Nickel sensitivity

Eye and Skin Contact. Some nickel salts and aqueous solutions of these salts, eg, the sulfate and chloride, may cause a primary irritant reaction of the eye and skin. The most common effect of dermal exposure to nickel is allergic contact dermatitis. Nickel dermatitis may occur in sensitized individuals following close and prolonged contact with nickel-containing solutions or metallic objects such as jewelry, particularly pierced earrings. It is estimated that 8—15% of the female human population and 0.2—2% of the male human population is nickel-sensitized (125). 

Although most nickel sensitization results from nonoccupational exposures, nickel dermatitis was historically a problem in workplaces where there was a high risk of continuous contact with soluble nickel, eg, in electroplating (qv) shops. Improved personal and industrial hygiene has largely eliminated this problem. However, there are a few occupations involving wet nickel work, particularly where detergents faciUtate the penetration of skin by nickel, where hand eczema may occur (126). 

Representative nickel-sensitive aquatic species show sublethal effects at 11.7 to 125 pg Ni/L. These effects include altered immunoregulatory mechanisms in tissues of the rainbow trout at 11.7 pg/L (Bowser etal. 1994), inhibited reproduction of daphnids at 30 pg/L, growth inhibition of freshwater and marine algae at 30 to 125 pg/L, reduced growth of rainbow trout at 35 pg/L, accumulation from the medium by mussels at 56 pg/L, and abnormal development of sea urchin embryos at 58 pg/L (NRCC 1981 WHO 1991 Outridge and Scheuhammer 1993 Table 6.7). 

Nickel selenide, 22 87 Nickel-selenium, 22 73t Nickel sensitization, 17 119 Nickel silicate, 17 89 Nickel silicate green olivine, formula and DCMA number, 7 347t Nickel silicides, 17 121 uses for, 17 123 Nickel-silver, 7 759... 

In many countries, nickel is the commonest sensitizer in women, causing nickel allergy incidence to be high in a series of reported patch tests [399,400]. Since 1930, the emphasis has shifted from sensitization at work to sensitization in the home by nickel-plated metal and objects made of nickel alloy. The age of onset has altered to teenagers and young women and the source is now cheap metal jewellery and fasteners on clothing such as jeans studs. Also sensitization in infancy has been reported. Nickel-sensitive patients do not... 

Nickel itch is a dermatitis resulting from sensitization to nickel the first symptom is usually pruritis, which occurs up to 7 days before skin eruption appears. The primary skin eruption is erythematous, or follicular it may be followed by superficial discrete ulcers that discharge and become crusted or by eczema. The eruptions may spread to areas related to the activity of the primary site such as the elbow flexure, eyelids, or sides of the neck and face. In the chronic stages, pigmented or depigmented plaques may be formed. Nickel sensitivity, once acquired, is apparently not lost of 100 patients with positive patch tests to nickel, all reacted to the metal when retested 10 years later. ... 

Veien NK Nickel sensitivity and occupational skin disease. Occup Med State of the Art Rev 9 81-95, 1994... 

McConnell LH, FinkJN, Schlueter DP, et al Asthma caused by nickel sensitivity. Ann Intern Med 78 888-890, 1973... 

Dermal Effects. Contact dermatitis, which results from dermal exposure to nickel, is the most prevalent effect of nickel in the general population (see Section 2.2.3.2). Several studies indicate that a single oral dose of nickel given as nickel sulfate can result in a flare-up in the dermatitis in nickel-sensitive individuals (Burrows et al. 1981 Christensen and Moller 1975 Cronin et al. 1980 ... 

Intermediate-duration studies suggest that longer term oral exposure can be tolerated by some nickel-sensitive individuals and may even serve to desensitize some individuals. Jordan and King (1979) found flaring of dermatitis in only 1/10 nickel-sensitive women given nickel sulfate at 0.007 mg/kg/day for 2 weeks. Patch test responses to nickel were reduced in nickel-sensitive women given one weekly dose of 0.05 or 0.07 (but not 0.007) mg nickel/kg as nickel sulfate for 6 weeks (Sjovall et al. 1987). 

Santucci et al. (1994) gave increasing daily doses of nickel (0.01-0.03 mg/kg/day) as nickel sulfate to eight nickel-sensitive women for up to 178 days. A significant clinical improvement in hand eczema was observed in all subjects after 1 month of treatment, and continued treatment resulted in healing of all dermal lesions except for those on the hands. Measurement of urine and serum nickel suggested a decrease in the absorption of nickel and an increase in the excretion of nickel with longer exposure. 

The Santucci et al. (1994) study indicates that a daily dose of 0.01-0.03 mg nickel/kg can be tolerated by some nickel-sensitive people and may also serve to reduce their sensitivity. Among 44 sensitive subjects treated with a regimen of 1-2 ng nickel sulfate every other day, or daily for up to 2-3 years,... 

Although most patch testing is done with nickel sulfate because it is less irritating than nickel chloride, exposure of the skin to nickel alloys results in the release of nickel chloride from the influence of human sweat. Therefore, nickel chloride is the more relevant form of nickel for examining threshold concentrations (Menne 1994). Menne and Calvin (1993) examined skin reactions to various concentrations of nickel chloride in 51 sensitive and 16 nonsensitive individuals. Although inflammatory reactions in the sweat ducts and hair follicles were observed at 0.01% and lower, positive reactions to nickel were not observed. To be scored as a positive reaction, the test area had to have both redness and infiltration, while the appearance of vesicles and/or a bullous reaction were scored as a more severe reaction. At 0.1%, 4/51 and 1/51 tested positive with and without 4% sodium lauryl sulfate. Menne et al. (1987) examined the reactivity to different nickel alloys in 173 nickel-sensitive individuals. With one exception (Inconel 600), alloys that released nickel into synthetic sweat at a rate of <0.5 pg/cmVweek showed weak reactivity, while alloys that released nickel at a rate of >1 pg/cm /week produced strong reactions. 

Nickel sensitivity has been induced in guinea pigs following skin painting or intradermal injection with nickel sulfate (Turk and Parker 1977 Wahlberg 1976 Zissu et al. 1987). As discussed in Section 22.2.2, nickel sensitivity can also be induced in mice if oral exposure to nickel is reduced (Moller 1984 van Hoogstraten et al. 1994). 

Higher serum nickel levels have been found in occupationally exposed individuals compared to nonexposed controls (Angerer and Lehnert 1990 Elias et al. 1989 Toijussen and Andersen 1979). Serum nickel levels were found to be higher in workers exposed to soluble nickel compounds compared to workers exposed to less-soluble nickel compounds (Toijussen and Andersen 1979). Concentrations of nickel in the plasma, urine, and hair were similar in nickel-sensitive compared to nonsensitive individuals (Spruit and Bongaarts 1977). 

Nickel sensitivity has also been induced in guinea pigs by skin painting or intradermal injection (Wahlberg 1976 Zissu et al. 1987) and in mice by dermal contact (Siller and Seymour 1994). Dermal effects in animals after dermal exposure to nickel included distortion of the epidermis and dermis, hyperkeratinization, atrophy of the dermis, and biochemical changes (Mathur et al. 1977, 1988). 

Based on human data, environmental exposure or exposure to nickel at hazardous waste sites could result in dermatitis in nickel-sensitized individuals. 

Veien and Menne (1990) have suggested that vasoactive substances found in food can enhance nickel sensitivity reactions. Foods that they suggested that nickel-sensitive people should avoid include beer, wine (especially red wine), herring, mackerel, tuna, tomatoes, onions, carrots, apples, and citrus fruits. The vasoactive substances may increase the amount of nickel that is able to reach the skin. 

Several chronic inhalation and oral studies and acute dermal studies in animals are reported in the literature. These studies exposed several species of animals to both soluble and less-soluble nickel compounds. The target organs were found to be the respiratory system for inhalation exposure and the respiratory system, gastrointestinal tract, hematological system, and kidneys for oral exposure at high levels. Reproductive and developmental effects were observed in animals after inhalation exposure and after oral exposure to nickel. Nickel sensitivity and dermatitis were also observed. 

The development of nickel sensitivity in mice has been shown to be related to both the concentration of the nickel solution applied to the skin and the duration of exposure (Siller and Seymour 1994). Male mice showed a weaker response than females, and further studies regarding the gender difference in the development of nickel sensitivity would be useful. 

Dose-response data for dermal exposure of humans or animals to nickel were not identified. The thresholds for nickel sensitivity identified for acute dermal exposure of humans (Menne and Calvin 1993 Menne et al. 1987) should be protective for longer term exposure. 

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