Urinary nickel (Ni) provides an indication of recent or ongoing exposure to the metal, and endogenous detoxification to a lesser extent. There is substantial evidence that Ni is an essential trace element.
However, excessive assimilation of Ni has been established to be nephrotoxic, and carcinogenic. The general population may be exposed to Ni from ambient air, water and food. With the exception of specific occupational exposures, most absorbed Ni comes from food and beverages, and intakes can vary depending upon geographical location and water supply. Extensive Ni exposure may occur with cigarette
Ni is present at relatively higher levels in a large number of foods and food products, including: hydrogenated oils (margarine), black tea, nuts and seeds, soy milk and chocolate milk, chocolate and cocoa powders, certain canned and processed foods, and certain grains such as oats, buckwheat, whole wheat, and wheat germ. Other sources of Ni include: urban air/particulate diesel exhaust, Ni-Cd batteries, non-
precious/ semiprecious dental materials, pigments (usually for ceramics or glass), arc welding, and nickel refining, metallurgical processes and electroplating.
Hair elemental analysis may confirm exposure to Ni over the past 2-4 months.
Chelation may acutely increase urinary excretion of Ni.
Urinary excretion of nickel bound to cysteine or other thiol compounds (such as glutathione) or to amino acids (histidine, aspartic acid, arginine) is the predominant mode of excretion. With the exception of specific occupational exposures, most absorbed Ni comes from food or drink, and intakes can vary by factors exceeding 100 depending upon geographical location, diet, and water supply. Nickel is present in a surprisingly large number of foods and food products, including: hydrogenated oils, black tea, nuts and seeds, soy milk and chocolate milk, chocolate and cocoa powders, certaincanned and processed foods, including meat and fish, certain grains, including: oats, buckwheat, whole wheat and wheat germ. 1 to 10% of dieatry Ni may be absorbed from the gastrointestinal tract into the blood. Urine reflects recent exposure to nickel and ay vary widely in nickel content from day to day.
Other sources of Ni include cigarettes (2 to 6 mcg Ni per average cigarett), diesel exhaust, Ni-Cd batteries, nonprecious, seminprecious dental materials, electroplating, plated objects, costume jewelry and pigments (usually for ceramics or glass), Arc welding, and metallurgical processes.
Most clinically relavant Ni exposures are manifested as dermatoses - contact dermatitis and atopic dermatitis. However, Ni hypersensitizes the immune system and may cause hyperallergenic responses to many different substances. Because Ni can displace zinc from binding sites on enzymes it can affect abnormal enzymatic activity. Nickel sensitivity is observed to be three to five times more prevelant in females than in males.
Other laboratory tests or possible clinical findings that may be associated with Ni exposure are; hair elements analysis, presentation of multiple allergic sensitivities, dermatitis, positive patch test for "Ni allergy", proteinuria, hyperaminoaciduria (by 24-hour urine amino acid analysis). Administration of EDTA or sulfhydryl agents (DMPS, DMSA, D-penicillamine) may increase urine Ni levels; such chelator- induced elevations may or may not be associated with adverse health effects.
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