Contact Dermatitis

Written by Dr Adrian Morris

What is Contact Dermatitis?

Contact dermatitis covers a range of delayed skin reactions that occur after direct skin contact with a sensitising agent or contact irritant.  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 T-cell mediated immune response 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 atopic people involved in the cleaning industry after frequent exposure and skin “insult” from detergents and water.  These agents remove the natural outer skin protective greases and irritate the skin.  This cumulative and progressive skin dryness, scaling and cracking leads to the typical exogenous dermatitis.  Solvents, detergents and cutting oils used in factories and workshops are triggers, as is urine ammonia residue in nappy rashes anddermatitis.

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.  Common in adult females (over 10% of females are Nickel allergic).  The lesions have 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 become thickened plaques with time.  These are limited to the site of exposure and resolve within weeks if the trigger is removed.  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:  Nickel in jewellery tends to affect the earlobes, wrists and fingers, hair dyes affect the scalp and face, leather shoe dyes 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 is leached from coins in 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. Occasionally contact dermatitis may develop into a generalised “id reaction” or auto-eczematisation remote from the original area of contact.

Contact Urticaria

Contact urticaria is an IgE mediated “wheal and flare” reaction occurring within minutes of protein allergen skin contact. This is often seen with chefs (fresh shrimps & 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

Photosensitive dermatitis develops almost exclusively in males in sun exposure areas after exposure to photo-toxins (psoralens) in foods (parsnip, celery, lime) and drugs (phenothiazines & thiazides) 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 presenting with a generalised and sometimes blistering dermatitis on the hands and feet.  It affects mainly females who are nickel allergic on patch testing.  It may improve 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 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

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. People using steroid creams may develop false negative results.

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 for a week. (Repeated Open Application Test (ROAT)).  Prick Tests are used to identify causes of Contact Urticaria.  Photopatch testing utilises ultra violet light over the test site to induce Photosensitive dermatitis

Management essentials:

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 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.
• Oral Steroids may be necessary for a few days if topical steroid creams fail to control.
• Antibiotics are used to treat any secondary skin infections.
• 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

Further reading.

1. Durham S., ABC of Allergies (BMJ 1998)

The photograph of contact dermatitis on the hand was reproduced from the ABC of Allergies (BMJ 1998)

.