Induction of myeloperoxidase deficiency in granulocytes in lead- intoxicated dogs

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.

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Induction of myeloperoxidase deficiency in granulocytes in lead- intoxicated dogs

Blood ◽

10.1182/blood.v53.4.588.bloodjournal534588 ◽

1979 ◽

Vol 53 (4) ◽

pp. 588-593

Author(s):

KC Caldwell ◽

L Taddeini ◽

RL Woodburn ◽

GL Anderson ◽

M Lobell

Keyword(s):

Enzyme Activity ◽

Lead Poisoning ◽

Clinical Signs ◽

Lead Toxicity ◽

Blood Lead ◽

Blood Lead Levels ◽

Red Cell ◽

Lead Levels ◽

Red Cell Membranes

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.

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Lead Toxicity in a Family as a Result of Occupational Exposure

Archives of Industrial Hygiene and Toxicology ◽

10.2478/10004-1254-59-2008-1861 ◽

2008 ◽

Vol 59 (2) ◽

pp. 127-133 ◽

Cited By ~ 4

Author(s):

Aryapu Raviraja ◽

Gaja Babu ◽

Anita Bijoor ◽

Geraldine Menezes ◽

Thuppil Venkatesh

Keyword(s):

Occupational Exposure ◽

Liver Function ◽

Lead Poisoning ◽

Lead Toxicity ◽

Blood Lead ◽

Blood Lead Levels ◽

Zinc Protoporphyrin ◽

Function Tests ◽

The Family ◽

Lead Levels

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.

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Fast Hemoglobin in Lead Poisoning

Blood ◽

10.1182/blood.v28.3.377.377 ◽

1966 ◽

Vol 28 (3) ◽

pp. 377-386 ◽

Cited By ~ 7

Author(s):

SAMUEL CHARACHE ◽

DAVID J. WEATHERALL

Keyword(s):

Lead Poisoning ◽

Molecular Species ◽

Hypochromic Anemia ◽

Blood Lead ◽

Blood Lead Levels ◽

Oxidized Glutathione ◽

Elevated Blood ◽

Lead Levels ◽

Elevated Blood Lead Levels

Abstract 1. An electrophoretically fast hemoglobin was found in approximately 40 per cent of preschool children with elevated blood lead levels. 2. Fast hemoglobin was found more often in lead-poisoned patients with hypochromic anemia than in patients with normochromic red cells. 3. Fast hemoglobin differed from hemoglobins produced in vitro by incubation with chromate or oxidized glutathione. It had electrophoretic properties similar to that found in a few patients receiving tolbutamide. 4. Fast hemoglobin could not be differentiated from normal hemoglobin A3 by any technic utilized. 5. Both lead and A3 hemoglobins were heterogeneous molecular species. 6. The mechanisms leading to the production of hemoglobin A3 and lead hemoglobin remain unknown.

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Delta-Aminolevulinic Acid Dehydratase Enzyme Activity and Susceptibility to Lead Toxicity in Uganda’s Urban Children

10.20944/preprints202112.0371.v1 ◽

2021 ◽

Author(s):

Ambrose Mukisa ◽

Denis M Kasozi ◽

Claire Aguttu ◽

Joseph Kyambadde

Keyword(s):

Enzyme Activity ◽

Aminolevulinic Acid ◽

Lead Toxicity ◽

Blood Lead ◽

Urban Children ◽

Sub Saharan Africa ◽

Nutrition Status ◽

Blood Lead Levels ◽

Acid Dehydratase ◽

Lead Levels

Rapid industrialization, urbanization, and population explosion in sub-Saharan Africa escalate environmental Lead levels with subsequent elevation of blood Lead levels in children. Nutrition status, age, and genetics govern one’s susceptibility to Lead toxicity. This study expounded this susceptibility by relating blood Lead levels, d-aminolevulinic acid dehydratase enzyme activity (ALAD), and genetic variations of proteins that code for ALAD enzyme in urban children of Uganda. Spectrophotometric analysis for blood Lead (BL), hemoglobin levels, and determination d-levels aminolevulinic acid dehydratase enzyme activity of the blood samples from 198 children were performed prior to a polymerase chain reaction and restriction fragment length digestion for ALAD polymorphism was done. Up to 99.5% of samples coded for the ALAD1 allele whereas 0.05% coded for ALAD2. Genotypes ALAD2-2 members had elevated BLL (mean 14.1 µg/dL) and reduced ALAD enzyme activity compared to others. This, therefore, implies that the majority of children hoard BL which may affect them later in life.

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Keep the 18-Month Health Supervision Visit

PEDIATRICS ◽

10.1542/peds.80.6.967 ◽

1987 ◽

Vol 80 (6) ◽

pp. 967-967

Author(s):

CONNIE LYBARGER ◽

NANCY MURPHY

Keyword(s):

Lead Poisoning ◽

Lead Toxicity ◽

Blood Lead ◽

Recent Change ◽

The Other ◽

Blood Lead Levels ◽

Health Supervision ◽

Lead Levels

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

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Blood lead levels and risk factors for lead poisoning among children in Jakarta, Indonesia

The Science of The Total Environment ◽

10.1016/s0048-9697(02)00297-8 ◽

2003 ◽

Vol 301 (1-3) ◽

pp. 75-85 ◽

Cited By ~ 36

Author(s):

Rachel Albalak ◽

Gary Noonan ◽

Sharunda Buchanan ◽

W.Dana Flanders ◽

Carol Gotway-Crawford ◽

...

Keyword(s):

Risk Factors ◽

Lead Poisoning ◽

Blood Lead ◽

Blood Lead Levels ◽

Lead Levels

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RAPID PROTOPORPHYRIN QUANTITATION FOR DETECTION OF LEAD POISONING

PEDIATRICS ◽

10.1542/peds.50.4.625 ◽

1972 ◽

Vol 50 (4) ◽

pp. 625-631

Author(s):

Larry P. Kammholz ◽

L. Gilbert Thatcher ◽

Frederic M. Blodgett ◽

Thomas A. Good

Keyword(s):

Lead Poisoning ◽

Glacial Acetic Acid ◽

Blood Lead ◽

Deficiency Anemia ◽

Blood Lead Levels ◽

X Ray ◽

Fluorescent Method ◽

Lead Levels ◽

Fluorescence Test

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.

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Question Regarding Need for Treatment

PEDIATRICS ◽

10.1542/peds.56.4.621b ◽

1975 ◽

Vol 56 (4) ◽

pp. 621-622

Author(s):

Arthur W. Kaemmer ◽

Byron R. Johnson

Keyword(s):

Mass Screening ◽

Lead Poisoning ◽

Blood Lead ◽

Blood Lead Levels ◽

Elevated Blood ◽

Screening Programs ◽

Environmental Lead ◽

Need For Treatment ◽

Lead Levels ◽

Elevated Blood Lead Levels

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

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Too Much Lead, Too Little Iron

PEDIATRICS ◽

10.1542/peds.82.3.395 ◽

1988 ◽

Vol 82 (3) ◽

pp. 395-395

Author(s):

MARGARET CLARK

Keyword(s):

Public Health ◽

Iron Deficiency ◽

Lead Poisoning ◽

Predictive Value ◽

Blood Lead ◽

Blood Lead Levels ◽

The Public ◽

Erythrocyte Protoporphyrin ◽

Lead Levels

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.

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INCIDENCE OF HIGH BLOOD LEAD LEVELS IN CHICAGO CHILDREN

PEDIATRICS ◽

10.1542/peds.44.5.661 ◽

1969 ◽

Vol 44 (5) ◽

pp. 661-667

Author(s):

Lorry A. Blanksma ◽

Henrietta K. Sachs ◽

Edward F. Murray ◽

Morgn J. O'Connell

Keyword(s):

Seasonal Variation ◽

Atomic Absorption ◽

Lead Poisoning ◽

Atomic Absorption Spectroscopy ◽

Screening Program ◽

Blood Lead ◽

Blood Lead Levels ◽

Children At Risk ◽

Lead Levels ◽

Poisoning In Children

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.

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