Chapter 13

Allergic Contact Dermatitis

David E. Cohen
Sharon E. Jacob
As the primary interface with the environment, the skin is placed in the precarious position of
routine exposure and assault from exogenous chemicals and physical agents. Fortunately,
most of these exposures result in no clinically apparent disease. However, in some
circumstances, a panoply of immunologic events results in the sensitization and subsequent
elicitation of allergic contact dermatitis (ACD).
The classic interpretation of the skin as a simple barrier to penetration by exogenous agents
underestimates the immunologic capacity of the integument. Modern concepts have divulged
the finely orchestrated interplay of host defenses that cope with these onslaughts. In the
1950s, Landsteiner and Chase
1
firmly established ACD as a form of cell-mediated
hypersensitivity. It was not until the latter half of the twentieth century, however, that the
fundamental role of intact lymphatic systems, cellular elements (Langerhans cells,
keratinocytes, and lymphoid cells), and specific cytokines in the sensitization and elicitation
phases of ACD became recognized (see Chap. 10).
1

Today we understand that these complex T-cell-mediated events are specifically and
sensitively targeted to one or more chemical entities. When the level of exposure exceeds the
thresholds of sensitization and elicitation, immunologic memory of the event is generated.
That being said, the frequent lack of an obvious causative culprit or temporal relationship
between the allergen and dermatitis leads to an intense detective and analytic exercise of
determining and subsequently avoiding the offending chemical entity.