J (2001). "Guidelines for care of contact dermatitis". Br. J. Dermatol. 145 (6): 877–85. doi:10.1046/j.1365-2133.2001.04499.x. PMID 11899139. S2CID 26038634.
  13. "Photocontact Dermatitis". Archived from the original on 21 April 2011. Retrieved 31 March 2011.
  14. Hristakieva, E.; Gancheva, D.; Gancheva, T. (2014). "Contact dermatitis in patient with chronic venous insufficiency". Trakia Journal of Sciences. 12 (3): 245–249. doi:10.15547/tjs.2014.03.005.
  15. Zug KA, Warshaw EM, Fowler JF Jr, Maibach HI, Belsito DL, Pratt MD, Sasseville D, Storrs FJ, Taylor JS, Mathias CG, Deleo VA, Rietschel RL, Marks J (2009). "Patch-test results of the North American Contact Dermatitis Group 2005–2006". Dermatitis : Contact, Atopic, Occupational, Drug. 20 (3): 149–60. doi:10.2310/6620.2009.08097. PMID 19470301. S2CID 24088485.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  16. DermNet dermatitis/contact-allergy
  17. 17.0 17.1 Rietschel RL (1997). "Mechanisms in irritant contact dermatitis". Clin. Dermatol. 15 (4): 557–9. doi:10.1016/S0738-081X(97)00058-8. PMID 9255462.
  18. 18.0 18.1 American Academy of Dermatology (February 2013), "Five Things Physicians and Patients Should Question", Choosing Wisely: an initiative of the ABIM Foundation, American Academy of Dermatology, archived from the original on 1 December 2013, retrieved 5 December 2013
  19. Sheth, V. M.; Weitzul, S. (2008). "Postoperative topical antimicrobial use". Dermatitis : Contact, Atopic, Occupational, Drug. 19 (4): 181–189. doi:10.2310/6620.2008.07094. PMID 18674453.
  20. 20.0 20.1 20.2 20.3 "Contact dermatitis Lifestyle and home remedies – Diseases and Conditions". Mayo Clinic. 2011-07-30. Archived from the original on 2016-12-01. Retrieved 2014-04-18.

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