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Lead toxicity developing brain

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,... [Pg.2614]

While the acceptable blood lead level set by the US Occupational Safety and Health Agency (OSHA) remained 50 //g/dL in 2007, that for children had been progressively lowered by the Center for Disease Control and Prevention (CDC) to 10 /(g/ dL by 1991. The disparity between acceptable blood lead levels in adults and children can be explained in part by the paucity of studies of lead toxicity in adults, and the increased sensitivity of the developing brain in children to toxins. The efforts of the lead industry to thwart public health regulation in the workplace contributed to the disparity in standards for children and adults. OSHA is reluctant to revise the occupational lead standard because of the risk of litigation. The mounting evidence of the impact of lower and lower lead levels on blood pressure and the kidneys in industry and the general public is reviewed in this chapter. [Pg.774]

Geist, C. R. and Mattes, B. R. (1979). Behavioral effects of postnatal lead acetate exposure in developing laboratory rats. Physiol. Psychol., 7, 399 Geist, C. R. and Praed, J. E. (1982). Chronic lead exposure of rats open-field performance. Perceptual Motor Skills, 55, 487 Gelman, B. G. and Michaelson, I. A. (1979). Neonatal lead toxicity and in vitro lipid peroxidation of rat brain. /. Toxicol. Env. Health, 5, 671 Gelman, B. G., Michaelson, I. A. and Bornschein, R. L. (1979). Brain lipofuscin concentration and oxidant defence enzymes in lead-poisoned neonatal rats. J. Toxicol. Env. Health, 5, 683... [Pg.138]

Sauerhoff, M. W. and Michaelson, I. A. (1973). Hyperactivity and brain catecholamines in lead-exposed developing rats. Science, 182, 1022 Scarborough, J. (1969). Roman Medicine. (New York Cornell University Press) Schlaepfer, W. W. (1969). Experimental lead neuropathy a disease of the supporting cells in the peripheral nervous system. J. Neuropathol. Exp. Neurol., 21, 401 Schroeder, H. A. and Mitchener, M. (1971). Toxic effects of trace elements on the reproduction of mice and rats. Arch. Env. Health, 23, 102 Schroeder, H. A. and Tipton, I. H. (1968). The human body burden of lead. Arch. Env. Health, 17, 965... [Pg.149]

This difference in attention to risk populations for lead neurotoxicity versus cardiovascular and cerebrovascular toxicity traces in part to what available data currently permit one to conclude comparatively about these serious adverse effects. Childhood Pb neurotoxicity is expressed through a myriad of developmental neurocognitive and neurobehavioral mechanisms centered on the developing brain for which adult neural analogs have not been as well conceptualized. [Pg.503]


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