Intoxication, lead

In children, entry of lead into the body occurs primarily by ingestion, although inhalation also contributes to body burden. Once lead intoxication proceeds to encephalopathy, the risk of death exists. Dose-response information on a pediatric population relating PbB levels with the occurrence of acute... 

Renal Effects. The characteristics of early or acute lead-induced nephropathy in humans include nuclear inclusion bodies, mitochondrial changes, and cytomegaly of the proximal tubular epithelial cells dysfunction of the proximal tubules (Fanconi s syndrome) manifested as aminoaciduria, glucosuria, and phosphaturia with hypophosphatemia and increased sodium and decreased uric acid excretion. These effects appear to be reversible. Characteristics of chronic lead nephropathy include progressive interstitial fibrosis, dilation of tubules and atrophy or hyperplasia of the tubular epithelial cells, and few or no nuclear inclusion bodies, reduction in glomerular filtration rate, and azotemia. These effects are irreversible. The acute form is reported in lead-intoxicated children, whose primary exposure is via the oral route, and sometimes in lead workers. The chronic form is reported mainly in lead workers, whose primary exposure is via inhalation. Animal studies provide evidence of nephropathy similar to that which occurs in humans, particularly the acute form (see Section 2.2.3.2). 

A study of 55 adolescents who had been treated for lead intoxication in early childhood (11-17 years earlier) revealed no evidence of chronic nephropathy, as evidenced by endogenous creatinine clearance, BUN, serum uric acid, and routine urinalysis (Chisolm et al. 1976). PbB levels during the acute poisoning episode ranged from 100 to 650 pg/dL all patients received immediate chelation therapy. At the time of the study, their PbB levels had decreased to less than 40 pg/dL. 

Zinc is in the active site of ALAD and can play a protective role in lead intoxication by reversing the enzyme-inhibiting effects of lead. Children with high PbB levels (50-67 pg/dL) were reported to consume less zinc than children with lower PbB (12-29 pg/dL) (Johnson and Tenuta 1979). In a group of 13 children, Markowitz and Rosen (1981) reported that the mean serum zinc levels in children with... 

Iron appeared to reduce the effects of orally or subcutaneously administered lead on blood enzyme and liver catalase activity (Bota et al. 1982). Treatment of pregnant hamsters with iron- or calcium-deficient diets in conjunction with orally administered lead resulted in embryonic or fetal mortality and abnormalities (ranting, edema) in the litters, while treatment with complete diets and lead did not (Carpenter 1982). Inadequate levels of iron in association with increased body burdens of lead enhanced biochemical changes associated with lead intoxication (Waxman and Rabinowitz 1966). Ferrous iron was reported to protect against the inhibition of hemoglobin synthesis and cell metabolism by lead it has been speculated that iron competes with lead uptake by the cell (Waxman and Rabinowitz 1966). In... 

People with Neurologic Dysfunction or Kidney Disease. This population is unusually susceptible to lead exposure. The neurologic and renal systems are the primary target organs of lead intoxication, which may become overburdened at much lower threshold concentrations to elicit manifestations of lead intoxication (Benetou-Marantidou et al. 1988 Chisolm 1962, 1968 Lilis et al. 1968 Pollock and Ibels 1986). 

Keogh JP University of Maryland at Baltimore, Baltimore, MD Validation of new biomarkers as predictors of long term health effects after lead intoxication National Institute of Environmental Health Sciences... 

Klein RF Department of Veterans Affairs, Medical Center, Portland, OR Chronic lead exposure impairs osteoblast function in vivo gain insight into the consequences of lead intoxication on the skeleton Department of Veterans Affairs, Research and Development... 

Lead intoxication has been observed in children, but rarely in adults, in residential settings (Sedman 1989). The geometric mean blood lead level (GM PbB) for children has dropped dramatically since the late 1970 s. Results of the CDC NHANES II and NHANES III, Phases I and II, study of blood lead levels for children aged 1-5 are summarized below (CDC 1997b, 1997d). 

Bhattacharya A, Smelser DT, Berger O, et al. 1998. The effect of succimer therapy in lead intoxication using postural balance as a measure A case study in a nine year old child. Neurotoxicology (Little Rock) 19(l) 57-64. 

Chiang HC, Chang PY. 1989. [Lead intoxication in shipscrapping employees in Taiwan.] Kao-hsiung I Hsueh K o Hsueh Tsa Chih 5 284-290. (Chinese)... 

Chisolm JJ Jr. 1962. Aminoaciduria as a manifestation of renal tubular injury in lead intoxication and a comparison with patterns of aminoaciduria seen in other diseases. J Pediatr 60 1-17. 

Chisolm JJ Jr. 1965. Chronic lead intoxication in children. Dev Med Child Neurol 7 529-536. 

Chisolm JJ Jr. 1968. The use of chelating agents in the treatment of acute and chronic lead intoxication in childhood. J Pediatr 73 1-38. 

Chowdhury AR, Rao RV, Gautam AK, et al. 1987. Functional changes of testes in lead intoxicated rats. Ind Health 25 55-62. 

Cullen MR, Kayne RD, Robins JM. 1984. Endocrine and reproductive dysfunction in men associated with occupational inorganic lead intoxication. Arch Environ Health 39 431-440. 

Flora SJS, Jeevaratnam K, Kumar D. 1993. Preventive effects of sodium molybdate in lead intoxication in rats. Ecotoxicol Environ Safety 26 133-137. 

Gerber GB, Maes J. 1978. Heme synthesis in the lead intoxicated mouse embryo. Toxicology 9 173-179. 

Hashmi NS, Kachru DN, Khandelwal S, et al. 1989a. Interrelationship between iron deficiency and lead intoxication Part 2. Biol Trace Elem Res 22 299-307. 

Holness DL, Nethercott JR. 1988. Acute lead intoxication in a group of demolition workers. Appllnd Hyg 3 338-341. 

Hryhirczuk DO, Rabinowitz RB, Hessl SM, et al. 1985. Elimination kinetics of blood lead in workers with chronic lead intoxication. Am J Ind Med 8 33-42. 

Ibels LS, Pollock CA. 1986. Toxicology management review Lead intoxication. Med Tox 1 387-410. 

Janin Y, Couinaud C, Stone A, et al. 1985. The "lead-induced colic" syndrome in lead intoxication. Surg Ann 17 287-307. 

MachleWR. 1935. Tetra-ethyl lead intoxication and poisoning by related compounds of lead. JAMA 105 578-585. 

Parras F, Patier JL, Ezpeleta C. 1987. Lead contaminated heroin as a source of inorganic lead intoxication. N Engl J Med 316 755. 

Pollock CA, lbels LS. 1986. Lead intoxication in paint removal workers on the Sidney Harbour Bridge. Med JAust 145 635-639. 

Rosen JF, Zarate-Salvador C, Trinidad EE. 1974. Plasma lead levels in normal and lead-intoxicated children. J Pediatr 84 45-48. 

Tejani A, Lancman L. RajkumarS. 1986. Progressive renal damage due to lead intoxication in early life. Int J Pediatr Nephrol 7 9-12. 

Tennekoon G, Aitchison CS, Frangia J, et al. 1979. Chronic lead intoxication Effects of developing optic nerve. Ann Neurol 5 558-564... 

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