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Plasma catecholamines where measured in 15 children with chronic lead poisoning and 15 matched controls by radioimmunassay. The data suggest that plasma catecholamines (norepinephrine and epinphrine) were significantly elevated in chronic lead poisoning. Plasma catecholamine elevation may well be important in the clinical finding of hyperactivity and hypertension associated with chronic lead poisoning.
Despite the widespread use of lead paint hazard control for children with lead poisoning, few controlled studies that estimate the effect of such control on children's blood lead levels have been published. This retrospective follow-up study examined the effects of lead hazard remediation and its timing on the blood lead levels of lead-poisoned children. From the New York City child blood lead registry, 221 children were selected who had an initial blood lead level of 20-44 micro g/dL between 1 July 1994 and 31 December 1996; were 6 months to 6 years of age; had a report of a follow-up blood lead test between 10 and 14 months after the initial test; had a lead-based paint hazard identified in the primary dwelling unit prior to the 10- to 14-month follow-up blood lead test; had resided or spent time at only one address with an identified lead-based paint hazard; and were not chelated. The decline in geometric mean blood lead levels from baseline to 10-14 months later was compared for children whose homes were remediated and whose homes were not remediated during the follow-up period. Regardless of remediation, geometric mean blood lead levels declined significantly from 24.3 micro g/dL at the initial diagnosis to 12.3 micro g/dL at the 10- to 14-month follow-up blood lead test (P<0.01). Among the 146 children whose homes were remediated the geometric mean blood lead levels declined 53% compared to 41% among the 75 children whose homes were not remediated by the follow-up blood lead test, a remediation effect of approximately 20% (P<0.01). After adjusting for potential confounders, the remediation effect was 11%, although it was no longer significant. Race was the only factor that appeared to confound the relationship: Black children had higher follow-up blood lead levels even after controlling for other factors, including the natural logarithm of the initial blood lead level. The effect of remediation appeared to be stronger for younger (10 to <36 months old) than for older (36 to 72 months old) children (P=0.06). While children in homes with earlier remediation (within less than 3 months) appeared to have greater declines in blood lead levels at the follow-up test than children in homes with later remediation (after 3 or more months), this trend was not significant when controlling for confounding factors. The findings of this study suggest that early identification of lead-poisoned children and timely investigation and abatement of hazards contribute to reducing blood lead levels. However, the apparent effect is modest and further research is needed to systematically test and improve the effectiveness of lead hazard controls.
Although lead poisoning (plumbism) has been recognized for centuries, lead exposures still occur frequently today because of its varied uses and persistence in the environment. Despite the awareness of the adverse effects of lead on adults, childhood plumbism was first reported only about a century ago. Young children are one of the most vulnerable groups to the adverse effects of lead because of their rapidly developing central nervous systems. Federal regulations in the 1970s have been successfully implemented to decrease the amount of environmental lead by decreasing the content of lead in gasoline and indoor paint. However, almost 30 years after these laws were passed, inner-city housing with leaded paint still exists. We describe three children living in New York City who developed plumbism from the ingestion of leaded paint chips.
Twenty-seven dogs with lead poisoning were admitted to the University of Pennsylvania Veterinary Hospital from July, 1963, to April, 1975. The major source of the lead was paint. A common history was ingestion of plaster or paint scrapings during room renovation. Most of the dogs were less than 1 year old and had clinical signs referable to the gastrointestinal or the nervous system, or both. The gastrointestinal signs, in order of frequency, were vomiting, anorexia, tender abdomen, diarrhea, and constipation. The neurologic signs, in order of frequency, were hysteria, convulsions, ataxia, blindness, and mydriasis. The finding of many nucleated erythrocytes without severe anemia was nearly pathognomonic for lead poisoning. Of 14 affected dogs subjected to abdominal radiography, 9 had evidence of ingested radiopaque material. A mean blood lead concentration of 18.8 mug/100 ml, with a range of 0 to 50 mug/100 ml, was found for 26 dogs that were hospitalized for problems unrelated to lead poisoning. Of the 27 dogs with lead poisoning, 22 had their blood analyzed for lead. This group had blood lead values ranging from 40 to 530 mug/100 ml. Seven of the affected dogs were monitored throughout their period of treatment with calcium ethylenediaminetetraacetate. The concentration of lead in the blood decreased quickly after the initiation of treatment but leveled off after 2 or 3 days. The initial rapid phase probably corresponded to the removal of weakly bound or extracellular lead, whereas the slow phase probably corresponded to strongly bound or intracellular lead.
The continued occurrence of occupational lead poisoning and overexposure in the United States represents a serious challenge to the occupational health community. We outline a proposed action strategy which integrates case-based surveillance, hazard surveillance, increased requirements for biological monitoring, and targeted educational activities, with a goal of eliminating occupational lead poisoning. The system provides a simple mechanism for monitoring compliance in lead-using employers, in order to identify employers for enforcement action. Lead poisoning should be viewed as an eradicable condition; successfully solving the persistent lead overexposure problem can serve as a model for approaching other occupational diseases.
The formation constants of lead chelates of the stereoisomers of 2,3-dimercaptosuccinic acid (DMSA) were determined from potentiometric titrations in the presence of the competing ligand, EDTA. The lead chelates formed at pH 7.4 with the stereoisomers of DMSA are the monomeric complexes PbL and HPbL. Formation of PbL and HPbL at pH 7.4 is independent of total concentrations of lead and DMSA present, and so is the concentration ratio of PbL:HPbL. Lead is completely chelated at pH 7.4 when the total concentration of ligand is equal to or greater than the total concentration of lead present. Lead tends to bind to a greater extent with rac- than with meso-DMSA, and the relative extent increases with an increase in the concentration ratio of ligand to lead and finally reaches a constant value of 45. The binding sites in the chelates, PbL, of the stereoisomers of DMSA are the two thiolate groups and one carboxylate group. rac-DMSA also forms a dimeric complex Pb2L2 in which both carboxylate groups of the ligands participate in binding with lead ions. The formation constants of the lead chelates of rac-DMSA were invariably found to be larger than those of the corresponding of meso-DMSA chelates, because in all the lead chelates of the stereoisomers of DMSA formed in solution, rac-DMSA existed in staggered anti conformations, whereas meso-DMSA preferred a staggered gauche conformation with respect to carboxylate groups in the ligands. The potential of using ZnL2 of rac-DMSA as a therapeutical lead chelator was assessed by considering its lead-mobilizing ability and its ability to deplete endogenous zinc; on this basis it is predicted that ZnL2 of rac-DMSA is a better chelator than meso-DMSA for the treatment of lead poisoning.
Lead poisoning existed and was already known in Antiquity but was forgotten, at least in the literature, until the end of the Middle Ages, where it was mentioned sporadically. In the 19th century this disease, which reached epidemic dimensions during the period of industrialization, was "rediscovered." Several comprehensive clinical articles appeared in the literature. The clinical picture deepened during the beginning of the 20th century, and preventive efforts were started. However, the concept of poisoning remained strictly clinical. During the latter half of the 20th century a new concept emerged: subclinical and early forms became recognized as undesirable effects. This led to a substantial lowering of hygienic standards. Pediatric poisoning has also been a serious problem during the 20th century. After the 1920s, environmental pollution by lead caused by the introduction of tetraethyl lead in gasoline became an alarming public health problem. The use became restricted in the 1980s; its effects on blood lead levels are now evident. Today's research focuses on the effects of low exposure, often with the aim of defining noneffect levels for different types of effects.
OBJECTIVE: To describe a series of patients with clinically significant lead poisoning. METHODOLOGY: A case series of nine patients with lead poisoning who required inpatient management, identified through a Clinical Toxicology Service. RESULTS: Nine children presented with clinically significant lead poisoning. The median serum lead was 2.5 micro mol/L (range 1.38-4.83). Eight of the children were exposed to lead-based paint, with seven due to dust from sanded lead paint during house renovations. Serial blood determinations suggested re-exposure in four of the patients, and in one of these patients the re-exposure was from a different source of lead. Eight of the patients required chelation therapy. CONCLUSIONS: Serious lead poisoning continues to occur and there appears to be complacency regarding the hazard posed by lead paint in old houses.
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A case of lead poisoning in a female art conservator is reported. The patient had experienced excessive lead exposure while restoring an antique Peruvian tapestry from the Chancay period (1000 to 1500 AD) using a powdered pigment (cinnabar), which had been recovered from the same tomb in which the tapestry was found. Over two months, prominent neurological, gastrointestinal, and diffuse muscular symptoms developed. Severe anemia accompanied by basophilic stippling of RBCs led to the diagnosis of lead poisoning, which was confirmed by markedly elevated blood lead levels (up to 130 micrograms/dL) and impairment of heme synthetic enzymes. The severity of the intoxication necessitated chelation therapy. Chemical analysis of the antique powdered pigment showed it to be the source of lead exposure, in that it contained about 1% lead.
Lead poisoning affects an estimated 890,000 young children in the United States annually (American Academy of Pediatrics [AAP], 1998). Extremely high levels in the child can cause mental retardation, coma, seizures, and death. Chronic low level exposure is more commonly seen with multiple effects, including learning disabilities, impaired growth, and hearing loss. Lead poisoning prevention efforts have significantly reduced the number of children affected by this serious health hazard. Health care providers need to continue their vigilant efforts to educate families living in older homes about the risks, screening, and treatment.
Lead poisoning affects children adversely worldwide. In the United States, elevated blood lead levels (BLLs) (>10 microg/dL) result primarily from exposure to lead-based paint or from associated lead-contaminated dust and soil; however, other sources of lead exposure, including folk remedies, Mexican terra cotta pottery, and certain imported candies, also have been associated with elevated BLLs in children. This report describes five cases in California of lead poisoning from atypical sources. Health-care providers should be aware of the potential hazards of certain food products, and community members should be educated about potential sources of lead poisoning for children.
47 lead-poisoned children, treated and without encephalopathy, are compared with sibling controls on perceptual-verbal pattern comparisons of subtests of the Wechsler Intelligence Scale for Children to determine whether there has been brain damage. Both groups of children do not differ significantly from each other on comparisons of these patterns, and they appear to be similar to each other in WISC functioning. The conclusion is that lead-poisoning, treated, and without encephalopathy, does not result in detectable brain damage by means of these pattern analyses.
Lead poisoning was demonstrated in two gray-headed woodpeckers (Picus canus) and one white-backed woodpecker (Dendrocopus leucotos) in Sweden; they had liver lead levels between 9.4 and 26.2 mg(-1) wet weight. At necropsy one gray-headed woodpecker showed signs of emaciation and the other one had severe traumatic injuries, caused by a cat. The white-backed woodpecker died in the transportation box during a translocation program. The source of the lead could not be determined, but it was suspected that it may have originated from lead pellets shot into trees and picked out by the woodpeckers during food search.
To determine the incidence of renal functional abnormalities after lead poisoning, we evaluated the parameters of renal tubular function in 134 children and young adults, 8-13 years after chelation therapy for severe lead poisoning. There was no evidence of hypertension or reduced kidney function as assessed by serum creatinine (Cr) concentrations. Urinary alpha-amino nitrogen (Uaan) concentrations were significantly increased compared with 19 healthy age-matched controls. Ninety-four children (70%) had aminoaciduria (Uaan/Cr >0.23). Urinary glucose excretion was also significantly higher than that of 2 historical controls. Thirty-two children (24%) had glycosuria (>125 mg/24 h). Fractional excretion of phosphate was normal in all children. We conclude that a partial Fanconi syndrome can persist up to 13 years after childhood lead poisoning.
OBJECTIVES: To determine the prevalence of elevated blood lead levels among children living in a rural area and to determine the effectiveness of the Centers for Disease Control and Prevention (CDC) Lead Risk Assessment Questionnaire and additional questionnaire items in correctly identifying rural children having elevated blood lead levels. RESEARCH DESIGN: Comparison of results of a questionnaire that is intended to identify children as being at low or high risk for lead poisoning with children's blood lead levels. SETTING: The three practice sites of the only pediatric group in a rural county of upstate New York. PATIENTS: A consecutive sample of 705 children ages 6 to 72 months who were seen for health supervision visits between June and September 1993. RESULTS: Sixty-nine percent of the children were considered to be at high risk for lead poisoning by the CDC questionnaire. Overall, 8.4% of the children in the study had blood lead levels of 10 micrograms/dL (0.48 mumol/L) or higher, and 2.1% had blood lead levels of 15 micrograms/dL (0.72 mumol/L) or higher. No significant difference was noted between the percentages of high- and low-risk children who had elevated blood lead levels. To devise a more effective lead risk assessment tool for children in this setting, the two items from the CDC questionnaire and the two additional items that had the greatest predictive utility were combined to form a short alternative questionnaire. The alternative questionnaire thus consisted of items concerning whether the child has a sibling or playmate with lead poisoning, whether the child lives near an industry that potentially may release lead, whether the child lives in rented or owner-occupied housing, and whether the child has a parent who is a migrant farm worker. Children categorized as high risk with the alternative questionnaire were much more likely to have elevated blood lead levels than those who were categorized as low risk. The alternative questionnaire was very effective in correctly identifying children with elevated blood lead levels. Eighty-eight percent of children having blood lead levels of 10 micrograms/dL or higher and 100% of children having blood lead levels of 15 micrograms/dL or higher were classified as high risk by the questionnaire. Children classified as low risk were very unlikely to have elevated blood lead levels; 98% of low-risk children had blood lead levels of less than 10 micrograms/dL, and 100% had blood lead levels of less than 15 micrograms/dL. CONCLUSIONS: These results suggest that the CDC lead risk assessment questionnaire is of limited benefit in identifying rural children with blood lead levels 10 micrograms/dL or higher or 15 micrograms/dL or higher. An alternative questionnaire, however, seems to have marked clinical utility for identifying rural children with elevated blood lead levels.
Lead intoxication has been reported to occur as a consequence of nonoccupational exposure, the source being mostly the leaching of lead from fluid containers in domestic use. Three such cases are described, for which the cause has been identified to be in the lining of the vat used to contain home-made wine. All cases are members of the same family.