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LEAD

 

The possible involvement of lipid peroxidation (LPO) in the lead (Pb) and cadmium (Cd) induced thyroid dysfunction with special reference to type-I iodothyronine 5'-monodeiodinase (5'-D) activity was studied in rat liver homogenate. Peroxidative reactions involving membrane components were found to be markedly stimulated by chronic administration of Pb and Cd in rats. Metal induced inhibition in 5'-D activity was also observed. Since LPO is primarily an outcome of free radical generation, we suggest metal induced free radical mediated inhibition of 5'-D activity in rat liver homogenate. In addition, serum triiodothyronine (T3) and thyroxine (T4) concentrations were also decreased by metals. lead induced inhibition of 5-D' activity.doc

Thirty men occupationally exposed to lead have been examined. The selection of subjects was based on increased lead poisoning indices as well as on the data proving there had been no thyroid disease incidence noted prior to the lead poisoning. Each of the subjects underwent determination of T4 concentration simultaneously with the measurement of three basic indicators of lead poisoning: ALA in urine and ZPP and Pb in blood. Three T4 concentration ranges have been obtained therefore all the cases have been divided into three groups: I increased T4 concentration: II normal T4 concentration; III decreased T4 concentration. In each group T4 concentrations have been compared with the poisoning indicators. The highest poisoning indicators have been found in group II exhibiting normal T4 concentrations (43.33% of cases). It differed significantly from group III (50.0% of cases) exhibiting decreased T4 concentrations. The determination values in group I (increased T4 concentrations) have been excluded from statistical calculations, as there were too few cases (6.67%). The discrepancy of T4 results, their pathological picture at lower values of poisoning indices evidence that the establishment of Pb effects upon thyroid function would call for the determination of a number of additional factors possibly affecting the mechanism handling this phenomenon.lead poisoning reduces T4 in exposed workers.doc

 

Food Chem Toxicol 1986 Sep;24(9):913-21

Survey of lead, cadmium and fluoride in human milk and correlation of levels with environmental and food factors.

Dabeka RW, Karpinski KF, McKenzie AD, Bajdik CD

Lead, cadmium and fluoride were determined in 210 samples of human milk and the mean and median levels and ranges found were 1.04 and 0.55 ng/g (range less than 0.05-15.8 ng/g) for lead, 0.08 and 0.06 ng/g (range less than 0.002-4.05 ng/g) for cadmium, and 7.08 and less than 4 ng/g (range less than 2-97 ng/g) for fluoride. For mothers taking no fluoride supplements and living in communities with fluoride (1 microgram/g) in the drinking-water, the mean fluoride level was 9.8 ng/g. Where no fluoride was present in the drinking-water, the mean level was 4.4 ng/g. Geometric means for all non-zero lead, cadmium and fluoride concentrations were 0.566, 0.063 and 12 ng/g, respectively. Statistical correlation of levels with some dietary and environmental factors showed that lead levels were most strongly correlated with the age of the house (P less than 0.001), with maternal exposure to heavy traffic for more than 5 yr (P = 0.011), and with coffee consumption (P = 0.034). Fluoride levels correlated strongly (P = 0.007) with the presence of fluoride in the drinking-water. Cadmium levels correlated strongly with exposure to cigarette smoke (P = 0.005 if the mother smoked and P = 0.003 if the father smoked and the mother did not smoke).

PMID: 3781438, UI: 87055560
 
Z Ernahrungswiss 1990 Mar;29(1):54-73

[The toxicological estimation of the heavy metal content (Cd, Hg, Pb) in food for infants and small children].

[Article in German]

Schumann K

Walther-Straub-Institut fur Pharmakologie und Toxikologie der Ludwig-Maximilians-Universitat, Munchen, FRG.

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.