As methylmercury is excreted in human milk and infants are particularly susceptible to toxicity due to this compound, the purpose of this study was to evaluate the possible transfer of methylmercury to infants via breast-feeding. In a community with a high intake of seafood, 583 children from a birth cohort were followed. The duration of nursing was recorded, and hair samples were obtained for mercury analysis at approximately 12 months of age. The hair mercury concentrations increased with the length of the nursing period, and those nursed throughout the first year showed the highest geometric mean (9.0 nmol/g or 1.8 microg/g). Human milk therefore seems to be an important source of methylmercury exposure in infants. An increasing time interval from weaning to hair sample collection was not associated with any detectable decrease in mercury concentrations. A slow or absent elimination of methylmercury during the first year after birth could explain this finding. In certain fishing communities, infants nursed for long periods may be at increased risk of developing methylmercury toxicity.
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This paper is the third in a series dealing with reference procedures for the measurement of catalytic activity concentrations of enzymes at 37 degrees C and the certification of reference preparations. Other parts deal with: Part 1. The Concept of Reference Procedures for the Measurement of Catalytic Activity Concentrations of Enzymes; Part 2. Reference Procedure for the Measurement of Catalytic Concentration of Creatine Kinase; Part 4. Reference Procedure for the Measurement of Catalytic Concentration of Alanine Aminotransferase; Part 5. Reference Procedure for the Measurement of Catalytic Concentration of Aspartate Aminotransferase; Part 6. Reference Procedure for the Measurement of Catalytic Concentration of gamma-Glutamyltransferase; Part 7. Certification of Four Reference Materials tamyltransferase, Lactate Dehydrogenase, Alanine Aminotransferase and Creatine Kinase at 37 degrees C. A document describing the determination of preliminary upper reference limits is also in preparation. The procedure described here is deduced from the previously described 30 degrees C IFCC reference method (1). Differences are tabulated and commented on in Appendix 1.
Umbilical cord tissue was obtained from 50 births in the Faroe Islands, where high mercury intake is due to ingestion of pilot whale meat. The mercury concentration correlated significantly with the frequency of maternal whale meat dinners during pregnancy and with mercury concentrations in umbilical cord blood and in maternal hair. The results were compared with published values for mercury in umbilical cord tissue from 12 infants diagnosed with congenital methylmercury poisoning in Minamata, Japan. From the regression coefficients obtained in the Faroese samples, the median umbilical cord mercury concentration of 4.95 nmol/g dry weight in Minamata would correspond to 668 nmol/l cord blood and 114 nmol/g maternal hair. These levels agree well with other evidence of susceptibility of the fetus to increased exposure to methylmercury.ImagesFigure 1.Figure 2.
Blood lead concentrations were measured in a group of children from a group of 9- to 10-year-old school children in Aarhus, Denmark. The study group was selected as a high-level and a low-level lead group, as identified by the lead concentration in the circumpulpal dentine in deciduous teeth shed 2-3 years previously. The validity of the blood sampling technique was investigated in adult volunteers, and lead was determined by electrothermal atomic absorption. Capillary blood sampling by a finger-stick method was preferred, as the slight contamination caused by this technique was deemed acceptable. The children with the highest dentine lead levels (n = 70), had blood lead concentrations of 0.08-0.63 mumol/l and a geometric mean of 0.28 mumol/l. The children with lowest dentine levels (n = 76) had blood lead concentrations of 0.08-0.70 mumol/l and a geometric mean of 0.18 mumol/l. The blood lead concentrations were compared with interview data on behaviour, family habits, diet, parents' tobacco smoking and occupation, water lead measurements, and traffic counts. A total of 20% of the variation in blood lead was explained by parents' tobacco smoking, the child's number in the sibship, gender, and consumption of canned food at home.
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