Childhood Lead Poisoning in Russia: A Site-specific Pediatric Blood Lead Evaluation

1997 ◽  
Vol 3 (4) ◽  
pp. 241-248 ◽  
Author(s):  
Carol H. Rubin ◽  
Emilio Esteban ◽  
Robert Jones ◽  
Gary Noonan ◽  
Elena Gurvich ◽  
...  
PEDIATRICS ◽  
1996 ◽  
Vol 97 (6) ◽  
pp. 916-917
Author(s):  
Mary Beth Miller ◽  
Steven C. Curry ◽  
Donald B. Kunkel ◽  
Patricia Arreola ◽  
Ernest Arvizu ◽  
...  

Lead compounds are used as coloring agents for numerous products. Two cases of children with elevated blood lead concentrations encountered by the authors suggested that pool cue chalk may serve as a source of environmental lead. The objective of this study was to determine lead content of various brands and colors of pool cue chalk. Atomic absorption analyses were conducted of 23 different types of pool cue chalk for lead content. Three of 23 types of pool cue chalk contained more than 7000 ppm (mg/kg) lead: one manufacturer's green and tangerine chalk and another manufacturer's green chalk. It was concluded that some brands of pool cue chalk contain relatively large amounts of lead and could contribute to childhood lead poisoning.


2019 ◽  
Vol 25 ◽  
pp. S51-S57 ◽  
Author(s):  
Shelley A. Bruce ◽  
Krista Y. Christensen ◽  
Marjorie J. Coons ◽  
Jeffrey A. Havlena ◽  
Jon G. Meiman ◽  
...  

PEDIATRICS ◽  
1972 ◽  
Vol 49 (3) ◽  
pp. 474-475
Author(s):  
Jane S. Lin-Fu

I read the AAP's recent statement, "Acute and Chronic Childhood Lead Poisoning,"1 with disappointment verging on alarm. The statement recommends that "the major emphasis . . . be placed on the testing of dwellings for lead-pigment paints . . . in order to identify high-risk areas." Yet many such areas, or "lead belts," have long been so correctly identified that 20 to 40% of young children screened from these areas have been shown to have blood lead values of 40 µg/100 ml or more.2


PEDIATRICS ◽  
1992 ◽  
Vol 89 (4) ◽  
pp. 614-618
Author(s):  
Deborah E. Glotzer ◽  
Howard Bauchner

Published recommendations (1985) for the management of childhood lead poisoning suggest the use of ethylenediaminetetraacetic acid (EDTA)provocation testing and chelation as the mainstay of treatment for blood lead levels between 25 and 55 μg/dL. Since 1985 evidence has accumulated indicating that (1) levels of blood lead less than 25 μg/dL are detrimental to cognitive development, (2) EDTA provocation testing may result in potentially harmful shifts in the body lead burden, and (3) oral agents such as penicillamine and 2,3-dimercaptosuccinic acid are effective in reducing elevated lead levels. To determine how this evidence impacts on the management of childhood lead poisoning, the authors surveyed the lead poisoning clinics of pediatric departments in the cities estimated by the United States Public Health Service to have the largest number of children affected by lead poisoning. Thirty (70%) of 43 surveys were completed. Respondents indicated that the lowest blood lead level for which they would use a chelating agent to reduce the lead burden was as follows: 50 μg/dL (3%), 45 μg/dL (3%), 40μg/dL (13%) 35 μg/dL (3%), 30 μg/dL (27%), 25 μg/dL (47%) and 20μg/dL (3%). For all blood lead levels from 20 through 55 μg/dL, EDTA was the most frequently recommended chelating agent (chelation and provocation testing). Fifteen percent of responding lead clinics do not use the provocation test under any circumstances. For a child with a negative EDTA provocation test, the percentage of respondents recommending the use of any chelation therapy ranged from 16% for blood lead levels of 25 through 29μg/dL to 66% for levels of 50 through 55 μg/dL. Orally active chelating agents are used by fewer than one third of the responding lead clinics and were selected as the chelating agent of choice at all blood lead levels from 25 through 55 μg/dL by at least one respondent. The results of this survey indicate the following: (1) There is a wide range of blood lead levels for which chelation therapy is recommended. (2) The majority of children with elevated lead burdens are managed using EDTA. (3) The EDTA provocation test continues to be widely used. (4) The majority of children with blood lead levels of 25 through 44 μg/dL with negative provocation tests do not receive chelation therapy. (5) Orally active chelating agents are used in the minority of lead clinics. (6) No common approach for the treatment of lead toxicity appears to exist. (7) In the majority of pediatric centers, current management of blood lead elevation does not appear to reflect new information regarding the effects and treatment of lead poisoning.


PEDIATRICS ◽  
1981 ◽  
Vol 67 (6) ◽  
pp. 904-906
Author(s):  
Alan R. Cohen ◽  
Margret S. Trotzky ◽  
Diane Pincus

Hematologic abnormalities in childhood lead poisoning may be due, in part, to the presence of other disorders, such as iron deficiency or thalassemia minor. In order to reassess increased lead burden as a cause of microcytic anemia, we studied 58 children with class III or IV lead poisoning, normal iron stores, and no inherited hemoglobinopathy. Anemia occurred in 12% and microcytosis in 21% of these children. The combination of anemia and microcytosis was found in only one of 58 patients (2%). When only children with class IV lead poisoning were studied, the occurrence of microcytosis increased to 46%. However, the combination of microcytosis and anemia was found in only one of these 13 more severely affected patients. Microcytic anemia was similarly uncommon in children with either blood lead concentration ≥ 50 µg/100 ml or erythrocyte protoporphyrin concentration ≥ 110 µg/100 ml. These data indicate that microcytosis and anemia occur much less commonly than previously reported in childhood lead poisoning uncomplicated by other hematologic disorders.


PEDIATRICS ◽  
1987 ◽  
Vol 79 (4) ◽  
pp. 582-583
Author(s):  
PHILIP J. LANDRIGAN ◽  
JOHN W. GRAEF

Great gains in the understanding and control of childhood lead poisoning have been made since this disease was first diagnosed in the early years of this century. Efforts of pediatricians, public health officials, and enlightened regulators have brought about substantial reductions in the lead content of paint, food, milk, water, air, and, most recently, gasoline. Significant decreases in children's blood lead levels and in the incidence of lead poisoning have resulted. Few American pediatricians trained in the past decade have ever seen a child with the coma, papilledema, and convulsions of acute lead encephalopathy. Despite these advances, the silent epidemic of childhood lead poisoning is not yet over. It is particularly well now that we function in this manner because some of the important issues that we are dealing with at this time are items that cannot be completed by this date. We will depend upon the new Executive Committee and new Executive Board to carry these issues to completion. Last year, I spoke to you with a great deal of concern about our problems in medical liability. I expressed a conviction that an independent research on this subject could contribute to a real resolution of the problem. We have pursued this plan during the year and I can tell you now that, at the instigation of the Academy, the Institute of Medicine of the National Academy of Sciences has held a feasibility study and a planning meeting during this year. This has lead to the formation of a proposal for the research that is now waiting only for the funding to proceed.


2007 ◽  
Vol 7 ◽  
pp. 479-492 ◽  
Author(s):  
Anne M. Rothweiler ◽  
Elena E. Cabb ◽  
Shawn L. Gerstenberger

One of the first steps in addressing the problem of childhood lead poisoning is to identify the possible sources of exposure in specific communities and target high-risk populations with appropriate interventions. Due to several factors, such as lack of funding and lack of blood lead reporting, little information exists regarding the occurrence of childhood lead poisoning and the prevalence of potential exposure sources in the state of Nevada. Following the recent establishment of a Nevada-based Lead Poisoning Program, we compiled the most current information available on Nevadans, and use this knowledge to suggest future research objectives and outreach activities for the state. Accordingly, we identify the characteristics of the vulnerable Nevada populations, explore possible sources of lead exposure unique to Nevada, and summarize the existing data on childhood lead poisoning. Emerging data indicates that Nevada is an area of rapid population growth, characterized by increasing immigration from Latin America, increasing numbers of children from low-income families with no health insurance. Also, childhood lead poisoning may arise from exposure to non-paint sources of lead. After presenting the Nevada statistics, we propose and recommend a set of research and outreach strategies that best suit the needs of Nevada residents.


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