Cobalt release from earrings and piercing jewellery - analytical results of a German survey.

BACKGROUND: Contact sensitization to cobalt is common. Some industrial exposures have been identified, but cobalt allergy is also often diagnosed in 'non-occupational' patients. Exposure of consumers is largely unexplained. OBJECTIVE: To present the analytical results on cobalt release from earrings and piercing jewellery sampled in a German Federal surveillance scheme. METHODS: Two German state laboratories analysed cobalt release, after immersion in artificial sweat according to EN 1811, along with nickel release in 87 pieces of jewellery, which were mostly taken apart for separate examination of piercing posts (n = 139), clasps (n = 51), and/or decorative items (n = 52). The distribution of cobalt release was described by the use of Kaplan-Meier analysis, taking into account that the majority of measurements were left-censored, that is, below the limit of quantification. RESULTS: Thirty-eight of 87 earrings and piercing jewellery items had at least one part releasing cobalt. The median cobalt release was estimated as 0.013 µg/cm(2) /week, and 75% of parts released up to 0.085 µg/cm(2) /week. Release varied somewhat between the three parts, with, for example, 22.1% of posts releasing ≥ 0.2 µg/cm(2) /week. CONCLUSIONS: Cobalt release from earrings and piercing jewellery, in particular from piercing posts, is considerable. Scientifically based exposure limits should be set, as in the case of nickel.

The phenolic acids from bacterial degradation of the mangiferin aglycone are quantified in the feces of pigs after oral ingestion of an extract of Cyclopia genistoides (honeybush tea).

Polyphenols are cleaved by bacterial enzymes to form phenolic acid metabolites in the colon, where they may exert physiologic effects. For norathyriol, the aglycone of mangiferin, one of the major phenolic compounds present in Cyclopia genistoides (honeybush), a further bacterial degradation is likely; but knowledge of the importance of this metabolic process is very limited. Based on a hypothesized cleavage of the middle ring of norathyriol, this study was designed to determine phenolic cleavage products in the feces of pigs fed an extract of C genistoides. Pigs received 74 mg mangiferin per kilogram of body weight daily for 11 days; feces fractions were collected on day 11 and on the first 2 days after the last intake of extract. Several phenolic acids were detected in the feces samples, including 3-hydroxyphenylacetic acid; 4-hydroxybenzoic acid; 3,4-dihydroxybenzoic acid; 3,4-dihydroxyphenylacetic acid; 2,4,6-trihydroxybenzoic acid; 3,4,5-trihydroxybenzoic acid (gallic acid); and phloroglucinol. However, in vivo formation was likely only for 3,4-dihydroxybenzoic acid; 3,4-dihydroxyphenylacetic acid; 2,4,6-trihydroxybenzoic acid; and 3,4,5-trihydroxybenzoic acid because these were not present in the blank feces, in the animals' normal diet, or in the C genistoides extract. The fact that these amounts were very low suggests further degradation of the metabolites by intestinal microflora or absorption of the cleavage products by the colon.

Mangiferin and hesperidin metabolites are absorbed from the gastrointestinal tract of pigs after oral ingestion of a Cyclopia genistoides (honeybush tea) extract.

Health-promoting properties such as antioxidative, anticarcinogenic, and cholesterol-lowering effects are described for mangiferin and hesperidin, the major phenolic compounds present in Cyclopia genistoides (honeybush). However, knowledge of their metabolic fate and their absorption from the gastrointestinal tract is very limited. The aim of this study was to determine the concentrations of mangiferin, hesperidin, and their metabolites in plasma, urine, and feces samples from pigs consuming an extract of Cyclopia genistoides. Pigs were administered up to 74 mg mangiferin per kilogram of body weight and 1 mg hesperidin per kilogram of body weight per day for 11 days. Plasma samples were collected at various time points on days 9 and 11 of the study and days 1 and 2 after termination of extract administration. Urine and feces were collected in fractions for 24 hours. In the plasma samples, the aglycone of mangiferin (norathyriol) was detected. Mean plasma concentrations ranged from 7.8 to 11.8 mumol/L. Six metabolites of mangiferin and hesperidin were detected in the urine, including methyl mangiferin, norathyriol, its monoglucuronide, hesperetin, hesperetin monoglucuronide, and eriodictyol monoglucuronide. Between 26.0% and 30.8% of the administered dose of hesperidin and only between 1.4% and 1.6% of mangiferin could be detected in the urine on days 9 and 11 of the study. Approximately 8.2% of the administered dose of mangiferin was determined in the feces. The main metabolite was norathyriol. Neither hesperidin nor metabolites ascribed to hesperidin intake were detected. The results suggest that formation of norathyriol from mangiferin occurs in vivo, and specific metabolites were identified in blood and excretion products in urine and feces. This study will aid in investigating the physiological functions of the parent compounds in vivo.