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Childhood lead exposure has devastating lifelong consequences, as even low-level exposure stunts intelligence and leads to delinquent behavior. However, these consequences may be more extensive than previously thought because childhood lead exposure may adversely affect normal-range personality traits. Personality influences nearly every aspect of human functioning, from well-being to career earnings to longevity, so effects of lead exposure on personality would have far-reaching societal consequences. In a preregistered investigation, we tested this hypothesis by linking historic atmospheric lead data from 269 US counties and 37 European nations to personality questionnaire data from over 1.5 million people who grew up in these areas. Adjusting for age and socioeconomic status, US adults who grew up in counties with higher atmospheric lead levels had less adaptive personality profiles: they were less agreeable and conscientious and, among younger participants, more neurotic. Next, we utilized a natural experiment, the removal of leaded gasoline because of the 1970 Clean Air Act, to test whether lead exposure caused these personality differences. Participants born after atmospheric lead levels began to decline in their county had more mature, psychologically healthy adult personalities (higher agreeableness and conscientiousness and lower neuroticism), but these findings were not discriminable from pure cohort effects. Finally, we replicated associations in Europeans. European participants who spent their childhood in areas with more atmospheric lead were less agreeable and more neurotic in adulthood. Our findings suggest that further reduction of lead exposure is a critical public health issue., Competing Interests: The authors declare no competing interest.

Even at low levels in blood, lead has been associated with reduced IQ scores, behavioural problems, learning impediments, aggression and violent behaviour. Since the 1980s, the South African Medical Research Council (SAMRC) has been investigating the sources of exposure to lead in South Africa (SA), the groups at highest risk of lead poisoning and a selection of the myriad associated health and social consequences. SAMRC research evidence contributed to the phasng out of leaded petrol, restrictions on lead in paint and other interventions. Subsequently, childhood blood lead levels in SA declined significantly. More recent studies have revealed elevated risks of lead exposure in subsistence fishing and mining communities, users of arms and ammunition, those ingesting certain traditional medicines, and users of certain ceramicware and artisanal cooking pots. Lead-related cognitive damage costs the SA economy ~USD17.7 (ZAR261.3) billion annually, justifying further SAMRC investment in lead exposure research in the country.

Exposure to lead is detrimental to children's development. YouTube is a form of social media through which people may learn about lead poisoning. The aim of this cross-sectional study was to analyze the variation in lead poisoning-related YouTube contents between different video sources. The 100 most viewed lead poisoning-related videos were manually coded, among which, 50 were consumer-generated, 19 were created by health care professionals, and 31 were news. The 100 videos had a total of more than 8.9 million views, with news videos accounting for 63% of those views. The odds of mentioning what lead poisoning is, how to remove lead, and specifically mentioning the danger in ages 1-5 because of rapid growth among videos created by health care professionals were 7.28 times (Odds ratio, OR = 7.28, 95% CI, 2.09, 25.37, p = 0.002); 6.83 times (OR = 6.83, 95% CI, 2.05, 22.75, p = 0.002) and 9.14 times (OR = 9.14, CI, 2.05, 40.70, p = 0.004) that of consumer-generated videos, respectively. In this study, professional videos had more accurate information regarding lead but their videos were less likely to be viewed compared to consumer-generated videos and news videos. If professional videos about lead poisoning can attract more viewers, more people would be better informed and could possibly influence policy agendas, thereby helping communities being affected by lead exposure.

Background: It is well known that lead exposure induces neurotoxic effects, which can result in a variety of neurocognitive dysfunction. Especially, occupational lead exposures in adults are associated with decreases in cognitive performance including working memory. Despite recent advances in human neuroimaging techniques, the neural correlates of lead-exposed cognitive impairment remain unclear. Therefore, this study was aimed to compare the neural activations in relation to working memory function between the lead-exposed subjects and healthy controls., Methodology/principal Findings: Thirty-one lead-exposed subjects and 34 healthy subjects performed an n-back memory task during MRI scan. We performed fMRI using the 1-back and 2-back memory tasks differing in cognitive demand. Functional MRI data were analyzed using within- and between-group analysis. We found that the lead-exposed subjects showed poorer working memory performance during high memory loading task than the healthy subjects. In addition, between-group analyses revealed that the lead-exposed subjects showed reduced activation in the dorsolateral prefrontal cortex, ventrolateral prefrontal cortex, pre supplementary motor areas, and inferior parietal cortex., Conclusions/significance: Our findings suggest that functional abnormalities in the frontoparietal working memory network might contribute to impairments in maintenance and manipulation of working memory in the lead-exposed subjects.

Background: Lead is a heavy metal and important environmental toxicant and nerve poison that can destruction many functions of the nervous system. Lead poisoning is a medical condition caused by increased levels of lead in the body. Lead interferes with a variety of body processes and is toxic to many organs and issues, including the central nervous system. It interferes with the development of the nervous system, and is therefore particularly toxic to children, causing potentially permanent neural and cognitive impairments. In this study, we investigated the relationship between lead poisoning and the intellectual and neurobehavioral capabilities of children., Methods: The background characteristics of the research subjects were collected by questionnaire survey. Blood lead levels were detected by differential potentiometric stripping analysis (DPSA). Intelligence was assessed using the Gesell Developmental Scale. The Achenbach Child Behavior Checklist (CBCL) was used to evaluate each child's behavior., Results: Blood lead levels were significantly negatively correlated with the developmental quotients of adaptive behavior, gross motor performance, fine motor performance, language development, and individual social behavior (P < 0.01). Compared with healthy children, more children with lead poisoning had abnormal behaviors, especially social withdrawal, depression, and atypical body movements, aggressions and destruction., Conclusion: Lead poisoning has adverse effects on the behavior and mental development of 2-4-year-old children, prescribing positive and effective precautionary measures.

More than 90% of body lead is stored in bone. The technique of K-X-Ray fluorescence developed in the 1990s has enabled the quantitative measurement of decades of cumulative lead in bone, whereas blood lead levels reflect only recent exposure to lead. Bone lead is mobilized into the blood like bone calcium, as in osteoporosis, and exposes the patient to increased lead load. Many studies have assessed the toxic effect of chronic exposure from childhood to old age in present or former workers in industrial lead, as well as in non-occupational citizens in whom social and environmental circumstances might have induced higher exposure levels. This review points to the effects of elevated levels of bone lead and the associated cognitive decline among the elderly, with lead toxicity being one of the possible causes of degenerative dementia. There is evidence of an association between increased bone lead levels and renal disease, degenerative diseases like cataract, and suggestive but not causal association with blood pressure and hypertension. Community surveys show increased mortality associated with exposure to lead. Removal of sources of lead exposure, for example the use of non-leaded petrol, has reduced lead levels in the population, and there are currently strong recommendations to further lower the present allowed blood lead level to minimize chronic cumulative lead toxicity.

Background: We carried out animal experiments based on the orthogonal design L(8)(2(7)) setting seven factors with two different levels of each and 10 groups of rats. The nutrients tested were tyrosine, glycine, methionine, taurine, ascorbic acid, thiamine and zinc., Objectives: The objective of this study was to explore the optimal combinations of nutrients for prevention or amelioration of lead-induced learning and memory impairment., Methods: Rats were supplemented with nutrients by gavage once a day in two experiments: one was simultaneous nutrient supplementation with lead acetate administration (800 mg l(-1)) for 8 weeks (prophylactic supplementation) and the other was nutrient supplementation for 4 weeks after the cessation of 4 weeks of lead administration (remedial supplementation). Morris water maze was initiated at ninth week. Rats were terminated for assays of levels of Pb in blood, activities of superoxide dismutase (SOD) and nitric oxide synthase (NOS) in hippocampus, levels of nitric oxide (NO) in hippocampus and expressions of Ca2+/calmodulin-dependent protein kinase II (CaMKII) and cyclic adenosine monophosphate (cAMP) response element-binding protein messenger RNA in hippocampus., Results: Results showed that in prophylactic supplementation, methionine, taurine, zinc, ascorbic acid and glycine were the effective preventive factors for decreasing prolonged escape latency, increasing SOD and NOS activities and NO levels in the hippocampus, respectively. On the other hand, in remedial supplementation, taurine was the effective factor for reversing Pb-induced decrease in activities of SOD, NOS and levels of NO., Conclusions: In conclusion, the optimum combinations of nutrients appear to be methionine, taurine, zinc, ascorbic acid and glycine for the prevention of learning and memory impairment, while taurine and thiamine appear to be the effective factors for reversing Pb neurotoxicity.

The transition to synthetic chemicals as a popular method of insect control in the United States was one of the most critical developments in the history of American agriculture. Historians of agriculture have effectively identified the rise and charted the dominance of early chemical insecticides as they came to define commercial agriculture between the emergence of Paris green in the 1870s and the popularity of DDT in the 1940s and beyond. Less understood, however, are the underlying mechanics of this transition. this article thus takes up the basic question of how farmers and entomologists who were once dedicated to an impressively wide range of insect control options ultimately settled on the promise of a chemically driven approach to managing destructive insects. Central to this investigation is an emphasis on the bureaucratic maneuverings of Leland O. Howard, who headed the Bureau of Entomology from 1894 to 1927. Like most entomologists of his era, Howard was theoretically interested in pursuing a wide variety of control methods--biological, chemical, and cultural included. In the end, however, he employed several tactics to streamline the government's efforts to almost exclusively support arsenic and lead-based chemical insecticides as the most commercially viable form of insect control. While Howard in no way "caused" the national turn to chemicals, this article charts the pivotal role he played in fostering that outcome.

Anecdotal observations suggest that neurological impairments associated with petrol (gasoline) sniffing resolve with abstinence, although these effects have not been proven empirically. Severe exposure to leaded petrol may induce a lead encephalopathy that extends beyond any acute intoxication and requires emergency hospital treatment. Previously, in chronic petrol sniffers, we showed neurological, saccadic, and cognitive abnormalities that were more severe in petrol sniffers with a history of hospitalization for lead encephalopathy, and that correlated with blood lead levels and the length of time of sniffing petrol. Ex-petrol sniffers showed a qualitatively similar but quantitatively less severe pattern of impairment. Petrol sniffing was stopped completely in one of the study communities by modifying social, occupational, and recreational opportunities. After 2 years, we obtained biochemical and neurobehavioral (neurological, saccade, and cognitive) data from all available participants of the earlier study including 10 nonsniffers and 29 chronic petrol sniffers, with six of these individuals previously receiving hospital treatment for lead encephalopathy. Here, we report that blood lead was reduced and that neurobehavioral impairments improved, and in many cases normalized completely. The most severe petrol-related neurobehavioral impairment was observed among individuals who had longer histories of abuse and higher blood lead levels, and among petrol sniffers with a history of lead encephalopathy. Those with the greatest extent of neurobehavioral impairment showed the greatest degree of improvement with abstinence, but were less likely to recover completely. This is the first direct evidence that neurological and cognitive impairment from chronic petrol sniffing ameliorates with abstinence and may recover completely.

Seventy-one-year-old identical twin brothers with chronic lead poisoning were identified from an occupational medicine clinic roster. Both were retired painters, but one brother (J.G.) primarily removed paint and had a history of higher chronic lead exposure. Patella and tibia bone lead concentrations measured by K-X-ray fluorescence in each brother were 5-10 times those of the general population and about 2.5 times higher in J.G. than in his brother (E.G.). Magnetic resonance spectroscopy (MRS) studies examined N-acetylaspartate:creatine ratios, a marker of neuronal density. Ratios were lower in J.G. than in his brother. Scores on neurocognitive tests that assess working memory/executive function were below expectation in both twins. Short-term memory function was dramatically worse in J.G. than in his brother. These results demonstrate some of the more subtle long-term neurologic effects of chronic lead poisoning in adults. In particular, they suggest the presence of frontal lobe dysfunction in both twins, but more dramatic hippocampal dysfunction in the brother with higher lead exposure. The MRS findings are consistent with the hypothesis that chronic lead exposure caused neuronal loss, which may contribute to the impairment in cognitive function. Although a causal relation cannot be inferred, the brothers were genetically identical, with similar life experiences. Although these results are promising, further study is necessary to determine whether MRS findings correlate both with markers of lead exposure and tests of cognitive function. Nevertheless, the results point to the potential utility of MRS in determining mechanisms of neurotoxicity not only for lead but also for other neurotoxicants as well.

Background: Lead is neurotoxic; yet, whether cognitive decline in older persons is associated with lead exposure is unknown. We studied whether lead exposure biomarkers are associated with cognitive test scores, as well as the modifying effects of age on the lead-cognition relationship., Methods: Lead exposure biomarkers and Mini-Mental Status Exam (MMSE) scores were measured among subjects in the Normative Aging Study. Multiple linear and logistic regression analyses were performed to examine the cross-sectional association of these 2 variables., Results: We found an odds ratio (OR) of 2.1 for MMSE <24 with an increase from the lowest to the highest quartile of patella lead levels (95% confidence interval [CI] = 1.1 to 4.1). From the lowest to the highest quartile of blood lead the OR for low MMSE was 3.4 (CI = 1.6 to 6.2). There was an interaction between lead biomarkers and age. Among subjects in the lowest quartile of patella lead levels, MMSE score decreased by 0.03 points per year (CI = -0.07 to 0.005), whereas in the highest quartile, MMSE score decreased by 0.13 points per year (CI = -0.19 to -0.07). Similar interactions were found between blood lead levels and age., Conclusions: Increased levels of lead in bone and blood are inversely associated with cognitive performance among older men. Lead exposure might accelerate age-associated cognitive decline.

Enormous effort has been focused over the last decade and a half on characterizing the behavioral effects of lead in the developing organism. While age-appropriate standardized measures of intelligence (IQ) have been the dependent variable most often used to assess lead-induced cognitive impairment in epidemiologic studies, researchers have also used a variety of other methods designed to assess specific behavioral processes sensitive to lead. Increased reaction time and poorer performance on vigilance tasks associated with increased lead body burden suggest increased distractibility and short attention span. Assessment of behavior on teachers' rating scales identified increased distractibility, impulsivity, nonpersistence, inability to follow sequences of directions, and inappropriate approach to problems as hallmarks of lead exposure. Robust deficits in learned skills such as reading, spelling, math, and word recognition have also been found. Spatial organizational perception and abilities seem particularly sensitive to lead-induced impairment. Assessment of complex tasks of learning and memory in both rats and monkeys has revealed overall deficits in function over a variety of behavioral tasks. Exploration of behavioral mechanisms responsible for these deficits identified increased distractibility perseveration, inability to inhibit inappropriate responding, and inability to change response strategy as underlying deficits. Thus, there is remarkable congruence between the epidemiologic and experimental literatures with regard to the behavioral processes identified as underlying the deficits inflicted by developmental lead exposure. However, careful behavioral analysis was required from researchers in both fields for such understanding to emerge.

The long term neurobehavioural consequences of childhood lead poisoning are not known. In this study adult subjects with a documented history of lead poisoning before age 4 and matched controls were examined with an abbreviated battery of neuropsychological tests including measures of attention, reasoning, memory, motor speed, and current mood. The subjects exposed to lead were inferior to controls on almost all of the cognitive tasks. This pattern of widespread deficits resembles that found in children evaluated at the time of acute exposure to lead rather than the more circumscribed pattern typically seen in adults exposed to lead. Despite having completed as many years of schooling as controls, the subjects exposed to lead were lower in lifetime occupational status. Within the exposed group, performance on the neuropsychological battery and occupational status were related, consistent with the presumed impact of limitations in neuropsychological functioning on everyday life. The results suggest that many subjects exposed to lead suffered acute encephalopathy in childhood which resolved into a chronic subclinical encephalopathy with associated cognitive dysfunction still evident in adulthood. These findings lend support to efforts to limit exposure to lead in childhood.

Over the 20-year period since the first issue of Environmental Health Perspectives was published, there has been considerable progress in the understanding of the potential toxicity of exposure to lead. Many of these advances have been reviewed in published symposia, conferences, and review papers in EHP. This brief review identifies major advances as well as a number of current concerns that present opportunities for prevention and intervention strategies. The major scientific advance has been the demonstration that blood lead (PbB) levels of 10-15 micrograms/dL in newborn and very young infants result in cognitive and behavioral deficits. Further support for this observation is being obtained by prospective or longitudinal studies presently in progress. The mechanism(s) for the central nervous system effects of lead is unclear but involve lead interactions within calcium-mediated intracellular messenger systems and neurotransmission. Effects of low-level lead exposure on blood pressure, particularly in adult men, may be related to the effect of lead on calcium-mediated control of vascular smooth muscle contraction and on the renin-angiotensin system. Reproductive effects of lead have long been suspected, but low-level effects have not been well studied. Whether lead is a carcinogen or its association with renal adenocarcinoma is a consequence of cystic nephropathy is uncertain. Major risk factors for lead toxicity in children in the United States include nutrition, particularly deficiencies of essential metals, calcium, iron, and zinc, and housing and socioeconomic status. A goal for the year 2000 is to reduce prevalence of blood lead levels exceeding 15 micrograms/dL.

A prospective methodology was used to assess the neurobehavioral effects of fetal and postnatal lead exposure during the first 2 years of life. Lead was measured in whole blood prenatally in mothers and at quarterly intervals in the infant. Prenatal blood lead levels were low (mean = 8.0 micrograms/dL). However, approximately 25% of the study infants had at least one serial blood lead level of 25 micrograms/dL or higher during the second year of life. Multiple regression and structural equation analyses revealed statistically significant relationships between prenatal and neonatal blood lead level and 3- and 6-month Bayley Mental and/or Psychomotor Development Index. However, by 2 years of age, no statistically significant effects of prenatal or postnatal lead exposure on neurobehavioral development could be detected. Data consistent with the hypothesis that a postnatal neurobehavioral growth catch-up occurred in infants exposed fetally to higher levels of lead are presented.

This article identifies four culturally shaped sources of lead exposure in human societies: modern and historic technological sources: food habits; culturally defined health beliefs; and beauty practices. Examples of these potential sources of lead poisoning are presented from current cultures. They include the use of lead-glazed cooking pottery in Mexican-American households; folk medical use of lead in Hispanic, Arabic, South Asian, Chinese, and Hmong communities; as well as the use of lead as a cosmetic in the Near East, Southeast Asia, and South Asia. Four interacting cultural conditions that create barriers to the reduction of lead exposure and lead poisoning are identified and discussed. These are knowledge deficiencies, communication resistance, cultural reinterpretations, and incongruity of explanatory models.

Up to 2 years of age, children with umbilical cord blood lead levels of 10 to 25 micrograms/dL achieve significantly lower scores on tests of cognitive development than do children with lower prenatal exposures. By age 5 years, however, they appear to have recovered from, or at least compensated for, this early insult. Change in performance between 24 and 57 months of age was examined in relation to level of postnatal lead exposure and various sociodemographic factors. Among children with high prenatal lead exposure, greater recovery of function was associated with lower blood level at 57 months, higher socioeconomic status, higher Home Observation for Measurement of the Environment scores, higher maternal IQ, and female gender. The difference between the scores at 57 months of children with optimal and less optimal values on these variables generally exceed 1/2 standard deviation. Higher prenatal lead exposure is associated with an increased risk of early cognitive deficit. Furthermore, the risk that a deficit will persist through the preschool years is increased among children with high prenatal exposure and either high postnatal exposure or less optimal sociodemographic characteristics.

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.

Five decades ago, lead toxicity in childhood was thought in nonlethal cases to be without residual effect. This misconception was corrected in 1943 by Randolph Byers, who began the modern era of lead neurotoxicology by asserting that lead not only killed cells, but interfered with the normal development of central nervous system neurons. The human data from Byers forward is reviewed, with particular attention on methodological issues that have emerged. The papers on human neurotoxicology presented at the NIEHS lead conference held in Research Triangle Park, NC, in 1974 are examined to demonstrate the progress made over the last 15 years. Seven methodological solecisms have clouded judgment over the question of lead toxicity at low dose: worship of the sacrament of p = 0.05; inaccurate causal modeling; drawing conclusions from studies with inadequate power; positing phantom covariates; underestimating the importance of "small" effects; demanding proof of causality; and evaluating studies in isolation. The principles behind these errors are discussed. Lead exposure is associated with hyperactivity, and hyperactivity is a risk factor for antisocial behavior. The relationship between lead exposure and antisocial behavior is estimated. A plan for the effective removal of one major lead source, housing stock, is presented.

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.

A prospective follow-up study on new lead workers who began work at a storage battery factory was carried out between 1975 and 1981. Psychological performances (eg, intelligence, memory, visuomotor functions, vigilance, and personality) were assessed before the commencement of exposure and after one, two, and four years of work. Of an initial number of 89 workers, 24 were available for the one-year, 16 for the two-year, and 11 for the four-year reexamination. The time-weighted average blood lead values ranged between 0.68 and 2.17 mumol/l (14 and 45 micrograms/100 ml, respectively). A reference group, nonexposed workers in a cable manufacturing plant and an electrical power plant, was similarly followed. Initially the average psychological performances were similar among the lead workers and the referents. For some of the psychological tests learning effect, which was clearly evident among the referents during the follow-up, was almost absent among the lead workers. The lead worker's visual intelligence and visuomotor functions in particular were impaired significantly after the first two years of follow-up. When the lead workers were divided into two groups according to the median time-weighted average of the blood lead values (1.30 mumol/l), the Block Design and the Santa Ana coordination tests were those which best separated the subgroups. Although the impairment of the lead workers' performance was rather slight and the dispersion in the psychological changes was wide, it was evident that some higher nervous functions were affected by lead levels above about 1.45 mumol/l.

A structured problem-solving task was used to evaluate the effects of lead (Pb) exposure on the activity patterns and attention of 18-month-old infants. After statistically controlling for the influence of the caretaker's attempts to support and teach the infant during the task, multivariate techniques were used to examine the residual variances to detect any effects of prenatal or postnatal Pb exposure. Contrary to expectations, no relationship was found between Pb exposure and measures of attention. Activity level was found to be negatively related to blood Pb level. The suggested suppression of behavior was inconsistent with reports of hyperactivity found in school children with elevated Pb level, but is consistent with observations of lethargy in infants with iron deficiency. To examine this alternative, free erythrocyte protoporphyrin (FEP) levels, which are elevated both in the presence of elevated Pb and in iron deficiency, were incorporated into the regression model. FEP was the best predictor of room movement, as indicated by a backward elimination analysis that removed all Pb measures from the model. However, none of the other measures of hematopoietic status were related to behavior. The suppression of activity level, if a reliable effect, is very small, and only weakly though significantly related to FEP level.

The relationship between postnatal lead (Pb) exposure and early sensorimotor development was prospectively investigated in a group of infants born to parents residing in lead-hazardous areas of Cincinnati, Ohio. Few significant relationships were found between current or cumulative infant blood Pb levels and indices of sensorimotor development during the first year of life. When important developmental covariates such as birth weight and home environment were included in the analyses, no significant relationship between Pb exposure and development remained. To date, there appears to be no evidence in these data that postnatal low-level Pb exposure increases an infant's risk for delays in early sensorimotor development.

In a cross sectional study of occupational exposure to inorganic lead 91 men performed a series of microcomputer based tasks assessing sensor motor reaction time, memory, attention, verbal reasoning, and spatial processing. Performance on the tasks was studied in relation to three ranges of blood lead concentration (low, less than 20 micrograms/dl; medium, 21-40 micrograms/dl; and high, 41-80 micrograms/dl) and exposure response correlations for blood lead concentration, zinc protoporphyrin (ZPP) (range 7-210 micrograms/dl), and urinary aminolaevulinic acid (ALA) (range 0.5-22.0 mg/l). The results show that the high group were impaired on most of the tasks used and, in general, the magnitude of the impairment correlated better with blood lead concentration than ZPP or urinary ALA. An examination of the patterns of task impairment indicated a general slowing of sensory motor reaction time which was relatively independent of the nature of the cognitive functions being tested. There was some evidence, however, suggesting mild impairment of attention, verbal memory, and linguistic processing. In general, workers with high blood lead concentrations showed clear impairment of sensory motor functions in the absence of correspondingly strong evidence for impaired processing and memory functions. It is argued that a general slowness in responding may underlie many previous reports of widespread cognitive impairment in lead workers.

To evaluate the effects of chronic lead exposure on the nervous system in adults, a set of neurobehavioural and electrophysiological tests was administered to 99 lead exposed foundry employees and 61 unexposed workers. Current and past blood lead concentrations were used to estimate the degree of lead absorption; all previous blood lead concentrations had been less than or equal to 90 micrograms/100 ml. Characteristic signs (such as wrist extensor weakness) or symptoms (such as colic) of lead poisoning were not seen. Sensory conduction in the sural nerve was not affected. By contrast, various neurobehavioural functions deteriorated with increasing lead burden. Workers with blood lead concentrations between 40 and 60 micrograms/100 ml showed impaired performance on tests of verbal concept formation, visual/motor performance, memory, and mood. Thus impairment in central nervous system function in lead exposed adults occurred in the absence of peripheral nervous system derangement and increased in severity with increasing lead dose.

Insidious neurotoxic effects of lead have been studied in a population of 42 lead-exposed workers and a reference group of 22 comparable workers with no lead exposure. The age of the individuals ranged from 18 to 50 years. The complete Wechler Adult Intelligence Scale, as well as psychomotor and memory tests, was included in the test battery. The exposure was assessed by means of the lead concentration in blood and hair and the ratio between zinc protoporphyrin and hemoglobin in the blood. Significant differences were found between the two groups of workers, especially concerning long-term memory, verbal and visuospatial abstraction, and psychomotor speed. Decreased performance in these tests was in most cases associated with indices of increased lead exposure, not only in the total population studied, but also within the lead-exposed group alone. Blood lead and zinc protoporphyrin appeared to correlate better with the intellectual impairment than did hair lead, and thus these analyses are probably better predictors for neurotoxic effects of lead. Age and exposure time were not found to be significant confounding factors in this study.

To evaluate critical exposure levels and the reversibility of lead neurotoxicity a group of lead exposed foundry workers and an unexposed reference population were followed up for three years. During this period, tests designed to monitor neurobehavioural function and lead dose were administered. Evaluations of 160 workers during the first year showed dose dependent decrements in mood, visual/motor performance, memory, and verbal concept formation. Subsequently, an improvement in the hygienic conditions at the plant resulted in striking reductions in blood lead concentrations over the following two years. Attendant improvement in indices of tension (20% reduction), anger (18%), depression (26%), fatigue (27%), and confusion (13%) was observed. Performance on neurobehavioural testing generally correlated best with integrated dose estimates derived from blood lead concentrations measured periodically over the study period; zinc protoporphyrin levels were less well correlated with function. This investigation confirms the importance of compliance with workplace standards designed to lower exposures to ensure that individual blood lead concentrations remain below 50 micrograms/dl.

The neuropsychological performance of a group of 49 workers occupationally exposed to lead was compared with a matched control group of 36 non-exposed workers. The psychometric measurements were composed of tests covering a broad range of different neuropsychological functions, particular emphasis being given to perceptual motor ability and attention concentration functioning. A questionnaire to assess subjective symptoms in mood, sleep disturbance, poor concentration and forgetfulness, somatic complaints, and social passivity was also included in the battery of tests. Compared with the controls, the performance of the lead workers was found to be significantly poorer for digit symbol, Bourdon-Wiersma, trail making test (part A), Santa Ana test, flicker fusion, and simple reaction time. In terms of subjective symptoms the exposed group also reported significantly more complaints of anxiety and depressed mood, poor concentration and forgetfulness, and other somatic complaints. These differences were observed among lead workers with a mean blood lead value of 2.35 mumol/l (SD 0.7).

Lead intoxication is a classical environmental hazard that can cause encephalopathy. During recent years several studies have suggested poor performances in psychological tests and increased numbers of subjective symptoms among workers with comparatively low blood lead concentrations. Forty-nine long-term lead-exposed male workers with time-weighted average blood lead concentrations between 1.3 and 3.3 mumol/l calculated from at least seven years' results have been compared with a referent group of 27 male industrial workers with normal blood lead concentrations and comparable intellectual backgrounds. Several indices of exposure were used. Both groups were examined with neuropsychological tests and a questionnaire covering neuropsychiatric symptoms. The exposed group performed less well in 11 of 14 non-verbal tests, and there were significant differences in tests of memory and reaction time. A non-linear dose-effect trend was indicated. The results are in accordance with those found in similar studies, and it is concluded that the blood lead concentration should be below 2.5 mumol/l to avoid the effects shown in this study.

Recent data have demonstrated health effects of lead in children at doses previously believed to be harmless. Data from epidemiological studies in many countries, and from experimental studies of animals given lead, demonstrate psychological impairment at blood lead concentrations of 0.5-0.7 mumol/L. Current estimates are that 17 per cent of American children (3-4 million) exceed the level of 0.7 mumol/L. Lead exposure is not a problem for urban poor children alone, but inner-city minorities have a higher rate of exposure. The overabundance of lead coexists in the same area with two serious shortages: affordable housing and jobs. It is argued that a program to train unemployed inner-city residents in safe de-leading, while expensive, makes hygienic, economic, and common sense.

Initial evaluations of 104 low-socioeconomic status black children screened by the local community health departments in North Carolina showed significant effects of lead in the range 6-59 micrograms/dl on IQ after controlling for concomitant social factors, such as socioeconomic status, home environment, and maternal IQ. The main concomitant variable was socioeconomic status, which was multicolinear with other social factors. Five years later, when all blood lead levels were 30 micrograms/dl or less, lead effects on IQ were no longer significant. The correlation between maternal and child IQ, which had been suppressed initially in children with higher lead levels, returned to expected levels when decreases in blood lead level occurred, while concomitant variables remained stable over the 5-year period.

A model for understanding the effects of lead on child development, which focuses on the ecology of childhood is presented. The methods used in 10 prospective, longitudinal studies of the effects of lead are summarized and preliminary results presented. Differences between studies lead to a conclusion that there should be more interinvestigator collaboration to ensure greater comparability across studies.

In 1932 Haury described lead-glaze pottery from the Southwest. In view of his report, it appeared desirable to find out whether the makers of such pottery suffered from lead poisoning. A series of 46 bone specimens from Kinishba, where lead-glaze pottery was made, and a control series of 33 specimens from Point of Pines, where such pottery is not known to have been made, were screened by X-ray and by X-ray diffraction. The 11 most promising specimens were then analyzed by atomic absorbtion spectrophotometry. Lead was found in quantities believed to be below the toxic range; concentrations in the control series from Point of Pines were, with few exceptions, higher than in the experimental series from Kinishba.