The Sequelae of Pica With and Without Lead Poisoning

Smith, Hugo Dunlap; Baehner, Robert L.; Carney, Thomas E.; Majors, William Joseph

doi:10.1001/archpedi.1963.02080040611011

Cited by 42 publications

(17 citation statements)

References 12 publications

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“…Information concerning behavioral effects of lead has been obtained from animal studies and from long-term psychological studies of children accidently poisoned by lead (9)(10)(11)(12)(13)(14)(15)(16).…”

Section: Discussionmentioning

confidence: 99%

“…Smith et al (10) likewise report that at least 25%b of the young children who survive an attack of acute lead encephalopathy sustain permanent brain damage. Subtle neurologic deficits and mental impairEnvironmental Health Perspectives (9).…”

Section: Introductionmentioning

confidence: 99%

“…Moncrieff et al (18), and, more recently by Gibson et al (14), and Millar et al (15) in patients with mental deficiency, and David et al (16) in hyperactive children. These studies (9)(10)(11)(12)(13)(14)(15)(16) were based on case histories of children who had ingested, intentionally or accidently, large amounts of lead from house paint, peeling wall plaster, toys, or poorly fired ceramicware and other eating utensils. The effect of relatively low level chronic exposure to lead on the brain of the young during their earliest period of life, when the brain is undergoing rapid growth and development into specialized function has not been investigated.…”

Section: Introductionmentioning

confidence: 99%

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

Michaelson¹,

Sauerhoff²

1974

Environ Health Perspect

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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 newborns 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 -y-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 exposure w...

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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

Michaelson¹,

Sauerhoff²

1974

Environ Health Perspect

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“…Sequelae to severe forms of poisoning such as encephalopathy are well established (1)(2)(3)(4). Although there is a substantial incidence of overexposure to lead among ghetto children as evidenced by elevated blood leads (5) and elevated tooth leads (6), there is little evidence relating to the question of whether overexposure in the absence of overt poisoning is harmful.…”

Section: Introductionmentioning

confidence: 99%

Follow-up of Children Overexposed to Lead

Albert¹,

Shore²,

Sayers³

et al. 1974

Environ Health Perspect

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The purpose of this study is to assess the nature and magnitude of the deleterious health effects of subclinical over-exposure to lead in children. The study stems from concerns about the impact on the health of children in city slums who ingest leaded paint without overt evidence of poisoning and the health implication of rising levels of lead in the environment from automotive emissions. The study sample was derived mainly from a registry of children on whom blood lead determinations had been made by the New York City Department of Health and was supplemented by siblings of the registry cases and children from a lead belt area who had extractions of deciduous teeth in dental clinics. Information was obtained through parental interview, medical records, and psychometric evaluation. The data show that deleterious health effects occur in children who were treated for severe lead poisoning and in children without diagnosed lead poisoning who had elevated blood leads (>0.06 mg-%). In the absence of diagnosed lead poisoning or elevated blood leads, excess lead exposure, measured in terms of high levels of lead in teeth, was not associated with deleterious health effects.

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“…Significantly elevated blood lead levels have been found in autistic children (Cohen et al 1976). Electroencephalographic abnormalities are seen as long as five years after treatment (Smith et al 1963). …”

Section: Learning and Behavioral Manifestationsmentioning

confidence: 99%

Effects of lead on collagen synthesis and renal function in the rat

Rodolfo-Sioson

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The Sequelae of Pica With and Without Lead Poisoning

Cited by 42 publications

References 12 publications

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

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

Follow-up of Children Overexposed to Lead

Effects of lead on collagen synthesis and renal function in the rat

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