Keep the 18-Month Health Supervision Visit

PEDIATRICS ◽  
1987 ◽  
Vol 80 (6) ◽  
pp. 967-967
Author(s):  
CONNIE LYBARGER ◽  
NANCY MURPHY

To the Editor.— In the April 1987 issue of Pediatrics, two important editorials were published. One, by Landrigan and Graef1 was on pediatric lead poisoning. The other, by Haggerty,2 was related to retaining the 18-month health supervision visit despite a recent change in immunization policies. We wish to point out a connection between these two commentaries; the 18-month health supervision visit provides an ideal opportunity to screen children for lead toxicity and to educate parents about lead poisoning. Blood lead levels previously thought to be safe have been found to be associated with irreversible neurologic damage.1

2008 ◽  
Vol 59 (2) ◽  
pp. 127-133 ◽  
Author(s):  
Aryapu Raviraja ◽  
Gaja Babu ◽  
Anita Bijoor ◽  
Geraldine Menezes ◽  
Thuppil Venkatesh

Lead Toxicity in a Family as a Result of Occupational ExposureThis article describes an entire family manufacturing lead acid batteries who all suffered from lead poisoning. The family of five lived in a house, part of which had been used for various stages of battery production for 14 years. Open space was used for drying batteries. They all drank water from a well located on the premises. Evaluation of biomarkers of lead exposure and/or effect revealed alarming blood lead levels [(3.92±0.94) μmol L-1], 50 % reduction in the activity of δ-aminolevulinic acid dehydratase [(24.67±5.12) U L-1] and an increase in zinc protoporphyrin [(1228±480) μg L-1]. Liver function tests showed an increase in serum alkaline phosphatase [(170.41±41.82) U L-1]. All other liver function test parameters were normal. Renal function tests showed an increase in serum uric acid [(515.81±86.29) μmol L-1] while urea and creatinine were normal. Serum calcium was low [(1.90±0.42) mmol L-1in women and (2.09±0.12) mmol L-1in men], while blood pressure was high in the head of the family and his wife and normal in children. Lead concentration in well water was estimated to 180 μg L-1. The family was referred to the National Referral Centre for Lead Poisoning in India, were they were received treatment and were informed about the hazards of lead poisoning. A follow up three months later showed a slight decrease in blood lead levels and a significant increase in haemoglobin. These findings can be attributed to behavioural changes adopted by the family, even though they continued producing lead batteries.


Blood ◽  
1979 ◽  
Vol 53 (4) ◽  
pp. 588-593 ◽  
Author(s):  
KC Caldwell ◽  
L Taddeini ◽  
RL Woodburn ◽  
GL Anderson ◽  
M Lobell

Abstract Lead interferes with heme synthesis in erythrocytes and has a deleterious effect on red cell membranes. We measured myeloperoxidase (MPO) enzyme activity in the granulocytes of dogs fed increasing quantities of lead. Concurrently, iodination capability and in vitro bactericidal activity were measured. Blood lead levels were monitored. Three of 4 dogs poisoned with lead developed significant decreases in MPO enzyme activity in their granulocytes. The decline in MPO activity correlated with cumulative lead toxicity as judged by blood lead levels and clinical signs of lead poisoning. Iodination ability in all 4 dogs decreased with cumulative lead toxicity. After discontinuation of lead administration, recovery of granulocyte MPO activity preceded recovery of iodination ability. This observation suggests the possibility of separate effects of lead on iodination ability and MPO activity. Moderate impairment of bactericidal capacity developed in 3 of 4 dogs with severe lead poisoning. Clinical infections were not observed during the course of the study.


Blood ◽  
1979 ◽  
Vol 53 (4) ◽  
pp. 588-593
Author(s):  
KC Caldwell ◽  
L Taddeini ◽  
RL Woodburn ◽  
GL Anderson ◽  
M Lobell

Lead interferes with heme synthesis in erythrocytes and has a deleterious effect on red cell membranes. We measured myeloperoxidase (MPO) enzyme activity in the granulocytes of dogs fed increasing quantities of lead. Concurrently, iodination capability and in vitro bactericidal activity were measured. Blood lead levels were monitored. Three of 4 dogs poisoned with lead developed significant decreases in MPO enzyme activity in their granulocytes. The decline in MPO activity correlated with cumulative lead toxicity as judged by blood lead levels and clinical signs of lead poisoning. Iodination ability in all 4 dogs decreased with cumulative lead toxicity. After discontinuation of lead administration, recovery of granulocyte MPO activity preceded recovery of iodination ability. This observation suggests the possibility of separate effects of lead on iodination ability and MPO activity. Moderate impairment of bactericidal capacity developed in 3 of 4 dogs with severe lead poisoning. Clinical infections were not observed during the course of the study.


2003 ◽  
Vol 301 (1-3) ◽  
pp. 75-85 ◽  
Author(s):  
Rachel Albalak ◽  
Gary Noonan ◽  
Sharunda Buchanan ◽  
W.Dana Flanders ◽  
Carol Gotway-Crawford ◽  
...  

PEDIATRICS ◽  
1972 ◽  
Vol 50 (4) ◽  
pp. 625-631
Author(s):  
Larry P. Kammholz ◽  
L. Gilbert Thatcher ◽  
Frederic M. Blodgett ◽  
Thomas A. Good

A rapid fluorescent method for estimation of free erythrocyte protoporphyrin (FEP) is described. Simple ethyl acetate-glacial acetic acid extractions are performed, fluorescence quantitated in a fluorimeter and expressed numerically by comparison with known coproporphyrin standards. Fifty-six children were studied and the extent of lead poisoning was evaluated initially and at different follow-up intervals. A clear relationship was shown between FEP fluorescence and blood lead levels. A correlation was also seen for the intensity of fluorescence and evidence for increased absorption of lead, as estimated by x-ray evidence of ingested lead and deposits in bone. Children with iron deficiency anemia also showed elevations of FEP fluorescence. This FEP fluorescence test allows for a rapid, numerical determination which appears to be useful as a screening test for lead intoxication. It can quickly select patients that may have markedly increased lead absorption and need prompt therapy or select those that at least require further studies for possible lead exposure or the presence of anemia.


PEDIATRICS ◽  
1975 ◽  
Vol 56 (4) ◽  
pp. 621-622
Author(s):  
Arthur W. Kaemmer ◽  
Byron R. Johnson

Dr. Greensher and his colleagues are to be congratulated for bringing to the readers' attention a most unusual source of lead poisoning. Inasmuch as many localities are initiating city-wide lead screening programs, it is obvious that pediatricians in this country will be seeing many children with abnormally elevated blood lead levels, and in many cases diligent efforts such as this will have to be undertaken to determine the exact source of the environmental lead. biggest problems with mass screening programs for lead poisoning are well outlined by Moriarty's article.2


PEDIATRICS ◽  
1988 ◽  
Vol 82 (3) ◽  
pp. 395-395
Author(s):  
MARGARET CLARK

In Reply.— We appreciate the work of Carraccio et al which confirms our findings that the anemia found in children with lead poisoning results from coexistent iron deficiency. The discrepancy between the two studies concerning the predictive value of blood lead in elevations of erythrocyte protoporphyrin bears further exploration. What is striking, however, is that in both series more than 50% of the variability in erythrocyte protoporphyrin remains unexplained. Now the public health focus is on detecting children with low blood lead levels—before even subtle CNS damage has occurred.


PEDIATRICS ◽  
1969 ◽  
Vol 44 (5) ◽  
pp. 661-667
Author(s):  
Lorry A. Blanksma ◽  
Henrietta K. Sachs ◽  
Edward F. Murray ◽  
Morgn J. O'Connell

The Chicago Board of Health in October 1986 began a mass-screening program using a blood lead test to detect lead poisoning in children. Atomic absorption spectroscopy made it possible to screen 5,000 specimens in 1 month, and to test a total of 68,744 children in 2 years. The incidence of high blood lead values was variable and seasonal it was lowest in November through January and highest in June. Control children exhibited the same seasonal variation in lead levels as did the children at-risk for lead poisoning. As a result of this program, 1,154 children were treated with chelates for lead poisoning in 1967 and 1968 at the Lead Poisoning Clinic, and the incidence of high blood lead levels among children living in the same areas declined from 8.5% in 1967 to 3.8% in 1968.


PEDIATRICS ◽  
1972 ◽  
Vol 49 (4) ◽  
pp. 606-608
Author(s):  
Paul Harris ◽  
Marshall R. Holley

Blood lead levels were determined on 24 mothers during labor and on the blood of their newborn offspring. The mean value for the mother's blood lead was 13.2 µg/100 gm (range 10 to 20) and for the cord blood 12.3 (range 10 to 20) µg/100 gm whole blood. These levels are lower than "normal" blood lead standards usually accepted in the diagnosis and treatment of childhood lead poisoning.


PEDIATRICS ◽  
1974 ◽  
Vol 54 (5) ◽  
pp. 626-628
Author(s):  
Richard W. Moriarty

The absence of fully effective treatment for lead encephalopathy, and the suggestive evidence that lead poisoning may cause brain damage even in the absence of overt encephalopathy, have led to massive efforts to prevent such damage. These preventive efforts have been directed toward screening to identify children who have absorbed an undue amount of lead from their environment, reducing their further exposure to lead, and removing already absorbed lead from those most in danger of developing ill effects. This approach has been codified in the Surgeon General's Report of 19701 which makes the following recommendations: 1. All young children who live in or visit old dilapidated buildings should have periodic blood lead determinations. 2. Any child with repeated blood lead levels over 40µg/100 ml whole blood should be considered to be at risk of lead poisoning, h ave current sources of exposure to lead investigated and corrected, and be followed closely to ensure that he does not develop higher blood lead levels or clinical symptoms. 3. All children with blood lead levels between 50 and 79µg/100 ml should have diagnostic tests for metabolic and clinical evidence of lead poisoning and be treated immediately if such evidence is present. 4. All children with blood lead levels over 80µg/100 ml should be hospitalized immediately and treated with chelating agents. Many aspects of this approach are subjects of current controversey, and the last word will not be written until much better knowledge of the natural history and ecology of lead poisoning is available.


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