Dermatologists use the terms “eczema” and “dermatitis” interchangeably to describe a varied pattern of inflammation which, when acute, is characterised by erythema and vesiculation, and, when chronic, by dryness, lichenification, and fissuring (fig 1). Contact dermatitis is the consequence of a pathological response to one or more external agents that may act either as irritants, where allergic T cell mechanisms are not involved, or as allergens, where cell mediated hypersensitivity initiates the proceedings. Many studies have shown that it is very difficult to distinguish allergic contact dermatitis from irritant and endogenous forms.1

Contact dermatitis is classified into a number of reaction patterns: acute irritant dermatitis is a severe eczematous reaction that results from a single overwhelming exposure, or a few brief exposures to strong irritants or a caustic agent. Chronic (cumulative) irritant dermatitis is characterised by eczematous changes that develop upon repeated exposure to weaker irritants, which are “wet”—for example, water, soaps, detergents, solvents, weak acids or alkalis—or “dry”, as in the case of environmental factors like low humidity, heat, air, and dusts.2 Many industrial substances are irritants and some are also allergens.

Allergic contact dermatitis is defined as a specific immune phenomenon that is the result of a T cell mediated immune response to a defined allergen, resulting in eczema or the exacerbation of a pre-existing dermatitis when the patient has been re-challenged with the allergenic material. Common allergens include chromate, rubber chemicals, preservatives, nickel, fragrances, epoxy resins and phenol-formaldehyde resins (box 1). In many cases, several aetiological elements are involved including allergens, irritants, and endogenous factors, especially atopic eczema.