Lead toxicity children

Rosen JF Montefiore Medical Center, Bronx, NY Treatment outcomes in moderately lead toxic children (human) National Institute of Environmental Health Sciences... 

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. 

Rosen JE, Markowitz ME, Bijur PE, Jenks ST, WiELOPOLSKi L, Kalee-Ezra JA and Siatkin DN (1991) Sequential measurements of bone lead content by L X-ray fluorescence in CaNa2EDTA-treated lead-toxic children. Environ Health Perspect 91 57-62. 

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).]... 

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]. 

There are no children In the reference area who had lead toxicity or whose blood lead level exceeded 29 pg/dl (Table XIII). The term "lead toxicity" Is defined here as a child with a blood-lead level > 30 pg/dl and an EP pg/dl. The term "lead toxicity" Is not used In a toxicological sense. 

Table XVII shows that 5.6 percent of black children living within 0.5 mile of RSR were found to have lead toxicity, and no child living beyond 0.5 mile of RSR was found to have lead toxicity.

Increased susceptibility of certain segments of the population, e.g., young children, may arise from increased tissue sensitivity, more complete absorption, altered distribution, or less developed or impaired defense mechanisms. The increased sensitivity of the child to lead toxicity is well documented (100, 101). In children, unlike the adult, renal tubular damage and encephalopathy are more common sequelae (76, 100). With arsenic exposure, children show significantly higher concentrations of the element in hair and urine than do adults (62). 

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,... 

Rick Nevin believes that lead poisoning accounts for much of the violent crime in the United States (Washington Post, July 8,2007). Exposure to lead as a child correlates with violent behavior later in life, according to studies of the association between lead poisoning and crime rates in nine different countries. Sixty-five to ninety percent or more of the substantial variation in violent crime in all these countries is explained by lead. Lead in US. paint and gasoline fumes has exposed toddlers to lead toxicity because they put their contaminated hands in their mouths. He believes that lead toxicity is not the only factor leading to crime, but is a big factor. 

Preparations containing >0,5% lead chromate are required to be labelled according to EU Guideline 67/548/EEC (Annex I) as toxic (Symbol skull and crossbones) and beside others with the Risk phrases R 40 (limited evidence of carcinogenic effect), R 61 (may cause harm to the unborn child) and R 62 (possible risk of impaired fertility). 

Other approaches to induce gastrointestinal discomfort have far more serious toxic effects. The chemical colchicine stops cell division (an antimitotic), producing severe nausea, vomiting, and dehydration, which can lead to delirium, neuropathy, and kidney failure. On the other hand, colchicine is used in the treatment of gout and has been studied as an anticancer agent because it stops cell division. Most toxic of all are plants that produce lectins, and the most toxic of these is the chemical ricin produced by castor beans. Only 5 to 6 seeds are necessary to kill a small child. Fortunately, following oral consumption much of the ricin is destroyed in the stomach. Ricin is extremely effective at stopping protein synthesis, so much so that direct exposure to only 0.1 pg/kg can be fatal. 

The risk assessor should be sensitive to certain dose-response patterns that are often encountered in studies on developmental toxicity. For example, the lowest effective doses in adults and young are often similar or may be the same, but the type of effects may be very different as well, the effects on the developing child may be permanent (or lead to latent effects), whereas the effects on the adult may be transient. Also, the end-points used in evaluating alterations in children s health may vary considerably. The difference between the maternal toxic dose and the developmental toxic dose may at times be related to the relative thoroughness with which end-points are evaluated. Also, the variability and level of severity within a particular end-point need to be defined, since end-point variability and level of severity can have a significant effect on the power of the study and the ability to establish an effect level. Approaches to carrying out dose-response assessments are described below. 

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