Nickel allergy is any of several allergic conditions provoked by exposure to the chemical element nickel. Nickel allergy often takes the form of nickel allergic contact dermatitis (Ni-ACD), a form of allergic contact dermatitis (ACD). Ni-ACD typically causes a rash that is red and itchy and that may be bumpy or scaly. The main treatment for it is avoiding contact with nickel-releasing metals, such as inexpensive jewelry. Another form of nickel allergy is a systemic form: systemic nickel allergy syndrome (SNAS) can mimic some of the symptoms of irritable bowel syndrome (IBS) and also has a dermatologic component.
Signs and symptoms The most common sign of nickel allergy is inflammation of the skin at an area that comes into regular contact with nickel. This often takes the form of a reddened patch of skin with raised bumps (papules) or small blisters (vesicles), and edema. People with chronic dermatitis tend to have dry, scaly, and cracked skin at the site of contact. These sites of inflammation (called "primary eruptions") can occur anywhere on the skin that contacts nickel, but are most common on the hands, face, or anywhere that contacts metal objects such as jewelry or metal clothes buttons. Particularly high levels of nickel exposure can cause irritated patches of skin to appear at other sites on the body (called "secondary eruptions"). These typically occur as blistering rashes on the hands, eyelids, and at the inside of flexing joints (inside the elbow, back of the knee, etc.). Ingestion of nickel may cause a systemic reaction, which can result in generalized inflammation of the skin across the body, small blisters in the hands, irritation inside the flexing joints (flexural eczema), and redness and irritation of both buttocks. Systemic contact dermatitis (SCD) is defined as a dermatitis occurring in an epi-cutaneously contact-sensitized person when exposed to haptens systemically such as orally, per rectum, intravesically, transcutaneously, intrauterinely, intravenously, or by inhalation. The pathophysiology of systemic nickel allergy syndrome (SNAS) is not well understood. The clinical course is determined by an immunological interplay between two types of T cells (Th1 and Th2 responses). SCD is often considered a subset of SNAS, but with only skin manifestations. SNAS presents with an array of symptoms ranging from respiratory to generalized skin rash to gastrointestinal symptoms. The gastrointestinal symptoms may mimic those of irritable bowel syndrome. A meta review evaluating SNAS found that 1% of patients sensitized to nickel reacted to the nickel content of a 'normal' diet, and with increasing doses of nickel more individuals reacted. SNAS is a multilayered immunological response demonstrating variance between individuals and doses of nickel exposure.
Causes
Nickel exposure Nickel is both naturally abundant – it is the fifth most common element on earth – and widely used in industry and commercial goods. Workplace nickel exposure is common in many industries, and the performance of normal work tasks can result in nickel skin levels sufficient to elicit dermatitis. Within the workplace, individuals may be exposed to significant amounts of nickel, airborne from the combustion of fossil fuels or from contact with tools that are nickel plated. Historically, workplaces where prolonged contact with soluble nickel has been high have shown high risks for allergic contact nickel dermatitis. For example, nickel dermatitis was common in the past among nickel platers. Outbreaks of nickel allergy from consumer goods have been documented throughout the 20th century, with jewelry, stocking suspenders, and metallic buttons on blue jeans each resulting in dermatitis at the point of contact. Nickel can also be present in food and drinking water; ingestion of increased nickel is not associated with systemic allergic disease, but is associated with flare-ups of dermatitis or aggravation of vesicular hand eczema. Similarly, aggravation of dermatitis has been reported in response to nickel-containing surgical implants or dental gear. The risk of an object eliciting nickel allergy is linked to the amount of nickel released by its surface (and not to its total nickel content). Suspected objects can be screened by wiping the surface with a 1% dimethylglyoxime solution that turns pink if more than 0.5 μg/cm2 per week is released by the surface. Various methods exist to test the skin or nails for nickel exposure, typically relying on wiping the skin, then quantifying the nickel on the wipe via mass spectrometry. Dietary nickel exposure may come from high-nickel foods, possibly canned food (via the packaging), possibly stainless steel cookware (whereas some grades of stainless steel contain more nickel than others), or plumbing (especially the first water run from the tap in the morning).
Physiology Nickel allergy results in a skin response after the skin comes in contact with an item that releases a large amount of nickel from its surface. It is commonly associated with nickel-containing belt buckles coming into prolonged contact with the skin. The skin reaction can occur at the site of contact, or sometimes spread beyond to the rest of the body. Free (released) nickel that is able to penetrate the skin is taken up by scavenger (dendritic) cells and then presented to the immune system T-Cells. With each subsequent exposure to nickel these T cells become stimulated and duplicate themselves. With enough exposure to nickel, the amassing clones of T-cells reach "threshold" and the skin develops a rash. The rash can appear as acute, subacute, or chronic eczema-like skin patches, primarily at the site of contact with the nickel (e.g., earlobe from nickel earrings). From the time of exposure, the rash usually appears within 12–120 hours and can last for 3–4 weeks or for the continued duration of nickel contact/exposure. Three simultaneous conditions must occur to trigger Ni-ACD:
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