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Results for “LEAD POISONING”

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PubMed1987

American Academy of Pediatrics Committee on Environmental Hazards and Committee on Accident and Poison Prevention: Statement on childhood lead poisoning.

Patterns of childhood lead poisoning have changed substantially in the United States. The mean blood lead level has declined, and acute intoxication with encephalopathy has become uncommon. Nonetheless, between 1976 and 1980, 780,000 children, 1 to 6 years of age, had blood lead concentrations of 30 micrograms/L or above. These levels of absorption, previously thought to be safe, are now known to cause loss of neurologic and intellectual function, even in asymptomatic children. Because this loss is largely irreversible and cannot fully be restored by medical treatment, pediatricians' efforts must be directed toward prevention. Prevention is achieved by reducing children's exposure to lead and by early detection of increased absorption. Childhood lead poisoning is now defined by the Academy as a whole blood lead concentration of 25 micrograms/L or more, together with an erythrocyte protoporphyrin level of 35 micrograms/dL or above. This definition does not require the presence of symptoms. It is identical with the new definition of the US Public Health Service. Lead poisoning in children previously was defined by a blood lead concentration of 30 micrograms/dL with an erythrocyte protoporphyrin level of 50 micrograms/dL. To prevent lead exposure in children, the Academy urges public agencies to develop safe and effective methods for the removal and proper disposal of all lead-based paint from public and private housing. Also, the Academy urges the rapid and complete removal of all lead from gasoline.(ABSTRACT TRUNCATED AT 250 WORDS)

Child↗
PubMed1984

Erythroid karyorrhexis in the peripheral blood smear in severe arsenic poisoning: a comparison with lead poisoning.

Three men with severe arsenic poisoning were hospitalized with working diagnoses, respectively, of peptic ulcer, pancreatitis, and viral gastroenteritis. In the first two patients, correct diagnosis was delayed until the return of heavy-metal screening tests ordered because of painful peripheral neuropathy in one and sudden flaccid paralysis, resembling Guillain-Barré syndrome, in the other. Both patients had coarsely stippled red blood cells with markedly abnormal nuclei in their peripheral blood smears. These distinctive hematologic features led to an early diagnosis in the third patient. The author's review of past cases of lead poisoning showed that red blood cell karyorrhexis also tends to occur in patients who consume illicit whiskey ("moonshine"). Karyorrhexis or marked dyserythropoiesis in the peripheral smear, not heretofore described in arsenic or lead poisoning, may indeed be a unique hematologic clue. Scrutiny of the peripheral blood and/or buffy coat smear in patients with perplexing gastrointestinal or neurologic symptoms may enable earlier diagnosis and better therapy of arsenic poisoning.

Adult↗
PubMed1986

delta-Aminolaevulinic acid dehydratase as an index of the presence and severity of lead poisoning in acute and chronic lead exposure.

The activity of delta-aminolaevulinic acid dehydratase (ALA-D; porphobilinogen synthase) was measured in whole blood from a group of workers with acute exposure to lead and with low blood lead levels, a group of workers with chronic lead exposure and high blood lead levels, and a group of people without undue environmental lead exposure. The activity of ALA-D was reduced significantly at low blood lead levels only if undue exposure to lead had occurred, and was thus a reflection of low level lead poisoning. In chronic lead exposure the enzyme was not invariably reactivated fully with dithiothreitol, indicating more severe enzyme poisoning. The one lead worker with symptomatic lead poisoning had the most marked enzyme suppression. Measurement of both ALA-D activity and blood lead levels was more useful than the measurement of blood lead levels alone in the diagnosis and assessment of the severity of lead poisoning.

Acute Disease↗
PubMedDate not supplied

Severe lead poisoning in pregnancy.

BACKGROUND: Lead freely crosses the placenta. Consequently, gestational lead poisoning is not only harmful to the woman but also to the developing fetus, invariably producing congenital lead poisoning. The scope and consequences of severe lead poisoning in pregnancy (blood lead level > or =45 microg/dL) have not been well characterized. METHODS: We reviewed our experience in the management of women with severe gestational lead poisoning. Additionally, we reviewed the literature on this disorder in an effort to identify patterns in etiology and outcome. RESULTS: Over a 3-year period treatment was provided to 7 severely lead-poisoned women. A 25-year review of the medical literature identified an additional 8 cases. Among these 15 women, 70% were Hispanic, all of whom developed lead poisoning from the ingestion of soil, clay, or pottery ("tierra"). Other sources of lead poisoning were paint chip ingestion (n = 2), household renovation, and use of a complementary-alternative medication (bone meal). Lead poisoning was discovered in the third trimester in 12 (86%) subjects after the women presented with subtle but characteristic findings of severe lead poisoning, including malaise, anemia, or basophilic stippling on blood smear; one woman was identified when she presented after a generalized seizure, having a blood lead level of 104 microg/dL. Five women received chelation therapy during pregnancy with CaNa(2) EDTA, dimercaprol, or succimer. At delivery mean maternal blood lead level was 55 microg/dL, whereas mean neonatal lead level was 74 microg/dL (P =.009). Thirteen neonates underwent chelation, all within the first 28 days of life. No infant in the current series had an identifiable birth defect. CONCLUSIONS: On the basis of this experience we conclude that severe lead poisoning in pregnant women has the following characteristics: 1) it most often occurs because of intentional pica, 2) its presenting features are subtle, often consisting only of malaise and anemia, and 3) blood lead levels in the neonate are higher than simultaneous maternal lead levels.

Female↗
PubMedDate not supplied

Maternal perceptions of lead poisoning in children with normal and elevated lead levels.

INTRODUCTION: The purpose of this study was to examine mothers' perceptions of the severity and susceptibility of their children to lead poisoning and to determine if a correlation existed between mothers' knowledge of lead poisoning and their children's blood lead levels. It was thought that mothers of children with lead poisoning (lead levels > or = 10 micrograms/dL) would score lower on a test of their perceptions and knowledge of lead poisoning than would mothers of children with normal lead levels (lead levels < or = 9 micrograms/dL). METHOD: A cross-sectional study comparing scores of a questionnaire completed by mothers whose children had elevated blood lead levels and mothers whose children had normal blood lead levels was conducted. RESULTS: No difference was found in the median test score between the 2 groups. For the correct responses on a question-by-question comparison, significant difference existed between groups; however, the percentage of correct responses was not always greater for the mothers of children with normal blood lead levels. DISCUSSION: Mothers' perceptions and knowledge of lead poisoning were not associated with their children's blood lead levels.

Adult↗
PubMed1997

Childhood lead poisoning on the US-Mexico border: a case study in environmental health nursing lead poisoning.

Human exposure to environmental hazards is a major public health problem along the US-Mexico border due to socioeconomic, cultural and political factors. Childhood lead exposure is endemic in areas of extreme poverty and substandard housing. Hispanic children of indigent, poorly-educated, disenfranchised families are at disproportionate risk. Risk management is contingent upon consideration of the interrelationships between socioeconomics, politics, and culture. This case study explains childhood lead poisoning in a colonia family living at subsistence level from such a perspective. The purpose of the study was to identify, explain, and ameliorate lead exposure pathways. Case study methodology was used to support or refute the proposition that these children were exposed to occupational lead. The children were the study sampling unit and the family a subunit. An embedded single case explanatory design was appropriate. Data were collected from exposure surveys, environmental and blood specimens, and review of medical records. Pattern-matching and explanation-building techniques were used to analyze data. The study illustrated how extreme poverty, lack of access to health services, social isolation, language and legal barriers, and hazardous occupations may be singularly common risk factors for Hispanic children on the US-Mexico border. The study is pertinent to public health nurses who work with this population.

Child↗
PubMed1952

LEAD poisoning.

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Lead↗
PubMed1997

Preventing lead poisoning in children.

Lead poisoning is the most significant and prevalent disease of environmental origin among US children. Despite over 100 years' knowledge of the special hazards of lead exposure for young children, it has taken over a century for effective primary prevention to be adopted. Obstacles to primary prevention have included deliberate campaigns by industry to prevent restrictions upon such uses on lead as plumbing, paints, and gasoline additives; influence of industrial support of biomedical research at major US medical schools: lack of appropriate policy mechanisms to identify and control lead exposures; and opposition to investing resources in lead poisoning prevention. The removal of lead from gasoline, which began in the United States in 1972 and was completed in 1995, has resulted in almost fourfold reductions in median blood lead levels in US children from 1976 to 1991. Increased screening and interventions to identify and abate lead sources, such as lead in housing, also contributed to this major public health success. Nevertheless, lead exposures remain prevalent, although increasingly less generally distributed. Perhaps because of the renewed "ghettoization" of lead, support for lead poisoning prevention has waned. Objections to investing public and private resources in screening and source abatement have challenged the continuing commitment of public health officials to prevention. The demonstrable success and social benefits of preventing lead toxicity are cited in support of continued preventive health policies.

Child Welfare↗