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Biomedical subjects

G Winneke

Publications and source records attributed to G Winneke.

At least 55 records · Page 3Linked to original sources
PubMed1991

Sensitive periods for behavioral toxicity of polychlorinated biphenyls: determination by cross-fostering in rats.

Polychlorinated biphenyls (PCBs) are transferred to developing organisms via the milk rather than through placental barriers. Recent epidemiological data, however, suggest a greater importance of the prenatal exposure period for the development of neuropsychological disorders. The relative effectiveness of pre- and postnatal PCB exposure was compared in a cross-fostering experiment in rats. Female Wistar rats were fed diets containing 0 or 30 mg PCB/kg. After birth half of the litters in each exposure group were nursed by dams of the other condition. Six different congeners were determined in the brains of the offspring at various ages. Internal exposure to higher chlorinated congeners peaked at weaning in groups with postnatal or permanent exposure, whereas the concentration of a low-chlorinated compound was lower at weaning than at birth or at later age stages. Brain tissue levels in prenatally treated rats declined with aging. In two behavioral paradigms, active avoidance learning and retention of a visual discrimination task, prenatally exposed rats exhibited alterations similar to those of permanently treated subjects, while postnatal exposure caused no detectable behavioral changes. These results support the above-mentioned epidemiological studies which related neurodevelopmental deficits in children to prenatal PCB exposure.

Animals↗
PubMed1990

Behavioral effects of pre- and postnatal exposure to a mixture of low chlorinated PCBs in rats.

Polychlorinated biphenyl (PCB)-treated Wistar rats were tested on three different behavioral paradigms. Animals were pre- and postnatally exposed to a technical mixture of PCBs with a chlorine content of 42%. Exposure levels were 0, 5, or 30 mg/kg diet. These conditions did not affect the health of the dams, the litter size or weight, or the physical development of the offspring. Relative liver weights in the offspring, however, were elevated in a dose-dependent manner. Open-field ambulation, active avoidance learning, and operant conditioning on a fixed interval 30-sec schedule (FI-30-sec) were used to evaluate PCB-induced behavioral alterations. Ambulation was increased in 30-mg-treated rats at Day 22, but not at Day 120. There were more avoidance responses and intertrial responses in the 30-mg group than in both other groups. On the FI-30-sec schedule slightly more reactions were emitted by the 30-mg group during the first 10 sec of the interval than by the other animals. More pronounced, however, were the differences between groups in the temporal pattern of responses within the 30-sec interval. It is concluded that in rats PCB exposure causes consistent alterations in all of the tested activity-dependent behaviors.

Animals↗
PubMed1990

Effects of lead on neurophysiological and performance measures: animal and human data.

This paper reports lead-induced changes in neuropsychological measures and behavioral performance measures in monkeys and children. Monkeys were pre- and postnatally exposed to lead via the diet. Blood lead levels at the time of testing were 9.3, 40.3, and 55.7 micrograms/dL in controls, and animals exposed to 350 ppm or 600 ppm lead acetate, respectively. Flash-evoked and brainstem auditory-evoked potentials were recorded in adult animals. Results indicate latency increases in both measures as well as amplitude decreases in the flash-evoked response. Delayed reaction time and serial choice reaction were determined as measures of behavioral performance in lead-exposed school-age children from two lead smelter areas. In addition, pattern-reversal-evoked potentials and nerve conduction velocity were investigated. Neither nerve conduction velocity nor latency of the pattern-reversal-evoked potential were consistently influenced by lead. Of the behavioral measures, serial choice reaction performance revealed a consistent lead-related deficit, which became more pronounced with increasing task difficulty.

Animals↗
PubMed1988

The effects of lead in laboratory animals and environmentally-exposed children.

Consistent association has been found in 4 independent studies between disruption of visual-motor integration and reaction performance and markers of lead exposure (blood, teeth) in children, but not for intelligence deficit; blood-lead levels were typically below 30 micrograms/dl in these children. In order to demonstrate the persistent nature of Pb-induced neurobehavioral deficit experimentally rats were studied after cessation of dietary Pb-exposure in a variety of behavioral tasks. Persistent retention-deficit was found for visual discrimination-learning and for radical arm-maze performance.

Adolescent↗
PubMed1985

Comparing the effects of perinatal and later childhood lead exposure on neuropsychological outcome.

Blood lead values (PbB) from cord blood and maternal samples as well as present PbB from venous blood samples were available for 114 six- to seven-year-old children living in or near the city of Nordenham (FRG). These children represented 30% of all children born between July 1975 and August 1976 in the district hospital (N = 383). The range of cord blood PbB was 4-31 micrograms/100 ml (mean = 8.2 micrograms/100 ml) and of maternal PbB was 4-30 micrograms/100 ml (mean = 9.3 micrograms/100 ml), whereas the range for present PbB was 3.9-22.8 micrograms/100 ml (mean = 8.2 micrograms/100 ml). The degree of correlation between maternal and cord blood PbB was 0.79, despite the poor technical quality of many cord blood samples as compared to maternal blood samples (less coagulation). These children were given a battery of neurophysiological and neuropsychological tests. The present report is restricted to psychological performance measures. The test battery covered intelligence (reduced Wechsler Intelligence Scale for Children), visual-motor performance (Bender Test, GFT), serial reaction performance (Wiener Reaction Device), and cued as well as choice reaction times. After correction for confounding by means of stepwise multiple-regression analysis, few significant associations between blood lead levels and performance deficit occurred. In general the degree of association was somewhat stronger for present PbB than for perinatal PbB: With increasing present PbB there was a borderline drop of performance IQ (P less than 0.1), as well as a significant disruption of serial reactions, which was more pronounced for the difficult (P less than 0.01) than for the easier version of the Wiener Device (P less than 0.05). A similar but less pronounced pattern of associations was observed for maternal PbB but not for cord blood PbB. Some influence of perinatal lead exposure on later performance can, thus, still be detected if, in addition to cord blood PbB, maternal PbB is taken into account as well.

Child↗
PubMed1984

Neuropsychological effects of lead in children: interactions with social background variables.

Following a short and selective summary of findings from psychological studies on lead-induced cognitive dysfunction in man, our own studies in lead-exposed children are briefly described in more detail. These studies, run in the cities of Duisburg and Stolberg, were based on tooth lead levels as the principal indicator of long-term cumulative lead exposure. From a comprehensive sample of neuropsychological outcome measures, only few significant findings emerged, namely lead-related deficits of visual-motor integration and of reaction performance, but not of general intelligence. Without exception, the observed lead effects were small compared to those of social background. An interesting interaction was found between lead exposure and social background for visual-motor integration and for reaction performance: for both these measures, but not for intelligence, the degree of association between performance deficit and lead exposure was more pronounced in socially disadvantaged children than in those from a more middle-class background. This finding was tentatively discussed within a transactional model of development. The common practice of simply controlling the effects of confounding social factors by analysis of covariance or related techniques appears doubtful in this context.

Achievement↗
PubMed1983

Neuropsychological studies in children with elevated tooth-lead concentrations. II. Extended study.

Results from neuropsychological tests, collected under double-blind-precautions, were evaluated for 115 schoolage children (mean age: 9.4 years) living in a lead smelter area (Stolberg, FRG). Tooth-lead concentrations (PbT) from shed incisor teeth as measures of longtime lead-exposure were available for these children (mean = 6.16 ppm; range: 1.9-38.5 ppm), and for 83 of them blood-lead concentrations (PbB) were available as well (mean = 14.3 micrograms/dl; range: 6.8-33.8 micrograms/dl). The following functional capacities were tested: intelligence (German WISC), perceptual-motor integration (Göttinger Formreproduktionstest = GFT, Diagnosticum for Cerebralschädigung = DCS), reaction performance (Wiener Determinationsgerät), finger-wrist tapping-speed, and repetitive cancellation-performance (Differentieller Leistungstest). In addition standardized behavior ratings were obtained by the examiners, the mothers, and the teachers. Multiple stepwise regression-analysis (forced solution) was calculated for outcome-variables and Pb-tooth, including age, sex, duration of labor, and socio-hereditary background as covariates. Significant (P less than 0.05) or near-significant (P less than 0.1) association was established between Pb-tooth and GFT-performance (errors), reaction-performance (false reactions), and four behavioral dimensions as rated by the mothers, namely distractability, restlessness, lack of information, and wasting of time; the proportion of explained variance never exceeded 6%, however. No significant association was found between PbT and WISC verbal-IQ after the effects of "socio-hereditary background" had been eliminated, although there was still a tendency for high level-children (PbT greater than 10 ppm) to be inferior to low level-children (PbT less than or equal to 4 ppm) by 4.6 IQ-points after correction for confounding. There was a near-significant, inverse relationship between finger-wrist tapping-speed and Pb-blood. The results are discussed within the framework of attention-deficit disorder, and compared to neurobehavioral Pb-effects from animal-experiments, which provide suggestive evidence for a causal relationship between developmental lead-exposure and certain neurobehavioral deficits.

Child↗
PubMed1982

Task dependent neurobehavioral effects of lead in rats.

In order to test neurobehavioral effects of low-level lead exposure during early development, Wistar-rats were given pre- and postnatal dietary lead as lead acetate in four concentrations: 0, 80, 250, and 750 ppm. These diets, known to give rise to blood lead-levels (PbB) of less than 5, 11, 18, and 31 micrograms/dl, resulted in erythrocyte ALAD-inhibition of 40, 73, and 83%, respectively. The animals were tested first at 70 to 100 days postnatal (PN 70-100) in a 2-way active avoidance-task, and then at PN 190-250 in a visual discrimination-task. Lead-exposure was associated with performance-disruption in the discrimination-task, significant (p less than 0.001) already for the 250 ppm-exposure, but with significant (p less than 0.05) performance-facilitation in the avoidance-task. If learning and retention in animals is taken as a measure of cognitive performance neurobehavioral lead-toxicity cannot easily be explained in terms of cognitive deficit. An interpretation in terms of emotional reactivity or behavioral disinhibition would seem more convincing, which covers the results from activity-studies as well. 70% ALAD-inhibition corresponds to PbBs of about 20 micrograms/dl in rats, and to about 40 micrograms/dl in children. Some implications of animal studies for neuropsychological results from Pb-exposed children are discussed.

Animals↗