Sunday 13 December 2009, 23:22

Allergy to metals

The mechanism of contact allergy to metals

Allergy to metals

Nickel is the main cause of metal-induced allergic contact dermatitis (ACD) and accounts for as much allergy as all other metals taken together.


However, the recent tendency to reduce nickel use in all products placed in direct and prolonged contact with the skin (such as jewellery and dentistry products) has led to an increased use of other metals such as cobalt,  chromium, palladium and gold. This in turn has lead to an increased incidence of ACD caused by other metals. Interestingly, many patients sensitive to nickel, are also sensitive to other metals. This may due to either cross-reactivity or multiple concurrent sensitization.


Contact allergy is a hypersensitive skin reaction resulting from contact with substances normally harmless to non-allergic individuals. It appears as a itchy, red and swollen rash (called allergic contact dermatitis or ACD) developing within hours to days on the sensitized skin.


In general terms, contact allergy is described as a hypersensitive delayed reaction, which is mediated by T cells (T lymphocytes). In the specific case of metal allergy, it has been possible to demonstrate that the hypersensitive reaction involves activation of metal-specific T cells, followed by proliferation and production of both Th-1 and Th2-type cytokines. These findings invalidate the initial hypothesis suggesting that ACD in humans was a reaction involving primarily Th1-type responses.


The mixed Th1- and Th2-type response induced by metals is characterized by the production of both Th1-type cytokines (interleukin 2 and interferon gamma) and Th2-tye cytokines (interleukins 4, 5 and 13). Th1-type cytokines are the biochemical hallmarks of delayed-type hypersensitivity, traditionally regarded as a cell-mediated reaction (antibody-independent response). On the contrary, Th2-type cytokines are associated with the promotion of IgE antibodies, traditionally involved in atopy and immediate allergic reactions.


Thus, the pathogenetic mechanism of ACD is more complex than thought previously, in that it involves both cell-mediated reactions and antibody-mediated reactions. Further research is needed to elucidate which interplay exists between these two hypersensitive reactions in the development of ACD.


By Chiara De Carli

Category: Allergy

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