Contact dermatitis covers a range of delayed skin reactions that occur after direct skin contact with a sensitising agent or contact irritant.
by Dr. Adrian Morris
This is common in adults in the workplace (Occupational Dermatitis) and occurs in cleaners, caterers, mechanics, hairdressers, nurses and food handlers. Triggers include hair products, jewellery, dyes in clothing, leather, rubber, glues, cement, raw food exposure, topical medications, sunscreens, cosmetics, fragrances and plants. Irritant contact dermatitis accounts for over 80% of all contact dermatitis. This occurs on the hands and other skin surfaces where chronic exposure to a cleaning agent or chemical induces a non-allergic localised skin irritation. Allergic contact dermatitis involves a delayed cell mediated allergy which develops after exposure to a metal or chemical in the environment. Contact Urticaria is a rapid onset localised urticaria seen in chefs and food handlers.
Irritant Contact Dermatitis
Irritant contact dermatitis is a common non-allergic condition which occurs on the hands of people involved in the cleaning industry after frequent exposure and skin “insult” from surfactants in detergents and water. These surfactants such as Sodium Lauryl Sulphate remove the natural outer skin protective greases and irritate the skin. This cumulative and progressive skin dryness, scaling and cracking leads to the typical irritant dermatitis. Solvents, detergents and cutting oils used in factories and workshops are triggers, as is urine ammonia residue in nappy rashes and dermatitis.
Allergic Contact Dermatitis
Allergic Contact Dermatitis develops after repeated allergen exposure and is a T cell mediated delayed skin hypersensitivity to common metals, dyes, rubber products and cosmetics. This allergy is common in adult females (over 15% of females are Nickel allergic). The lesions are sharply demarcated, occurring at the site of allergen exposure (or contact) and develop over 48 hours. Initially there is redness and itching, followed by crusted vesicles and blisters, which becomes thickened skin with time. Allergies are limited to the site of exposure and resolve within weeks after allergen removal. Many allergens causing contact dermatitis are chemicals (or haptens) that have to bind to a carrier protein to trigger a delayed immune response. Certain specific areas of skin are primarily affected by this allergy: Nickel in jewellery tends to affect the earlobes, wrists and fingers, hair dyes affect the scalp and face, leather shoe dyes or rubber affect the feet and nail varnish or cosmetics affect the face and neck. Minimal perspiration can elute contact allergens through several layers of clothing. Nickel from coins leaches from pockets and leather shoe dyes or rubber through socks. Arm-pit contact dermatitis is triggered by formaldehyde and perfumes in deodorants. Paraphenylenediamine (PPD) added to darken Henna products is a potent skin sensitiser. It is often found in the cheaper Henna-based skin tattoos and many hair products. Methylisothiazolinone (MI) a preservative in “wet wipes” and emollients is a growing problem. As are Paraben preservatives and Fragrances added to creams. Lanolin (wool alcohol) although often suspected is a less likely cause for contact dermatitis. Chlorhexidine surgical cleaning solvent may trigger contact dermatitis in health care workers. Occasionally localised contact dermatitis may develop into a generalised symmetrical “id reaction” or auto-eczematisation remote from the original area of contact.
Contact urticaria is an IgE mediated “wheal and flare” allergy reaction occurring within minutes of protein allergen skin contact. This is often seen with chefs (fresh shrimps, potato & garlic) and animal handlers, as well as medical staff after latex rubber exposure. Up to 10% of healthcare workers are now latex allergic and present with contact dermatitis, allergic rhinitis, asthma and even anaphylaxis.
Photosensitive dermatitis often develops in males in sun exposure areas after contact with potential photo-toxins (psoralens) in foods (parsnip, celery, lime) and drugs (phenothiazines & diuretics) as well as topical sunscreens (para-aminobenzoic acid) and fragrances (musk or oil of Bergamot) in cologne.
“Systemic” contact dermatitis
Systemic contact dermatitis is a controversial condition with a non-specific generalised dermatitis and blistering of the hands. It affects mainly females with allergy to nickel on patch testing and the dermatitis is presumably nickel-induced (“id” reaction). It has been suggested that the condition improves on a diet low in Nickel-containing foodstuffs and by avoiding nickel in cooking utensils.
Identifying the cause:
Always have a high index of suspicion of occupational contact dermatitis in those workers dealing with food, detergents and solvents with frequent exposure to water, cleaning agents and oils. Enquire about the exact nature of the occupation and chemicals in the workplace. “What exactly does your job involve?” When do symptoms get worse and what alleviates them? Enquire about trigger activities, hobbies, reactions to soaps or cosmetics, non-prescription creams and other cleaning agents.
Occupations most at risk for allergic contact dermatitis include: Hairdressers, cement workers, food processors, florists, printers, chefs, builders, nurses, motor mechanics, painters, laundry workers, animal handlers and pharmaceutical factory workers.
Diagnostic Tests: Patch Tests
Individuals react to a substance days after exposure; this is called a Delayed Hypersensitivity Reaction. This delay in reaction time makes identification of the causative allergen very difficult.
Patch Testing is the cornerstone of diagnosing allergic contact dermatitis. The various suspected allergens (in a white soft paraffin base) are placed on the skin (in Finn chambers) and kept in position for 48 hours (2 days). The patches are then removed and the reactions assessed. These are again reassessed after a further 48 hours (2 days), as irritant (but not allergic) reactions will disappear by this time. Reactions are graded 0 (no reaction) to 3+ (redness with blistering) for each allergen. False positive results may occur with the “angry back” or “excited skin” syndrome of non-specific hypersensitivity. False negative results may occur if the person is using cortisone creams.
The European Standard Contact Dermatitis Testing Series (“TRUE Test”) Includes extracts of Nickel, Wool alcohols (Lanolin), Neomycin, Chromate, Benzocaine, Fragrance mix, Colophony, Epoxy resin, Quinoline mix, Balsam of Peru, Thiuram mix, Ethylenediamine, Cobalt, Formaldehyde, Paraben mix, Carba mix, Black Rubber mix, Phenylenediamine, Mercapto mix, Thiomersal, Kathon CG and Quaternium-15. “TRUE Test” is available commercially from Diagenics in the UK and this test is available at our Surrey Allergy Clinics.
Other standard allergen series are available for Medicament, Steroid, Footwear, Dental & Hairdressing related contact allergens.
Another useful contact dermatitis test is the Open application test: This involves applying the suspected allergen twice daily to the skin of the forearm or behind the ear for a week. (Repeated Open Application Test or ROAT). Prick Tests are used to identify causes of Contact Urticaria. Photopatch testing utilises ultra violet light over the skin test site to induce Photosensitive dermatitis
A THOROUGH and EXHAUSTIVE ALLERGY HISTORY with PATCH TESTING followed by AVOIDANCE of implicated ALLERGEN and PROTECTION of SKIN with BARRIER CREAMS.
Avoidance of the implicated contact allergen is imperative as contact allergy is usually life-long. Occupational contact dermatitis should be discussed with the employer and reported as an occupational disease. The worker should be protected from further exposure or relocated to a less exposed work-station.
- Topical steroid creams are the mainstay of the acute treatment. Get control with a potent steroid and wean to a less potent steroid cream. Only use dilute hydrocortisone (0,5%) on the face and skin creases. Remember some people can become allergic to topical steroids (bear in mind if the steroid cream aggravates the condition).
- Oral Steroids may be necessary for a few days if steroid creams fail to control
- Antibiotics are used to treat any secondary skin infections (Fucidic acid or Mupirocin)
- Oral antihistamines are usually ineffective but will reduce itch in contact urticaria
- Potassium Permanganate (1: 10 000) daily soaks and Icthammol 10% in glycerine dressings are used to treat weepy lesions.
Avoid all topical skin sensitisers such as antihistamine creams (mepyramine, antazoline, diphenhydramine), neomycin, benzocaine and tea tree oil.
Common Contact Allergens
|Nickel||Earrings, clothing clasps, coins, spectacles, jewellery|
|Cobalt||Jewellery, dental plates, prostheses, polish stripper|
|Chromate||Cement, leather, bleaches, matches, tattoos|
|Formaldehyde||Shampoo, cosmetics, newsprint, deodorant, clothing|
|Paraphenylenediamine||Colouring in hair dyes, henna and textiles|
|Ethylenediamine||Preservative in creams, paints, rubber, antifreeze|
|Mercaptobenzothiazole||Rubber (boots & gloves), catheters, glues|
|Thiurams||Rubber, fungicides, hair dye, stockings, clothing dyes|
|Balsam of Peru||Perfumes & cosmetics|
|Colophony||Sticking plaster, solder flux, polish, varnishes|
|Parabens||Preservatives in cosmetics and creams|
|Epoxy resins||Glues, surface coatings, PVC products|
|Topical medicated creams||Antibiotics: Neomycin, quinoline, chloramphenicol Antihistamines: Antazoline, Anaesthetics: Benzocaine|
|Wool alcohols||Lanolin, cosmetics, skin creams & emollients|
|Plant photo-toxins||Parsnip, celery, parsley, fennel, orange|
|Plant allergens Compositae||Primula, Poison Ivy, Tulip bulbs, Onion & Garlic, Dahlia, Chrysanthemums and Feverfew|
- Durham S., ABC of Allergies (British Medical Journal 1998)
- du Vivier A., Atlas of Clinical Dermatology 3rd Ed Ch 4 (Churchill Livingston 2008)
- Bourke J, Coulson I, English J. Guidelines for care of contact dermatitis Br Journal Dermatology 2001; 145: 877-85