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PubMedDate not supplied

Insecticide poisoning of peafowls and lead poisoning in a cockatoo.

The deaths of peafowls and a cockatoo were respectively traced to insecticide and lead toxicities. The specific insecticide could not be identified but was demonstrated in the liver by use of fruit flies. The liver of the cockatoo contained 7.1 ppm of lead. The source was presumably a plastic feeder painted with a leaded paint.

Animals↗
PubMed2001

[Lead poisoning in adults. Experience of the Poison Control Center of Marseille from 1993 to 2000].

OBJECTIVE: Report the experience of the Marseille's anti-poison center with lead poisoning adults. PATIENTS AND METHODS: Between 1993 and 2000, 45 adults patients consulted the poison Centre of Marseille for a history of lead exposure (9 women, 36 men, average age 44 YO, between 22 an 76 YO). The lead sources were mostly occupational (welding, heavy metal industries...), but some were environmental (shooting as a hobby, hunting,...). RESULTS: Ninety-one percent of the patients presented with a clinical feature of possible lead intoxication (asthenia, abdominal pain, anaemia, seizures,...). For 22 patients, calcitetracemate provocation test was negative. 6 patients with a positive test refused to be treated. 16 patients with a positive test were treated with chelation therapy (average lead blood level 566 micrograms/l--mini 320 micrograms/l, maxi 943 micrograms/l--and average lead urine elimination 3,011 micrograms/24 H--mini 789 micrograms/24 H, maxi 7,229 micrograms/24 H. 58 cures were done (1 to 12 cures for each patient). The average quantities of lead eliminated in the urine during the chelation therapy was 30,912 micrograms +/- 29,059 micrograms by case. For 12 patients who stopped the lead exposure after the diagnosis of lead poisoning, the chelaion therapy permitted to decrease the lead blood level of 69%. For 4 patients still exposed during the treatment, the lead blood level decrease of 7% only. For the 16 treated patiEnts, a clinical improvement was noted, and no adverse effects of chelation therapy was observed during the 58 cures.

Adult↗
PubMed1989

Lead poisoning among household members exposed to lead-acid battery repair shops in Kingston, Jamaica.

To investigate the risk of lead poisoning among household members exposed to 'backyard' battery repair shops (BBRS) in Kingston, Jamaica, environmental and blood lead (PbB) were measured at 24 households (112 individuals) with a BBRS worker or located at a BBRS premises and at 18 neighbourhood control households (74 individuals). Elevated PbB (greater than or equal to 25 micrograms per decilitre [micrograms/dl]) was common among subjects of all ages living at BBRS premises, especially among children less than age 12, 43% of whom had PbB greater than 70 micrograms/dl. Potentially hazardous soil and house dust lead levels were also common at BBRS premises, where 84% of yards had soil lead levels above 500 parts per million (geometric mean 3388 parts per million [ppm] at BBRS premises households with a BBRS worker). Geometric mean blood and environmental lead levels were significantly lower at control households, where less than 10% of subjects in all age groups had elevated PbB (maximum 33 micrograms/dl). Sharing a premises with a BBRS was a stronger determinant of household blood lead and environmental contamination than was the presence of a BBRS worker in a household. Blood lead levels were associated with soil and house dust lead levels in all age groups. We conclude that small battery repair shops, which have also been described in other developing countries, create a high lead poisoning risk for nearby residents.

Adolescent↗
PubMedDate not supplied

[Acute lead poisoning in cows due to feeding of lead contaminated ash residue].

In a dairy herd of 21 cows which were on pasture during the day at the end of May 2002, four eight years old cows were suddenly inappetent and showed severe diarrhoea consisting of black discolorate feces. A few days after the onset of the disease, three affected cows exhibited neurological disorders. These cows were admitted to the IInd Medical Clinic of the University for Veterinary Medicine in Vienna. Following clinical signs were observed: circulatory weakness, anorexia, atony of the rumen, diarrhoea and in accordance with acute lead poisoning typical signs of the central nervous system. One cow died and the other two animals were euthanized. Results of blood testing were anaemia, basophil spotting of erythrocytes, increase of liver enzymes and CK, hypocalcaemia, decrease of potassium and phosphate. The cerebrospinal fluid of two cows showed increased CK-, LDH- and AST-values. The lead contents of whole blood samples were between 0.486 and 0.928 mg/kg, of liver samples 13.3 to 114.4 mg/kg, of kidney samples 172.2 to 448 mg/kg and of rumen content 59 mg/kg fresh matter. At necropsy, enteritis, liver fluke disease and severe interstitial and alveolar pulmonary emphysema were found. Pathohistologically typical ischaemic necrosis of neurons predominantly at the tips of the gyri, disseminated petechial hemorrhages and moderate diffuse neovascularisation, but no acid-fast intranucleolar inclusion bodies in the renal tubules were observed. As causative agent of the acute lead poisoning a residue on combustion, taken up by the cows on the pasture, was confirmed. The ash residue was formed by combustion of three tires which contained 450 g heavy weights of 96.5% lead for wheel balance. The lead content of the ash residue was between 2.9 and 28 g/kg dry matter.

Animal Feed↗
PubMed2001

Fatal pediatric lead poisoning--New Hamphshire, 2000.

Fatal pediatric lead poisoning is rare in the United States because of multiple public health measures that have reduced blood lead levels (BLLs) in the population. However, the risk for elevated BLLs among children remains high in some neighborhoods and populations, including children living in older housing with deteriorated leaded paint. This report describes the investigation of the first reported death of a child from lead poisoning since 1990 (1). The investigation implicated leaded paint and dust in a home environment as the most likely source of the poisoning. Lead poisoning can be prevented by correcting lead hazards, especially in older housing, and by screening children at risk according to established guidelines (2).

Child, Preschool↗
PubMed2002

Assessment of cleaning to control lead dust in homes of children with moderate lead poisoning: treatment of lead-exposed children trial.

In this article we describe the assessment and control of lead dust exposure in the Treatment of Lead-exposed Children (TLC) Trial, a clinical trial of the effects of oral chelation on developmental end points in urban children with moderately elevated blood lead levels. To reduce potential lead exposure from settled dust or deteriorated paint during the drug treatment phase of the trial, the homes of 765 (98%) of the randomized children (both active and placebo drug treatment groups) were professionally cleaned. Lead dust measurements were made in a sample of 213 homes before and after cleaning. Geometric mean dust lead loadings before cleaning were 43, 29, 308, and 707 micro g/ft2 in the kitchen floor, playroom floor, playroom windowsill, and playroom window well samples respectively. Following cleaning, floor dust lead loadings were reduced on average 32% for paired floor samples (p < 0.0001), 66% for windowsills (p < 0.0001), and 93% for window wells (p < 0.0001). Cleaning was most effective for 146 homes with precleaning dust lead levels above the recommended clearance levels, with average reductions of 44%, 74%, and 93% for floors (p < 0.0001), windowsills (p < 0.0001), and window wells (p < 0.0001), respectively. Despite these substantial reductions in dust lead loadings, a single professional cleaning did not reduce the lead loadings of all dust samples to levels below current federal standards for lead in residential dust. Attainment of dust levels below current standards will require more intensive cleaning and lead hazard reduction strategies.

Chelating Agents↗
PubMed1990

[Morphological changes in the nervous system in lead poisoning. I. Experimentally induced lead neuropathy].

A morphological study on experimental model of lead (Pb) neuropathy (by the method of Pentschev, A., 1966) was described. Dense inclusions in Schwann's cells and satellite cells of the sensory ganglia were found by an electron microscope in the examined peripheral nerves (n. ischiadicus) and sensory ganglia (g. lumbale and g. trigeminale--Gasseri). These finding supported direct toxic action of Pb on these structures and proved their participation in the pathogenesis of developing neuropathy.

Animals↗
PubMed1993

[Morphological changes in the nervous system in lead poisoning. II. Experimental lead-induced encephalopathy].

The morphological investigation in an experimental model of lead (Pb) encephalopathy (according to the method of A. Pentschew, 1966) is presented. Electron microscopy-dense inclusions are found out in the nuclei and cytoplasm of astrocytes and in some ependyma cells in the investigated cortical and subcortical (paraventricular) structure of the brain and spinal cord. This confirms the direct toxic action of Pb on these structures and proves their participation in pathogeneses of the developing encephalopathy. The established inclusions in the ependyma and the data about a disturbance of the blood-brain barrier give a reason to be proposed the possibility for a penetration of Pb in the nervous system not only through a blood but also through a cerebrospinal fluid way.

Animals↗
PubMed1998

[Lead poisoning caused by lead-glazed ceramic household article, initially assumed to be of occupational origin].

The authors observed serious lead intoxication of a 18 year old female ceramic apprentice caused by tea with lemon stored in a glazed ceramic teapot made by the patient herself. The case history suggests: 1. the need of warning people to avoid the use of ceramic tablewares made by insufficient technology for alimentary purposes. 2. Patient with lead exposure can have also alimentary intoxication. 3. It seems advisable to perform screening tests of the ceramic apprentices who use lead glazes in order to detect the eventual increased absorption of lead in time.

Adolescent↗
PubMed2006

Validation of a 20-year forecast of US childhood lead poisoning: Updated prospects for 2010.

We forecast childhood lead poisoning and residential lead paint hazard prevalence for 1990-2010, based on a previously unvalidated model that combines national blood lead data with three different housing data sets. The housing data sets, which describe trends in housing demolition, rehabilitation, window replacement, and lead paint, are the American Housing Survey, the Residential Energy Consumption Survey, and the National Lead Paint Survey. Blood lead data are principally from the National Health and Nutrition Examination Survey. New data now make it possible to validate the midpoint of the forecast time period. For the year 2000, the model predicted 23.3 million pre-1960 housing units with lead paint hazards, compared to an empirical HUD estimate of 20.6 million units. Further, the model predicted 498,000 children with elevated blood lead levels (EBL) in 2000, compared to a CDC empirical estimate of 434,000. The model predictions were well within 95% confidence intervals of empirical estimates for both residential lead paint hazard and blood lead outcome measures. The model shows that window replacement explains a large part of the dramatic reduction in lead poisoning that occurred from 1990 to 2000. Here, the construction of the model is described and updated through 2010 using new data. Further declines in childhood lead poisoning are achievable, but the goal of eliminating children's blood lead levels > or =10 microg/dL by 2010 is unlikely to be achieved without additional action. A window replacement policy will yield multiple benefits of lead poisoning prevention, increased home energy efficiency, decreased power plant emissions, improved housing affordability, and other previously unrecognized benefits. Finally, combining housing and health data could be applied to forecasting other housing-related diseases and injuries.

Child, Preschool↗
PubMed1994

Preventing childhood lead poisoning.

Of all the neurotoxins, lead is the longest known and best understood. Because we know so much about what it does, where it is, and what is required to remove it from the presence of children, lead poisoning should also be one of the easiest diseases to eradicate. Despite this, progress in the primary prevention of childhood lead poisoning has been halting and erratic. In this paper, I outline the rapidly advancing state of knowledge on the epidemiology and toxicology of lead, examine some of the reasons for the gap between what is known and what has been accomplished, and outline the steps toward authentic primary prevention. Eradication of childhood lead poisoning is a realizable goal. Its importance is unquestioned; former Secretary of the Department of Health and Human Services Louis Sullivan declared in 1991 that it is the most serious environmental disease of North American children.

Child↗