Lead Poisoning in Children

Moncrieff, Alan; O, Koumides; Clayton, Barbara E.; Patrick, A. D.; Renwick, A. G.; Roberts, G. E.

doi:10.1136/adc.39.203.1

Cited by 174 publications

(32 citation statements)

References 19 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%

“…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%

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

Michaelson¹,

Sauerhoff²

1974

Environ Health Perspect

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“…However, pica, a behavior often found to occur in the absence of social consequences, is not acceptable at any level in any stimulus context due to health risks. These risks include intestinal blockage, poisoning, and parasitic infection (Fisher, Piazza, Bowman, Kurtz, Sherer, & Lachman, 1994;Foxx & Martin, 1975;Moncrieff, Koumides, Clayton, Patrick, Renwick, & Roberts, 1964). Therefore, successful assessment and treatment of automatically reinforced pica is of particular importance.…”

Section: Introductionmentioning

confidence: 99%

Functional assessment and treatment of pica: a single‐case experiment

Rapp

Dozier

Carr

2001

Behavioral Interventions

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The pica of a 6-year-old girl diagnosed with autism was initially shown to persist in the absence of socially mediated consequences. In an attempt to provide a competing source of oral stimulation, we used a stimulus preference assessment to identify food items that were subsequently presented noncontingently. However, the noncontingent schedule could not be thinned to a practical variation while still maintaining reductions in pica. A subsequent multielement evaluation of response blocking and verbal reprimands demonstrated that neither intervention both produced and maintained low levels of pica. Verbal reprimands were then used in conjunction with noncontingent food presentation, but this intervention did not produce signi®cant reductions in pica. Suppression of pica was ultimately obtained in both a clinic setting and in the child's natural environment using contingent, varied auditory stimulation. The results are discussed in the context of the`least restrictive alternative' model of treatment selection.

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“…test results in children, have been diagnosed (Byers and Lord 1943, Mellins and Jenkins 1955, Jenkins and Mellins 1957, Byers 1959, Cohen and Ahrens 1959, Smith 1964, Moncrieff et al 1964, Gibson et al 1967, Pueschel 1974, Beattie et al 1975, Landrigan et al 1975). …”

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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Lead Poisoning in Children

Cited by 174 publications

References 19 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

Functional assessment and treatment of pica: a single‐case experiment

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

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