| pubmed-article:6832395 | pubmed:abstractText | Environmental sources of lead are multiple, and a number of factors influence their toxicity. However, with the exception of tetramethyl and tetraethyl lead, the particular compound of lead seems to have relatively little influence on toxicity compared with the particle size of the source and the route and frequency of exposure. Susceptibility to lead toxicity is greater among immature animals and very young children because of their higher levels of lead ingestion, greater absorption from the gastrointestinal tract, higher percent lead retention in tissues, and greater reactivity of organs, particularly the central nervous system. Marginal nutritional status also increases susceptibility to lead toxicity. Dietary factors influencing toxicity of lead include total calories, calcium, iron, zinc, fat, ascorbic acid, and protein. Although vitamin D, specifically the metabolite 1,25-dihydroxycholecalciferol, increases lead absorption in vitamin D-deficient animals, clinical studies have shown that lead-burdened children have reduced rather than elevated plasma 1,25-dihydroxycholecalciferol levels. Bioavailability of lead, as shown by tissue lead concentrations, is not always an adequate predictor of lead toxicity. For example, concurrent exposure to cadmium results in higher toxicity of lead to the hematopoietic system, but lowers tissue lead levels substantially. Low dietary calcium increases the total body burden of lead but disproportionately increases the deposition of lead in nonosseous tissues. | lld:pubmed |
