Metal Allergy—A Review on Exposures, Penetration, Genetics, Prevalence, and Clinical Implications

Abstract

The prevalence of metal allergy is high in the general population, and it is estimated that up to 17% of women and 3% of men are allergic to nickel and that 1-3% are allergic to cobalt and chromium. Among dermatitis patients, the prevalence of metal allergy is even higher. Metal allergy is mainly an environmental disorder although null mutations in the filaggrin gene complex were recently found to be associated with nickel allergy and dermatitis. Environmental metal exposures include jewelry, buttons, clothing fasteners, dental restorations, mobile phones, and leather. Although consumer exposure is responsible for most cases of metal allergy, the importance of occupational metal exposure remains present and should always be taken into consideration when one interprets allergic patch test reactions to metals. Traditionally, nickel, cobalt, and chromium have been the most important contact allergens. However, recently, gold and palladium have drawn much attention as the prevalence of contact allergy to these metals is high. Palladium allergy is mainly a result of cross-sensitization to nickel, whereas gold allergy is rarely clinically relevant when one takes its high prevalence into account. The epidemiology of metal allergy has recently changed in Europe as nickel allergy among ear-pierced Danish women has decreased following regulatory intervention on nickel release from consumer products. In the United States, the prevalence of nickel allergy is still increasing, which may be explained by the absence of regulation. The prevalence of chromium allergy is increasing in the United States, Singapore, and Denmark among dermatitis patients. This increase is significantly associated with leather exposure in Denmark. Metal allergy may result in allergic contact dermatitis and systemic allergic (contact) dermatitis. Furthermore, metal allergy has been associated with device failure following insertion of intracoronary stents, hip and knee prostheses, as well as other implants. This area is in need of more research.

Metal assisted peptide bond hydrolysis: Chemistry, biotechnology and toxicological implications

“…The contact or oral exposure to nickel metal or Ni(II) salts causes allergy in sensitized individuals. Also in this case, the soluble Ni(II) species are thought to be the toxic agents [120,121]. Implants made of alloys containing nickel, such as stainless steel, give rise to both types of nickel toxicity by means of a slow release of Ni(II) ions [122,123].…”

Contact hypersensitivity to nickel in patients with atopic dermatitis

“…It can be found in jewelry, metal buttons, zippers, glasses frames, coins, metal parts of watches, belt buckles and mobile phones [17]. In 1994 the European Union issued a decree specifying the limits of nickel excretion by items that have direct contact with human skin at 0.5 μg/cm 2 /week.…”

“…In spite of these precautions, nickel remains the most common contact allergen in the European population. It is responsible for ACD in 65 million people [17,18] -17% of women and 3% of men [19]. Risk of hypersensitivity development is increased when direct exposure to the hapten occurs within skin deprived of an epithelial barrier.…”

“…Występuje w biżuterii, metalowych guzikach, zamkach błyskawicznych, oprawkach okularów, monetach, metalowych częściach zegarków, sprzączkach od paska czy telefonach komórkowych [17]. W 1994 r. w Unii Europejskiej wydano zarządzenie określające limity wydzielania niklu przez produkty mające kontakt ze skórą do 0,5 μg/cm 2 /tydzień.…”

Cardiotoxicity of Palladium Compounds / Kardiotoksičnost Jedinjenja Paladijuma

“…Previous studies conducted on rats and rabbits have shown that palladium has toxic effects on the kidney (14,15), liver (16,17), produces de terioration of the general condition of experimental animals (2,18) and could cause allergy in animals (14,(19)(20)(21) and humans (22)(23)(24)(25)(26). Clinical signs of acute poisoning include death, tonic and clonic convulsions, ataxia, tiptoe gait, reduced intake of food and water, weakness and abdominal distension in animals (2,18).…”