A Study of Pica in Relation to Lead Poisoning

Greenberg, Morris; Jacobziner, H; McLaughlin, Mary C.; Fuerst, Harold T.; Pellitteri, Ottavio

doi:10.1542/peds.22.4.756

Cited by 27 publications

(1 citation statement)

References 12 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It is now well recognized that inorganic lead produces not only clinically definable encephalopathies and neuropathies, but also various behavioral changes indicative of cerebral dysfunction. However, only within the past fifty years has attention been called to its effects in children (2,8) in whom toxicity can easily be overlooked until clinically recognizable encephalopathy occurs (4).…”

Section: Introductionmentioning

confidence: 99%

Animal Models of Human Disease: Severe and Mild Lead Encephalopathy in the Neonatal Rat

Michaelson¹,

Sauerhoff²

1974

Environmental Health Perspectives

View full text Add to dashboard Cite

Inorganic lead produces cerebral dysfunction and clinically definable encephalopathies in man. To date there have been few studies on the biochemical changes in brain following exposure to inorganic lead. Studies correlating toxicity with behavioral and brain neurochemical changes following lead exposure have been hindered because adult laboratory animals are resistant to the central nervous system effects of lead poisoning. Such studies have been impeded by lack of suitable experimental models until Pentschew and Garro showed that brain lesions develop in neonatal rats when a pregnant rat newly delivered of her litter is placed on a 4% lead carbonate containing diet. Lead passes into the developing sucklings via maternal milk. Lead-poisoned new-borns have pronounced retardation of growth and during the fourth week of ilfe develop the severe signs of lead encephalopathy, namely, extensive histological lesions of the cerebellum, brain edema, and paraplegia. There is an approximate 85-fold increase in the lead concentration of both the cerebellum and cerebral cortex relative to controls, but edema and gross vascular changes are confined to the cerebellum. Ingested lead had little effect on RNA, DNA, and protein concentrations of developing rat cerebellum and cerebral cortex. However, there was a reduction of between 10 and 20% in the DNA content of the cerebellum around 3 weeks of age in the lead-exposed sucklings. This suggests a failure of cell multiplication in this part of the brain.A critical evaluation of this experimental approach indicated that under similar dietary conditions experimental lactating rats eat 30% less food than controls resulting in: (a) sustained loss in body weight of nursing mothers and that (b) offsprings who develop paraplegia and cerebellar damage do so after gaining access to lead containing diet. We have studied mothers' food consumption and body weight changes and blood, milk, and brain lead content; and newborns' body and brain weight changes, blood and brain lead content, and brain serotonin (5HT), norepinephrine (NE), dopamine (DA), and gamma-aminobutyric acid (GABA). We have found that a lactating mother rat eating 5% lead acetate (2.73% Pb) produced milk containing 25 ppm lead. When the mothers' diet is changed at day 16 from 5% PbAc to one containing 25 ppm Pb, and neonates allowed free access to the solid diet, the sucklings still have retarded body growth but do not develop paraplegia or grossly apparent vascular damage of the cerebellum. However, during the fourth week these animals exhibit a less severe form of "encephalopathy" consisting of hyperactivity, tremors, and stereotype behavior. Pair-fed controls coetaneous to experimental groups do not display such activities. There was no change in brain 5HT, GABA, or NE, but a 15-20% decrease in brain DA. Change in DA relative to other monoamines suggests a relationship between CNS dysfunction due to lead and DA metabolism in the brain.The experimental design as discribed provides a model of CNS dysfunction due to lead exposu...

show abstract

Section: Introductionmentioning

confidence: 99%

Animal Models of Human Disease: Severe and Mild Lead Encephalopathy in the Neonatal Rat

Michaelson¹,

Sauerhoff²

1974

Environmental Health Perspectives

View full text Add to dashboard Cite

show abstract

Myocardial Changes in Lead Poisoning

Kline¹

1960

Arch Pediatr Adolesc Med

View full text Add to dashboard Cite

Angina pectoris in patients with chronic lead poisoning has been mentioned briefly in the literature since 1829, when Andral, as quoted by Hirschfeld,5 described symptoms of palpitation, dyspnea, and generalized precordial discomfort in such patients.Hirschfeld,5 in 1926, coined the term "angina pectoris saturnina" and believed that this was the result of spasm of the coronary vessels brought about by the effects of lead. The patients whom he described were between 20 and 30 years old.There were no autopsies. Sporadic cases appeared in the literature since that time (Sessa and Guarino11). More recently, Read and Williams 8 studied a case of lead poisoning in which the patient had complained of substernal pain. The electrocardiograph revealed marked depression of the conduction system and T-wave abnormalities. The patient subsequently recovered, and thereafter his electrocardiographs were within normal limits. In two other patients with plumbism Read and Williams found bradycardia.Recently a 2-year-old child died at the Michael Reese Hospital with the diagnosis of acute lead poisoning. A complete autopsy was performed, and changes were encoun¬ tered in the myocardium characteristic of subacute interstitial myocarditis. A review of previous autopsy records disclosed four more children who had suffered from lead poisoning. Numerous sections of the heart in these cases were examined, and myocardial changes were found in all.It is the purpose of this study to draw attention to the myocardial involvement in cases of lead poisoning. The myocardial lesions per se seem to have been responsible

show abstract