The development of nickel ACD requires that an individual become immunologically sensitized to nickel. This is termed the induction phase or sensitization phase and the length of this phase varies greatly between individuals. It can range from 1-3 weeks to develop, following days to weeks of intimate contact in a piercing or on the skin with a form of nickel that can re-lease a sufficient amount of solubilized nickel ions onto the skin. The quantity of nickel ions that is sufficient to induce sensitivity varies with the individual. If the skin is already damaged, sensitization may be induced more quickly and by lower amounts of the solubilized nickel. Temperature, the presence of other allergic conditions, gender, and age may also be determining factors for 1) susceptibility, 2) the amount of nickel ions required for a reaction, and 3) the time to develop sensitization to nickel. Induction of nickel sensitization most commonly originates from body piercing but is also more likely if skin exposure is combined with irritants and/or moist skin.
A nickel-sensitized individual, when re-exposed to nickel ions on the skin in sufficient amounts, may have an allergic response within a matter of hours. This is termed the elicitation phase, which often occurs at a lower concentration of nickel ions than required for inducing sensitization in the first place. The elicitation of nickel ACD usually occurs at the site of exposure but can occur in skin remote from the site of contact with nickel where previous nickel sensitization reactions have occurred.(2)
Whilst systemic elicitation of ACD in individuals sensitized by direct skin contact is well documented for a small proportion of nickel-sensitized individuals, there exists some controversy(3) about the ability to sensitize individuals when nickel exposure is oral, intravenous, or inhaled. Only about 1-10% of dietary nickel is absorbed by the body. Average daily-ingested intake of nickel is about 200 micrograms. A few studies have shown that nickel-sensitive individuals orally given >5,000 micrograms nickel (as NiSO4) as a single dose had a nickel ACD response. While such exposures are in excess of those encountered in normal diets, some researchers suggest that dietary control of nickel intake may help in the ongoing treatment of nickel ACD caused by other sources. These researchers have correctly identified foods high in nickel content (e.g., nuts, chocolate, beans), but they have sometimes incorrectly advocated the avoidance of cutlery, bowls, etc. made from stainless steel, which do not release significant amounts of nickel.
A correlation between dermal nickel sensitization and asthma due to respiratory exposure to soluble nickel has not been demonstrated. This lack of association is likely the result of different immunological mechanisms of the two types of allergy. Respiratory sensitization is known to be a type 1 mediated immunological reaction, whereas skin sensitization involves a type 4 reaction.
2. Occupational Medicine. 1994. 3rd Edition, ed. by Zenz, C.; Dickerson, O.B.; Horvath, E.P. (Eds). St. Louis: Mosby.
3. Menné, T.; Veien, N.; Sjolin, K-E.; Maibach, H.I. 1994. Systemic contact dermatitis. Amer. J. of Contact Dermatitis 5(1): 1-12.