[The toxicological estimation of the heavy metal content (Cd, Hg, Pb) in food for infants and small children].
There are differences between young and adult organisms regarding toxokinetic aspects and clinical manifestations of heavy metal intoxications. Chronically, toxic Cd intake causes a microcytotic hypochromic anemia in young rats at lower exposure levels and after shorter exposure periods than in adult animals. Cd absorption is increased by co-administration of milk and in conjunction with iron deficiency. After long exposure periods toxic Cd concentrations accumulate in the kidney cortex; this process starts very early in life. In 3-year-old children Cd concentrations in the kidney can reach up to one-third of those found in adults. Hg++ and methyl-Hg can cause Hg encephalopathia, and frequently cause mental retardation in adults. Correspondingly, Hg++ accumulation in the brains of suckling rats is approx. 10 times higher than in grown animals. Milk increases the bioavailability of Hg++. In suckling rats Hg is bound to a greater extent to ligands in the erythrocytes. Methyl-Hg concentrations in breast milk reach 5% of those in maternal plasma and that is a severe hazard for breastfed children of exposed mothers. Toxic Pb concentrations can lead to Pb encephalopathia. A high percentage of surviving children have seizures and show signs of mental retardation. Anemia and reduced intelligence scores were recently observed in children after exposure to very low levels of Pb. Pb absorption is increased in children and after co-administration of milk. There are no definite proofs for carcinogenesis or mutagenesis after oral exposure to Cd, Hg, and Pb in man. Heavy metal concentrations were found in the same order of magnitude in commercial infant formulas and in breast milk. When infant formulas are reconstituted with contaminated tap water, however, Pb and Cd concentrations can be much higher. The average heavy metal uptake from such diets exceeds the provisional tolerable weekly intake levels set by the WHO for adults, calculated on the basis of an average food intake and a downscaled body weight. These considerations do not even provide for differences in absorption and distribution or for the increased sensitivity of children to heavy metal exposure. However, dilution effects for essential heavy metals were observed in fast-growing young children; this effect might be extrapolated to toxic metals. These theoretical considerations are compared with epidemiological evidence. A health statistic from Baltimore shows a decline of Pb intoxications in infants. This observation correlates with a simultaneous decline in exposure to Pb which was due, for example, to decreased use of lead dyes in house paints and the abolition of tin cans for infant food.(ABSTRACT TRUNCATED AT 400 WORDS)
Walther-Straub-Institut für Pharmakologie und Toxikologie der Ludwig-Maximilians-Universität, München, FRG.
K
K
Schümann
D000818:Animals; D002104:Cadmium / Q000032:analysis* / Q000493:pharmacokinetics / Q000633:toxicity; D002105:Cadmium Poisoning / Q000209:etiology; D002675:Child, Preschool; D005506:Food Contamination; D006801:Humans; D007223:Infant; D007225:Infant Food / Q000032:analysis*; D007854:Lead / Q000032:analysis* / Q000493:pharmacokinetics / Q000633:toxicity; D007855:Lead Poisoning / Q000209:etiology; D008628:Mercury / Q000032:analysis* / Q000493:pharmacokinetics / Q000633:toxicity; D008630:Mercury Poisoning / Q000209:etiology; D008895:Milk, Human / Q000032:analysis
D002104:Cadmium; D007854:Lead; D008628:Mercury
Zur toxikologischen Beurteilung der Schwermetallgehalte (Cd, Hg, Pb) in Säuglings- und Kleinkindnahrung.