Matilda S. McIntire

Air lead: relation to lead in blood of black school children deficient in glucose-6-phosphate dehydrogenase.

Forty-four black children at two elementary schools within 0.7 mile of a battery plant had significantly higher (P < .001) concentrations of lead in their bloods (34.1 � 9.7, micrograms per 100 milliliters, mean � standard deviation) than 122 students (26.3 � 7.1) at seven schools 1 to 3 miles distant; 5 months later there was a comparable difference between red cell lead values (54.1 � 18.5 versus 37.4 � 12.6). Among the blacks, those deficient in glucose-6-phosphate dehydro-genase had a higher (P < .005) concentration of lead in the blood after correction for anemia (32.9 � 9.7) than the nondeficient (25.7 � 8.8), and a higher concentration in the red cells (47.3 � 14.7 as compared to 35.6 � 15.8, P < .001); the enzyme effect was independent of geographic location.

Erythrocyte Nucleotides in Children—Increased Blood Lead and Cytidine Triphosphate

Summary: The erythrocyte nucleotides of 25 children, 1–5 years old, with normal and increased blood leads, were assayed by anion-exchange high-performance liquid chromatography. Red blood cells of the 12 children with blood lead (PbB) below 30 μ/dl (20.3 ± 6 μ/dl, X ± S.D.) had normal levels of activity of pyrimidine 5‘-nucleotidase (P5N) and their erythrocytes were virtually free of pyrimidine nucleotides except for small amounts of UMP and UDP. The purine nucleotides, predominantly ATP and GTP, were present at values similar to adults. In the 13 children with PbB 30–72 μ/dl (45.3 ± 14.3 μ/dl), total cytidine phosphates (CMP, CDP, CTP) were significantly (P < 0.001) increased from trace values to 8.31 ± 6.21 nmoles/1010 erythrocytes. The purine nucleotides were unchanged. P5N activity was 143.3 ± 22.0 units/g hemoglobin in children with PbB < 30 μ/dl and 75.4 ± 24.2 units (P < 0.001) in the high lead subjects. There was a logarithmic correlation of erythrocyte cytidine phosphates with PbB (r = 0.89, P < 0.001) and an inverse correlation of cytidine phosphates with ln P5N activity (r = 0.59, P < 0.001), of ln P5N with PbB (r = 0.64, P < 0.001) and of ln P5N with ln erythrocyte zinc protoporphyrin (Protoporphyrin IX) (r = 0.57, P < 0.001).Speculation: The accumulation of small amounts of erythrocyte CTP in children with increased lead exposure but with blood concentrations of leads as low as 30 μg/dl supports a lower threshold for the consequences of lead induced inhibition of pyrimidine 5′-nucleotidase (P5N) than indicated by earlier, less sensitive assays of nucleotides in adults with lead poisoning. The presence of CTP as the predominant pyrimidine nucleotide is similar to the profile in congenital deficiency of P5N but the nucleotides accumulate with less suppression of P5N than found in congenital deficiency. The significance of increased red cell cytidine phosphates at low levels of lead exposure is unknown but it appears to relate to suppression of P5N activity early in red cell maturation, and thus provides an index of antecedant lead exposure that correlates with erythrocyte zinc protoporphyrin.

Persistent dystonia in a brain-damaged child after ingestion of phenothiazine

Persistent dystonia in a 10-year-old mentally retarded girl followed an assumedintoxication with trifluoperazine and chlorpromazine. It would appear that in children, as in adults, this infrequent event of irreversible neurotoxicity occurs almost exclusively in subjects with antecedent brain damage.

How Effective is Safety Packaging

Of 96 ingestions involving safety packaging, 82% involved misuse. The package in some way was unacceptable to the consumer--it was too difficult to open or too difficult to close. Nonacceptance by the elderly was not a significant factor. In only 18% of the safety packaged ingestions, did the child upen the package. The child was more likely to be able to open the screw-cap and the strip-pack. The pop-off and press-lift were not opened by any child but were types misused only by parents. The older child with a record of prior poisoning was most likely to open a safety package. These children would appear to represent a hard core of risk subjects refractory even to safety packaging. Safety packaging has had a dramatic effect on the morbidity and mortality of accidental poisoning. There are two remaining problems that require further study: 1. The analysis of technical factors impeding consumer acceptance and child proofing. The ideal package is so easily handled by the adult that misuse does not occur, but is too difficult for the child to open. 2. The personality characteristics of the safety-package-resistant child. Safety packaging, as implemented by the Comsumer Product Safety Commission, has had remarkable success. Education did not reduce accidental poisoning; safety packaging does. Pediatricians, pharmacists, and toxicologists must work with industry and the Consumer Product Safety Commission to complete the goal of elimination of accidental poisoning.

Neurologic sequelae of poisoning in children

A detailed psychometric-psychologic-neurologic evaluation, carried ourt18 months to 14 years after an acute episode of poisoning, revealed no over-all difference between 41 children who had had acute central nervous system (CNS) intoxications and 41 paired control patients who had ingested a toxic agent but had had no acute CNS symptoms. Of the 8 children in the, study group who had had convulsions of variable duration, 6 have Binet scores below 90 (p

Effect of anemia on blood and tissue lead in rats

The effect of anemia on the lead content of blood, red cells, and tissue was studied in rats given oral lead, 54 mg/kg‐day for 6 days. The 16 rats made anemic (hematocrit, 26%) by bleeding on days 1, 3, and 5 had significantly higher concentrations of lead in the kidney, liver, red cells, blood, and brain (but not in the bone marrow). Increases in blood lead in anemic subjects were correlated with the concentrations in red cells, kidney, and liver. The greater increase in the lead content of all tissues of the anemic rats is consistent with increased lead absorption in anemia and is considered relevant to the clinical coexistence of anemia and lead poisoning.

Insecticide poisoning of childhood: Follow-up evaluation

T :i-i E o c c u R R E N C E Of late sequelae t o insecticide poisoning by the cholinesterase inhibitors and the chlorinated hydrocarbons has yet to be fully evaluated. Almost no attention has been given to this possibility in children who might, because of developmental immaturity, be particularly susceptible to neurologic sequelae. During the years from 1952 to 1963, 31 children, aged 11 months to 6 years, were hospitalized at Childrens Memorial Hospital, Omaha, with acute insecticide poisoning. Chlorinated hydrocarbons were responsible for 19 exposures; 4 of the 5 children exposed to concentrated solutions (above 5 per cent) had convulsions; 3 of the 19 had other central nervous system symptoms. Convulsions also occurred in the one child exposed to diazanon. The 11 miscellaneous

A BRIEF GUIDE TO THE MENTAL DEVELOPMENT OF PRESCHOOL CHILDREN.

Mental retardation affects twice as many children as any other chronic disorder. Since the general physician treats the majority of the children in the United States, he should be able to detect signs of subnormal mental development.A series of simple tests is suggested to aid in evaluating mental development. These procedures will not provide a complete psychologic assessment, but they will indicate whether a more comprehensive evaluation is necessary.

EFFECT OF ANEMIA ON BLOOD AND TISSUE LEAD OF RATS

Despite the epldemiologic coexistence of anemia and plumbism, the contribution of preexisting anemia to the risk for lead poisoning is incompletely defined. Rats were given oral lead, 54 mg/kg/day × 7. One group of 16 was made anemic (A) by bleeding off 25% of the blood volume on days 1, 3, and 5: sham phlebotomy was done on the same days in 12 non-anemic (NA) animals. Blood lead (Pb-B) and red cell lead (Pb-Rbc) were comparable until after day 5 when the hematocrit (Hct) of A dropped below 30%. At sacrifice on day 7 the comparable values, mean ± SE, were significantly different (*, p < .01) in the anemic (A) rats .These generalized increases support an increased absorption of lead in anemia consistent with the clinical predilection to lead toxicity of children and adults with low levels of hemoglobin.

NORMAL URBAN INCREASES IN RED CELL LEAD AND DEPRESSION OF RED CELL MEMBRANE Na/K ATPase

Na/K ATPase of the red cell membrane was investigated as evidence of a biochemical effect of moderate, “subtoxic” increases in blood lead.Na/K ATPase averaged 62% (61.7 ± 10.4) of total red cell membrane ATPase in 49 urban and suburban boys, ages 10-18, with a whole blood lead (Pb-B) of 10-32 μg% and a mean red cell lead (Pb-Rbc) of 33 μg% (33.4 ± 12.2). Within this group it was unaffected by age, race or hematocrit. Mean Na/K ATPase in 10 adult controls with Pb-B of 9-26 μg% was 70% (69.7 ± 6.47%). In 10 lead workers with a Pb-B of 55-102 μg% and mean Pb-Rbc of 121 μg% (120.6 ± 16.4%) the mean Na/K ATPase was 32% (32.1 ± 6.8%).The correlation coefficient of Pb-rbc with NaA ATPase in the 49 students and the 10 lead workers was 0.75, with the regression equation of y (Na/K ATPase) = 71.9% = 0.316 Pb-rbc. The linear correlation of red cell lead with Na/K ATPase at normal urban levels of blood lead suggests a significant health effect based on the known association of decreased enzyme activity with increased red cell permeability and loss of intracellular potassium.