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Treatment of lead poisoning in wild geese.

Twenty-seven wild geese (Anser albifrons) suffering from lead poisoning caused by ingestion of lead shot were treated with disodium calcium ethylenediaminetetraacetate. The concentration of lead in blood ranged from 0.4 to 23.0 micrograms/ml, with a mean concentration of 5.6 micrograms/ml. In 22 of the birds, 1 to 48 lead pellets (mean, 10.5 pellets/bird) were seen on radiographs of their gizzards. Eleven of 27 birds recovered 3 to 8 weeks after the initiation of treatment. In the birds that recovered, the lead pellets were rapidly eroded as the birds recovered their appetites in response to treatment, and disappeared radiographically between treatment days 17 and 52. The birds that did not survive died within 4 weeks, despite decreased concentrations of lead in blood. Of these 16 birds, 15 had radiographic evidence of impaction of the proventriculus at the first examination and no evidence of resolution of the impaction at the time of death. In contrast, only 2 of the 11 geese that recovered had impaction of the proventriculus at the time of admission. Thus, the condition of the proventriculus seems to be the first consideration to evaluate in the prognosis of lead poisoning in geese.

Animals↗

Lead poisoning from ingestion of a toy necklace--Oregon, 2003.

Although ingestion of dust from lead-based paint is the most common source of lead exposure among children in the United States, lead also can be present in unsuspected objects. Ingestion of these objects can result in elevated blood lead levels (BLLs). This report describes an investigation by the Deschutes County Health Department and the Oregon Department of Human Services of lead poisoning in a boy who swallowed a medallion pendant from a necklace sold in a toy vending machine. The investigation resulted in a nationwide recall in September 2003 of the implicated toy necklace. Clinicians and caregivers should consider lead poisoning in any child who ingests, or puts in his mouth, a metal object. Cases of lead poisoning should be reported immediately to public health authorities to prevent other children from being exposed to the same sources of lead.

Child, Preschool↗

Long term mortality study of chromate pigment workers who suffered lead poisoning.

Long term mortality was studied in a group of 57 chromate pigment workers who suffered clinical lead poisoning, mostly between 1930 and 1945. One death was attributed to lead poisoning and there were significant excesses of deaths from nephritis (observed/expected 3/0.24) and cerebrovascular disease (9/2.20), as well as non-significant excesses for respiratory diseases (7/3.59) and accidents and violence (3/1.13). The deaths from nephritis followed long spells of service exceeding 10 years. Poisoning appeared to have more adverse long term effects on older workers: 15 men aged 40 or over at the time of acute poisoning experienced generally high mortality, and 30 years later or by the end of 1981 only two survived instead of the seven expected. The risk of cerebrovascular disease appeared to be unrelated to duration of exposure and affected even men employed for under one year. Excluding the 57 lead poisoned men, other contemporary workers at the factories showed no excess mortality from cerebrovascular disease.

Adult↗

[Chronic lead poisoning in children today. A pathology of poverty and social exclusion].

Despite the recognition of lead poisoning in children as a major public health problem in France since the 1980's, the setting-up of systematic detection of lead poisoning at a national level has not yet been done. The main source of intoxication in children is in paintings containing ceruse in housing built before 1948. Moderate chronic poisoning, although leading to irreversible lesions, particularly of the central nervous system, remains usually unnoticed. The biological diagnosis is mainly based upon blood lead level, completed by the protoporphyrine-zinc level. Large scale identification of dangerous housing and the control of rehabilitation are the only means available to decrease the incidence of lead posioning. Targeted screening is difficult because it concerns children excluded from classical health care systems. Prevention and long-term treatment requires elimination of the source of lead intoxication after an environmental inquiry. This raises the problems of rehousing and follow-up of intoxicated children.

Child↗

Lyssaviral infection and lead poisoning in black flying foxes from Queensland.

Pteropid lyssaviral infection, lead poisoning, and the difficulties in diagnosing pteropid lyssaviral infection using histopathological examination of tissues are described in wild black flying foxes (Pteropus alecto) from northern Queensland (Australia). An adult female P. alecto showed aggression before death in January 1995. Lead poisoning was diagnosed due to the presence of intranuclear lead inclusion bodies in renal proximal convoluted tubular epithelium and high concentrations of lead in renal and hepatic tissues, 370.03 +/- 7.35 ppm and 16.76 +/- 0.53 ppm, respectively. Renal inclusion bodies were composed of lead, calcium, phosphorus, and possibly sulphur; some inclusions had their granules arranged in concentric bands. This bat also had a moderate concentration (8.09 +/- 0.18 ppm) of cadmium in renal tissue. An adult male P. alecto presented with ascending paralysis before it died in May 1996. Pteropid lyssaviral infection was diagnosed subsequently in both bats in September 1996 by immunofluorescent and immunoperoxidase antibody tests for rabies on brains and viral culture from brains. Neither bat had gross or microscopic lesions of the brain that suggested a lyssaviral infection, apart from occasional, subtle, eosinophilic cytoplasmic inclusions in the neurones of the brain stem of the female. These cases illustrate the need for a specific test to detect pteropid lyssavirus such as an immunofluorescent antibody test for lyssavirus rather than histopathological examination of tissues.

Animals↗

An esoteric occupational hazard for lead poisoning.

A case of life threatening lead poisoning was diagnosed clinically in a Jewish scribe and verified by appropriate laboratory studies. The special ink used by the scribe was found to contain lead in appreciable amounts. Eleven more asymptomatic subjects, both scribes and manufacturers of the ink, were studied and five were found to have subclinical lead overload. Handling or production of this ink is a potential hazard for lead intoxication.

Adult↗

[Evaluation of the screening strategy for lead poisoning in 1-to-3-year-old children monitored in maternal-child welfare centers in Paris].

A procedure for screening for lead poisoning was implemented since 1987 in the maternal and child health centers of 6 Paris "arrondissements". It relies on a screening of the children through environmental and clinical information. Our study aimed at evaluating this procedure and at estimating the prevalence of lead poisoning in the children aged 1 to 3 years old attending free maternal and child health centers in Paris. We did a cross-sectional survey of a sample of 512 children. A questionnaire concerning each child's risk factors was answered by the paediatric nurses of the clinics. Potential lead poisoning cases were detected by capillary determining of free erythrocyte protoporphyrins (FEP). Blood lead level (PbB) was measured in children with FEP > or = 350 micrograms/l. The prevalence rate of lead poisoning was estimated at 1.9% +/- 1.7% for a PbB threshold > or = 250 micrograms/l and at 9.6% +/- 3.5% for a PbB threshold > or = 150 micrograms/l. The detection procedure identified 4 children out of 5 with a PbB > or = 250 micrograms/l and 2 children out of 3 with a PbB > or = 150 micrograms/l.

Child, Preschool↗

[Lead poisoning after ingestion of ayurvedic drugs].

HISTORY AND CLINICAL FINDINGS: A 60-year-old woman suffering from rheumatoid arthritis and taking methotrexate was admitted with recurrent episodes of nausea, vomiting, constipation, loss of appetite, myalgia and backache, sternal chest pain, costal and jaw pain. On examination the epigastrium was tender to palpation and nonrigid. INVESTIGATIONS: Laboratory tests showed normocytic anemia (with a hemoglobin concentration of 8.6 g/dl), elevated blood urea and creatinine levels, hyponatremia, hypochloremia, hemolysis and polychromasia, anisocytosis, poikilocytosis and basophilic stippling of several red cells. On gastroscopy an ulcer was excluded, ultrasound scan of abdomen, X-ray of chest and pelvis showed no abnormalities. The electrocardiogram showed a right bundle branch block and left anterior hemiblock. DIAGNOSIS, TREATMENT, AND COURSE: In the differential diagnosis of anemia with basophilic stippling and abdominal discomfort, lead poisoning was found. Whole-blood lead concentration was markedly raised to 852 micro g/l (normal < 100 micro g/l). Lead poisoning was the result of the use of ayurvedic drugs during a period of 7.5 months prior to admission to the authors' hospital. CONCLUSION: Heavy metal poisoning, especially lead poisoning, should be considered in the differential diagnosis in patients with unspecific clinical symptoms taking traditional Indian remedies.

Anemia↗

[Involvement of free radicals in lead poisoning].

The following proves that free radicals are involved in lead poisoning: An enolamine form of 5-aminolevulinic acid (ALA), a haem precursor which accumulates in the body of lead poisoned patients undergoes fast autooxidation with concomitant generation of reactive oxygen species. The transmembrane potential and calcium ions fluxes of isolated rat mitochondria are strongly affected by ALA. This toxic effect is inhibited by antioxidant enzymes. Induction of antioxidant enzymes' activity was observed in lead-exposed workers.

Animals↗

[Chronic lead poisoning].

Epidemiologic studies have shown a steady decrease in the blood lead concentrations in populations from developed countries. This decrease is due to the promulgation of legislative measures designed to reduce sources of environmental lead exposure. As a result, during the last several years, lead poisoning has been reported with a minor frequency. We describe here three patients with chronic lead poisoning owing to chronic ingestion of water contaminated by lead pipes.

Chronic Disease↗

Wisconsin children at risk for lead poisoning.

The 1999 US Government Accounting Agency (GAO) report to Congress documented that among children in the United States, those served by federal health care programs had high rates of lead poisoning but low rates of blood lead testing. To further explore these findings, the Wisconsin Department of Health and Family Services initiated matching the state's blood lead test data file with the Medicaid eligibility file, and with the WIC Program enrollment file. This article examines data analyzed from the matched files for the year 1999. The results of the analysis of Wisconsin data shadowed the national findings contained in the GAO report. About half of the Wisconsin children enrolled in Medicaid and WIC have been screened, the majority of lead poisoned children in Wisconsin receive Medicaid (80%) and WIC (60%) services. Additional data collected by the department on the physical and environmental health of severely lead-poisoned children indicates that lead-coated surfaces and deterioration were identified as the primary source and cause of the poisoning. These findings support the Wisconsin recommendations for blood lead testing of 1 and 2 year olds living in older or renovated housing, and all children enrolled in Medicaid or WIC.

Child↗

[A "historical" case of lead poisoning via drinking water: diagnostic and therapeutic issues].

INTRODUCTION: It is likely that lead poisoning via drinking water is often overlooked because of its supposed rarity and nonspecific early symptoms, which result in delayed management. EXEGESIS: One case of severe lead poisoning via drinking water is reported. The diagnosis was long missed and a particularly long chelating treatment was required. The clinical features included lead colic, a Burton's lead line, anemia, polyneuritis and arterial hypertension. Eighteen courses of calcium EDTA were required to obtain 'biological recovery'. The poisoning was linked to a very long water supply lead pipe and potomania secondary to alcohol withdrawal. CONCLUSION: This case report illustrates how difficult the early recognition of lead poisoning can be, and underlines the need to inquire about a toxic aetiology, particularly via the environment, of otherwise unexplained pathological conditions.

Chelating Agents↗

Public policy and child lead poisoning: implementation of Title X.

Nurses who care for pediatric patients in all settings must be aware of the critical effects of lead poisoning in children. Lead causes toxic effects in the human body, especially in children. These hazards have led to government involvement related to the issues of lead poisoning. Currently, governmental programs are set up under Title X: The Residential Lead Based Paint Hazard Reduction Act of 1992. However, the political changes and potential cuts in government spending may affect programs such as Title X. Because of this and their important role in child health, pediatric nurses should understand the political process, the implementation of such programs, and effects of potential funding cuts.

Child↗

[Renal failure caused by mercury and lead poisoning in the calf (author's transl)].

The renal lesions in three calves with mercury poisoning (phenylmercuric acetate) and two calves with lead poisoning are described. In addition of slight tubular degeneration, glomerulonephritis occurred in the animals with mercury poisoning. Moreover, uraemia, oedema and haemorrhages were present. Lesions of the brain not were found. In the animals with lead poisoning, chronic renal tubular changes and characteristic intranuclear inclusion bodies in the proximal tubular cells were observed. The juxtamedullary glomeruli showed proliferative mesangial lesions. In one calf, the cerebral cortex showed oedema, necrosis of neurons and an increase in glial cells.

Animals↗

[A little known source of lead poisoning: rasp and file manufacture (author's transl)].

Seventy-two subjects employed in rasp manufacturing and, especially, manual "engraving" were studied by the authors, mainly in order to find out whether lead poisoning could be induced by their particular working activity. Twelve subjects (16.7%) were found to have standard biological parameters for lead (blood lead, urinary delta-ALA and urinary coproporphyin levels) within normal limits. Twenty-five (34.7%) showed hematochemical and urinary signs of increased lead absorption, and 35 (48.6%) marks of lead poisoning, more or less severe. The manufacturing process was then studied and working places were inspected too. Finally, lead poisoning was found to be due to a small lead block, used by hand-engravers in order to avoid damages to the already engraved surfaces of the rasps. This survey leads therefore to the conclusion that rasp manual engraving has to be included among the working activities which can induce lead poisoning.

Female↗

[Microenvironmental lead poisoning].

Authors describe two cases of lead poisoning of unusual origin. A 43 year old male patient bought some waste metal in order to build a fence around his new house for saving money. He removed the old corroded coat of paint using a grinder without any protection. Consequently, he had got grave lead intoxication with colic and anemia. Another 34 year old unemployed male person moulded leaded chessmen in his own kitchen. This activity resulted in serious intoxication of the patient and highly increased lead absorption of the family members. In addition to the exploration of professional exposure the authors stress also the significance of the clearing up of occasional lead-related hobbies and home activities in case of lead intoxication of unknown origin.

Adult↗