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Three groups of rhesus monkeys (N = 4/group) were administered daily doses of lead acetate dissolved in milk throughout the first year of life. The doses of lead administered were 0.9 mg/kg/day (high lead group), 0.3 mg/kg/day (low lead group), and no added dietary lead (control group). These doses resulted in mean blood lead concentrations over the first year of 65, 32 and 4 micrograms/dl for the high lead, low lead and control groups, respectively. Lead administration was terminated at the end of the first year and blood lead concentrations fell steadily over the next 44 months. At no time were overt signs of toxicity apparent. The effects of prior lead exposure on a fixed-interval (FI) schedule of food presentation were examined beginning at 33 months of age, at which time blood lead concentrations of all animals were less than 12 micrograms/dl. Acquisition of the bar press response varied widely among individual monkeys and no group differences were observed. Throughout 20 sessions of responding under an FI 60 sec food schedule, the lead treated animals had a significantly lower index of curvature (IC) than controls indicating a less pronounced positively accelerated pattern of responding. The magnitude and consistency of this effect were directly related to the dose of lead administered. Overall FI response rate, running rate and postreinforcement pause duration were not altered by lead treatment. Pentobarbital (2.5-10 mg/kg) decreased IC and increased response rate; these effects were not altered by lead treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Binghamton heterogeneous (HET) stock mice were exposed to 0.5% lead acetate solution from conception through adulthood. Activity was measured in an open field, shuttle-box, and the home cage. Independent groups of animals were tested at several ages in the light (day) and dark (night). Despite significant blood-lead level differences between the control and lead treated animals, developmental and activity differences between groups were restricted to selected measures. The lead-treatment appeared to alter only jumping in the open field and some consummatory behaviors observed in the home cage. This research does not provide support for a model which proposes a simple, direct relationship between low-level lead toxicity and hyperactive behavior. It is suggested that future research focus on the specific conditions under which activity is measured. Animal parallels to a human "hyperactive disorder" may need to be reformulated in terms of attention deficits which mark the childhood disorder.

Rats exposed to lead via the maternal milk were tested at maturity on three different visual discrimination tasks. Starting at parturition the dams were given either tap water, 0.20% sodium acetate, 0.02% lead acetate, or 0.20% lead acetate in the drinking water. At weaning, the pups from all the groups were placed on normal chow and tap water. At 20 days of age, the concentration of lead in the blood and brain of the high lead-exposed offspring was approximately 6 times that of controls (11 microgram% vs 66 microgram%). A significant deficit was found in the ability of the high lead-exposed group to acquire a simultaneous visual discrimination task conducted in an operant chamber. No significant differences were observed in the ability of lead-exposed rats to acquire either a successive visual discrimination task or a cued go/no-go discrimination. Thee results suggest that early lead exposure can affect certain behavioral processes and that the effects may persist even after the rat has reached maturity.

Suckling rats were exposed to one of three solutions, 2.6 x 10(-3) M lead acetate, 5 x 10(-3) M acetic acid or water, from parturition until the pups were 18 days old. Male offspring from dams on acetic acid demonstrated above normal preweaning body weights and were significantly less active than normals in the open field by day 44. The preweaning body weights and ambulation of offspring from dams on lead acetate fell between the results for normal and acetic acid rats. These results indicate that the role of the acetic acid component cannot be discounted when lead acetate is the compound utilized in behavioral studies aimed at examining an effect by lead on laboratory rats.

The effect of zinc deficiency on the toxicity of dietary lead in rats, as measured by body weight changes, tissue lead retention, and choice behavior in a complex maze was studied. Weanling rats were fed a zinc-free semipurified diet which was supplemented via drinking solutions with either 2 or 20 ppm zinc and 0, 10, or 100 ppm lead. During exposure, choice behavior was quantified in a radial maze. After a 3-week period on diet, the animals' physical development was assessed, and the retention of lead and zinc in bone and brain were determined by atomic absorption spectroscopy. Zinc deficiency slowed rats' weight gain, did not affect relative organ weights, increased the retention of lead in both calvarium and in brain, and reduced the accuracy of performance in the maze. Lead exposure at 100 ppm reduced body weight and increased relative organ weights, and reduced maze accuracy at both 10 and 100 ppm. Neither treatment affected the rats' running speed through the maze. Lead exposure and zinc deficiency exerted additive effects on body weight. The two treatments did not interact in the behavioral assay.

Children attending non-remedial first and second grades were classified according to the concentration of lead in their shed deciduous teeth. Children in the lowest and highest tenth percentile were studied with a detailed neuropsychological battery under blind conditions. Thirty-nine non-lead covariates were controlled either by matching or in the biostatistical analysis. High lead children tended to have significantly lower IQ scores particularly on the verbal scales of the WISC-R, impaired auditory and language processing, increased reaction times at longer intervals of delay. Their teachers who were blind to the dentine lead levels found an increased incidence of disordered classroom behavior in direct relationship to the concentration of lead in their teeth. Quantitative electroencephalographic analysis demonstrated decreased midline alpha and increased midline delta in high lead subjects. Four years later a subsample of these children was followed up and observed during quiet classroom activity. High lead children tended to spend more time off tasks staring at classmates, out the window or at the observer. These observations demonstrate that lead at doses below those which are associated with frank clinical symptoms produce deficits in intelligence, attention, auditory-language function and disordered classroom behavior.

Five studies dealing with long term occupational exposure to carbon disulfide, a mixture of organic solvents, toluene, styrene and lead are reviewed. All of the studies were cross-sectional, comprising either a comparison between exposed and nonexposed groups or the determination of exposure-response relationships, or both. The tests for the cognitive functions were known clinical intelligence and memory tests. The perceptual and psychomotor tasks were the Santa Ana test, the Bourdon-Wiersma test for visual-motor speed and accuracy, the Symmetry Drawing test and the Mira test. In four of the five studies the neurotoxic effect involved both cognitive and psychomotor functions. In the carbon disulfide group, psychomotor retardation was the most pronounced effect: in the group exposed to solvent mixtures the main effects were seen in the cognitive functions. The effects of styrene were limited to perceptual and psychomotor disturbances. As the most sensitive methods have varied from study to study, the continued use of broad and diverse psychological methodology in studies dealing with long term neurotoxic effects is proposed.

The study was designed to determine whether lead ingestion by nursing rats would affect dam-pup interaction. Dams were exposed to diets with 0.0, 0.2, 0.4 or 1.0 percent by weight metallic lead. Mean blood-lead levels of pups at weaning were 3, 19, 40 and 57 micrograms/100 ml of blood respectively. Maternal behavior was assessed by videotaping behavior for complete 24 hour periods on alternate days from birth to weaning. Analysis of data revealed that lead affected dams nursed for longer periods than normal and offspring were slower to explore their environment. It was concluded that altered maternal behavior was related to delays in pup development and the functional isolation of experimental pups from their environment may be the antecedent to altered behavior later in maturity.

Rhesus monkeys were pre- and postnatally exposed to 0, 350, or 600 ppm lead acetate in the diet. Blood lead levels of the mothers were less than 1, 24.4, and 37.4 micrograms/100 g blood, respectively, while those of the offspring were substantially higher, at least in the early stages of development. At the age of 12-15 months the animals were tested for group activity levels in an unfamiliar environment. No substantial lead-related alterations of activity occurred neither for group activity nor for the activity of individual animals. There were, however significant dose-related impairments of pattern discrimination learning set formation, while in simple discrimination learning during the early training phases deficits were seen in the high lead group only. Emotional alterations of these animals may account for this result, whereas true cognitive deficits are likely to underly the impairment of learning set formation seen in the low lead group. It is concluded that the effects of lead in cognitive tasks are not secondary to changes of general activity level.

The social behavior of infant rhesus monkeys during the first year of life was examined under a variety of lead (Pb) exposure conditions in four separate experiments. Daily ingestion of PB acetate in milk for one year elevated blood Pb levels to 30-100 microgram/dl, suppressed play, increased social clinging, and exacerbated the disruption of social behavior caused by changing the play environment midway through the year of observation. The presence of control monkeys in social test-groups reduced the magnitude of Pb-induced social behavior changes. In contrast to daily postnatal Pb exposure, chronic exposure to Pb during gestation had no measurable effect on postnatal social development, and acute, transient postnatal Pb exposure (producing blood Pb levels > 200 microgram/dl during month 2 of life) affected only the monkeys' response to the change in the plan environment. These data suggest that daily ingestion of Pb, and not a previously-acquired tissue burden, was responsible for the long-term changes in social development observed. The results are discussed in the general context of primate social development, which is thought to require adequate interactive play for appropriate social integration and reproductive behavior at maturity.

Using a prospective, follow-up approach a group of storage battery plant workers was tested by means of a number of psychodiagnostic tests, as e.g., subtests of the WAIS and WMS, Bourdon-Wiersma test, Santa Ana test, before and two years after entering lead-works. Their performance was compared with that of an age-equivalent group of non-exposed controls. Blood lead levels of the lead group increased from an initial 15.3 +/- 6.7 micrograms/dl (Mean +/- SD) to a final 30.5 +/- 9.6 micrograms/dl after two years, whereas the corresponding PbB-value of the controls was 10.5 +/- 3.7 micrograms/dl and 10.3 +/- 4.0 micrograms/dl, respectively. In the primary psychological examination there were no detectable performance differences between the exposed and controls. Whereas the control group displayed pronounced performance improvement due to training for most of the tests over the two-year period, a sizeable portion of the exposed group exhibited even performance deterioration. Group-comparisons were tested by the non-parametric ch 2-test and two-sided Kolmogorov-Smirnov test. The most sensitive indicators of psychological impairment among the lead workers were Block Design test, Santa Ana coordination test and Digit Span test. It is concluded that the impairment of CNS function, as evidenced by differential test performance, was caused by lead exposure. No exact threshold for impaired performances could be estimated.

In 1977, a hair sample was taken from 26 newborn babies and their mothers and analysed for lead and cadmium. Six years later, each of these 26 children was given a psychometric test (McCarthy Scales of Children's Abilities). Statistical analysis shows a significant negative relationship between the degree of in utero exposure to cadmium and lead and the child's motor and perceptual abilities. Any effect on memory or verbal skills was not statistically significant. Allowing for the confounding variables does not consistently affect these results.

Exposure of rhesus monkeys to lead during the first year after birth resulted in cognitive deficits when the monkeys were tested as adults (5-6 years of age). A pronounced lead-related deficit was detected in the test of Delayed Spatial Alternation (DSA), and a much less robust effect was detected in the Hamilton Search Task (HST). Both tests provided examples of "windows of sensitivity" to the effect of lead, where the behavioral criterion was challenging enough to elicit a deficit in lead-treated monkeys while still being within the capabilities of the controls. The lead-induced deficit in DSA was most pronounced after short intertrial delays, suggesting that the effect was probably not due to a mnemonic dysfunction, but rather may have been due to deficits in strategy or attention. The lose-shift type of error accounted for most of the lead-related DSA deficit, indicating that the lead-treated monkeys perseverated on an alternation strategy even when it was not rewarded. These results indicate that exposure to lead during the first year after birth can result in very long-term and possibly permanent cognitive deficits.

Male rats were chronically treated via drinking water with 50 or 500 ppm sodium acetate or 50 or 500 ppm lead acetate from weaning. Behavioral testing on a fixed-ratio (FR) schedule of reinforcement began at 55 days of age. A series of increasing ratio values was studied. The lower exposure level was without effect at any ratio value. The 500 ppm concentration decreased response rates over the first 15-20 sessions of FR5 and FR25, after which rates reached control levels. Changes in response rate derived primarily from longer interresponse times (IRTs) and decreased running rates. Differences in performance were not evident at FR values of 50 and 100. The 50 ppm concentration produced blood lead (PbB) values averaging 30.3 micrograms/dl; the 500 ppm concentration produced PbBs of 58-94 micrograms/dl. Zinc protoporphyrin levels resulting from 500 ppm exposure differed from controls even after one month of exposure, and continued to increase over eight months of exposure, to 72 micrograms/dl. Comparison of these data to previous studies from this laboratory of FI performance in which the identical exposure protocol was employed, suggests that FR response rates are less sensitive than FI to disruption by lead.