In lead toxicity

Lolin Y, O Gorman P. 1988. An intra-erythrocytic low molecular weight lead-binding protein in acute and chronic lead exposure and its possible protective role in lead toxicity. Ann Clin Biochem 25 688-697. 

Rosen JF. 1989. Metabolic abnormalities in lead toxic children Public health implications. Bull N Y Acad Med 65 1067-1084. 

Saenger P, Markowitz ME, Rosen JF. 1984. Depressed excretion of 6P-hydroxycortisol in lead-toxic children. J Clin Endocrinol Metab 58 363-367. 

Thomasino JA, Zuroweste E, Brooks SM, et al. 1977. Lead, zinc and erythrocyte delta-aminolevulinic acid dehydratase Relationships in lead toxicity. Arch Environ Health 32 244-247. 

Gurer, H., Ozgunes, H., Oztezcan, S., and Ercal, N. 1999. Antioxidant role of alpha-lipoic acid in lead toxicity. Tree Radical Biology and Medicine 27(1-2) 75-81. 

Acute lead toxicity produces appetite loss and vomiting. Chronic toxicity leads to renal malfunction, anemia, gout, and nervous system disorders, including brain damage in children. (Lead inhibits development in fetal and child brains.) The effects are more serious for a patient deficient in calcium, zinc, or iron (see Figure 2). Available Pb + affects the structure and function of the bone marrow, where it inhibits several enzymes involved in heme synthesis. It also affects mitochondrial functions in diverse ways. It has proven difficult, however, to specify critical interactions in lead toxicity. Pb + is not particularly carcinogenic but quite toxic. Acute toxicity is dealt with by infusion of Ca +-EDTA,... 

To gain insight into the impact of environmental and occupational factors (e.g., as in epidemiologic studies, such as in lead toxicity or carpal timnel syndrome). 

In iron deficiency where iron is unavailable for incorporation into heme in the developing reticulocytes or where incorporation is inhibited as in lead toxicity, protoporphyrin IX accumulates in the red cells. This can be measured by extraction into ethyl acetate-acetic acid and then back-extracted into HCl. After neutralization, an ether extraction followed by differential extraction into HCl allows separation of protoporphyrin and coproporphyrin. 

M. R. Moore, in Lead Toxicity History and Environmental Impact (R. Lansdown and W. Yule, eds.), Johns Hopkins University EYess, Baltimore, 1986, p. 54 ff. 

FIGURE 22.1 Chronology of guidelines for deetines in lead toxicity thresholds in young children. Source Mushak (1992a). Elsevier Inc. Reprinted with permission. 

Rosen JF, Markowitz ME, Bijur PE, Jenks ST, Wielopolski L, Kalef-Ezra JA, Slatkin DN (1989) L-X-Ray fluorescence of cortical bone lead compared with the CaNaj-EDTA test in lead-toxic children Public health implications. Proc Natl Acad Sci 86 685-689. [Erratum Proc Natl Acad Sci 86(19) 7595 (1989).]... 

Subcellular mechanisms in lead toxicity Significance in childhood encephalopathy, neurological sequelae, and late dementias. In Neurotoxicology, edited by L. Roizin, H. Shiraki, and N. Arcevic (ed.) p. 289. New York Raven Press (1977). 

Depending on the level of lead exposure, children have been reported to have symptoms such as ataxia, convulsions, headache, and learning disabilities and tend to exhibit hyperactive behaviors. Encephalopathy has been reported in lead-toxic children. Learning and behavioral deficits in children have been reported. Blood levels of less than 10 micrograms per decUiter, which are comparatively low, could result in such deficits in children. Blood lead levels have demonstrated an inverse relation to the neuropsychological performance of children. Children 2 to 4 years of age had slower mental development as blood lead levels increased [4,6,9]. 

Lead has a high affinity for bone, partly due to its antagonistic relationship with calcium. The greatest amount of lead in the body is the skeleton, which acts as a reservoir for lead. The influence of lead upon bone must be considered from the perspective of vitamin the metabolism of which is significantly altered in lead toxicity. Bone structure is in a constant state of self-renewal, with continual controlled destruction, reduction, and rebuilding. Lead is known to influence the various biochemical and physiological events involved with this process. 

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