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PubMedDate not supplied

Pathogenetic considerations of pica in lead poisoning.

An important factor associated with lead poisoning in children is the habit of eating non-food substances, a condition termed pica. In search for underlying mechanisms involved in the pathogenesis of pica, this investigation presents evidence in support of the hypothesis that in many families failure of normal mother-child interaction, paternal deprivation, culturally dependent maternal oral interests and significant stress factors in the home where abundant lead-containing material is available are etiologically related to the development of pica in lead poisoning. Other factors, which have been thought to be associated with pica, are nutritional deficiencies and maladaptive behavior patterns. A multifocal treatment approach is considered to be most effective.

Child↗
PubMed1994

[Lead poisoning in pregnancy].

Endemic areas of lead poisoning have recently been rediscovered raising an important public health problem, particularly for pregnant women and their offspring. Theoretically, pregnant women can no longer be exposed to occupational sources with the application of public health regulations but other sources including water contamination, wall paint, industrial wastes and automobile exhaust fumes cannot be ignored. The placental barrier is permeable to free serum lead and levels in cord blood reaches 5 to 10% of the maternal blood level. In addition, lead may be released from maternal bone reserves during pregnancy and thus become a major source of intoxication for the fetus. Lead content in fetal organs increases with gestational age and may affect the nervous system and calcium dependent organs. Moderate lead levels of 100 micrograms/L can inhibit fetal haeme and erythropoiesis. Besides the classical signs of lead poisoning, pregnant women risk spontaneous abortion and increased blood pressure. Manifestations in the fetus and newborn include prematurity, fetal hypotrophy and malformations. Other manifestations are not seen until several years after birth and include retarded mental development and muscular and behaviour disorders. Diagnosis is based on screening tests which should be used in cases of suspected accidental or environmental intoxication. Tests should include assay of zinc protoporphyrins and aminolevulinic acid dehydrase. A search for the source of the contamination should be undertaken when blood levels above 250 micrograms/L are observed. Treatment with metal chelators is not recommendable (except in extreme life-threatening cases) during pregnancy due to their teratogenic effect. Prevention is the only adequate treatment.

Bone and Bones↗
PubMed1997

Intracranial vascular calcifications, glioblastoma multiforme, and lead poisoning.

A 72-year-man with previous lead poisoning presented with raised intracranial pressure and localizing neurologic signs. CT scans showed a high-grade glioma and extensive intracranial calcifications, which proved to be vascular in distribution on postmortem examination. The latter findings support the concept of dystrophic calcification following lead-induced cerebrovascular injury. Lead poisoning should be considered in the differential diagnosis of unexplained intracranial calcifications. There is also evidence from previous studies to suggest a causative relationship between lead poisoning and development of glioma.

Aged↗
PubMed1984

Chronic renal failure with gout: a marker of chronic lead poisoning.

EDTA (calcium disodium edetate) lead mobilization and x-ray fluorescence (XRF) finger bone lead tests were done in 42 patients with chronic renal failure and without persisting lead intoxication. Nineteen of 23 patients with gout and 8 of 19 without gout had positive EDTA lead mobilization tests. Those patients with gout excreted significantly more excess lead chelate than those without gout. In the gout group 17 patients denied any childhood or industrial exposure to lead. They had a greater number of positive tests and excreted significantly more excess lead chelate than 14 patients with neither gout nor lead exposure. These results confirm that gout in the presence of chronic renal failure is a useful marker of chronic lead poisoning. Of 27 patients with positive lead mobilization tests, only 13 had elevated XRF finger bone lead concentrations (sensitivity 48%). Three of 15 patients with negative lead mobilization tests had elevated XRF finger bone lead concentrations (specificity 80%). Although the XRF finger bone lead test is a convenient noninvasive addition to the diagnostic evaluation of patients with chronic renal failure and gout, its application is limited due to the lack of sensitivity of the method.

Aged↗
PubMed1992

Prevalence of radiographic evidence of paint chip ingestion among children with moderate to severe lead poisoning, St Louis, Missouri, 1989 through 1990.

Although experts once believed that ingesting chips of lead-based paint was the major cause of lead poisoning among children, conventional wisdom now holds that lead-contaminated dust and soil are the major routes of exposure. Data from a childhood lead-poisoning treatment clinic were examined to assess the frequency with which children ingest paint chips. For this study, the reports on abdominal radiographs of 90 children with moderate to severe lead poisoning who had received their first chelation treatment during 1989 or 1990 were reviewed. According to a radiologist's evaluation, 13 of 90 abdominal radiographs (14%; 95% confidence interval [CI] 7% to 22%) showed evidence of paint chip ingestion. Of 46 children with blood lead levels greater than or equal to 55 micrograms/dL, 12 (26%) had radiographs that showed paint chips, whereas only 1 (2%) of 44 children with blood lead levels less than 55 micrograms/dL had such radiographs (prevalence ratio = 11.5; 95% CI 1.6 to 84.6). The actual proportion of children with moderate to severe lead poisoning who have consumed leaded-paint chips is likely to be higher than this estimate based on radiographic evidence. While lead-contaminated dust is a major source of lead exposure, ingestion of leaded-paint chips clearly remains an important source of exposure among children with moderate to severe lead poisoning.

Acute Disease↗
PubMed1983

Increase of delta-aminolevulinic acid dehydratase (ALAD) in rat erythrocytes in lead poisoning.

The well known fact that the activity of delta-aminolevulinic acid dehydratase (ALAD: EC 4.2.1.24) is reduced in red cells of animals with lead poisoning was found to be upset, by using a modified method of Gibson's original procedure, for determination of activated ALAD activity. The modified method involves addition of 0.2 mM Zn2+ and then preheating the enzyme solution at 60 degrees C for 5 min before following Gibson's original procedure. With this methodological modification, the ALAD activity of erythrocytes of rats poisoned with lead was found increased. Furthermore, the enzyme was purified from the peripheral blood of lead-poisoned rats. ALAD protein in peripheral blood was also determined by single radial immuno diffusion using rabbit anti-serum raised against rat liver ALAD. As the result, the ALAD activity obtained from the modified method was found to be directly proportional to the absolute amount of enzyme proteins determined both by chemically and immunochemically. The modified method for measuring true ALAD content in blood cells in lead poisoning is more reliable than previous ones.

Animals↗
PubMed1986

Occupational lead poisoning in Ohio: surveillance using workers' compensation data.

To determine the utility of workers' compensation (WC) data in a system for the surveillance of occupational lead poisoning, we reviewed workers' compensation claims for lead poisoning in Ohio. For the period 1979 through 1983, 92 (81 per cent) of the 114 claims attributed to lead met our case definition of lead poisoning. The likelihood that a company had a case of lead poisoning was strongly correlated with the number of claims against the company. Thirty companies accounted for the 92 cases; two companies accounted for 49 per cent of these. Inspection by the Occupational Safety and Health Administration (OSHA) occurred at 14 of these companies, all of which were cited for violations of the OSHA lead standard. Comparison of the Standard Industrial Classification (SIC) codes for the 14 companies inspected by OSHA with the 15 companies not inspected by OSHA revealed that OSHA inspected battery manufacturers, non-ferrous foundries, secondary smelters, and primary lead smelters, but not bridge painters, manufacturers of electronic components, mechanical power transmission equipment, pumps, and paints, nor a sheriff's office where firing range slugs were remelted to make new bullets. Neither the number of cases of lead poisoning at a company nor the size of a company was related to the likelihood of being inspected by OSHA. Claims for WC appear to be a useful adjunct to an occupational lead poisoning surveillance system; their usefulness should be compared to that of other systems such as laboratory reports of elevated blood lead levels in adults.

Adult↗
PubMed2003

Chronic lead poisoning in an adult battery worker.

BACKGROUND: Lead poisoning is a common environmental health hazard in developing countries. Incidences of lead poisoning are seen in all age groups, especially in adults working in lead-based industries, where many still remain unaware of the adverse effects of exposure to unusually high levels of lead. METHODS: We report the case of an adult battery worker, who initially received symptomatic treatment because of clinical misdiagnosis. Later, he was treated with appropriate chelators, which helped to decrease blood lead levels drastically. However, being unable to change his occupation, he continues to be exposed to potentially lethal doses of lead. CONCLUSIONS: A key role for health agencies, besides providing opportunities for diagnosis and therapy, should be to increase public awareness about this widespread environmental hazard through education, documentation and communication.

Adult↗
PubMed1999

[The effects of lead poisoning on expression of nerve growth factor gene of submandibular gland in mice].

OBJECTIVE: To study the toxicity of lead poisoning to submandibular gland and its effects on nerve growth factor (NGF) gene expression in mice. METHODS: An experimental model with lead poisoning was established and its histopathological changes in the submandibular gland of mice were observed under light and electronic microscopes. Effects of lead poisoning on expression of NGF mRNA in submandibular gland were analyzed quantitatively by human NGF DNA probe labelled with digoxin with in situ hybridization. RESULTS: Body weight of the mice with experimental lead poisoning reduced, and their lead levels in blood and submandibular gland increased. Lobular atrophy, fibrous hypertrophy, angiectasis of the stroma and enlargement of lobule interstitial in mouse submandibular gland with lead poisoning could be found under light and electron microscopes. Their rough surfaced endoplasmic reticulum was extended and mitochondrion swollen. Graphic analysis showed that diameters of the secretory striate ducts and granular tubules decreased in the mice with lead poisoning. Results of in situ hybridization indicated that hybridized signals in the granular and secretory striate ducts and granular tubules reduced significantly, and NGF mRNA expression decreased. CONCLUSION: Lead is toxic to the submandibular gland of mice and can affect their NGF gene expression.

Animals↗
PubMedDate not supplied

[Changes in the kinetic characteristics of reactions catalyzed by erythrocyte delta-aminolevulinate dehydratase in experimental lead poisoning in rats].

An increase in values of both kinetic parameters (Km and Vmax) of the delta-aminolevulinate dehydratase reaction was observed in blood of rats poisoned with lead. The Km value of the reaction was increased, while Vmax--decreased, after addition of Pb2+ into rat blood in vitro. The results obtained as well as the data published in literature suggest that a compensatory mechanism appears to function in vivo, where a substrate, delta-aminolevulenic acid, plays a triggering role.

Aminolevulinic Acid↗
PubMed2001

[Lead poisoning in calves due to old white lead paint].

A case of poisoning by chronic ingestion of lead in calves with a peracute clinical course is described. The source of lead was a prime coat of white lead on old white painted doors. These doors originated from an institution for aged people and had been used as pen walls for fattening calves. About 12 weeks later five animals died within hours after onset of CNS-symptoms. The post mortem examination of three animals revealed one with multifocal laminar edema and mild vasculitis in the cerebrocortex, one with acid fast intranuclear inclusion bodies in the renal tubular epithelial cells and one without lesions. Liver, kidney and abomasal contents of two animals were analysed for lead content. The concentration was diagnostic for lead poisoning in one case only.

Abomasum↗
PubMed1988

Recurrent lead poisoning in a child with immobilization osteoporosis.

Lead poisoning associated with progressive osteoporosis in patients who have been previously lead poisoned has been described but poorly documented. We managed a 4-year-old child with a prior history of plumbism who developed recurrent blood lead elevations (as high as 70 mcg/dl), requiring multiple courses of EDTA, after acute paraplegia from transverse myelitis. The patient was hospitalized throughout these periods of chelation. No exogenous sources of lead were found. Calcium, phosphate, magnesium, alkaline phosphatase and parathyroid hormone levels remained normal while vitamin D levels were depressed. Metabolic studies revealed negative calcium balance with an elevated urinary calcium:creatinine ratio. Long-bone radiographs were remarkable for progressive osteoporosis with no evidence of metallic foreign bodies. This case illustrates that bone, the major repository of lead, can become a source of significant lead level elevations in conditions associated with accelerated resorption.

Child, Preschool↗
PubMed1999

The association between state housing policy and lead poisoning in children.

OBJECTIVES: This study examined the effect of an active program of household lead paint hazard abatement, applied over 22 years, on childhood lead poisoning in Massachusetts. METHODS: A small areas analysis was used to compare screening blood lead levels of children in Worcester County, Mass (n = 27,590), with those in Providence County, RI (n = 19,071). Data were collapsed according to census tract. RESULTS: The percentage of children with lead poisoning (blood lead level > or = 20 micrograms/dL [Pe20]) was, on average, 3 times higher in Providence County census tracts (3.2% vs 0.9% in Worcester County census tracts, P < .0001), despite similar percentages of pre-1950s housing in both counties. The ratio of Pe20 in Providence vs Worcester County census tracts was 2.2 (95% confidence interval = 1.8, 2.7), after adjustment for differences in housing, sociodemographic, and screening characteristics. This estimate was robust to alternative regression methods and sensitivity analyses. CONCLUSIONS: Massachusetts policy, which requires lead paint abatement of children's homes and places liability for lead paint poisoning on property owners, may have substantially reduced childhood lead poisoning in that state.

Child↗