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Sample records for postnatal lead exposure

  1. The Yugoslavia Prospective Lead Study: contributions of prenatal and postnatal lead exposure to early intelligence.

    PubMed

    Wasserman, G A; Liu, X; Popovac, D; Factor-Litvak, P; Kline, J; Waternaux, C; LoIacono, N; Graziano, J H

    2000-01-01

    To investigate associations between the timing of lead (Pb) exposure on early intelligence, we examined the results of psychometric evaluations at ages 3, 4, 5, and 7 years, from 442 children whose mothers were recruited during pregnancy from a smelter town and a non-lead-exposed town in Yugoslavia. We compared the relative contribution of prenatal blood lead (BPb) with that of relative increases in BPb in either the early (0-2 years) or the later (from 2 years on) postnatal period to child intelligence measured longitudinally at ages 3 and 4 (McCarthy GCI), 5 (Wechsler Preschool and Primary Scale of Intelligence-Revised, WPPSI-R IQ), and 7 (Wechsler Intelligence Scale for Children-version III, WISC-III IQ), controlling for: Home Observation for Measurement of the Environment (HOME) quality; maternal age, intelligence, education, and ethnicity; and birthweight and gender. Elevations in both prenatal and postnatal BPb were associated with small decrements in young children's intelligence.

  2. Longitudinal analyses of prenatal and postnatal lead exposure and early cognitive development

    SciTech Connect

    Bellinger, D.; Leviton, A.; Waternaux, C.; Needleman, H.; Rabinowitz, M.

    1987-04-23

    In a prospective cohort study of 249 children from birth to two years of age, we assessed the relation between prenatal and postnatal lead exposure and early cognitive development. On the basis of lead levels in umbilical-cord blood, children were assigned to one of three prenatal-exposure groups: low (less than 3 micrograms per deciliter), medium (6 to 7 micrograms per deciliter), or high (greater than or equal to 10 micrograms per deciliter). Development was assessed semiannually, beginning at the age of six months, with use of the Mental Development Index of the Bayley Scales of Infant Development (mean +/- SD, 100 +/- 16). Capillary-blood samples obtained at the same times provided measures of postnatal lead exposure. Regression methods for longitudinal data were used to evaluate the association between infants' lead levels and their development scores after adjustment for potential confounders. At all ages, infants in the high-prenatal-exposure group scored lower than infants in the other two groups. The estimated difference between the overall performance of the low-exposure and high-exposure groups was 4.8 points (95 percent confidence interval, 2.3 to 7.3). Between the medium- and high-exposure groups, the estimated difference was 3.8 points (95 percent confidence interval, 1.3 to 6.3). Scores were not related to infants' postnatal blood lead levels. It appears that the fetus may be adversely affected at blood lead concentrations well below 25 micrograms per deciliter, the level currently defined by the Centers for Disease Control as the highest acceptable level for young children.

  3. Sex-based differences in gene expression in hippocampus following postnatal lead exposure

    SciTech Connect

    Schneider, J.S. Anderson, D.W.; Sonnenahalli, H.; Vadigepalli, R.

    2011-10-15

    The influence of sex as an effect modifier of childhood lead poisoning has received little systematic attention. Considering the paucity of information available concerning the interactive effects of lead and sex on the brain, the current study examined the interactive effects of lead and sex on gene expression patterns in the hippocampus, a structure involved in learning and memory. Male or female rats were fed either 1500 ppm lead-containing chow or control chow for 30 days beginning at weaning.Blood lead levels were 26.7 {+-} 2.1 {mu}g/dl and 27.1 {+-} 1.7 {mu}g/dl for females and males, respectively. The expression of 175 unique genes was differentially regulated between control male and female rats. A total of 167 unique genes were differentially expressed in response to lead in either males or females. Lead exposure had a significant effect without a significant difference between male and female responses in 77 of these genes. In another set of 71 genes, there were significant differences in male vs. female response. A third set of 30 genes was differentially expressed in opposite directions in males vs. females, with the majority of genes expressed at a lower level in females than in males. Highly differentially expressed genes in males and females following lead exposure were associated with diverse biological pathways and functions. These results show that a brief exposure to lead produced significant changes in expression of a variety of genes in the hippocampus and that the response of the brain to a given lead exposure may vary depending on sex. - Highlights: > Postnatal lead exposure has a significant effect on hippocampal gene expression patterns. > At least one set of genes was affected in opposite directions in males and females. > Differentially expressed genes were associated with diverse biological pathways.

  4. Early Postnatal Lipopolysaccharide Exposure Leads to Enhanced Neurogenesis and Impaired Communicative Functions in Rats

    PubMed Central

    Dai, Xuemei; Roller, Anna; Carter, Kathleen; Paul, Ian; Bhatt, Abhay J.; Lin, Rick C. S.; Fan, Lir-Wan

    2016-01-01

    Perinatal infection is a well-identified risk factor for a number of neurodevelopmental disorders, including brain white matter injury (WMI) and Autism Spectrum Disorders (ASD). The underlying mechanisms by which early life inflammatory events cause aberrant neural, cytoarchitectural, and network organization, remain elusive. This study is aimed to investigate how systemic lipopolysaccharide (LPS)-induced neuroinflammation affects microglia phenotypes and early neural developmental events in rats. We show here that LPS exposure at early postnatal day 3 leads to a robust microglia activation which is characterized with mixed microglial proinflammatory (M1) and anti-inflammatory (M2) phenotypes. More specifically, we found that microglial M1 markers iNOS and MHC-II were induced at relatively low levels in a regionally restricted manner, whereas M2 markers CD206 and TGFβ were strongly upregulated in a sub-set of activated microglia in multiple white and gray matter structures. This unique microglial response was associated with a marked decrease in naturally occurring apoptosis, but an increase in cell proliferation in the subventricular zone (SVZ) and the dentate gyrus (DG) of hippocampus. LPS exposure also leads to a significant increase in oligodendrocyte lineage population without causing discernible hypermyelination. Moreover, LPS-exposed rats exhibited significant impairments in communicative and cognitive functions. These findings suggest a possible role of M2-like microglial activation in abnormal neural development that may underlie ASD-like behavioral impairments. PMID:27723799

  5. Histological study on hippocampus, amygdala and cerebellum following low lead exposure during prenatal and postnatal brain development in rats.

    PubMed

    Barkur, Rajashekar Rao; Bairy, Laxminarayana K

    2016-06-01

    Neuropsychological studies in children who are exposed to lead during their early brain development have shown to develop behavioural and cognitive deficit. The aim of the present study was to assess the cellular damage in hippocampus, amygdala and cerebellum of rat pups exposed to lead during different periods of early brain development. Five groups of rat pups were investigated. (a) Control group (n = 8) (mothers of these rats were given normal drinking water throughout gestation and lactation), (b) pregestation lead-exposed group (n = 8) (mothers of these rats were exposed to 0.2% lead acetate in the drinking water for one month before conception), (c) gestation lead-exposed group (n = 8) (exposed to 0.2% lead acetate in the drinking water through the mother throughout gestation [gestation day 01 to day 21]), (d) lactation lead-exposed group (n = 8) (exposed to 0.2% lead acetate in the drinking water through the mother throughout lactation [postnatal day 01 to day 21]) and (e) gestation and lactation lead-exposed group (n = 8) (exposed to 0.2% lead acetate throughout gestation and lactation). On postnatal day 30, rat pups of all the groups were killed. Numbers of surviving neurons in the hippocampus, amygdala and cerebellum regions were counted using cresyl violet staining technique. Histological data indicate that lead exposure caused significant damage to neurons of hippocampus, amygdala and cerebellum regions in all lead-exposed groups except lactation lead-exposed group. The extent of damage to neurons of hippocampus, amygdala and cerebellum regions in lactation lead-exposed group was comparable to gestation and lactation groups even though the duration of lead exposure was much less in lactation lead-exposed group. To conclude, the postnatal period of brain development seems to be more vulnerable to lead neurotoxicity compared to prenatal period of brain development. © The Author(s) 2014.

  6. Valproic Acid Exposure during Early Postnatal Gliogenesis Leads to Autistic-like Behaviors in Rats

    PubMed Central

    Mony, Tamanna Jahan; Lee, Jae Won; Dreyfus, Cheryl; DiCicco-Bloom, Emanuel; Lee, Hee Jae

    2016-01-01

    Objective We reported that postnatal exposure of rats to valproic acid (VPA) stimulated proliferation of glial precursors during cortical gliogenesis. However, there are no reports whether enhanced postnatal gliogenesis affects behaviors related to neuropsychiatric disorders. Methods After VPA treatment during the postnatal day (PND) 2 to PND 4, four behavioral test, such as open field locomotor test, elevated plus maze test, three-chamber social interaction test, and passive avoidance test, were performed at PND 21 or 22. Results VPA treated rats showed significant hyperactive behavior in the open field locomotor test (p<0.05). Moreover, the velocity of movement in the VPA group was increased by 69.5% (p<0.01). In the elevated plus maze test, VPA exposed rats expressed significantly lower percentage of time spent on and of entries into open arms more than the control group (p<0.05). Also, both sociability and social preference indices with strangers in the three-chamber social interaction test were significantly lower in the VPA exposed rats (p<0.05). Conclusion Our results suggest that altered glial cell development is another locus at which pathogenetic factors can operate to contribute to the neurodevelopmental disorder. PMID:27776385

  7. Differential Effect of Postnatal Lead Exposure on Gene Expression in the Hippocampus and Frontal Cortex

    PubMed Central

    Schneider, J.S.; Mettil, W.; Anderson, D.W.

    2011-01-01

    Although developmental lead exposure is known to have detrimental effects on a variety of cognitive functions that depend on the integrity of the hippocampus and frontal cortex, little is known about how low levels of lead exposure affect expression of key families of genes in these structures. The present study examined the effects of exposure to environmentally-relevant levels of lead during the sensitive early post-weaning period in the rat on the expression profiles of a select number of neurobiologically relevant genes (i.e., genes for neurotrophic factors, NMDA receptors, metabotropic glutamate receptors, synaptic function/plasticity, cell signaling, and transcription/regulation) in the rat hippocampus and frontal cortex. Exposure to lead (180 and 375 ppm lead acetate in food for 30 days) significantly increased blood lead levels (5.8 to 10.3 μg/dl) and significantly affected expression of many of the genes examined. In many instances, lead exposure had different effects on the same gene depending on the brain region in which the expression of that gene was examined. Gene expression in the frontal cortex was often more sensitive to modification than gene expression in the hippocampus. These results suggest that even past infancy, exposures to low levels of lead can have significant effects on gene expression in frontal cortex and the hippocampus with the potential to exert long-term effects on behavior and cognition. PMID:22160880

  8. Effect of postnatal lead exposure on the development of sympathetic innervation of the heart. [Rats

    SciTech Connect

    Abreu, M.E.

    1983-01-01

    To determine possible mechanisms for this Pb-induced cardiotoxicity, several neutrochemical parameters indicative of cardiac sympathetic innervation were measured in developing rats. Presynaptic indices of nerve terminal development which were studied included steady-state levels of norepinephrine, neuronal uptake and vesicular storage of /sup 3/H-norepinephrine. Analysis of postsynaptic development was accomplished by quantitating the density of ..beta..-adrenergic receptors and by measuring the activity of adenylate cyclase. Rat pups were exposed to Pb from birth to weaning (21 days) via the milk of dams whose drinking water contained 0.2% Pb acetate. This method and level of Pb treatment had no effect on body or heart weight development, however, it did result in a seven-fold increase in the blood Pb content (70-75 ..mu..g/dl) of the treated pups during the period of exposure. Pb exposure accelerated the development of sympathetic innervation of the heart as detected by significant increases in the vesicular uptake of /sup 3/H-norepinephrine and the steady-state concentration of norepinephrine measured at postnatal day 4. On the other hand, ontogeny of the neutronal uptake of /sup 3/H-norepinephrine in the heart and in the forebrain was not affected by Pb treatment. The apparent premature development of sympathetic innervation induced by Pb treatment was not reflected in significant alterations in either the density or the affinity of ..beta..-adrenergic receptor sites determined by the binding kinetics of /sup 3/H-dihydroalprenolol.

  9. Sex-based differences in gene expression in hippocampus following postnatal lead exposure.

    PubMed

    Schneider, J S; Anderson, D W; Sonnenahalli, H; Vadigepalli, R

    2011-10-15

    The influence of sex as an effect modifier of childhood lead poisoning has received little systematic attention. Considering the paucity of information available concerning the interactive effects of lead and sex on the brain, the current study examined the interactive effects of lead and sex on gene expression patterns in the hippocampus, a structure involved in learning and memory. Male or female rats were fed either 1500 ppm lead-containing chow or control chow for 30 days beginning at weaning.Blood lead levels were 26.7±2.1 μg/dl and 27.1±1.7 μg/dl for females and males, respectively. The expression of 175 unique genes was differentially regulated between control male and female rats. A total of 167 unique genes were differentially expressed in response to lead in either males or females. Lead exposure had a significant effect without a significant difference between male and female responses in 77 of these genes. In another set of 71 genes, there were significant differences in male vs. female response. A third set of 30 genes was differentially expressed in opposite directions in males vs. females, with the majority of genes expressed at a lower level in females than in males. Highly differentially expressed genes in males and females following lead exposure were associated with diverse biological pathways and functions. These results show that a brief exposure to lead produced significant changes in expression of a variety of genes in the hippocampus and that the response of the brain to a given lead exposure may vary depending on sex. Copyright © 2011 Elsevier Inc. All rights reserved.

  10. Early postnatal lead exposure: behavioral effects in common tern chicks (Sterna Hirundo)

    SciTech Connect

    Burger, J.; Gochfeld, M.

    1985-01-01

    Exposure to lead early in life is known to affect behavioral and intellectual development. To develop an animal model the authors chose the common tern, Sterna hirundo, a species whose early developmental landmarks are well known. One potential for avian models lies in the reliance of birds on visual and acoustic rather than olfactory (and ultrasonic) modes of communication. One randomly chosen member from each of 8 pairs of young common tern chicks was injected with lead nitrate solution at a concentration of 0.2 mg/g. The pairs were not siblings but were matched for age (+/-1 d) and weight (+/-3 g). The second member of each pair was injected with an equal volume of sterile saline. Behavioral tests performed examined locomotion, balance and righting response, feeding tasks and begging, depth perception and response on a visual cliff, and behavioral thermoregulation. In each pair the control chick was heavier at 4 wk of age. For most behavioral measures, except begging and movement on a stationary incline, the lead-injected chicks performed less well than the control chicks. When presented with a novel feeding situation (reversal of fish position), the lead-injected chicks required significantly more time to eat the same number of fish. The single injection of lead, thus, affected a variety of behavioral patterns, with effects apparent within 5 d after injection.

  11. Prenatal and postnatal effects of low-level lead exposure: integrated summary of a report to the U.S. Congress on childhood lead poisoning.

    PubMed

    Mushak, P; Davis, J M; Crocetti, A F; Grant, L D

    1989-10-01

    This article provides an integrated summary of a report to Congress from the Federal government (ATSDR) on childhood lead poisoning in the United States, with particular reference to low-level lead exposure and its effects on the fetus and the preschool child. As mandated by Section 118(f)(1)(C) of the 1986 Superfund Amendments and Reauthorization Act (SARA), ATSDR has examined the full spectrum of human in utero and postnatal lead toxicity, with emphasis on low-level neurotoxicity and adverse impacts on growth indices in risk populations. Especially important has been assessment of the relative persistence of these effects in later life as discernible from a number of longitudinal studies now under way around the world. Included in the Congressional report were discussions of dose-effect and dose-response relationships using blood lead levels as the indicator of lead dose.

  12. Prenatal and postnatal effects of low-level lead exposure: Integrated summary of a report to the US congress on childhood lead poisoning

    SciTech Connect

    Mushak, P. ); Davis, M.; Grant, L.D. ); Crocetti, A.F. )

    1989-10-01

    This article provides an integrated summary of a report of Congress from the Federal government (ATSDR) on childhood lead poisoning in the United States, with particular reference to low-level lead exposure and its effects on the fetus and the preschool child. As mandated by Section 118(f)(1)(C) of the 1986 Superfund Amendments and Reauthorization Act (SARA), ATSDR has examined the full spectrum of human in utero postnatal lead toxicity, with emphasis on low-level neurotoxicity and adverse impacts on growth indices in risk populations. Especially important has been assessment of the relative persistence of these effects in later life as discernible from a number of longitudinal studies now under way around the world. Include in the Congressional report were discussions of dose-effect and dose-response relationships using blood lead levels as the indicator of lead dose.

  13. Early Postnatal Exposure to Cigarette Smoke Leads to Later Airway Inflammation in Asthmatic Mice

    PubMed Central

    Huang, Fei; Cheng, Hang; Zhang, Yu-tong; Ju, Yang-hua; Li, Ya-nan

    2017-01-01

    Background and objective Asthma is one of the most common airway inflammatory diseases. In most cases, asthma development is related to ubiquitous harmful environmental exposure factors in early-life. Previous studies have indicated that smoking can promote asthma development and increase the difficulty of asthma control. The aim of this study was to determine the effects of early-life CS exposure on ovalbumin (OVA)-sensitized asthmatic mice. Methods Pathological and immunological functions were analyzed in an adult asthma mice model in which mice were sensitized with OVA combined with early-life CS exposure. Results Mice exposed to CS for only 5 weeks demonstrated significantly reduced pulmonary compliance, increased airway inflammation, and augmented cellular and humoral immune responses. In addition, CS inhalation was sufficient to facilitate OVA sensitization and challenge asthmatic development. Meanwhile, CS exposure amplified regulatory T cell-mediated immunity inhibition, but still did not offset the increased effector T cell-mediated inflammatory response. Conclusion Early-life CS exposure is significantly associated with later pulmonary injury and aggravation of T-cell immunologic derangement in asthmatic mice. PMID:28135326

  14. Prenatal and early postnatal NOAEL-dose clothianidin exposure leads to a reduction of germ cells in juvenile male mice.

    PubMed

    Yanai, Shogo; Hirano, Tetsushi; Omotehara, Takuya; Takada, Tadashi; Yoneda, Naoki; Kubota, Naoto; Yamamoto, Anzu; Mantani, Youhei; Yokoyama, Toshifumi; Kitagawa, Hiroshi; Hoshi, Nobuhiko

    2017-07-07

    Neonicotinoids are pesticides used worldwide. They bind to insect nicotinic acetylcholine receptors (nAChRs) with high affinity. We previously reported that clothianidin (CTD), one of the latest neonicotinoids, reduced antioxidant expression and induced germ cell death in the adult testis of vertebrates. Here, we investigated the male reproductive toxicity of prenatal and early postnatal exposure to CTD, because it is likely that developmental exposure more severely affects the testis compared to adults due to the absence of the blood-testis barrier. Pregnant C57BL/6 mice were given water gel blended with CTD (0, 10 or 50 mg/kg/day; no-observed-adverse-effect-level [NOAEL for mice]: 47.2 mg/kg/day) between gestational day 1 and 14 days post-partum. We then examined the testes of male offspring at postnatal day 14. The testis weights and the numbers of germ cells per seminiferous tubule were decreased in the CTD-50 group, and abnormal tubules containing no germ cells appeared. Nevertheless, the apoptotic cell number and proliferative activity were not significantly different between the control and CTD-exposed groups. There were no significant differences in the androgen-related parameters, such as the Leydig cell volume per testis, the Sertoli cell number and the tubule diameter. The present study is the first demonstration that in utero and lactational exposures to CTD at around the NOAEL for mice reduce the germ cell number, but our findings suggest that these exposures do not affect steroidogenesis in Leydig cells during prenatal or early postnatal life.

  15. Prenatal and early postnatal NOAEL-dose clothianidin exposure leads to a reduction of germ cells in juvenile male mice

    PubMed Central

    YANAI, Shogo; HIRANO, Tetsushi; OMOTEHARA, Takuya; TAKADA, Tadashi; YONEDA, Naoki; KUBOTA, Naoto; YAMAMOTO, Anzu; MANTANI, Youhei; YOKOYAMA, Toshifumi; KITAGAWA, Hiroshi; HOSHI, Nobuhiko

    2017-01-01

    Neonicotinoids are pesticides used worldwide. They bind to insect nicotinic acetylcholine receptors (nAChRs) with high affinity. We previously reported that clothianidin (CTD), one of the latest neonicotinoids, reduced antioxidant expression and induced germ cell death in the adult testis of vertebrates. Here, we investigated the male reproductive toxicity of prenatal and early postnatal exposure to CTD, because it is likely that developmental exposure more severely affects the testis compared to adults due to the absence of the blood-testis barrier. Pregnant C57BL/6 mice were given water gel blended with CTD (0, 10 or 50 mg/kg/day; no-observed-adverse-effect-level [NOAEL for mice]: 47.2 mg/kg/day) between gestational day 1 and 14 days post-partum. We then examined the testes of male offspring at postnatal day 14. The testis weights and the numbers of germ cells per seminiferous tubule were decreased in the CTD-50 group, and abnormal tubules containing no germ cells appeared. Nevertheless, the apoptotic cell number and proliferative activity were not significantly different between the control and CTD-exposed groups. There were no significant differences in the androgen-related parameters, such as the Leydig cell volume per testis, the Sertoli cell number and the tubule diameter. The present study is the first demonstration that in utero and lactational exposures to CTD at around the NOAEL for mice reduce the germ cell number, but our findings suggest that these exposures do not affect steroidogenesis in Leydig cells during prenatal or early postnatal life. PMID:28579575

  16. Bcl-xL-mediated remodeling of rod and cone synaptic mitochondria after postnatal lead exposure: Electron microscopy, tomography and oxygen consumption

    PubMed Central

    Perkins, Guy A.; Scott, Ray; Perez, Alex; Ellisman, Mark H.; Johnson, Jerry E.

    2012-01-01

    Purpose Postnatal lead exposure produces rod-selective and Bax-mediated apoptosis, decreased scotopic electroretinograms (ERGs), and scotopic and mesopic vision deficits in humans and/or experimental animals. Rod, but not cone, inner segment mitochondria were considered the primary site of action. However, photoreceptor synaptic mitochondria were not examined. Thus, our experiments investigated the structural and functional effects of environmentally relevant postnatal lead exposure on rod spherule and cone pedicle mitochondria and whether Bcl-xL overexpression provided neuroprotection. Methods C57BL/6N mice pups were exposed to lead only during lactation via dams drinking water containing lead acetate. The blood [Pb] at weaning was 20.6±4.7 µg/dl, which decreased to the control value by 2 months. To assess synaptic mitochondrial structural differences and vulnerability to lead exposure, wild-type and transgenic mice overexpressing Bcl-xL in photoreceptors were used. Electron microscopy, three-dimensional electron tomography, and retinal and photoreceptor synaptic terminal oxygen consumption (QO2) studies were conducted in adult control, Bcl-xL, lead, and Bcl-xL/lead mice. Results The spherule and pedicle mitochondria in lead-treated mice were swollen, and the cristae structure was markedly changed. In the lead-treated mice, the mitochondrial cristae surface area and volume (abundance: measure correlated with ATP (ATP) synthesis) were decreased in the spherules and increased in the pedicles. Pedicles also had an increased number of crista segments per volume. In the lead-treated mice, the number of segments/crista and fraction of cristae with multiple segments (branching) similarly increased in spherule and pedicle mitochondria. Lead-induced remodeling of spherule mitochondria produced smaller cristae with more branching, whereas pedicle mitochondria had larger cristae with more branching and increased crista junction (CJ) diameter. Lead decreased dark- and light

  17. Infantile postnatal exposure to lead (Pb) enhances tau expression in the cerebral cortex of aged mice: relevance to AD.

    PubMed

    Bihaqi, Syed Waseem; Bahmani, Azadeh; Adem, Abdu; Zawia, Nasser H

    2014-09-01

    The sporadic nature in over 90% of Alzheimer's disease (AD) cases, the differential susceptibility and course of illness, and latent onset of the disease suggest involvement of an environmental component in the etiology of late onset AD (LOAD). Recent reports from our lab have demonstrated that molecular alterations favor abundant tau phosphorylation and immunoreactivity in the frontal cortex of aged primates with infantile lead (Pb) exposure (Bihaqi and Zawia, 2013). Here we report that developmental Pb exposure results in elevation of protein and mRNA levels of tau in aged mice. Western blot analysis revealed aberrant site-specific tau hyperphosphorylation accompanied by elevated cyclin dependent kinase 5 (CDK5) levels in aged mice with prior Pb exposure. Mice with developmental Pb exposure also displayed altered protein ratio of p35/p25 with more Serine/Threonine phosphatase activity at old age. These changes favored increase in tau phosphorylation, thus providing evidence that neurodegenerative diseases may be in part due to environmental influences that occur during development. Copyright © 2014 Elsevier Inc. All rights reserved.

  18. Neurotoxicity from prenatal and postnatal exposure to methylmercury

    PubMed Central

    Grandjean, Philippe; Weihe, Pal; Debes, Frodi; Choi, Anna L.; Budtz-Jørgensen, Esben

    2014-01-01

    The extent to which postnatal methylmercury exposure contributes to neurobehavioral delays is uncertain. Confounding may occur because the child's dietary exposure likely correlates with the mother's. This conundrum was examined in the Faroese birth cohort 1 born in 1986–1987. Exposure parameters included mercury concentrations in maternal hair at parturition, cord blood, and child blood and hair at the age-7 clinical examination (N = 923). In regression analyses, the child's current blood-mercury at age 7 (N = 694) showed only weak associations with the neuropsychological test variables, but visuospatial memory revealed a significant negative association. Mutual adjustment caused decreases of the apparent effect of the prenatal exposure. However, such adjustment may lead to underestimations due to the presence of correlated, error-prone exposure variables. In structural equation models, all methylmercury exposure parameters were instead entered into a latent exposure variable that reflected the total methylmercury load. This latent exposure showed significant associations with neurodevelopmental deficits, with prenatal exposure providing the main information. However, postnatal methylmercury exposure appeared to contribute to neurotoxic effects, in particular in regard to visuospatial processing and memory. Thus, addition in the regression analysis of exposure information obtained at a different point in time was not informative and should be avoided. Further studies with better information on exposure profiles are needed to characterize the effects of postnatal methylmercury exposure. PMID:24681285

  19. Antenatal exposure to the selective serotonin reuptake inhibitor fluoxetine leads to postnatal metabolic and endocrine changes associated with type 2 diabetes in Wistar rats

    SciTech Connect

    De Long, Nicole E.; Barry, Eric J.; Pinelli, Christopher; Wood, Geoffrey A.; Hardy, Daniel B.; Morrison, Katherine M.; Taylor, Valerie H.; Gerstein, Hertzel C.; Holloway, Alison C.

    2015-05-15

    Hypothesis: 10–15% of women take antidepressant medications during pregnancy. A recent clinical study reported that the use of selective serotonin reuptake inhibitor antidepressants during pregnancy is linked with an increased risk of postnatal obesity. While obesity is often associated with fatty liver, dyslipidemia and inflammation, to date, the effects of perinatal exposure to SSRIs on these outcomes are unknown. Methods: Female nulliparous Wistar rats were given vehicle (N = 15) or fluoxetine hydrochloride (FLX 10 mg/kg/d; N = 15) orally for 2 weeks prior to mating until weaning. We assessed glucometabolic changes and hepatic pathophysiology in the offspring. Results: Fluoxetine exposed offspring demonstrated altered glucose homeostasis without any alterations to beta cell mass. FLX-exposed offspring had a significant increase in the number of offspring with mild to moderate NASH and dyslipidemia. There was also increased inflammation of the liver in FLX-exposed offspring; males had significant elevations in TNFα, IL6 and monocyte chemoattractant protein 1 (MCP1), while female offspring had higher expression of TNFα, and increased macrophage infiltration (MCP1). Limitations: This is an animal study. Further research examining the metabolic outcomes of children exposed to antidepressants in utero are required, given the increase in childhood obesity and psychiatric medication use during pregnancy. Conclusion: These data demonstrate that fetal and neonatal exposure to FLX results in evidence of increased adiposity, fatty liver and abnormal glycemic control. Since these are all hallmarks of the metabolic syndrome, this raises concerns regarding the long term metabolic sequelae of fetal exposure to SSRIs in human populations. - Highlights: • Antenatal exposure to fluoxetine results in postnatal adiposity in the offspring. • Offspring exposed to fluoxetine have abnormal glycemic control in adulthood. • Maternal exposure to fluoxetine causes fatty liver in

  20. Prenatal immunotoxicant exposure and postnatal autoimmune disease.

    PubMed Central

    Holladay, S D

    1999-01-01

    Reports in humans and rodents indicate that immune development may be altered following perinatal exposure to immunotoxic compounds, including chemotherapeutics, corticosteroids, polycyclic hydrocarbons, and polyhalogenated hydrocarbons. Effects from such exposure may be more dramatic or persistent than following exposure during adult life. For example, prenatal exposure to the insecticide chlordane or to the polycyclic aromatic hydrocarbon benzo[(italic)a(/italic)]pyrene produces what appears to be lifelong immunosuppression in mice. Whether prenatal immunotoxicant exposure may predispose the organism to postnatal autoimmune disease remains largely unknown. In this regard, the therapeutic immunosuppressant cyclosporin A (CsA) crosses the placenta poorly. However, lethally irradiated rodents exposed to CsA postsyngeneic bone marrow transplant (i.e., during re-establishment of the immune system) develop T-cell-mediated autoimmune disease, suggesting this drug may produce a fundamental disruption in development of self-tolerance by T cells. The environmental contaminant 2,3,7, 8-tetrachlorodibenzo-(italic)p(/italic)-dioxin (TCDD) crosses the placenta and produces fetal thymic effects (italic)in vivo(/italic) similar to effects of CsA in fetal thymic organ culture, including inhibited thymocyte maturation and reduced expression of thymic major histocompatability complex class II molecules. These observations led to the suggestion that gestational exposure to TCDD may interfere with normal development of self-tolerance. Possibly supporting this hypothesis, when mice predisposed to development of autoimmune disease were treated with TCDD during gestation, postnatal autoimmunity was exacerbated. Similar results have been reported for mice exposed to diethylstilbestrol during development. These reports suggest that prenatal exposure to certain immunotoxicants may play a role in postnatal expression of autoimmunity. PMID:10502532

  1. [Pre and postnatal tobacco exposure and bronchiolitis].

    PubMed

    Cano Fernández, J; Zabaleta Camino, C; de la Torre Montes de Neira, E; Yep Chullen, G A; Melendi Crespo, J M; Sánchez Bayle, M

    2003-02-01

    To determine the influence of pre- and postnatal tobacco exposure in the development of bronchiolitis. A questionnaire was given to the parents of children hospitalized between August 2001 and August 2002. It included items on parental smoking habits and maternal smoking during pregnancy. Clinical, analytical and radiological criteria were used to diagnose bronchiolitis. Of 450 children, 123 (27.3 %) were diagnosed with bronchiolitis. The control group was composed of 327 children. A total of 61.6 % of the children had at least one parent who smoked and 32.9 % of these children developed bronchiolitis; 39.1 % had non-smoking parents and 18.2 % were hospitalized with bronchiolitis (OR 2.20 [1.39-3.47]). Of the entire group of children studied, 35.3 % had mothers who smoked and 37.7 % of these children had bronchiolitis compared with 21.4 % of children whose mothers were non-smokers (OR 2.22 [1.45-3.39]). A total of 49.6 % had fathers who smoked, and 32.3 % of these children were diagnosed with bronchiolitis compared with 22 % of children whose fathers were non-smokers (OR 1.65 [1.10-2.57]). Forty-four percent of children whose mothers smoked during pregnancy were hospitalized with bronchiolitis compared with only 20.9 % of non-exposed children (OR 2.96 [1.90-4.62]). The large number of mothers who smoked during pregnancy (27.8 %) was notable. Multivariant analysis with logistic regression was performed and the only variable that remained statistically significant was smoking during pregnancy (p < 0.00001; OR 3.27 [1.39-7.71]). Maternal smoking during pregnancy seems to be the main risk factor for the subsequent development of bronchiolitis

  2. Alterations in central monoamine systems after postnatal lead acetate treatment in rats

    SciTech Connect

    Luthman, J. Univ. of Colorado Health Sciences Center, Denver, CO ); Lindqvist, E.; Olson, L. ); Gerhardt, G.A.; Hoffer, B.H. )

    1994-04-01

    The present study was undertaken to investigate the effect of postnatal lead exposure on central monoamine systems. Newborn male Sprague-Dawley rats were given 1 or 8 mg/kg lead acetate intraperitoneally for 20 days postnatally. Two groups of control rats received sodium acetate, or sodium acetate in oversized litters to compensate for lead-induced malnutrition in the high lead dose group, while nontreated animals also served as controls. At Day 21 or 51 regional tissue levels of monoamines were determined using HPLC techniques. No major changes were seen after the lead exposures in the levels of dopamine, noradrenaline, and serotonin, or metabolites of dopamine and serotonin, when compared to respective control groups. On the other hand, in the control group given sodium acetate in oversized litters some alterations of the monoamine levels were observed in frontal cortex and striatum at Day 21 compared to controls. At Day 51, the striatal homovanillic acid and 5-hydroxyindoleacetic acid levels were higher in the low lead dose group compared to those in the controls, No other changes in the monoamine levels were seen at Day 51. At 50-70 days postnatally, potassium-stimulated dopamine overflow was studied in striatum with in vivo chronoamperometry. In the high lead dose group the amplitudes of signals were lower in both the dorsal and ventral striatum compared to the controls, while no difference was seen in the clearance time of dopamine. The capacity of the dopamine terminals to respond to repeated stimulation was not affected by the lead exposure. Thus, the steady-state levels of monoamines were essentially unaltered after postnatal lead exposure in rats, while functional aspects of striatal dopamine transmission were affected after exposure to the higher dose of lead. These findings support the hypothesis that lead-induced changes in motor skills and exploratory behavior may be related to altered dopamine neurotransmission. 77 refs., 3 figs., 2 tabs.

  3. Food Exposures to Lead

    PubMed Central

    Kolbye, Albert C.; Mahaffey, Kathryn R.; Fiorino, John A.; Corneliussen, Paul C.; Jelinek, Charles F.

    1974-01-01

    Exposures to lead have emanated from various sources, including food, throughout human history. Occupational and environmental exposures (especially pica) appear to account for much of the identified human disease, however, food-borne exposures deserve further investigation. Lead residues in food can result from: biological uptake from soils into plants consumed by food animals or man, usage of lead arsenate pesticides, inadvertent addition during food processing, and by leaching them improperly glazed pottery used as food storage or dining utensils. Estimates of total dietary exposure should reflect frequency distribution data on lead levels in specific food commodities in relation to the quantities actually ingested by various sample populations to distinguish degrees of risk associated with particular dietary habits. Earlier estimates of average total dietary intake of lead by adults have been reported to range from above 500 μg/day downward with more recent estimates suggesting averages of 200 μg/day or lower. The strengths and weaknesses of these data are discussed along with analytical and sampling considerations. FDA programs related to food surveillance, epidemiology, and toxicological investigation are briefly described. PMID:4406646

  4. Prenatal and Postnatal Cell Phone Exposures and Headaches in Children

    PubMed Central

    Sudan, Madhuri; Kheifets, Leeka; Arah, Onyebuchi; Olsen, Jorn; Zeltzer, Lonnie

    2013-01-01

    Objective Children today are exposed to cell phones early in life, and may be at the greatest risk if exposure is harmful to health. We investigated associations between cell phone exposures and headaches in children. Study Design The Danish National Birth Cohort enrolled pregnant women between 1996 and 2002. When their children reached age seven years, mothers completed a questionnaire regarding the child’s health, behaviors, and exposures. We used multivariable adjusted models to relate prenatal only, postnatal only, or both prenatal and postnatal cell phone exposure to whether the child had migraines and headache-related symptoms. Results Our analyses included data from 52,680 children. Children with cell phone exposure had higher odds of migraines and headache-related symptoms than children with no exposure. The odds ratio for migraines was 1.30 (95% confidence interval: 1.01–1.68) and for headache-related symptoms was 1.32 (95% confidence interval: 1.23–1.40) for children with both prenatal and postnatal exposure. Conclusions In this study, cell phone exposures were associated with headaches in children, but the associations may not be causal given the potential for uncontrolled confounding and misclassification in observational studies such as this. However, given the widespread use of cell phones, if a causal effect exists it would have great public health impact. PMID:23750182

  5. Prenatal and Postnatal Cell Phone Exposures and Headaches in Children.

    PubMed

    Sudan, Madhuri; Kheifets, Leeka; Arah, Onyebuchi; Olsen, Jorn; Zeltzer, Lonnie

    2012-12-05

    Children today are exposed to cell phones early in life, and may be at the greatest risk if exposure is harmful to health. We investigated associations between cell phone exposures and headaches in children. The Danish National Birth Cohort enrolled pregnant women between 1996 and 2002. When their children reached age seven years, mothers completed a questionnaire regarding the child's health, behaviors, and exposures. We used multivariable adjusted models to relate prenatal only, postnatal only, or both prenatal and postnatal cell phone exposure to whether the child had migraines and headache-related symptoms. Our analyses included data from 52,680 children. Children with cell phone exposure had higher odds of migraines and headache-related symptoms than children with no exposure. The odds ratio for migraines was 1.30 (95% confidence interval: 1.01-1.68) and for headache-related symptoms was 1.32 (95% confidence interval: 1.23-1.40) for children with both prenatal and postnatal exposure. In this study, cell phone exposures were associated with headaches in children, but the associations may not be causal given the potential for uncontrolled confounding and misclassification in observational studies such as this. However, given the widespread use of cell phones, if a causal effect exists it would have great public health impact.

  6. Preterm cerebellar growth impairment after postnatal exposure to glucocorticoids

    PubMed Central

    Tam, Emily W. Y.; Chau, Vann; Ferriero, Donna M.; Barkovich, A. James; Poskitt, Kenneth J.; Studholme, Colin; Fok, Eric D.-Y.; Grunau, Ruth E.; Glidden, David V.; Miller, Steven P.

    2012-01-01

    With improving survival rates of preterm newborns, adverse cognitive outcomes are increasingly recognized. Adverse cognitive outcomes are associated with decreased cerebellar volumes, and modifiable risk factors for these adverse outcomes should be identified. Animal models demonstrate reduced preterm cerebellar growth after exposure to glucocorticoids. Preterm neonates were prospectively studied with serial MRI examinations near birth and again near term-equivalent age. Adjusting for associated clinical factors, antenatal bethamethasone was not associated with changes in cerebellar volume. Postnatal exposure to clinically routine doses of hydrocortisone or dexamethasone were associated with impaired cerebellar, but not cerebral, growth. Modifying postnatal risk factors for impaired cerebellar development, and particularly glucocorticoid exposure, may help to decrease risk for adverse neurological outcome after preterm birth. PMID:22013125

  7. Prenatal and postnatal cocaine exposure predict teen cocaine use

    PubMed Central

    Delaney-Black, Virginia; Chiodo, Lisa M.; Hannigan, John H.; Greenwald, Mark K.; Janisse, James; Patterson, Grace; Huestis, Marilyn A.; Partridge, Robert T.; Ager, Joel; Sokol, Robert J.

    2015-01-01

    Preclinical studies have identified alterations in cocaine and alcohol self-administration and behavioral responses to pharmacological challenges in adolescent offspring following prenatal exposure. To date, no published human studies have evaluated the relation between prenatal cocaine exposure and postnatal adolescent cocaine use. Human studies of prenatal cocaine-exposed children have also noted an increase in behaviors previously associated with substance use/abuse in teens and young adults, specifically childhood and teen externalizing behaviors, impulsivity, and attention problems. Despite these findings, human research has not addressed prior prenatal exposure as a potential predictor of teen drug use behavior. The purpose of this study was to evaluate the relations between prenatal cocaine exposure and teen cocaine use in a prospective longitudinal cohort (n = 316) that permitted extensive control for child, parent and community risk factors. Logistic regression analyses and Structural Equation Modeling revealed that both prenatal exposure and postnatal parent/caregiver cocaine use were uniquely related to teen use of cocaine at age 14 years. Teen cocaine use was also directly predicted by teen community violence exposure and caregiver negativity, and was indirectly related to teen community drug exposure. These data provide further evidence of the importance of prenatal exposure, family and community factors in the intergenerational transmission of teen/young adult substance abuse/use. PMID:20609384

  8. Prenatal and postnatal cocaine exposure predict teen cocaine use.

    PubMed

    Delaney-Black, Virginia; Chiodo, Lisa M; Hannigan, John H; Greenwald, Mark K; Janisse, James; Patterson, Grace; Huestis, Marilyn A; Partridge, Robert T; Ager, Joel; Sokol, Robert J

    2011-01-01

    Preclinical studies have identified alterations in cocaine and alcohol self-administration and behavioral responses to pharmacological challenges in adolescent offspring following prenatal exposure. To date, no published human studies have evaluated the relation between prenatal cocaine exposure and postnatal adolescent cocaine use. Human studies of prenatal cocaine-exposed children have also noted an increase in behaviors previously associated with substance use/abuse in teens and young adults, specifically childhood and teen externalizing behaviors, impulsivity, and attention problems. Despite these findings, human research has not addressed prior prenatal exposure as a potential predictor of teen drug use behavior. The purpose of this study was to evaluate the relations between prenatal cocaine exposure and teen cocaine use in a prospective longitudinal cohort (n=316) that permitted extensive control for child, parent and community risk factors. Logistic regression analyses and Structural Equation Modeling revealed that both prenatal exposure and postnatal parent/caregiver cocaine use were uniquely related to teen use of cocaine at age 14 years. Teen cocaine use was also directly predicted by teen community violence exposure and caregiver negativity, and was indirectly related to teen community drug exposure. These data provide further evidence of the importance of prenatal exposure, family and community factors in the intergenerational transmission of teen/young adult substance abuse/use.

  9. PRENATAL EXPOSURE TO ETHANOL AFFECTS POSTNATAL NEUROGENESIS IN THALAMUS

    PubMed Central

    Mooney, Sandra M.; Miller, Michael W.

    2010-01-01

    The number of neurons in the ventrobasal thalamus (VB) in the adolescent rat is unaffected by prenatal exposure to ethanol. This is in sharp contrast to other parts of the trigeminal-somatosensory system which exhibit 30–35% fewer neurons after prenatal ethanol exposure. The present study tested the hypothesis that prenatal ethanol exposure affects dynamic changes in the numbers of VB neurons; such changes reflect the sum of cell proliferation and death. Neuronal number in the VB was determined during the first postnatal month in the offspring of pregnant Long-Evans rats fed an ethanol-containing diet or pair-fed an isocaloric non-alcoholic liquid diet. Offspring were examined between postnatal day (P) 1 and P30. The size of the VB and neuronal number were determined stereologically. Prenatal exposure to ethanol did not significantly alter neuronal number on any individual day, nor was the prenatal generation of VB neurons affected. Interestingly, prenatal ethanol exposure did affect the pattern of the change in neuronal number over time; total neuronal number was stable in the ethanol-treated pups after P12, but it continued to rise in the controls until P21. In addition, the rate of cell proliferation during the postnatal period was greater in ethanol-treated animals. Thus, the rate of neuronal acquisition is altered by ethanol, and by deduction there appears to be less ethanol-induced neuronal loss in the VB. A contributor to these changes is a latent effect of ethanol on postnatal neurogenesis in the VB and the apparent survival of new neurons. PMID:20170653

  10. Prenatal exposure to ethanol affects postnatal neurogenesis in thalamus.

    PubMed

    Mooney, Sandra M; Miller, Michael W

    2010-06-01

    The number of neurons in the ventrobasal thalamus (VB) in the adolescent rat is unaffected by prenatal exposure to ethanol. This is in sharp contrast to other parts of the trigeminal-somatosensory system, which exhibit 30-35% fewer neurons after prenatal ethanol exposure. The present study tested the hypothesis that prenatal ethanol exposure affects dynamic changes in the numbers of VB neurons; such changes reflect the sum of cell proliferation and death. Neuronal number in the VB was determined during the first postnatal month in the offspring of pregnant Long-Evans rats fed an ethanol-containing diet or pair-fed an isocaloric non-alcoholic liquid diet. Offspring were examined between postnatal day (P) 1 and P30. The size of the VB and neuronal number were determined stereologically. Prenatal exposure to ethanol did not significantly alter neuronal number on any individual day, nor was the prenatal generation of VB neurons affected. Interestingly, prenatal ethanol exposure did affect the pattern of the change in neuronal number over time; total neuronal number was stable in the ethanol-treated pups after P12, but it continued to rise in the controls until P21. In addition, the rate of cell proliferation during the postnatal period was greater in ethanol-treated animals. Thus, the rate of neuronal acquisition is altered by ethanol, and by deduction, there appears to be less ethanol-induced neuronal loss in the VB. A contributor to these changes is a latent effect of ethanol on postnatal neurogenesis in the VB and the apparent survival of new neurons.

  11. Lead exposure and neurobehavior development in later infancy

    SciTech Connect

    Dietrich, K.N.; Succop, P.A.; Bornschein, R.L.; Hammond, P.B.; Buncher, C.R.; Berger, O. ); Krafft, K.M. )

    1990-11-01

    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 {mu}g/dL). However, approximately 25% of the study infants had at least one serial blood lead level of 25 {mu}g/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.

  12. Lead exposure and neurobehavioral development in later infancy.

    PubMed Central

    Dietrich, K N; Succop, P A; Bornschein, R L; Krafft, K M; Berger, O; Hammond, P B; Buncher, C R

    1990-01-01

    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. PMID:2088739

  13. Developmental programming: interaction between prenatal BPA exposure and postnatal adiposity on metabolic variables in female sheep.

    PubMed

    Veiga-Lopez, Almudena; Moeller, Jacob; Sreedharan, Rohit; Singer, Kanakadurga; Lumeng, Carey; Ye, Wen; Pease, Anthony; Padmanabhan, Vasantha

    2016-02-01

    Among potential contributors for the increased incidence of metabolic diseases is the developmental exposure to endocrine-disrupting chemicals such as bisphenol A (BPA). BPA is an estrogenic chemical used in a variety of consumer products. Evidence points to interactions of BPA with the prevailing environment. The aim of this study was to assess the effects of prenatal exposure to BPA on postnatal metabolic outcomes, including insulin resistance, adipose tissue distribution, adipocyte morphometry, and expression of inflammatory markers in adipose tissue as well as to assess whether postnatal overfeeding would exacerbate these effects. Findings indicate that prenatal BPA exposure leads to insulin resistance in adulthood in the first breeder cohort (study 1), but not in the second cohort (study 2), which is suggestive of potential differences in genetic susceptibility. BPA exposure induced adipocyte hypertrophy in the visceral fat depot without an accompanying increase in visceral fat mass or increased CD68, a marker of macrophage infiltration, in the subcutaneous fat depot. Cohens effect size analysis found the ratio of visceral to subcutaneous fat depot in the prenatal BPA-treated overfed group to be higher compared with the control-overfed group. Altogether, these results suggest that exposure to BPA during fetal life at levels found in humans can program metabolic outcomes that lead to insulin resistance, a forerunner of type 2 diabetes, with postnatal obesity failing to manifest any interaction with prenatal BPA relative to insulin resistance and adipocyte hypertrophy.

  14. Developmental programming: interaction between prenatal BPA exposure and postnatal adiposity on metabolic variables in female sheep

    PubMed Central

    Veiga-Lopez, Almudena; Moeller, Jacob; Sreedharan, Rohit; Singer, Kanakadurga; Ye, Wen; Pease, Anthony

    2015-01-01

    Among potential contributors for the increased incidence of metabolic diseases is the developmental exposure to endocrine-disrupting chemicals such as bisphenol A (BPA). BPA is an estrogenic chemical used in a variety of consumer products. Evidence points to interactions of BPA with the prevailing environment. The aim of this study was to assess the effects of prenatal exposure to BPA on postnatal metabolic outcomes, including insulin resistance, adipose tissue distribution, adipocyte morphometry, and expression of inflammatory markers in adipose tissue as well as to assess whether postnatal overfeeding would exacerbate these effects. Findings indicate that prenatal BPA exposure leads to insulin resistance in adulthood in the first breeder cohort (study 1), but not in the second cohort (study 2), which is suggestive of potential differences in genetic susceptibility. BPA exposure induced adipocyte hypertrophy in the visceral fat depot without an accompanying increase in visceral fat mass or increased CD68, a marker of macrophage infiltration, in the subcutaneous fat depot. Cohens effect size analysis found the ratio of visceral to subcutanous fat depot in the prenatal BPA-treated overfed group to be higher compared with the control-overfed group. Altogether, these results suggest that exposure to BPA during fetal life at levels found in humans can program metabolic outcomes that lead to insulin resistance, a forerunner of type 2 diabetes, with postnatal obesity failing to manifest any interaction with prenatal BPA relative to insulin resistance and adipocyte hypertrophy. PMID:26646100

  15. Preterm cerebellar growth impairment after postnatal exposure to glucocorticoids.

    PubMed

    Tam, Emily W Y; Chau, Vann; Ferriero, Donna M; Barkovich, A James; Poskitt, Kenneth J; Studholme, Colin; Fok, Eric D-Y; Grunau, Ruth E; Glidden, David V; Miller, Steven P

    2011-10-19

    As survival rates of preterm newborns improve as a result of better medical management, these children increasingly show impaired cognition. These adverse cognitive outcomes are associated with decreases in the volume of the cerebellum. Because animals exhibit reduced preterm cerebellar growth after perinatal exposure to glucocorticoids, we sought to determine whether glucocorticoid exposure and other modifiable factors increased the risk for these adverse outcomes in human neonates. We studied 172 preterm neonatal infants from two medical centers, the University of British Columbia and the University of California, San Francisco, by performing serial magnetic resonance imaging examinations near birth and again near term-equivalent age. After we adjusted for associated clinical factors, antenatal betamethasone was not associated with changes in cerebellar volume. Postnatal exposure to clinically routine doses of hydrocortisone or dexamethasone was associated with impaired cerebellar, but not cerebral, growth. Alterations in treatment after preterm birth, particularly glucocorticoid exposure, may help to decrease risk for adverse neurological outcome after preterm birth.

  16. DETERMINANTS OF RESIDENTIAL LEAD EXPOSURE

    EPA Science Inventory

    The phase-out of leaded gasoline, and the accompanying decrease in lead emissions, resulted in a dramatic decline in mean blood lead levels from the late 1970s through the early 1990s. Nonetheless, lead exposures remain a public health concern. Long-term exposures to even low...

  17. DETERMINANTS OF RESIDENTIAL LEAD EXPOSURE

    EPA Science Inventory

    The phase-out of leaded gasoline, and the accompanying decrease in lead emissions, resulted in a dramatic decline in mean blood lead levels from the late 1970s through the early 1990s. Nonetheless, lead exposures remain a public health concern. Long-term exposures to even low...

  18. Cocaine Exposure In Utero Alters Synaptic Plasticity in the Medial Prefrontal Cortex of Postnatal Rats

    PubMed Central

    Lu, Hui; Lim, Byungkook

    2009-01-01

    Cocaine exposure during pregnancy causes abnormality in fetal brain development, leading to cognitive dysfunction of the offspring, but the underlying cellular mechanism remains mostly unclear. In this study, we examined synaptic functions in the medial prefrontal cortex (mPFC) of postnatal rats that were exposed to cocaine in utero, using whole-cell recording from mPFC layer V pyramidal neurons in acute brain slices. Cocaine exposure in utero resulted in a facilitated activity-induced long-term potentiation (LTP) of excitatory synapses on these pyramidal neurons and an elevated neuronal excitability in postnatal rat pups after postnatal day 15 (P15). This facilitated LTP could be primarily attributed to the reduction of GABAergic inhibition. Biochemical assays of isolated mPFC tissue from postnatal rats further showed that cocaine exposure in utero caused a marked reduction in the surface expression of GABAA receptor subunits α1, β2, and β3, but had no effect on glutamate receptor subunit GluR1. Both facilitated LTP and reduced surface expression of GABAA receptors persisted in rats up to at least P42. Finally, the behavioral consequence of cocaine exposure in utero was reflected by the reduction in the sensitivity of locomotor activity in postnatal rats to cocaine and the dopamine receptor agonist apomorphine. Since the mPFC is an important part of the reward circuit in the rat brain and plays important roles in cognitive functions, these findings offer new insights into the cellular mechanism underlying the adverse effects of cocaine exposure in utero on brain development and cognitive functions. PMID:19812341

  19. Effects of postnatal aluminum lactate exposure on neuromotor maturation in the rat

    SciTech Connect

    Bernuzzi, V.; Desor, D.; Lehr, P.R.

    1989-03-01

    In alkaline or neutral soils, aluminum is insoluble, but its solubility progressively increases with acidity, so acid precipitations have a considerable influence in mobilizing aluminum in natural waters, leading to higher alimentary ingestion of this element. In normal subjects aluminum is absorbed by the gastrointestinal tract and is excreted in urine. But even discrete renal failure may lead to Al accumulation in various tissues. Certain neurologic diseases have been related to Al intoxication. In patients undergoing chronic hemodialysis and ingesting aluminum-containing drugs, Al exposure is considered to be the causal factor for a high incidence of dialysis encephalopathy. Microcytic anemia and osteomalacia usually appeared before the neurologic symptoms. The authors have recently reported that the surviving pups of rats treated with aluminum during gestation showed a delay in their neuromotor development, as well as weight delay during the first postnatal week. This paper examines the effects of postnatal aluminum lactate exposure on mortality, weight evolution and neuromotor maturation in the rat.

  20. Postnatal ethanol exposure disrupts signal detection in adult rats.

    PubMed

    Woolfrey, Kevin M; Hunt, Pamela S; Burk, Joshua A

    2005-01-01

    Human prenatal ethanol exposure that occurs during a period of increased synaptogenesis known as the "brain growth spurt" has been associated with significant impairments in attention, learning, and memory. The present experiment assessed whether administration of ethanol during the brain growth spurt in the rat, which occurs shortly after birth, disrupts attentional performance. Rats were administered 5.25 g/kg/day ethanol via intragastric intubation from postnatal days (PD) 4-9, sham-intubation, or no intubation (naïve). Beginning at PD 90, animals were trained to asymptotic performance in a two-lever attention task that required discrimination of brief visual signals from trials with no signal presentation. Finally, manipulations of background noise and inter-trial interval duration were conducted. Early postnatal ethanol administration did not differentially affect acquisition of the attention task. However, after rats were trained to asymptotic performance levels, those previously exposed to ethanol demonstrated a deficit in detection of signals but not of non-signals compared to sham-intubated and naïve rats. The signal detection deficit persisted whenever these animals were re-trained in the standard task, but further task manipulations failed to interact with ethanol pretreatment. The present data support the hypothesis that early postnatal ethanol administration disrupts aspects of attentional processing in the rat.

  1. Pre- and Postnatal Exposure to Low Dose Glufosinate Ammonium Induces Autism-Like Phenotypes in Mice

    PubMed Central

    Laugeray, Anthony; Herzine, Ameziane; Perche, Olivier; Hébert, Betty; Aguillon-Naury, Marine; Richard, Olivier; Menuet, Arnaud; Mazaud-Guittot, Séverine; Lesné, Laurianne; Briault, Sylvain; Jegou, Bernard; Pichon, Jacques; Montécot-Dubourg, Céline; Mortaud, Stéphane

    2014-01-01

    Glufosinate ammonium (GLA) is one of the most widely used herbicides in agriculture. As is the case for most pesticides, potential adverse effects of GLA have not been studied from the perspective of developmental neurotoxicity. Early pesticides exposure may weaken the basic structure of the developing brain and cause permanent changes leading to a wide range of lifelong effects on health and/or behavior. Here, we addressed the developmental impact of GLA by exposing female mice to low dose GLA during both pre- and postnatal periods and analyzed potential developmental and behavioral changes of the offspring during infancy and adulthood. A neurobehavioral test battery revealed significant effects of GLA maternal exposure on early reflex development, pup communication, affiliative behaviors, and preference for social olfactory cues, but emotional reactivity and emotional memory remained unaltered. These behavioral alterations showed a striking resemblance to changes seen in animal models of Autistic Spectrum Disorders. At the brain level, GLA maternal exposure caused some increase in relative brain weight of the offspring. In addition, reduced expression of Pten and Peg3 – two genes implicated in autism-like deficits – was observed in the brain of GLA-exposed pups at postnatal day 15. Our work thus provides new data on the link between pre- and postnatal exposure to the herbicide GLA and the onset of autism-like symptoms later in life. It also raises fundamental concerns about the ability of current safety testing to assess risks of pesticide exposure during critical developmental periods. PMID:25477793

  2. Impact of Early Postnatal Androgen Exposure on Voice Development

    PubMed Central

    Grisa, Leila; Leonel, Maria L.; Gonçalves, Maria I. R.; Pletsch, Francisco; Sade, Elis R.; Custódio, Gislaine; Zagonel, Ivete P. S.; Longui, Carlos A.; Figueiredo, Bonald C.

    2012-01-01

    Background The impact of early postnatal androgen exposure on female laryngeal tissue may depend on certain characteristics of this exposure. We assessed the impact of the dose, duration, and timing of early androgen exposure on the vocal development of female subjects who had been treated for adrenocortical tumor (ACT) in childhood. Methods The long-term effects of androgen exposure on the fundamental vocal frequency (F0), vocal pitch, and final height and the presence of virilizing signs were examined in 9 adult (age, 18.4 to 33.5 years) and 10 adolescent (13.6 to 17.8 years) female ACT patients. We also compared the current values with values obtained 0.9 years to 7.4 years after these subjects had undergone ACT surgery, a period during which they had shown normal androgen levels. Results Of the 19 subjects, 17 (89%) had been diagnosed with ACT before 4 years of age, 1 (5%) at 8.16 years, and 1 (5%) at 10.75 years. Androgen exposure (2 to 30 months) was sufficiently strong to cause pubic hair growth in all subjects and clitoromegaly in 74% (14/19) of the subjects, but did not reduce their height from the target value. Although androgen exposure induced a remarkable reduction in F0 (132 Hz) and moderate pitch virilization in 1 subject and partial F0 virilization, resulting in F0 of 165 and 169 Hz, in 2 subjects, the majority had normal F0 ranging from 189 to 245 Hz. Conclusions Female laryngeal tissue is less sensitive to androgen exposure between birth and adrenarche than during other periods. Differential larynx sensitivity to androgen exposure in childhood and F0 irreversibility in adulthood are age-, concentration-, duration-, and timing-dependent events that may also be affected by exposure to inhibitory or stimulatory hormones. Further studies are required to better characterize each of these factors. PMID:23284635

  3. Impact of early postnatal androgen exposure on voice development.

    PubMed

    Grisa, Leila; Leonel, Maria L; Gonçalves, Maria I R; Pletsch, Francisco; Sade, Elis R; Custódio, Gislaine; Zagonel, Ivete P S; Longui, Carlos A; Figueiredo, Bonald C

    2012-01-01

    The impact of early postnatal androgen exposure on female laryngeal tissue may depend on certain characteristics of this exposure. We assessed the impact of the dose, duration, and timing of early androgen exposure on the vocal development of female subjects who had been treated for adrenocortical tumor (ACT) in childhood. The long-term effects of androgen exposure on the fundamental vocal frequency (F0), vocal pitch, and final height and the presence of virilizing signs were examined in 9 adult (age, 18.4 to 33.5 years) and 10 adolescent (13.6 to 17.8 years) female ACT patients. We also compared the current values with values obtained 0.9 years to 7.4 years after these subjects had undergone ACT surgery, a period during which they had shown normal androgen levels. Of the 19 subjects, 17 (89%) had been diagnosed with ACT before 4 years of age, 1 (5%) at 8.16 years, and 1 (5%) at 10.75 years. Androgen exposure (2 to 30 months) was sufficiently strong to cause pubic hair growth in all subjects and clitoromegaly in 74% (14/19) of the subjects, but did not reduce their height from the target value. Although androgen exposure induced a remarkable reduction in F0 (132 Hz) and moderate pitch virilization in 1 subject and partial F0 virilization, resulting in F0 of 165 and 169 Hz, in 2 subjects, the majority had normal F0 ranging from 189 to 245 Hz. Female laryngeal tissue is less sensitive to androgen exposure between birth and adrenarche than during other periods. Differential larynx sensitivity to androgen exposure in childhood and F0 irreversibility in adulthood are age-, concentration-, duration-, and timing-dependent events that may also be affected by exposure to inhibitory or stimulatory hormones. Further studies are required to better characterize each of these factors.

  4. In utero and postnatal exposure to arsenic alters pulmonary structure and function

    SciTech Connect

    Lantz, R. Clark Chau, Binh; Sarihan, Priyanka; Witten, Mark L.; Pivniouk, Vadim I.; Chen, Guan Jie

    2009-02-15

    In addition to cancer endpoints, arsenic exposures can also lead to non-cancerous chronic lung disease. Exposures during sensitive developmental time points can contribute to the adult disease. Using a mouse model, in utero and early postnatal exposures to arsenic (100 ppb or less in drinking water) were found to alter airway reactivity to methacholine challenge in 28 day old pups. Removal of mice from arsenic exposure 28 days after birth did not reverse the alterations in sensitivity to methacholine. In addition, adult mice exposed to similar levels of arsenic in drinking water did not show alterations. Therefore, alterations in airway reactivity were irreversible and specific to exposures during lung development. These functional changes correlated with protein and gene expression changes as well as morphological structural changes around the airways. Arsenic increased the whole lung levels of smooth muscle actin in a dose dependent manner. The level of smooth muscle mass around airways was increased with arsenic exposure, especially around airways smaller than 100 {mu}m in diameter. This increase in smooth muscle was associated with alterations in extracellular matrix (collagen, elastin) expression. This model system demonstrates that in utero and postnatal exposure to environmentally relevant levels of arsenic can irreversibly alter pulmonary structure and function in the adults.

  5. In Utero and Postnatal Exposure to Arsenic Alters Pulmonary Structure and Function

    PubMed Central

    Lantz, R. Clark; Chau, Binh; Sarihan, Priyanka; Witten, Mark L.; Pivniouk, Vadim I.; Chen, Guan Jie

    2009-01-01

    In addition to cancer endpoints, arsenic exposures can also lead to non-cancerous chronic lung disease. Exposures during sensitive developmental time points can contribute to the adult disease. Using a mouse model, in utero and early postnatal exposures to arsenic (100 ppb or less in drinking water) were found to alter airway reactivity to methacholine challenge in 28 day old pups. Removal of mice from arsenic exposure 28 days after birth did not reverse the alterations in sensitivity to methacholine. In addition, adult mice exposed to similar levels of arsenic in drinking water did not show alterations. Therefore, alterations in airway reactivity were irreversible and specific to exposures during lung development. These functional changes correlated with protein and gene expression changes as well as morphological structural changes around the airways. Arsenic increased the whole lung levels of smooth muscle actin in a dose dependent manner. The level of smooth muscle mass around airways was increased with arsenic exposure, especially around airways smaller than 100 μm in diameter. This increase in smooth muscle was associated with alterations in extracellular matrix (collagen, elastin) expression. This model system demonstrates that in utero and postnatal exposure to environmentally relevant levels of arsenic can irreversibly alter pulmonary structure and function in the adults. PMID:19095001

  6. Lead Aprons Are a Lead Exposure Hazard.

    PubMed

    Burns, Kevin M; Shoag, Jamie M; Kahlon, Sukhraj S; Parsons, Patrick J; Bijur, Polly E; Taragin, Benjamin H; Markowitz, Morri

    2017-05-01

    To determine whether lead-containing shields have lead dust on the external surface. Institutional review board approval was obtained for this descriptive study of a convenience sample of 172 shields. Each shield was tested for external lead dust via a qualitative rapid on-site test and a laboratory-based quantitative dust wipe analysis, flame atomic absorption spectrometry (FAAS). The χ(2) test was used to test the association with age, type of shield, lead sheet thickness, storage method, and visual and radiographic appearance. Sixty-three percent (95% confidence interval [CI]: 56%-70%) of the shields had detectable surface lead by FAAS and 50% (95% CI: 43%-57%) by the qualitative method. Lead dust by FAAS ranged from undetectable to 998 μg/ft(2). The quantitative detection of lead was significantly associated with the following: (1) visual appearance of the shield (1 = best, 3 = worst): 88% of shields that scored 3 had detectable dust lead; (2) type of shield: a greater proportion of the pediatric patient, full-body, and thyroid shields were positive than vests and skirts; (3) use of a hanger for storage: 27% of shields on a hanger were positive versus 67% not on hangers. Radiographic determination of shield intactness, thickness of interior lead sheets, and age of shield were unrelated to presence of surface dust lead. Sixty-three percent of shields had detectable surface lead that was associated with visual appearance, type of shield, and storage method. Lead-containing shields are a newly identified, potentially widespread source of lead exposure in the health industry. Copyright © 2016 American College of Radiology. Published by Elsevier Inc. All rights reserved.

  7. Association between prenatal and postnatal tobacco smoke exposure and allergies in young children.

    PubMed

    Tanaka, Keiko; Miyake, Yoshihiro

    2011-06-01

    Many studies have shown a positive association between environmental tobacco smoke (ETS) exposure and allergic disorders, whereas epidemiological evidence of the effect of maternal smoking during pregnancy on allergic diseases is inconsistent. We investigated the independent and joint effects of in utero exposure to maternal smoking and postnatal ETS exposure at home on allergic disorders among Japanese children. Study subjects were 1951 children aged 3 years. Data on maternal smoking during pregnancy and postnatal exposure to ETS at home, allergic symptoms, and potential confounders were collected through the use of a questionnaire. Outcomes were defined according to the criteria of the International Study of Asthma and Allergies in Childhood (ISAAC). The prevalence values of symptoms of wheeze, asthma, and eczema in the previous 12 months were 22.0%, 8.8%, and 17.2%, respectively. We found that postnatal ETS exposure at home in the absence of in utero exposure to maternal smoking was associated with a higher prevalence of wheeze (adjusted odds ratio (OR) = 1.30, 95% confidence interval (CI): 1.01-1.67). In contrast, in utero exposure without subsequent postnatal ETS exposure at home or exposure to postnatal ETS at home in addition to in utero exposure to maternal smoking was not associated with the prevalence of wheeze. No measurable associations were observed between fetal, postnatal, or joint exposure and the prevalence of asthma or eczema. Data from this study indicate that ETS at home may be associated with a higher prevalence of wheeze among young Japanese children.

  8. Early postnatal exposure of mice to side-steam tobacco smoke increases neuropeptide Y in lung

    PubMed Central

    Benders, K. B.; Hunter, D. D.; Dey, R. D.

    2012-01-01

    Our recent study showed that prenatal and early postnatal exposure of mice to side-steam tobacco smoke (SS), a surrogate to environmental tobacco smoke (ETS), leads to increased airway responsiveness and sensory innervation later in life. However, the underlying mechanism initiated in early life that affects airway responses later in life remains undefined. The concomitant increase in nerve growth factor (NGF) after exposures suggests that NGF may be involved the regulation of airway innervation. Since NGF regulates sympathetic nerve responses, as well as sensory nerves, we extended previous studies by examining neuropeptide Y (NPY), a neuropeptide associated with sympathetic nerves. Different age groups of mice, postnatal day (PD) 2 and PD21, were exposed to either SS or filtered air (FA) for 10 consecutive days. The level of NPY protein in lung and the density of NPY nerve fibers in tracheal smooth muscle were significantly increased in the PD2–11SS exposure group compared with PD2–11FA exposure. At the same time, the level of NGF in lung tissue was significantly elevated in the PD2–11SS exposure groups. However, neither NPY (protein or nerves) nor NGF levels were significantly altered in PD21–30SS exposure group compared with the PD21–30FA exposure group. Furthermore, pretreatment with NGF antibody or K252a, which inhibits a key enzyme (tyrosine kinase) in the transduction pathway for NGF receptor binding, significantly diminished SS-enhanced NPY tracheal smooth muscle innervation and the increase in methacholine-induced airway resistance. These findings show that SS exposure in early life increases NPY tracheal innervation and alters pulmonary function and that these changes are mediated through the NGF. PMID:22003086

  9. Reducing lead exposure in children

    SciTech Connect

    Farfel, M.R.

    1985-01-01

    The near elimination of lead-related childhood fatalities and encephalopathy by the 1970s and the sharp decline in mean blood lead levels nationwide documented between 1976 and 1980 are two milestones in the fight against lead poisoning. In the case of the latter, we know the antecedents, such as controls on the sale, use, and lead content of lead paint, improved chelation therapy, and increased awareness and case finding; however, the antecedents' relative contributions are not known due to a lack of evaluation. Similarly, the effect of a variety of social-welfare programs has not been evaluated. Since the 1970s, our perception of the problem of lead toxicity and consequently its control has changed. First steps have been made toward attaining one primary preventive objective, controlling the multiple sources of new inputs of lead to the biosphere that contribute to asymptomatic lead toxicity. The lead content of widely used commodities has been reduced (canned foods and gasoline) or virtually eliminated (paint). The benefits of passive measures used to attain reductions in lead exposure have been documented to a greater extent than those of active programs. The best example of a successful primary and passive preventive measure is the availability of lead-free gasoline since 1974, which largely accounts for decreases in ambient air lead concentrations nationwide and the recent shift to lower values in the distribution curve of children's blood lead levels. The latter provides a margin of safety for children before known toxic levels are reached. The contribution of reductions in dietary lead to changes in blood lead levels has not been well documented. Studies also show the benefits of the use of lead-free paint in new housing. Compared to children living in older homes with deteriorating lead paint, those living in lead-free homes are at low risk for lead toxicity.

  10. Sensory Neural Responses to Ozone Exposure during Early Postnatal Development in Rat Airways

    PubMed Central

    Hunter, Dawn D.; Wu, Zhongxin; Dey, Richard D.

    2010-01-01

    Airway infections or irritant exposures during early postnatal periods may contribute to the onset of childhood asthma. The purpose of this study was to examine critical periods of postnatal airway development during which ozone (O3) exposure leads to heightened neural responses. Rats were exposed to O3 (2 ppm) or filtered air for 1 hour on specific postnatal days (PDs) between PD1 and PD29, and killed 24 hours after exposure. In a second experiment, rats were exposed to O3 on PD2–PD6, inside a proposed critical period of development, or on PD19–PD23, outside the critical period. Both groups were re-exposed to O3 on PD28, and killed 24 hours later. Airways were removed, fixed, and prepared for substance P (SP) immunocytochemistry. SP nerve fiber density (NFD) in control extrapulmonary (EXP) epithelium/lamina propria (EPLP) increased threefold, from 1% to 3.3% from PD1–PD3 through PD13–PD15, and maintained through PD29. Upon O3 exposure, SP-NFD in EXP–smooth muscle (SM) and intrapulmonary (INT)-SM increased at least twofold at PD1–PD3 through PD13–PD15 in comparison to air exposure. No change was observed at PD21–PD22 or PD28–PD29. In critical period studies, SP-NFD in the INT-SM and EXP-SM of the PD2–PD6 O3 group re-exposed to O3 on PD28 was significantly higher than that of the group exposed at PD19–PD23 and re-exposed at PD28. These findings suggest that O3-mediated changes in sensory innervation of SM are more responsive during earlier postnatal development. Enhanced responsiveness of airway sensory nerves may be a contributing mechanism of increased susceptibility to environmental exposures observed in human infants and children. PMID:20118220

  11. Postnatal Environmental Tobacco Smoke Exposure Related to Behavioral Problems in Children.

    PubMed

    Chastang, Julie; Baïz, Nour; Cadwallader, Jean Sébastien; Cadwalladder, Jean Sébastien; Robert, Sarah; Dywer, John L; Dywer, John; Charpin, Denis André; Caillaud, Denis; de Blay, Frédéric; Raherison, Chantal; Lavaud, François; Annesi-Maesano, Isabella

    2015-01-01

    The purpose of this study was to examine the association between pre and post environmental tobacco smoke (ETS) exposure and behavioral problems in schoolchildren. In the cross-sectional 6 cities Study conducted in France, 5221 primary school children were investigated. Pre- and postnatal exposure to secondhand tobacco smoke at home was assessed using a parent questionnaire. Child's behavioral outcomes (emotional symptoms and conduct problems) were evaluated by the Strengths and Difficulties Questionnaire (SDQ) completed by the parents. ETS exposure during the postnatal period and during both pre- and postnatal periods was associated with behavioral problems in children. Abnormal emotional symptoms (internalizing problems) were related to ETS exposure in children who were exposed during the pre- and postnatal periods with an OR of 1.72 (95% Confidence Interval (CI)= 1.36-2.17), whereas the OR was estimated to be 1.38 (95% CI= 1.12-1.69) in the case of postnatal exposure only. Abnormal conduct problems (externalizing problems) were related to ETS exposure in children who were exposed during the pre- and postnatal periods with an OR of 1.94 (95% CI= 1.51-2.50), whereas the OR was estimated to be 1.47 (95% CI=1.17-1.84) in the case of postnatal exposure only. Effect estimates were adjusted for gender, study center, ethnic origin, child age, low parental education, current physician diagnosed asthma, siblings, preterm birth and single parenthood. Postnatal ETS exposure, alone or in association with prenatal exposure, increases the risk of behavioral problems in school-age children.

  12. The effects of prenatal and postnatal (via nursing) exposure to alcohol in rats

    SciTech Connect

    Nekvasil, N.; Baggio, C. )

    1992-02-26

    Pregnant and post-partum rats were given daily doses of 20% alcohol during days 13-21 gestation and postnatal days 3-12, respectively. Following exposure, all rat pups, were tested for balance, blood pressure, right and left cerebral hemisphere weights, and cerebellar weight. Results were grouped according to exposure and gender. The postnatal group was the only one to demonstrate difficulties with balance. The mean arterial pressure in males exposed postnatally was significantly lower than the control and prenatal males. Females exposed postnatally had a significantly higher blood pressure than control females. Within the postnatal group, males had a significantly lower blood pressure than the females. Prenatal and control females differed significantly for left cerebral hemisphere (LCH) weight with the prenatal weighing less. Male pups exposed prenatally had significantly heavier LCH than the postnatal and control males. For both males and females, postnatal LCH weights did not differ from those of the control pups. Within the prenatal group, the LCH weight in females was significantly lower than in males. Mean cerebellar weights were significantly lower in postnatal animals compared to control animals. A major finding of this study is that the effect of alcohol exposure on rat pups depends on gender and developmental age.

  13. Gestational and Early Postnatal Exposure to Simulated High Altitude Does Not Modify Postnatal Body Mass Growth Trajectory in the Rat

    PubMed Central

    Champin, Graciela M.; Bozzini, Clarisa; Alippi, Rosa M.

    2014-01-01

    Abstract Bozzini, Carlos E, Graciela M. Champin, Clarisa Bozzini, and Rosa M. Alippi. Gestational and Early Postnatal Exposure to Simulated High Altitude Does Not Modify Postnatal Body Mass Growth Trajectory in the Rat. High Alt Med Biol 15:418–421, 2014.—Postnatal hypoxia blunts body mass growth. It is also known that the quality of the fetal environment can influence the subsequent adult phenotype. The main purpose of the study was to determine whether gestational hypoxia and early postnatal hypoxia are able to blunt growth when the offspring is raised under normoxia. Hypobaric hypoxia was induced in simulated high altitude (SHA) chambers in which air was maintained at 380 mmHg (5450 m). Mature Sprague-Dawley rats of both sexes were divided in normoxic (NX) and hypoxic (HX) groups and, in the case of the HX group, maintained for 1 month at 5450 m. Mating was then allowed under NX or HX conditions. Offspring were NX-NX, NX-HX, HX-HX, or HX-NX: the first term indicates NX or HX during both gestation and the first 30 days of life; the second term indicates NX or HX during postnatal life between days 30 and 133. Body mass (g) was measured periodically and body mass growth rate (BMGR, g/d) was estimated between days 33 and 65 of postnatal life. Results can be summarized as follows: 1) BM was significantly higher in NX than in HX rats at weaning; 2) BMGR was not significantly different between NX-NX and HX-NX rats, and between HX-HX and NX-HX animals; and 3) BMGR was significantly higher in rats living under NX conditions than in those living under HX conditions during postnatal life. Data suggest that that hypobaric hypoxia during gestational and early postnatal development of rats does not alter the regulation of body mass growth in rats when compared to that seen under sea-level conditions. PMID:25184739

  14. Prenatal Versus Postnatal Tobacco Smoke Exposure and Intensive Care Use in Children Hospitalized With Bronchiolitis.

    PubMed

    Stevenson, Michelle D; Mansbach, Jonathan M; Mowad, Eugene; Dunn, Michelle; Clark, Sunday; Piedra, Pedro A; Sullivan, Ashley F; Camargo, Carlos A

    2016-07-01

    Among children hospitalized with bronchiolitis, we examined the associations between in utero exposure to maternal cigarette smoking, postnatal tobacco smoke exposure, and risk of admission to the intensive care unit (ICU). We performed a 16-center, prospective cohort study of hospitalized children aged <2 years with a physician admitting diagnosis of bronchiolitis. For 3 consecutive years, from November 1, 2007 until March 31, 2010, site teams collected data from participating families, including information about prenatal maternal smoking and postnatal tobacco exposure. Analyses used chi-square, Fisher's exact, and Kruskal-Wallis tests and multivariable logistic regression. Among 2207 enrolled children, 216 (10%) had isolated in utero exposure to maternal smoking, 168 (8%) had isolated postnatal tobacco exposure, and 115 (5%) experienced both. Adjusting for age, sex, race, birth weight, viral etiology, apnea, initial severity of retractions, initial oxygen saturation, oral intake, and postnatal tobacco exposure, children with in utero exposure to maternal smoking had greater odds of being admitted to the ICU (adjusted odds ratio [aOR] 1.51, 95% confidence interval [CI] 1.14-2.00). Among children with in utero exposure to maternal smoking, those with additional postnatal tobacco exposure had a greater likelihood of ICU admission (aOR 1.95, 95% CI 1.13-3.37) compared to children without postnatal tobacco smoke exposure (aOR 1.47, 95% CI 1.05-2.04). Maternal cigarette smoking during pregnancy puts children hospitalized with bronchiolitis at significantly higher risk of intensive care use. Postnatal tobacco smoke exposure may exacerbate this risk. Health care providers should incorporate this information into counseling messages. Copyright © 2016 Academic Pediatric Association. Published by Elsevier Inc. All rights reserved.

  15. Postnatal arsenic exposure and attention impairment in school children.

    PubMed

    Rodríguez-Barranco, Miguel; Gil, Fernando; Hernández, Antonio F; Alguacil, Juan; Lorca, Andres; Mendoza, Ramón; Gómez, Inmaculada; Molina-Villalba, Isabel; González-Alzaga, Beatriz; Aguilar-Garduño, Clemente; Rohlman, Diane S; Lacasaña, Marina

    2016-01-01

    additional evidence that postnatal arsenic exposure impairs neurological function in children. Copyright © 2015 Elsevier Ltd. All rights reserved.

  16. Prenatal epoxiconazole exposure effects on rat postnatal development.

    PubMed

    de Castro, Vera L S S; Maia, Aline H

    2012-04-01

    Although some studies have pointed out to embryo/fetal toxicity, knowledge about the potential toxicity of the fungicide epoxiconazole is still limited. Once the results of these previous studies have raised some concern, this study studied the effects of epoxiconazole maternal exposure on the physical endpoints in the development of rat pups. To accomplish that, the effects of epoxiconazole (50.0, 100.0, and 150.0  mg/kg) were examined when rats were exposed at two different developmental stages: during the first 6 days of pregnancy or in the organogenesis period (6-15 days). After parturition, pups were tested for growth and maturational milestones. Maternal exposure to the fungicide, independently of phase, resulted in significantly early mean time to vaginal opening and delayed time to testes descent in pups. Weight gain rate in pups and their mothers was not affected for the tested exposure period. The findings of this study emphasize that epoxiconazole maternal exposure may lead to alterations in developmental patterns in nursing pups, consistent with the known influence of epoxiconazole on steroid hormone synthesis.

  17. A systematic review of neurodevelopmental effects of prenatal and postnatal organophosphate pesticide exposure.

    PubMed

    González-Alzaga, B; Lacasaña, M; Aguilar-Garduño, C; Rodríguez-Barranco, M; Ballester, F; Rebagliato, M; Hernández, A F

    2014-10-15

    Agricultural and residential use of organophosphate (OP) pesticides has increased in recent decades after banning some persistent pesticides. Although there is evidence of the effects of OPs on neurodevelopment and behaviour in adults, limited information is available about their effects in children, who might be more vulnerable to neurotoxic compounds. This paper was aimed at analysing the scientific evidence published to date on potential neurodevelopmental and behavioural effects of prenatal and postnatal exposure to OPs. A systematic review was undertaken to identify original articles published up to December 2012 evaluating prenatal or postnatal exposure to OPs in children and effects on neurodevelopment and/or behaviour. Articles were critically compared, focusing on the methodology used to assess exposure and adverse effects, as well as potential contributing factors that may modify both exposure and outcomes, such as genetic susceptibility to certain enzymes involved in OPs metabolisation (e.g. paraoxonase-1) and gender differences. Twenty articles met the inclusion criteria, 7 of which evaluated prenatal exposure to OPs, 8 postnatal exposure and 5 both pre- and postnatal exposure. Most of the studies evaluating prenatal exposure observed a negative effect on mental development and an increase in attention problems in preschool and school children. The evidence on postnatal exposure is less consistent, although 2 studies found an increase in reaction time in schoolchildren. Some paraoxonase-1 polymorphisms could enhance the association between OPs exposure and mental and psychomotor development. A large variability in epidemiological designs and methodologies used for assessing exposure and outcome was observed across the different studies, which made comparisons difficult. Prenatal and to a lesser extent postnatal exposure to OPs may contribute to neurodevelopmental and behavioural deficits in preschool and school children. Standardised methodologies are

  18. Early postnatal diazepam exposure alters sex differences in the rat brain.

    PubMed

    Segovia, S; Pérez-Laso, C; Rodríguez-Zafra, M; Calés, J M; Del Abril, A; De Blas, M R; Collado, P; Valencia, A; Guillamón, A

    1991-06-01

    The volume and neuron number of the sexually dimorphic accessory olfactory bulb and locus coeruleus are altered by early postnatal exposure (from the day of birth to postnatal day 16) to diazepam. After diazepam treatment, both volume and neuron number were decreased in the male accessory olfactory bulb and in the female locus coeruleus. These results indicate that early postnatal diazepam administration can bear gender-dependent teratogenic effects upon sexually dimorphic nuclei and suggest that endogenous benzodiazepines may be involved in the sexual differentiation of the brain.

  19. Detrimental effects of postnatal exposure to propofol on memory and hippocampal LTP in mice.

    PubMed

    Wang, Yuan-Lin; Chen, Xin; Wang, Zhi-Ping

    2015-10-05

    Acute effects of propofol on memory and hippocampal long-term potentiation (LTP) in adult animals were reported. However, long-term effect of early postnatal application of propofol on memory was not totally disclosed. In this study, experiments were designed to verify the mechanisms underlying the long-term detrimental effects of propofol on memory and hippocampal synaptic plasticity. A consecutive propofol protocol from postnatal day 7 was applied to model anesthesia, long term memory and hippocampal synaptic plasticity were detected 2 months later. Our results showed that repeated propofol exposure in early phase affect the memory in the adult phase. Through recording the field excitatory postsynaptic potentials (fEPSPs) at Schaffer colletaral-CA1 synapses, both of basal synaptic transmission and hippocampal LTP were decreased after propofol application. While LTD induced by low frequency stimulation and 3,5-dihydroxyphenylglycine (3,5-DHPG) were not affected. Through analyzing the ultrastructure of dendrite in CA1 region, we found that propofol application decreased the spine density, which was consistent with the decrease of PSD-95 expression. In addition, p-AKT level was reduced after first propofol application. Intracerebroventricular injection of Akt inhibitor could mimic the propofol effects on basal synaptic transmission, hippocampal LTP and memory. Taken together, these results suggested that propofol possibly decreased AKT signaling pathway to restrict the spine development, finally leading to hippocampal LTP impairment and memory deficit.

  20. Effects of occupational lead exposure.

    PubMed

    Wang, Y L; Lu, P K; Chen, Z Q; Liang, Y X; Lu, Q M; Pan, Z Q; Shao, M

    1985-01-01

    Fifty-three workers in a battery factory, 52 solderers in a television factory, and 50 embroidery workers (a reference group) were studied. The average air lead levels of the three workplaces were 0.578 mg/m3, 0.002 mg/m3, and 0.001 mg/m3, respectively. Adverse effects in terms of clinical manifestations and biochemical criteria were evident among the battery factory workers. A significant dose-response relationship existed between the toxic effects and the air lead levels. The solderers showed no apparent abnormalities in comparison with the embroidery workers. The early clinical manifestations were dysfunction of the central nervous system, indigestion, arthralgia, and myalgia in the extremities. A positive association was observed between the prevalence of fatigue, mild abdominal pain, and arthralgia and the blood lead (PbB), urinary lead (PbU), and zinc protoporphyrin (ZPP) levels. The symptomatic threshold values of PbB, PbU, and ZPP were 30 micrograms/dl (1.5 mumol/l), 0.045 mg/l (0.2 mumol/l), and 40 micrograms/dl (0.7 mumol/l), respectively. The PbB, PbU, free erythrocyte protoporphyrin, and ZPP levels and the blood aminolevulinic dehydratase ratio could be used as indicators of lead exposure, although ZPP is preferred for a preventive monitoring program. The motor and sensory conduction velocities of the median nerve were slower in the exposed groups than in the reference group. No effects on behavioral function were observed among the solderers.

  1. Prenatal tobacco smoke and postnatal secondhand smoke exposure and child neurodevelopment.

    PubMed

    Herrmann, Melissa; King, Katherine; Weitzman, Michael

    2008-04-01

    To review the recent scientific literature examining the association of prenatal tobacco and postnatal secondhand smoke exposure and child neurodevelopment. Low birth weight and decreased in-utero brain growth are two of multiple potential etiologic pathways proposed as mediating the effects of prenatal tobacco smoke exposure on child neurodevelopment. These negative effects of prenatal exposure have been consistently demonstrated in animal models, and in humans have been found as early as the newborn period. The literature on both prenatal and postnatal exposure is remarkably consistent in showing associations with increased rates of behavior problems, including irritability, oppositional defiant behavior, conduct disorders and attention deficit hyperactivity disorder. A more rudimentary literature also suggests deficits in intelligence quotient. Recent studies have focused on elucidating the complex interaction among tobacco exposure, genetics and environmental factors. Questions still remain about the relative roles of prenatal vs. postnatal exposure and the potential role of genetic and social confounders, limiting the ability to infer a causal nature to these associations at this time. The consistency of findings across studies is, however, highly suggestive of a causal relationship between environmental tobacco exposure and adverse behavioral and cognitive outcomes in children. Prenatal tobacco and postnatal secondhand smoke exposure is consistently associated with problems in multiple domains of children's neurodevelopment and behavior.

  2. [Effects of early postnatal exposure to dieldrin on synaptic development of striatum in mice].

    PubMed

    Gao, Ye; Wang, Qu-nan; Wu, Shan

    2012-02-01

    To investigate the effects of early postnatal exposure to dieldrin on striatum synaptic development in lactation, adolescence and adulthood of mice. The pups were divided into 5 groups randomly. Three groups were exposed to dieldrin (0.01% DMSO solution) at doses of 0.2, 2.0 and 20.0 microg/kg and two control groups were exposed to DMSO or saline by intraperitoneal injection of every other day from postnatal days (PND) 3 to PND13. The striatum were isolated from brain in lactation (PND14), adolescence (PND36) and adulthood (PND98). Western blot assay was used to detect the expression levels of striatal synaptic proteins. The postnatal exposure to dieldrin could reduce the level of growth associated protein (GAP43) of striatum in lactation in a dose-dependent manner. In adolescence, the level of glial fibrillary acidic protein (GFAP) in striatum increased and the levels of tyrosine hydroxylase (TH), GAP43 and post-synaptic density protein 95 (PSD95) decreased with exposure doses. The level of Synapsin I decreased in adolescence male mice. The changes of expression levels of GFAP, TH and PSD95 proteins lasted to adulthood. Early postnatal exposure to dieldrin could affect the expression level of GAP43 protein in striatum. The expression levels of TH and PSD95 proteins in striatum decreased in adolescence and adulthood. These results indicated that the early postnatal exposure to dieldrin may persistently interfere in the striatal synaptic development.

  3. Neonatal lead exposure impairs development of rodent barrel field cortex

    PubMed Central

    Wilson, Mary Ann; Johnston, Michael V.; Goldstein, Gary W.; Blue, Mary E.

    2000-01-01

    Childhood exposure to low-level lead can permanently reduce intelligence, but the neurobiologic mechanism for this effect is unknown. We examined the impact of lead exposure on the development of cortical columns, using the rodent barrel field as a model. In all areas of mammalian neocortex, cortical columns constitute a fundamental structural unit subserving information processing. Barrel field cortex contains columnar processing units with distinct clusters of layer IV neurons that receive sensory input from individual whiskers. In this study, rat pups were exposed to 0, 0.2, 1, 1.5, or 2 g/liter lead acetate in their dam's drinking water from birth through postnatal day 10. This treatment, which coincides with the development of segregated columns in the barrel field, produced blood lead concentrations from 1 to 31 μg/dl. On postnatal day 10, the area of the barrel field and of individual barrels was measured. A dose-related reduction in barrel field area was observed (Pearson correlation = −0.740; P < 0.001); mean barrel field area in the highest exposure group was decreased 12% versus controls. Individual barrels in the physiologically more active caudoventral group were affected preferentially. Total cortical area measured in the same sections was not altered significantly by lead exposure. These data support the hypothesis that lead exposure may impair the development of columnar processing units in immature neocortex. We demonstrate that low levels of blood lead, in the range seen in many impoverished inner-city children, cause structural alterations in a neocortical somatosensory map. PMID:10805810

  4. Prenatal Exposure to Respiratory Syncytial Virus Alters Postnatal Immunity and Airway Smooth Muscle Contractility during Early-Life Reinfections

    PubMed Central

    Harford, Terri J.; Agrawal, Vandana; Yen-Lieberman, Belinda; Rezaee, Fariba; Piedimonte, Giovanni

    2017-01-01

    Maternal viral infections can have pathological effects on the developing fetus which last long after birth. Recently, maternal-fetal transmission of respiratory syncytial virus (RSV) was shown to cause postnatal airway hyperreactivity (AHR) during primary early-life reinfection; however, the influence of prenatal exposure to RSV on offspring airway immunity and smooth muscle contractility during recurrent postnatal reinfections remains unknown. Therefore, we sought to determine whether maternal RSV infection impairs specific aspects of cell-mediated offspring immunity during early-life reinfections and the mechanisms leading to AHR. Red fluorescent protein-expressing recombinant RSV (rrRSV) was inoculated into pregnant rat dams at midterm, followed by primary and secondary postnatal rrRSV inoculations of their offspring at early-life time points. Pups and weanlings were tested for specific lower airway leukocyte populations by flow cytometry; serum cytokine/chemokine concentrations by multiplex ELISA and neurotrophins concentrations by standard ELISA; and ex vivo lower airway smooth muscle (ASM) contraction by physiological tissue bath. Pups born to RSV-infected mothers displayed elevated total CD3+ T cells largely lacking CD4+ and CD8+ surface expression after both primary and secondary postnatal rrRSV infection. Cytokine/chemokine analyses revealed reduced IFN-γ, IL-2, IL-12, IL-17A, IL-18, and TNF-α, as well as elevated nerve growth factor (NGF) expression. Prenatal exposure to RSV also increased ASM reactivity and contractility during early-life rrRSV infection compared to non-exposed controls. We conclude that maternal RSV infection can predispose offspring to postnatal lower airways dysfunction by altering immunity development, NGF signaling, and ASM contraction during early-life RSV reinfections. PMID:28178290

  5. Prenatal and postnatal exposure to cell phone use and behavioral problems in children.

    PubMed

    Divan, Hozefa A; Kheifets, Leeka; Obel, Carsten; Olsen, Jørn

    2008-07-01

    The World Health Organization has emphasized the need for research into the possible effects of radiofrequency fields in children. We examined the association between prenatal and postnatal exposure to cell phones and behavioral problems in young children. Mothers were recruited to the Danish National Birth Cohort early in pregnancy. When the children of those pregnancies reached 7 years of age in 2005 and 2006, mothers were asked to complete a questionnaire regarding the current health and behavioral status of children, as well as past exposure to cell phone use. Mothers evaluated the child's behavior problems using the Strength and Difficulties Questionnaire. Mothers of 13,159 children completed the follow-up questionnaire reporting their use of cell phones during pregnancy as well as current cell phone use by the child. Greater odds ratios for behavioral problems were observed for children who had possible prenatal or postnatal exposure to cell phone use. After adjustment for potential confounders, the odds ratio for a higher overall behavioral problems score was 1.80 (95% confidence interval = 1.45-2.23) in children with both prenatal and postnatal exposure to cell phones. Exposure to cell phones prenatally-and, to a lesser degree, postnatally-was associated with behavioral difficulties such as emotional and hyperactivity problems around the age of school entry. These associations may be noncausal and may be due to unmeasured confounding. If real, they would be of public health concern given the widespread use of this technology.

  6. Parental smoking and children's respiratory health: independent effects of prenatal and postnatal exposure

    PubMed Central

    Pattenden, Sam; Antova, Temenuga; Neuberger, Manfred; Nikiforov, Bojidar; De Sario, Manuela; Grize, Leticia; Heinrich, Joachim; Hruba, Frantiska; Janssen, Nicole; Luttmann‐Gibson, Heike; Privalova, Larissa; Rudnai, Peter; Splichalova, Anna; Zlotkowska, Renata; Fletcher, Tony

    2006-01-01

    Objectives Adverse effects have been reported of prenatal and/or postnatal passive exposure to smoking on children's health. Uncertainties remain about the relative importance of smoking at different periods in the child's life. We investigate this in a pooled analysis, on 53 879 children from 12 cross‐sectional studies—components of the PATY study (Pollution And The Young). Methods Effects were estimated, within each study, of three exposures: mother smoked during pregnancy, parental smoking in the first two years, current parental smoking. Outcomes were: wheeze, asthma, “woken by wheeze”, bronchitis, nocturnal cough, morning cough, “sensitivity to inhaled allergens” and hay fever. Logistic regressions were used, controlling for individual risk factors and study area. Heterogeneity between study‐specific results, and mean effects (allowing for heterogeneity) were estimated using meta‐analytical tools. Results There was strong evidence linking parental smoking to wheeze, asthma, bronchitis and nocturnal cough, with mean odds ratios all around 1.15, with independent effects of prenatal and postnatal exposures for most associations. Conclusions Adverse effects of both pre‐ and postnatal parental smoking on children's respiratory health were confirmed. Asthma was most strongly associated with maternal smoking during pregnancy, but postnatal exposure showed independent associations with a range of other respiratory symptoms. All tobacco smoke exposure has serious consequences for children's respiratory health and needs to be reduced urgently. PMID:16885578

  7. Lead exposure in a firing range.

    PubMed Central

    Novotny, T; Cook, M; Hughes, J; Lee, S A

    1987-01-01

    We report lead exposure in four employees of a privately owned shooting range, one of whom had neurological toxicity due to lead. Increasing time worked at the range was associated with elevation of blood lead. This incident emphasizes the risk of airborne lead exposure to employees of firing ranges. PMID:3618861

  8. POSTNATAL DISPOSITION OF TCDD IN LONG EVANS RATS FOLLOWING GESTATIONAL EXPOSURE

    EPA Science Inventory

    POSTNATAL DISPOSITION OF TCDD IN LONG EVANS RATS FOLLOWING GESTATIONAL EXPOSURE.
    J J Diliberto', J T Hamm'.2, F McQuaid', and L S Birnbaum'. 'US EPA, ORD/NHEERL/ETD, RTP, NC; 2Curriculum in Toxicology, University of North Carolina, Chapel Hill, NC.
    2,3,7,8-Tetrachlorodibenz...

  9. Exposure to perfluorooctane sulfonate during pregnancy in rat and mouse. II: postnatal evaluation

    EPA Science Inventory

    The postnatal effects of in utero exposure to perfluorooctane sulfonate (PFOS, C8F17SO3-) were evaluated in the rat and mouse. Pregnant Sprague-Dawley rats were given 1, 2, 3, 5, or 10 mg/kg PFOS daily by gavage from gestation day (GD) 2 to GD 21; pregnant CD-1 mice were treated ...

  10. The Long-Term Economic Impact of in Utero and Postnatal Exposure to Malaria

    ERIC Educational Resources Information Center

    Barreca, Alan I.

    2010-01-01

    I use an instrumental-variables identification strategy and historical data from the United States to estimate the long-term economic impact of in utero and postnatal exposure to malaria. My research design matches adults in the 1960 Decennial Census to the malaria death rate in their respective state and year of birth. To address potential…

  11. Exposure to perfluorooctane sulfonate during pregnancy in rat and mouse. II: postnatal evaluation

    EPA Science Inventory

    The postnatal effects of in utero exposure to perfluorooctane sulfonate (PFOS, C8F17SO3-) were evaluated in the rat and mouse. Pregnant Sprague-Dawley rats were given 1, 2, 3, 5, or 10 mg/kg PFOS daily by gavage from gestation day (GD) 2 to GD 21; pregnant CD-1 mice were treated ...

  12. Exposure to Lipopolysaccharide in Utero Alters the Postnatal Metabolic Response in Heifers

    USDA-ARS?s Scientific Manuscript database

    This study was designed to determine the effect of prenatal lipopolysaccharide (LPS) exposure on the postnatal metabolic response to an LPS challenge in beef heifers. Pregnant crossbred cows (n = 50) were assigned to a prenatal immune stimulation (PIS; n = 25; administered 0.1 micrograms/kg BW LPS s...

  13. In Utero Exposure to Lipopolysaccharide Alters the Postnatal Acute Phase Response in Beef Heifers

    USDA-ARS?s Scientific Manuscript database

    This study was designed to determine the potential effect of prenatal lipopolysaccharide (LPS) exposure on the postnatal acute phase response (APR) to an LPS challenge in heifers. Pregnant crossbred cows (n = 50) were separated into prenatal immune stimulation (PIS; n = 25; administered 0.1 microgr...

  14. The Long-Term Economic Impact of in Utero and Postnatal Exposure to Malaria

    ERIC Educational Resources Information Center

    Barreca, Alan I.

    2010-01-01

    I use an instrumental-variables identification strategy and historical data from the United States to estimate the long-term economic impact of in utero and postnatal exposure to malaria. My research design matches adults in the 1960 Decennial Census to the malaria death rate in their respective state and year of birth. To address potential…

  15. Risk of Childhood Overweight after Exposure to Tobacco Smoking in Prenatal and Early Postnatal Life

    PubMed Central

    Ajslev, Teresa Adeltoft; Andersen, Camilla Schou; Dalgård, Christine; Sørensen, Thorkild I. A.

    2014-01-01

    Objective To investigate the association between exposure to mothers smoking during prenatal and early postnatal life and risk of overweight at age 7 years, while taking birth weight into account. Methods From the Danish National Birth Cohort a total of 32,747 families were identified with available information on maternal smoking status in child's pre- and postnatal life and child's birth weight, and weight and height at age 7 years. Outcome was overweight according to the International Obesity Task Force gender and age specific body mass index. Smoking exposure was categorized into four groups: no exposure (n = 25,076); exposure only during pregnancy (n = 3,343); exposure only postnatally (n = 140); and exposure during pregnancy and postnatally (n = 4,188). Risk of overweight according to smoking status as well as dose-response relationships were estimated by crude and adjusted odds ratios using logistic regression models. Results Exposure to smoking only during pregnancy, or both during pregnancy and postnatally were both significantly associated with overweight at 7 years of age (OR: 1.31, 95% CI: 1.15–1.48, and OR: 1.76, 95% CI: 1.58–1.97, respectively). Analyses excluding children with low birth weight (<2,500 gram) revealed similar results. A significant prenatal dose-response relationship was found. Per one additional cigarette smoked per day an increase in risk of overweight was observed (OR: 1.02, 95% CI: 1.01–1.03). When adjusting for quantity of smoking during pregnancy, prolonged exposure after birth further increased the risk of later overweight in the children (OR 1.28, 95% CI:1.09–1.50) compared with exposure only in the prenatal period. Conclusions Mother's perinatal smoking increased child's OR of overweight at age 7 years irrespective of birth weight, and with higher OR if exposed both during pregnancy and in early postnatal life. Clear dose-response relationships were observed, which emphasizes the need for prevention of

  16. Intrauterine and early postnatal exposure to outdoor air pollution and lung function at preschool age.

    PubMed

    Morales, Eva; Garcia-Esteban, Raquel; de la Cruz, Oscar Asensio; Basterrechea, Mikel; Lertxundi, Aitana; de Dicastillo, Maria D Martinez López; Zabaleta, Carlos; Sunyer, Jordi

    2015-01-01

    Effects of prenatal and postnatal exposure to air pollution on lung function at preschool age remain unexplored. We examined the association of exposure to air pollution during specific trimesters of pregnancy and postnatal life with lung function in preschoolers. Lung function was assessed with spirometry in preschoolers aged 4.5 years (n=620) participating in the INfancia y Medio Ambiente (INMA) cohort. Temporally adjusted land use regression (LUR) models were applied to estimate individual residential exposures to benzene and nitrogen dioxide (NO₂) during specific trimesters of pregnancy and early postnatal life (the first year of life). Recent and current (1 year and 1 week before lung function testing, respectively) exposures to NO₂ and nitrogen oxides (NOx) were also assessed. Exposure to higher levels of benzene and NO₂ during pregnancy was associated with reduced lung function. FEV1 estimates for an IQR increase in exposures during the second trimester of pregnancy were -18.4 mL, 95% CI -34.8 to -2.1 for benzene and -28.0 mL, 95% CI -52.9 to -3.2 for NO₂. Relative risk (RR) of low lung function (<80% of predicted FEV1) for an IQR increase in benzene and NO₂ during the second trimester of pregnancy were 1.22, 95% CI 1.02 to 1.46 and 1.30, 95% CI 0.97 to 1.76, respectively. Associations for early postnatal, recent and current exposures were not statistically significant. Stronger associations appeared among allergic children and those of lower social class. Prenatal exposure to residential traffic-related air pollution may result in long-term lung function deficits at preschool age. Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions.

  17. Developmental Effects of Lead Exposure in Children.

    ERIC Educational Resources Information Center

    Tesman, Johanna Rich; Hills, Amanda

    1994-01-01

    This report presents an overview of research on childhood lead exposure and poisoning, and the related social issues. The report first summarizes the history of lead poisoning and its prevalence in the United States, and discusses the basis for recent changes in guidelines for lead exposure by the Centers for Disease Control (CDC). The report then…

  18. Temporal pattern in the effect of postnatal blood lead level on intellectual development of young children.

    PubMed

    Schnaas, L; Rothenberg, S J; Perroni, E; Martínez, S; Hernández, C; Hernández, R M

    2000-01-01

    To determine the temporal pattern of the effect of postnatal blood lead level on the General Cognitive Index (GCI) of the McCarthy Scales of Children's Abilities, we used data from 112 children of the Mexico City Prospective Lead Study with complete evaluations from 36 to 60 months of age at 6-month intervals. We measured blood lead level every 6 months from 6 to 54 months. We controlled for 5-min Apgar, birth weight, birth order, sex, socioeconomic level, maternal IQ, and maximum maternal educational level in a repeated measures ANCOVA using child blood lead level grouped by 6-18 month (geometric mean 10.1 microg/dl, range 3.5-37.0 microg/dl), 24-36 month (geometric mean 9.7 microg/dl, range 3.0-42.7 microg/dl), and 42-54 month (geometric mean 8.4 microg/dl, range 2.5-44.8 microg/dl) averages. There were significant interactions between the 6-18 month blood lead level and age with GCI as the endpoint and between 24-36 month blood lead level and age. The regression coefficient of blood lead at 6-18 months became more negative with age until 48 months, when the rate of decline moderated (linear polynomial contrast p=0. 047). The regression coefficient of blood lead at 24-36 months with CGI became more negative as well from 36 to 48 months but then started decreasing toward zero from 48 to 60 months (quadratic polynomial contrast p=0.019). Significant between-subjects lead effects on GCI were found for 24-36 month blood lead level at 48 months (p=0.021) and at 54 months (p=0.073). The greatest effect (at 48 months) was a 5.8-point GCI decrease with each natural log unit increase in blood lead. Significant between-subjects lead effects on GCI were found for 42-54 month blood lead level at 54 months (p=0. 040) and at 60 months (p=0.060). The effect of postnatal blood lead level on GCI reaches its maximum approximately 1-3 years later, and then becomes less evident. Four to five years of age appears to be a critical period for the manifestation of the earlier postnatal

  19. Time To Pregnancy and occupational lead exposure

    PubMed Central

    Joffe, M; Bisanti, L; Apostoli, P; Kiss, P; Dale, A; Roeleveld, N; Lindbohm, M; Sallmen, M; Vanhoorne, M; Bonde, J

    2003-01-01

    Background: Lead exposure is known to be harmful to the male reproductive system, including impairment of fertility. However, it is unclear whether currently existing low levels of exposure have this effect. Aims: To study retrospectively current workers in lead using industries (battery manufacture, smelting, etc), and in non-lead using control industries, in four European countries, with Time To Pregnancy as the outcome variable, as part of the EU funded Asclepios Project. Methods: Exposure assessment was mainly by blood lead values, which were available from the late 1970s, supplemented by imputed values where necessary. Three exposure models were studied: (1) short term (recent) exposure; (2) total duration of work in a lead using industry; and (3) cumulative exposure. A Cox proportional hazards model with discrete ties was used for the statistical analysis, with covariates for both partners. Results: A total of 1104 subjects took part, of whom 638 were occupationally exposed to lead at the relevant time. Blood lead levels were mainly less than 50 µg/dl. No consistent association of Time To Pregnancy with lead exposure was found in any of the exposure models, although reduced fertility was observed in one category each in models (2) and (3). Conclusions: This basically negative result is unlikely to be due to the misclassification of key variables, to insufficient statistical power, or to bias, for example, response bias. If any impairment of male reproductive function exists at the levels of occupational lead exposure now current, it does not appear to reduce biological fertility. PMID:14504363

  20. Time To Pregnancy and occupational lead exposure.

    PubMed

    Joffe, M; Bisanti, L; Apostoli, P; Kiss, P; Dale, A; Roeleveld, N; Lindbohm, M-L; Sallmén, M; Vanhoorne, M; Bonde, J P

    2003-10-01

    Lead exposure is known to be harmful to the male reproductive system, including impairment of fertility. However, it is unclear whether currently existing low levels of exposure have this effect. To study retrospectively current workers in lead using industries (battery manufacture, smelting, etc), and in non-lead using control industries, in four European countries, with Time To Pregnancy as the outcome variable, as part of the EU funded Asclepios Project. Exposure assessment was mainly by blood lead values, which were available from the late 1970s, supplemented by imputed values where necessary. Three exposure models were studied: (1) short term (recent) exposure; (2) total duration of work in a lead using industry; and (3) cumulative exposure. A Cox proportional hazards model with discrete ties was used for the statistical analysis, with covariates for both partners. A total of 1104 subjects took part, of whom 638 were occupationally exposed to lead at the relevant time. Blood lead levels were mainly less than 50 microg/dl. No consistent association of Time To Pregnancy with lead exposure was found in any of the exposure models, although reduced fertility was observed in one category each in models (2) and (3). This basically negative result is unlikely to be due to the misclassification of key variables, to insufficient statistical power, or to bias, for example, response bias. If any impairment of male reproductive function exists at the levels of occupational lead exposure now current, it does not appear to reduce biological fertility.

  1. Prenatal cadmium exposure alters postnatal immune cell development and function.

    PubMed

    Hanson, Miranda L; Holásková, Ida; Elliott, Meenal; Brundage, Kathleen M; Schafer, Rosana; Barnett, John B

    2012-06-01

    Cadmium (Cd) is generally found in low concentrations in the environment due to its widespread and continual use, however, its concentration in some foods and cigarette smoke is high. Although evidence demonstrates that adult exposure to Cd causes changes in the immune system, there are limited reports of immunomodulatory effects of prenatal exposure to Cd. This study was designed to investigate the effects of prenatal exposure to Cd on the immune system of the offspring. Pregnant C57Bl/6 mice were exposed to an environmentally relevant dose of CdCl(2) (10ppm) and the effects on the immune system of the offspring were assessed at two time points following birth (2 and 7weeks of age). Thymocyte and splenocyte phenotypes were analyzed by flow cytometry. Prenatal Cd exposure did not affect thymocyte populations at 2 and 7weeks of age. In the spleen, the only significant effect on phenotype was a decrease in the number of macrophages in male offspring at both time points. Analysis of cytokine production by stimulated splenocytes demonstrated that prenatal Cd exposure decreased IL-2 and IL-4 production by cells from female offspring at 2weeks of age. At 7weeks of age, splenocyte IL-2 production was decreased in Cd-exposed males while IFN-γ production was decreased from both male and female Cd-exposed offspring. The ability of the Cd-exposed offspring to respond to immunization with a S. pneumoniae vaccine expressing T-dependent and T-independent streptococcal antigens showed marked increases in the levels of both T-dependent and T-independent serum antibody levels compared to control animals. CD4(+)FoxP3(+)CD25(+) (nTreg) cell percentages were increased in the spleen and thymus in all Cd-exposed offspring except in the female spleen where a decrease was seen. CD8(+)CD223(+) T cells were markedly decreased in the spleens in all offspring at 7weeks of age. These findings suggest that even very low levels of Cd exposure during gestation can result in long term detrimental

  2. Fetal lead exposure: antenatal factors

    SciTech Connect

    Ernhart, C.B.; Wolf, A.W.; Sokol, R.J.; Brittenham, G.M.; Erhard, P.

    1985-10-01

    It was hypothesized that maternal blood lead level at delivery and cord blood lead level of the neonate would be affected by maternal use of alcohol, history of alcohol abuse, and smoking. The possibility that iron status, as reflected in maternal serum ferritin, would be related to lead level was also explored. The maternal history of alcohol abuse was unrelated to lead level in 208 samples of maternal blood and 178 samples of cord blood. However, alcohol use during pregnancy was related in a dose-response fashion to maternal and to cord blood lead level. This effect was significant with and without control of maternal smoking. The effect of maternal smoking and serum thiocyanate on maternal and cord blood lead level were also highly significant with and without control of the maternal drinking variable. Serum ferritin was marginally related to lead level for white women and for black infants, but tests of the dichotomized maternal ferritin variable did not yield a significant linkage with maternal or cord blood lead level. The results further support recommendations that women abstain from alcohol consumption and cigarette smoking in pregnancy.

  3. Adult Neuropsychological Performance Following Prenatal and Early Postnatal Exposure to Tetrachloroethylene (PCE)-contaminated Drinking Water

    PubMed Central

    Janulewicz, Patricia A; White, Roberta F; Martin, Brett M; Winter, Michael R; Weinberg, Janice M; Vieira, Veronica; Aschengrau, Ann

    2012-01-01

    This population-based retrospective cohort study examined adult performance on a battery of neuropsychological tests in relation to prenatal and early postnatal exposure to tetrachloroethylene (PCE)-contaminated drinking water on Cape Cod, Massachusetts. Subjects were identified through birth records from 1969 through 1983. Exposure was modeled using pipe network information from town water departments, a PCE leaching and transport algorithm, EPANet water flow modeling software, and a Geographic Information System (GIS). Results of crude and multivariate analyses among 35 exposed and 28 unexposed subjects showed no association between prenatal and early postnatal exposure and decrements on tests that assess abilities in the domains of omnibus intelligence, academic achievement or language. The results were suggestive of an association between prenatal and early postnatal PCE exposure and diminished performance on tests that assessed abilities in the domains of visuospatial functioning, learning and memory, motor, attention and mood. Because the sample size was small, most findings were not statistically significant. Future studies with larger sample sizes should be conducted to further define the neuropsychological consequences of early developmental PCE exposure. PMID:22522125

  4. Regional Myelin and Axon Damage and Neuroinflammation in the Adult Mouse Brain After Long-Term Postnatal Vanadium Exposure.

    PubMed

    Azeez, Idris A; Olopade, Funmilayo; Laperchia, Claudia; Andrioli, Anna; Scambi, Ilaria; Onwuka, Silas K; Bentivoglio, Marina; Olopade, James O

    2016-09-01

    Environmental exposure to vanadium occurs in areas of persistent burning of fossil fuels; this metal is known to induce oxidative stress and oligodendrocyte damage. Here, we determined whether vanadium exposure (3 mg/kg) in mice during the first 3 postnatal months leads to a sustained neuroinflammatory response. Body weight monitoring, and muscle strength and open field tests showed reduction of body weight gain and locomotor impairment in vanadium-exposed mice. Myelin histochemistry and immunohistochemistry for astrocytes, microglia, and nonphosphorylated neurofilaments revealed striking regional heterogeneity. Myelin damage involved the midline corpus callosum and fibers in cortical gray matter, hippocampus, and diencephalon that were associated with axonal damage. Astrocyte and microglial activation was identified in the same regions and in the internal capsule; however, no overt myelin and axon damage was observed in the latter. Double immunofluorescence revealed induction of high tumor necrosis factor (TNF) immunoreactivity in reactive astrocytes. Western blotting analysis showed significant induction of TNF and interleukin-1β expression. Together these findings show that chronic postnatal vanadium exposure leads to functional deficit and region-dependent myelin damage that does not spare axons. This injury is associated with glial cell activation and proinflammatory cytokine induction, which may reflect both neurotoxic and neuroprotective responses. © 2016 American Association of Neuropathologists, Inc. All rights reserved.

  5. Prenatal cadmium exposure alters postnatal immune cell development and function

    SciTech Connect

    Hanson, Miranda L.; Holásková, Ida; Elliott, Meenal; Brundage, Kathleen M.; Schafer, Rosana; Barnett, John B.

    2012-06-01

    Cadmium (Cd) is generally found in low concentrations in the environment due to its widespread and continual use, however, its concentration in some foods and cigarette smoke is high. Although evidence demonstrates that adult exposure to Cd causes changes in the immune system, there are limited reports of immunomodulatory effects of prenatal exposure to Cd. This study was designed to investigate the effects of prenatal exposure to Cd on the immune system of the offspring. Pregnant C57Bl/6 mice were exposed to an environmentally relevant dose of CdCl{sub 2} (10 ppm) and the effects on the immune system of the offspring were assessed at two time points following birth (2 and 7 weeks of age). Thymocyte and splenocyte phenotypes were analyzed by flow cytometry. Prenatal Cd exposure did not affect thymocyte populations at 2 and 7 weeks of age. In the spleen, the only significant effect on phenotype was a decrease in the number of macrophages in male offspring at both time points. Analysis of cytokine production by stimulated splenocytes demonstrated that prenatal Cd exposure decreased IL-2 and IL-4 production by cells from female offspring at 2 weeks of age. At 7 weeks of age, splenocyte IL-2 production was decreased in Cd-exposed males while IFN-γ production was decreased from both male and female Cd-exposed offspring. The ability of the Cd-exposed offspring to respond to immunization with a S. pneumoniae vaccine expressing T-dependent and T-independent streptococcal antigens showed marked increases in the levels of both T-dependent and T-independent serum antibody levels compared to control animals. CD4{sup +}FoxP3{sup +}CD25{sup +} (nTreg) cell percentages were increased in the spleen and thymus in all Cd-exposed offspring except in the female spleen where a decrease was seen. CD8{sup +}CD223{sup +} T cells were markedly decreased in the spleens in all offspring at 7 weeks of age. These findings suggest that even very low levels of Cd exposure during gestation can

  6. Reduced Notch signalling leads to postnatal skeletal muscle hypertrophy in Pofut1cax/cax mice.

    PubMed

    Al Jaam, Bilal; Heu, Katy; Pennarubia, Florian; Segelle, Alexandre; Magnol, Laetitia; Germot, Agnès; Legardinier, Sébastien; Blanquet, Véronique; Maftah, Abderrahman

    2016-09-01

    Postnatal skeletal muscle growth results from the activation of satellite cells and/or an increase in protein synthesis. The Notch signalling pathway maintains satellite cells in a quiescent state, and once activated, sustains their proliferation and commitment towards differentiation. In mammals, POFUT1-mediated O-fucosylation regulates the interactions between NOTCH receptors and ligands of the DELTA/JAGGED family, thus initiating the activation of canonical Notch signalling. Here, we analysed the consequences of downregulated expression of the Pofut1 gene on postnatal muscle growth in mutant Pofut1(cax/cax) (cax, compact axial skeleton) mice and differentiation of their satellite cell-derived myoblasts (SCDMs). Pofut1(cax/cax) mice exhibited muscle hypertrophy, no hyperplasia and a decrease in satellite cell numbers compared with wild-type C3H mice. In agreement with these observations, Pofut1(cax/cax) SCDMs differentiated earlier concomitant with reduced Pax7 expression and decrease in PAX7(+)/MYOD(-) progenitor cells. In vitro binding assays showed a reduced interaction of DELTA-LIKE 1 ligand (DLL1) with NOTCH receptors expressed at the cell surface of SCDMs, leading to a decreased Notch signalling as seen by the quantification of cleaved NICD and Notch target genes. These results demonstrated that POFUT1-mediated O-fucosylation of NOTCH receptors regulates myogenic cell differentiation and affects postnatal muscle growth in mice.

  7. Reduced Notch signalling leads to postnatal skeletal muscle hypertrophy in Pofut1cax/cax mice

    PubMed Central

    Al Jaam, Bilal; Heu, Katy; Pennarubia, Florian; Segelle, Alexandre; Magnol, Laetitia; Germot, Agnès; Blanquet, Véronique; Maftah, Abderrahman

    2016-01-01

    Postnatal skeletal muscle growth results from the activation of satellite cells and/or an increase in protein synthesis. The Notch signalling pathway maintains satellite cells in a quiescent state, and once activated, sustains their proliferation and commitment towards differentiation. In mammals, POFUT1-mediated O-fucosylation regulates the interactions between NOTCH receptors and ligands of the DELTA/JAGGED family, thus initiating the activation of canonical Notch signalling. Here, we analysed the consequences of downregulated expression of the Pofut1 gene on postnatal muscle growth in mutant Pofut1cax/cax (cax, compact axial skeleton) mice and differentiation of their satellite cell-derived myoblasts (SCDMs). Pofut1cax/cax mice exhibited muscle hypertrophy, no hyperplasia and a decrease in satellite cell numbers compared with wild-type C3H mice. In agreement with these observations, Pofut1cax/cax SCDMs differentiated earlier concomitant with reduced Pax7 expression and decrease in PAX7+/MYOD− progenitor cells. In vitro binding assays showed a reduced interaction of DELTA-LIKE 1 ligand (DLL1) with NOTCH receptors expressed at the cell surface of SCDMs, leading to a decreased Notch signalling as seen by the quantification of cleaved NICD and Notch target genes. These results demonstrated that POFUT1-mediated O-fucosylation of NOTCH receptors regulates myogenic cell differentiation and affects postnatal muscle growth in mice. PMID:27628322

  8. Lead Exposure Hazard Management Guide

    DTIC Science & Technology

    1993-12-01

    one of the most common and preventable pediatric health problems in the United States today. Children are particularly susceptible to lead’s toxic...that have large percentages of children without lead poisoning problems can suspend the universal screening PROGRAM by submitting a letter of request, to...be frequented/used by children under the age of seven. Air Force Policy prioritizes specific facilities as follows: child development centers, annexes

  9. Relationship between prenatal lead exposure and infant blood lead levels.

    PubMed

    Archer, Natalie P; Bradford, Carrie M; Klein, David M; Barnes, Jim; Smith, L J; Villanacci, John F

    2012-10-01

    Recent literature has shown that analyzing newborn dried blood spots (DBS) may be effective in assessing some prenatal environmental exposures, such as exposure to lead. The purpose of this study was to evaluate the relationship between prenatal exposure to lead (as measured by newborn DBS results) and blood lead levels (BLLs) in infants 6 months of age or younger, using public health registry data for infants born in Texas from July 2002 through July 2006. The Texas Child Lead Registry (TCLR) was used to identify infants with documented elevated BLLs of 10 μg/dL or higher as well as infants with documented low BLLs. BLLs for these children were compared to their corresponding newborn DBS results using Pearson correlation coefficients and exact logistic regression models. Overall, a significant but weak positive correlation was found between infant BLLs and corresponding newborn DBS lead levels (r = 0.48). However, the odds of an infant with an elevated newborn DBS lead level having an elevated BLL at 6 months of age or younger were much greater than for an infant with a low newborn DBS lead level of <5 μg/dL (adjusted odds ratio 27.95, 95% CI: 5.52-277.28). Although an association was observed between newborn DBS lead levels and BLLs in infants tested between 0 to 6 months of age, our findings suggest that prenatal exposure may not be the only significant source of lead exposure for infants ≤6 months of age.

  10. Psychiatric epidemiologic study of occupational lead exposure

    SciTech Connect

    Parkinson, D.K.; Ryan, C.; Bromet, E.J.; Connell, M.M.

    1986-02-01

    The association of occupational lead exposure with neuropsychiatric functioning was evaluated using data collected in 1982 in eastern Pennsylvania from 288 lead-exposed workers and 181 nonexposed subjects. Both current and cumulative exposure indices were used. After controlling for age, education, and income, few meaningful differences between exposed and control workers were found on either neuropsychologic or psychosocial variables. Dose-response analyses indicated that among lead-exposed workers, cumulative and current exposure were unrelated to neuropsychologic performance. The only meaningful associations occurred between exposure and level of conflict in interpersonal relationships. The results thus give evidence against hypotheses suggesting adverse neuropsychologic effects.

  11. Environmental lead exposure and the kidney

    SciTech Connect

    Bernard, B.P.; Becker, C.E.

    1988-01-01

    Lead and its components remain widely distributed in the environment and in some workplaces. Lead serves no useful physiological function, yet is potentially toxic to several organ systems. For many years human health effects have been recognized after heavy lead exposure. Recently more subtle human effects have been suggested invoking nervous system, reproductive and kidney function. Assessing lead body burden and dose-response relationships of this metal by blood lead determination, porphyrin assessments, chelation testing or bone lead studies may be difficult. Quantitative assessment of subtle changes in kidney function by routine BUN, creatinine, or urinalysis also poses problems. There is now mounting evidence that chronic low level environmental lead exposure may subtly effect kidney function. This paper first examines the history of lead and kidney function and then examines critically the evidence associating low-level environmental lead exposure and effects on renal function. 119 references.

  12. Postnatal Exposure to Methyl Mercury from Fish Consumption: a Review and New Data from the Seychelles Child Development Study

    PubMed Central

    Myers, Gary J.; Thurston, Sally W.; Pearson, Alexander T.; Davidson, Philip W.; Cox, Christopher; Shamlaye, Conrad F.; Cernichiari, Elsa; Clarkson, Thomas W.

    2009-01-01

    Background Fish is an important source of nutrition worldwide. Fish contain both the neurotoxin methyl mercury (MeHg) and nutrients important for brain development. The developing brain appears to be most sensitive to MeHg toxicity and mothers who consume fish during pregnancy expose their fetus prenatally. Although brain development is most dramatic during fetal life, it continues for years postnatally and additional exposure can occur when a mother breast feeds or the child consumes fish. This raises the possibility that MeHg might influence brain development after birth and thus adversely affect children’s developmental outcomes. We reviewed postnatal MeHg exposure and the associations that have been published to determine the issues associated with it and then carried out a series of analyses involving alternative metrics of postnatal MeHg exposure in the Seychelles Child Development Study (SCDS) Main Cohort. Methods The SCDS is a prospective longitudinal evaluation of prenatal MeHg exposure from fish consumption. The Main Cohort includes 779 subjects on whom recent postnatal exposure data were collected at the 6, 19, 29, 66, and 107 month evaluations. We examined the association of recent postnatal MeHg exposure with multiple 66 and 107-month outcomes and then used three types of alternative postnatal exposure metrics to examine their association with the children’s intelligence quotient (IQ) at 107 months of age. Results Recent postnatal exposure at 107 months of age was adversely associated with four endpoints, three in females only. One alternative postnatal metric was beneficially associated with 9-year IQ in males only. Conclusions We found several associations between postnatal MeHg biomarkers and children’s developmental endpoints. However, as has been the case with prenatal MeHg exposure in the SCDS Main Cohort study, no consistent pattern of associations emerged to support a causal relationship. PMID:19442817

  13. Effects of intrauterine substance and postnatal violence exposure on aggression in children.

    PubMed

    Barthelemy, Olivier J; Richardson, Mark A; Rose-Jacobs, Ruth; Forman, Leah S; Cabral, Howard J; Frank, Deborah A

    2016-01-01

    During the cocaine epidemic of the 1980s and early 1990s, many expressed fears that children with intrauterine cocaine exposure (IUCE) would grow up to be unusually violent. The present study examines the relationship of caregiver reports of school-age children's aggressive behavior with IUCE and postnatal exposure to violence. Respondents were 140 low-income, primarily African American children, ages 8-11, and each child's current primary caregiver from a longitudinal study evaluating potential long term sequelae of IUCE. Multiple regression analyses were used to investigate the independent and interactive effects of level of IUCE (None (n = 69), Lighter (n = 47), Heavier (n =  24)) and exposure to violence (Violence Exposure Scale for Children-Revised) on aggressive behavior (Child Behavior Checklist), while also controlling for other intrauterine substance exposures and additional contextual factors. Children's self-reported exposure to violence was significantly positively associated with caregivers' reports of aggressive behavior (β = 2.17, P = .05), as was concurrent caregiver's psychiatric distress (β = .15, P = .003). However, neither IUCE nor its interaction with exposure to violence showed a significant association with aggressive behavior. Findings suggest the importance of postnatal social environment rather than IUCE in predicting aggressive behavior in childhood. © 2015 Wiley Periodicals, Inc.

  14. Detrimental effects of tobacco smoke exposure during development on postnatal lung function and asthma.

    PubMed

    Wang, Lei; Pinkerton, Kent E

    2008-03-01

    Exposure to environmental tobacco smoke (ETS) during fetal development and early postnatal life is perhaps the most ubiquitous and hazardous of children's environmental exposures. The developing lung is highly susceptible to ETS. A large body of literature links both prenatal maternal smoking and children's ETS exposure to decreased lung growth. This review summarizes the state of the knowledge, including both human epidemiology and laboratory animal experiments, linking ETS, lung development, and respiratory outcomes. Important issues discussed include lung development and lung function and asthma in relation to ETS exposure during critical windows of growth. Prenatal exposure to ETS is associated with impaired lung function and increased risk of developing asthma, whereas postnatal exposure mainly acts to trigger respiratory symptoms and asthma attacks, but it also plays an important role in the occurrence of asthma in children. This review provides evidence that avoidance of ETS exposure both before and after birth is beneficial to long-term respiratory health, because airway function in later life is believed to be largely determined by lung development occurring in utero and in early infancy.

  15. Lead absorption in cows: biological indicators of ambient lead exposure

    SciTech Connect

    Karacic, V.; Prpic-Majic, D.; Skender, L.

    1984-03-01

    In order to determine actual lead exposure from residual amounts of lead in the environmental soil following the introduction of effective engineering emission controls in a lead smeltery, the absorption of lead in cows grazing in the vicinity was investigated. Four groups of cows were examined: two groups of cows exposed to different ambient lead concentration, compared with two normal groups of cows. In each cow aminolevulinic acid dehydratase (ALAD), erythrocyte protoporphyrin (EP) and blood lead (Pb-B) were determined, two years prior to and four years after the technical sanitation of the lead emission source. The results demonstrated normalization of ALAD, EP and Pb-B after the technical sanitation. In spite of normalization, biological indicators ALAD and Pb-B determined four years after the technical sanitation showed increased lead absorption in comparison with the results of the control group. This indirectly indicates lead contamination of the environment from residual amounts of lead in the soil.

  16. Prenatal and Postnatal Exposure to Persistent Organic Pollutants and Infant Growth: A Pooled Analysis of Seven European Birth Cohorts.

    PubMed

    Iszatt, Nina; Stigum, Hein; Verner, Marc-André; White, Richard A; Govarts, Eva; Murinova, Lubica Palkovicova; Schoeters, Greet; Trnovec, Tomas; Legler, Juliette; Pelé, Fabienne; Botton, Jérémie; Chevrier, Cécile; Wittsiepe, Jürgen; Ranft, Ulrich; Vandentorren, Stéphanie; Kasper-Sonnenberg, Monika; Klümper, Claudia; Weisglas-Kuperus, Nynke; Polder, Anuschka; Eggesbø, Merete

    2015-07-01

    Infant exposure to persistent organic pollutants (POPs) may contribute to obesity. However, many studies so far have been small, focused on transplacental exposure, used an inappropriate measure to assess postnatal exposure through breastfeeding if any, or did not discern between prenatal and postnatal effects. We investigated prenatal and postnatal exposure to POPs and infant growth (a predictor of obesity). We pooled data from seven European birth cohorts with biomarker concentrations of polychlorinated biphenyl 153 (PCB-153) (n = 2,487), and p,p'-dichlorodiphenyldichloroethylene (p,p'-DDE) (n = 1,864), estimating prenatal and postnatal POPs exposure using a validated pharmacokinetic model. Growth was change in weight-for-age z-score between birth and 24 months. Per compound, multilevel models were fitted with either POPs total exposure from conception to 24 months or prenatal or postnatal exposure. We found a significant increase in growth associated with p,p'-DDE, seemingly due to prenatal exposure (per interquartile increase in exposure, adjusted β = 0.12; 95% CI: 0.03, 0.22). Due to heterogeneity across cohorts, this estimate cannot be considered precise, but does indicate that an association with infant growth is present on average. In contrast, a significant decrease in growth was associated with postnatal PCB-153 exposure (β = -0.10; 95% CI: -0.19, -0.01). To our knowledge, this is the largest study to date of POPs exposure and infant growth, and it contains state-of-the-art exposure modeling. Prenatal p,p'-DDE was associated with increased infant growth, and postnatal PCB-153 with decreased growth at European exposure levels.

  17. Overview of radon, lead and asbestos exposure

    SciTech Connect

    Demers, R. )

    1991-11-01

    Reducing the incidence of diseases caused by exposure to radon, lead and asbestos is a major public health challenge. Radon gas, which usually enters a home through the foundation, can cause lung cancer. Exposure to lead through paint, auto emissions and other sources can cause neurologic deficits, as well as anemia, abnormal vitamin D metabolism, nephropathy, hypertension and reproductive abnormalities. Asbestos, which is used in a vast number of products, is primarily associated with parenchymal asbestosis, pleural fibrosis, mesothelioma and lung cancer. The family physician can play a pivotal role in providing information about hazardous exposure, sources of exposure, epidemiology and disease prevention.29 references.

  18. DIETARY EXPOSURE OF CHILDREN TO LEAD

    EPA Science Inventory

    Children are the most susceptible population to lead exposure because 1) they have more opportunity for contact with lead sources due to their activities, 2) lead adsorption occurs more readily in a child as compared to an adult, and 3) the child's development is more vulnerable ...

  19. DIETARY EXPOSURE OF CHILDREN TO LEAD

    EPA Science Inventory

    Children are the most susceptible population to lead exposure because 1) they have more opportunity for contact with lead sources due to their activities, 2) lead adsorption occurs more readily in a child as compared to an adult, and 3) the child's development is more vulnerable ...

  20. High lead exposure in two leaded bronze ingot foundry workers.

    PubMed

    Song, Yoojun; Suh, Chunhui; Kim, Shin-Ae; Kim, Nami; Kim, Sung-Min; Jeong, Seong-Wook; Kim, Se-Yeong; Kim, Kun-Hyung; Kim, Jeong-Ho; Son, Byung-Chul; Lee, Chae-Kwan; Lee, Jong-Tae

    2014-01-01

    Awareness about lead poisoning in South Korea has increased; however, occupational exposures occurring in small-scale businesses have not been thoroughly investigated. We report two cases of high lead exposure in a leaded bronze ingot foundry. Two employees, a 54-year-old primary operator and a 46-year-old assistant, at a small-scale metalworking company who had been employed for 18 years and 1 month, respectively, showed elevated blood lead levels (61.1 μg/dL and 51.7 μg/dL, respectively) at an occupational health checkup. Neither worker complained of abnormal symptoms nor signs related to lead poisoning. Health assessment follow-ups were conducted and biological exposure indices of lead were calculated every four weeks. After the initial follow-up assessment, both workers were relocated from the foundry process to the metalworking process. In addition, a localized exhaust system was installed after the second follow-up. Foundry workers in a small-scale businesses might be at high risk of lead exposure because these businesses might be vulnerable to poor industrial hygiene. Therefore, regular occupational health checkups are required.

  1. Maternal Dexamethasone Exposure Alters Synaptic Inputs to Gonadotropin-Releasing Hormone Neurons in the Early Postnatal Rat

    PubMed Central

    Lim, Wei Ling; Idris, Marshita Mohd; Kevin, Felix Suresh; Soga, Tomoko; Parhar, Ishwar S.

    2016-01-01

    Maternal dexamethasone [(DEX); a glucocorticoid receptor agonist] exposure delays pubertal onset and alters reproductive behavior in the adult offspring. However, little is known whether maternal DEX exposure affects the offspring’s reproductive function by disrupting the gonadotropin-releasing hormone (GnRH) neuronal function in the brain. Therefore, this study determined the exposure of maternal DEX on the GnRH neuronal spine development and synaptic cluster inputs to GnRH neurons using transgenic rats expressing enhanced green fluorescent protein (EGFP) under the control of GnRH promoter. Pregnant females were administered with DEX (0.1 mg/kg) or vehicle (VEH, water) daily during gestation day 13–20. Confocal imaging was used to examine the spine density of EGFP–GnRH neurons by three-dimensional rendering and synaptic cluster inputs to EGFP–GnRH neurons by synapsin I immunohistochemistry on postnatal day 0 (P0) males. The spine morphology and number on GnRH neurons did not change between the P0 males following maternal DEX and VEH treatment. The number of synaptic clusters within the organum vasculosum of the lamina terminalis (OVLT) was decreased by maternal DEX exposure in P0 males. Furthermore, the number and levels of synaptic cluster inputs in close apposition with GnRH neurons was decreased following maternal DEX exposure in the OVLT region of P0 males. In addition, the postsynaptic marker molecule, postsynaptic density 95, was observed in GnRH neurons following both DEX and VEH treatment. These results suggest that maternal DEX exposure alters neural afferent inputs to GnRH neurons during early postnatal stage, which could lead to reproductive dysfunction during adulthood. PMID:27630615

  2. Blood pressure and industrial lead exposure.

    PubMed

    Maheswaran, R; Gill, J S; Beevers, D G

    1993-03-15

    The association between environmental lead exposure and raised blood pressure remains controversial. This association was examined in a cross-sectional study in 1981 on 809 male workers who were occupationally exposed to lead in a factory manufacturing car lead accumulator batteries in Birmingham, United Kingdom. Lead exposure was assessed by blood lead levels, blood zinc protoporphyrin levels, and years of industrial exposure to lead. The geometric mean blood lead level was 31.6 micrograms/dl with minimum and maximum values of 0 microgram/dl and 98 micrograms/dl, respectively. Unadjusted systolic blood pressure rose with increasing blood lead levels (analysis of variance, F = 3.3, p < 0.05) from 127 mmHg (95% confidence interval (CI) 123.5-130.5) in men with blood lead levels less than 21 micrograms/dl to 133 mmHg (95% CI 128.7-137.3) in men with levels exceeding 50 micrograms/dl. Following adjustment for the confounding effects of age, body mass index, and alcohol consumption, however, the effect of blood lead on systolic pressure was diminished (analysis of variance, F = 1.3, not significant) to 129 mmHg and 132 mmHg in the respective categories. There was no association between diastolic blood pressure and blood lead. Zinc protoporphyrin levels and years of industrial lead exposure did not raise adjusted systolic or diastolic pressure. In conclusion, subject to the limitations inherent in a cross-sectional survey, the findings are consistent with a weak effect of industrial lead exposure on systolic blood pressure, within the range of exposures observed in this study.

  3. Cell proliferation and cell death are disturbed during prenatal and postnatal brain development after uranium exposure.

    PubMed

    Legrand, M; Elie, C; Stefani, J; N Florès; Culeux, C; Delissen, O; Ibanez, C; Lestaevel, P; Eriksson, P; Dinocourt, C

    2016-01-01

    The developing brain is more susceptible to neurotoxic compounds than adult brain. It is also well known that disturbances during brain development cause neurological disorders in adulthood. The brain is known to be a target organ of uranium (U) exposure and previous studies have noted that internal U contamination of adult rats induces behavioral disorders as well as affects neurochemistry and neurophysiological properties. In this study, we investigated whether depleted uranium (DU) exposure affects neurogenesis during prenatal and postnatal brain development. We examined the structural morphology of the brain, cell death and finally cell proliferation in animals exposed to DU during gestation and lactation compared to control animals. Our results showed that DU decreases cell death in the cortical neuroepithelium of gestational day (GD) 13 embryos exposed at 40mg/L and 120mg/L and of GD18 fetuses exposed at 120mg/L without modification of the number of apoptotic cells. Cell proliferation analysis showed an increase of BrdU labeling in the dentate neuroepithelium of fetuses from GD18 at 120mg/L. Postnatally, cell death is increased in the dentate gyrus of postnatal day (PND) 0 and PND5 exposed pups at 120mg/L and is associated with an increase of apoptotic cell number only at PND5. Finally, a decrease in dividing cells is observed in the dentate gyrus of PND21 rats developmentally exposed to 120mg/L DU, but not at PND0 and PND5. These results show that DU exposure during brain development causes opposite effects on cell proliferation and cell death processes between prenatal and postnatal development mainly at the highest dose. Although these modifications do not have a major impact in brain morphology, they could affect the next steps of neurogenesis and thus might disrupt the fine organization of the neuronal network.

  4. Human biomonitoring issues related to lead exposure.

    PubMed

    Nieboer, Evert; Tsuji, Leonard J S; Martin, Ian D; Liberda, Eric N

    2013-10-01

    Lead as a toxic environmental metal has been an issue of concern for 30-40 years. Even though the exposures experienced by the general public have been significantly reduced, so have the acceptable blood lead concentrations assessed to safeguard health (specifically of children). The impact of these concurrent changes are reviewed and discussed in terms of the following: blood lead as the primary biomarker of exposure; pertinent toxicokinetic issues including modelling; legacy and newer sources of this toxic metal; improvements in lead quantification techniques and its characterization (chemical forms) in exposure media; and in vivo markers of lead sources. It is concluded that the progress in the quantification of lead and its characterization in exposure media have supported the efforts to identify statistical associations of lead in blood and tissues with adverse health outcomes, and have guided strategies to reduce human exposure (especially for children). To clarify the role of lead as a causative factor in disease, greater research efforts in biomarkers of effect and susceptibility seem timely.

  5. Occupational lead exposure and blood pressure.

    PubMed Central

    Parkinson, D K; Hodgson, M J; Bromet, E J; Dew, M A; Connell, M M

    1987-01-01

    Recent community studies have suggested that low level lead exposure is significantly associated with blood pressure in the general population. This finding is inconsistent with the results of recent occupational studies of lead exposed workers, although the occupational studies contained serious methodological weaknesses. The present study examined the relation between occupational lead exposure and diastolic and systolic blood pressure in randomly selected samples of 270 exposed and 158 non-exposed workers. Four exposure indicators were examined: employment at a lead battery plant nu a control plant, current blood lead value, current zinc protoporphyrin value, and time weighted average blood lead value. After controlling for other known risk factors such as age, education, income, cigarette usage, alcohol consumption, and exercise, the associations between exposure and blood pressure were small and non-significant. In the absence of a biologically feasible hypothesis regarding the mechanism by which low level lead exposure would influence blood pressure the present findings challenge the validity of the general population association. PMID:3689706

  6. Gestational medication use, birth conditions, and early postnatal exposures for childhood asthma.

    PubMed

    Chen, Yang-Ching; Tsai, Ching-Hui; Lee, Yungling

    2012-01-01

    Our aim is to explore (1) whether gestational medication use, mode of delivery, and early postnatal exposure correlate with childhood asthma, (2) the dose responsiveness of such exposure, and (3) their links to early- and late-onset asthma. We conducted a matched case-control study based on the Taiwan Children Health Study, which was a nationwide survey that recruited 12-to-14-year-old school children in 14 communities. 579 mothers of the participants were interviewed by telephone. Exclusive breastfeeding protected children from asthma. Notably, childhood asthma was significantly associated with maternal medication use during pregnancy, vacuum use during vaginal delivery, recurrent respiratory tract infections, hospitalization, main caregiver cared for other children, and early daycare attendance. Exposure to these factors led to dose responsiveness in relationships to asthma. Most of the exposures revealed a greater impact on early-onset asthma, except for vacuum use and daycare attendance.

  7. Gestational Medication Use, Birth Conditions, and Early Postnatal Exposures for Childhood Asthma

    PubMed Central

    Chen, Yang-Ching; Tsai, Ching-Hui; Lee, Yungling

    2012-01-01

    Our aim is to explore (1) whether gestational medication use, mode of delivery, and early postnatal exposure correlate with childhood asthma, (2) the dose responsiveness of such exposure, and (3) their links to early- and late-onset asthma. We conducted a matched case-control study based on the Taiwan Children Health Study, which was a nationwide survey that recruited 12-to-14-year-old school children in 14 communities. 579 mothers of the participants were interviewed by telephone. Exclusive breastfeeding protected children from asthma. Notably, childhood asthma was significantly associated with maternal medication use during pregnancy, vacuum use during vaginal delivery, recurrent respiratory tract infections, hospitalization, main caregiver cared for other children, and early daycare attendance. Exposure to these factors led to dose responsiveness in relationships to asthma. Most of the exposures revealed a greater impact on early-onset asthma, except for vacuum use and daycare attendance. PMID:22203862

  8. Postnatal hyperoxia exposure differentially affects hepatocytes and liver haemopoietic cells in newborn rats.

    PubMed

    Marconi, Guya Diletta; Zara, Susi; De Colli, Marianna; Di Valerio, Valentina; Rapino, Monica; Zaramella, Patrizia; Dedja, Arben; Macchi, Veronica; De Caro, Raffaele; Porzionato, Andrea

    2014-01-01

    Premature newborns are frequently exposed to hyperoxic conditions and experimental data indicate modulation of liver metabolism by hyperoxia in the first postnatal period. Conversely, nothing is known about possible modulation of growth factors and signaling molecules involved in other hyperoxic responses and no data are available about the effects of hyperoxia in postnatal liver haematopoiesis. The aim of the study was to analyse the effects of hyperoxia in the liver tissue (hepatocytes and haemopoietic cells) and to investigate possible changes in the expression of Vascular Endothelial Growth Factor (VEGF), Matrix Metalloproteinase 9 (MMP-9), Hypoxia-Inducible Factor-1α (HIF-1α), endothelial Nitric Oxide Synthase (eNOS), and Nuclear Factor-kB (NF-kB). Experimental design of the study involved exposure of newborn rats to room air (controls), 60% O2 (moderate hyperoxia), or 95% O2 (severe hyperoxia) for the first two postnatal weeks. Immunohistochemical and Western blot analyses were performed. Severe hyperoxia increased hepatocyte apoptosis and MMP-9 expression and decreased VEGF expression. Reduced content in reticular fibers was found in moderate and severe hyperoxia. Some other changes were specifically produced in hepatocytes by moderate hyperoxia, i.e., upregulation of HIF-1α and downregulation of eNOS and NF-kB. Postnatal severe hyperoxia exposure increased liver haemopoiesis and upregulated the expression of VEGF (both moderate and severe hyperoxia) and eNOS (severe hyperoxia) in haemopoietic cells. In conclusion, our study showed different effects of hyperoxia on hepatocytes and haemopoietic cells and differential involvement of the above factors. The involvement of VEGF and eNOS in the liver haemopoietic response to hyperoxia may be hypothesized.

  9. Prenatal lead exposure enhances methamphetamine sensitization in rats.

    PubMed

    Clifford, P Shane; Hart, Nigel; Thompson, Jeff; Buckman, Sam; Wellman, Paul J; Bratton, Gerald R; Nation, Jack R

    2009-08-01

    Adult female rats were exposed to lead-free sodium acetate via gavage [0 mg (vehicle control)] or to 16 mg lead as lead acetate for 30 days prior to breeding. Following confirmation of breeding, the female animals continued to be exposed to their respective doses throughout gestation and lactation. When weaned, 16 control and 16 lead-exposed offspring were placed on regular water and food (lead-exposure was discontinued) until postnatal day (PND) 70. At this time, one-half of the control animals and one-half of the lead-treatment animals received intraperitoneal (i.p.) injections of the vehicle (saline) for 10 successive days and the remaining animals in each exposure conditions received daily injections of 1.0 mg/kg (+)-methamphetamine (METH) for 10 days (N=8/group). Locomotion in automated chambers was monitored daily for 45 min post-injection. Subsequently, during dose-effect testing, all animals received consecutive daily i.p. injections of 0, 1.0, 2.0, and then 4.0 mg/kg METH. The results of the experiment showed that both control and lead-exposed animals exhibited heightened locomotor activity (i.e. behavioral sensitization) to the repeated administration of 1.0 mg/kg METH. More importantly, animals developmentally (perinatally) exposed to lead showed more rapid sensitization than did their control counterparts. These data indicate that early lead exposure increases sensitivity to the locomotor-stimulating effects of METH. In contrast, identically exposed lead animals exhibit diminished METH dose-effect responding when tested in an intravenous (i.v.) self-administration paradigm [Rocha A., Valles R., Bratton G.R., Nation J.R. Developmental lead exposure alters methamphetamine self-administration in the male rat: acquisition and reinstatement. Drug Alcohol Depend 2008a;95:23-29, Rocha A., Valles R., Hart N., Bratton G.R., Nation J.R. Developmental lead exposure attenuates methamphetamine dose-effect self-administration performance and progressive ratio

  10. Comparison Impairments of Spatial Cognition and Hippocampal Synaptic Plasticity Between Prenatal and Postnatal Melamine Exposure in Male Adult Rats.

    PubMed

    An, Lei; Zhang, Tao

    2016-02-01

    Our previous investigation showed that melamine in offspring hippocampus appeared to not be the critical factor for cognitive defects. The present study was to investigate whether the cognitive impairments induced by prenatal and postnatal melamine exposure and persisted into adulthood, and to evaluate the differences of the exposures in affecting hippocampus-depended cognition and synaptic plasticity. Wistar rats were exposed to melamine through the whole gestational period or from postnatal day (PD) 21 to PD41, and then tested on PD90. The experiments of water maze and hippocampal synaptic plasticity in vivo were performed to assess the effects on spatial cognition and synaptic impairments. The results indicated that cognitive defects were induced by exposures to either prenatal or postnatal melamine, whereas there was a more serious damage in prenatal. Histological evidence further showed that there were the detrimental effects of both prenatal and postnatal effects. Paired-pulse facilitation ratio and post-tetanic potentiation were severely impacted in prenatal-exposed rats but not postnatal-exposed ones. Both exposures to prenatal and postnatal melamine impaired long-term potentiation, while there was severe damage to prenatal animals. These data suggest that the detrimental effects of prenatal and postnatal melamine on cognition and hippocampal synaptic plasticity could persist into adulthood, and the impairment of prenatal exposure was to some extent more severe. Hence, prenatal and postnatal exposures to melamine may have different effects on hippocampus-dependent learning and memory, which would most likely result from differentially adversely properties on the hippocampal CA1 synaptic function.

  11. Lead exposure in outdoor firearm instructors

    SciTech Connect

    Tripathi, R.K.; Sherertz, P.C.; Llewellyn, G.C.; Armstrong, C.W. )

    1991-06-01

    This study was conducted to determine lead exposure of firearm instructors at an outdoor firing range, while cadets were firing nonjacketed and jacketed lead ammunitions. The breathing zone air for lead exceeded the Occupational Safety and Health Administration standard of 50 micrograms/m3 for two instructors during firing exercises using nonjacketed bullets. The use of totally copper-jacketed bullets reduced the breathing zone lead levels by 92 percent for instructor {number sign}1 and by 96 percent for instructor {number sign}2; subsequent blood lead levels showed a significant decline in both instructors.

  12. Neurohumoral blood pressure regulation in lead exposure

    SciTech Connect

    Boscolo, P.; Carmignani, M.

    1988-06-01

    Previous human studies demonstrated that lead exposure may modify the metabolism of catecholamines and of hormones controlled by the hypothalamo-pituitary axis and may affect the kallikrein-kinin system. This paper reports unpublished data on the plasma renin activity of lead-exposed workers; these results are in agreement with those of previous human and experimental studies suggesting that the synthesis or release of renin is increased after short and moderate exposure to inorganic lead and reduced whenever the exposure is prolonged. Previous experimental investigations demonstrated that lead may act on the cardiovascular system, with effects on the renin-angiotensin system, on the reactivity to stimulation of peripheral catecholaminergic receptors, on sympathetic and vagal tone, and on reactivity to the stimulation of baroreceptors. This paper reports the results of a study on male Sprague-Dawley rats that received 0, 15, 30, and 60 ..mu..g/mL of lead in drinking water for 18 months. Blood pressure was increased in the rats receiving 30 and 60 ppm of lead; cardiac inotropism was augmented only in those receiving the higher dose of the metal, and heart rate was not modified. Cardiovascular responses to agonists indicated that lead exposure affects the renin-angiotensin system and induces sympathetic hyperactivity be acting on central and peripheral sympathetic junctions increasing the responsiveness to stimulation of ..cap alpha../sub 2/-adrenoreceptors and by increasing the reactivity to stimulation of cardiac and vascular ..beta..-adrenergic and dopaminergic receptors.

  13. Sources of lead exposure in Mexico City.

    PubMed Central

    Romieu, I; Palazuelos, E; Hernandez Avila, M; Rios, C; Muñoz, I; Jimenez, C; Cahero, G

    1994-01-01

    Many countries, including Mexico, are facing a largely unrecognized epidemic of low-level lead poisoning. Mexico is the sixth largest lead-producing country in the world, and 40% of its production is used locally in different industrial processes that cause lead contamination of the environment. The major sources and pathways of lead exposure among the Mexican population are gasoline emissions, lead-glazed ceramics, leaded paint, and lead in canned foods and beverages. In this paper we present evidence for the presence of lead in different environmental media and its impact on blood lead levels of the Mexican population. Although during the last few years important measures have been implemented to decrease lead exposure, our findings suggest that lead poisoning is still an important problem in Mexico. There is an urgent need for regulatory policies that implement stricter control to protect the Mexican population. There is also a need to develop adequate programs to reduce the lead burden and the associated health effects in the population that has been chronically exposed. Images Figure 1. PMID:7523102

  14. Sources of lead exposure in Mexico City.

    PubMed

    Romieu, I; Palazuelos, E; Hernandez Avila, M; Rios, C; Muñoz, I; Jimenez, C; Cahero, G

    1994-04-01

    Many countries, including Mexico, are facing a largely unrecognized epidemic of low-level lead poisoning. Mexico is the sixth largest lead-producing country in the world, and 40% of its production is used locally in different industrial processes that cause lead contamination of the environment. The major sources and pathways of lead exposure among the Mexican population are gasoline emissions, lead-glazed ceramics, leaded paint, and lead in canned foods and beverages. In this paper we present evidence for the presence of lead in different environmental media and its impact on blood lead levels of the Mexican population. Although during the last few years important measures have been implemented to decrease lead exposure, our findings suggest that lead poisoning is still an important problem in Mexico. There is an urgent need for regulatory policies that implement stricter control to protect the Mexican population. There is also a need to develop adequate programs to reduce the lead burden and the associated health effects in the population that has been chronically exposed.

  15. Peri, pre and postnatal morphine exposure: exposure-induced effects and sex differences in the behavioural consequences in rat offspring.

    PubMed

    Timár, Julia; Sobor, Melinda; Király, Kornél P; Gyarmati, Susanna; Riba, Pál; Al-Khrasani, Mahmoud; Fürst, Susanna

    2010-02-01

    This study investigated the behavioural consequences of peri, pre and postnatal morphine (MO) exposure in rats. From gestational day 1 dams were treated with either saline or MO subcutaneously once a day (5 mg/kg on the first 2 days, 10 mg/kg subsequently). Spontaneous locomotor activity in a new environment (habituation) and antinociceptive effects of MO were measured separately in male and female pups after weaning and also in late adolescence or adulthood. The rewarding effect of MO was assessed by conditioned place preference in adult animals. Both exposure-induced and sex differences were observed. A significant delay in habituation to a new environment and decreased sensitivity to the antinociceptive effect of MO were found in male offspring of MO-treated dams. In contrast, the place preference induced by MO was enhanced in the MO-exposed adult animals and this effect was more marked in females. Prenatal exposure to MO resulted in more marked changes than the postnatal exposure through maternal milk. The results indicate that a medium MO dose administered once-daily results in long-term consequences in offspring and may make them more vulnerable to MO abuse in adulthood.

  16. Association of prenatal exposure to maternal smoking and postnatal exposure to household smoking with dental caries in 3-year-old Japanese children.

    PubMed

    Tanaka, Keiko; Miyake, Yoshihiro; Nagata, Chisato; Furukawa, Shinya; Arakawa, Masashi

    2015-11-01

    Epidemiological studies of the association between smoking exposure and dental caries are limited. The purpose of this cross-sectional study was to examine the association between prenatal and postnatal secondhand smoke (SHS) exposure and the prevalence of dental caries in primary dentition in young Japanese children. Study subjects were 6412 children aged 3 years. Information on exposure to maternal smoking during pregnancy and postnatal SHS exposure at home was collected via parent questionnaire. Children were classified as having dental caries if one or more primary teeth had decayed or had been filled. Compared with never smoking during pregnancy, maternal smoking in the first trimester of pregnancy was significantly associated with an increased prevalence of dental caries in children (adjusted odds ratio=1.37, 95% confidence interval: 1.03-1.80). Postnatal SHS exposure was also positively associated with dental caries, with a significant positive exposure-response relationship. Compared with children not exposed to prenatal maternal smoking or postnatal SHS at home, those exposed to both prenatal and postnatal smoking had higher odds of dental caries (adjusted odds ratio=1.62, 95% confidence interval: 1.23-2.11). Our findings suggest that maternal smoking during pregnancy and postnatal SHS exposure may be associated with an increased prevalence of dental caries in primary dentition. Copyright © 2015. Published by Elsevier Inc.

  17. Lead exposure among lead-acid battery workers in Jamaica.

    PubMed

    Matte, T D; Figueroa, J P; Burr, G; Flesch, J P; Keenlyside, R A; Baker, E L

    1989-01-01

    To assess lead exposure in the Jamaican lead-acid battery industry, we surveyed three battery manufacturers (including 46 production workers) and 10 battery repair shops (including 23 battery repair workers). Engineering controls and respiratory protection were judged to be inadequate at battery manufacturers and battery repair shops. At manufacturers, 38 of 42 air samples for lead exceeded a work-shift time-weighted average concentration of 0.050 mg/m3 (range 0.030-5.3 mg/m3), and nine samples exceeded 0.50 mg/m3. Only one of seven air samples at repair shops exceeded 0.050 mg/m3 (range 0.003-0.066 mg/m3). Repair shop workers, however, had higher blood lead levels than manufacturing workers (65% vs. 28% with blood lead levels above 60 micrograms/dl, respectively). Manufacturing workers had a higher prevalence of safe hygienic practices and a recent interval of minimal production had occurred at one of the battery manufacturers. Workers with blood lead levels above 60 micrograms/dl tended to have higher prevalences of most symptoms of lead toxicity than did workers with lower blood lead levels, but this finding was not consistent or statistically significant. The relationship between zinc protoporphyrin concentrations and increasing blood lead concentrations was consistent with that described among workers in developed countries. The high risk of lead toxicity among Jamaican battery workers is consistent with studies of battery workers in other developing countries.

  18. Programming Effects of Prenatal Glucocorticoid Exposure with a Postnatal High-Fat Diet in Diabetes Mellitus

    PubMed Central

    Sheen, Jiunn-Ming; Hsieh, Chih-Sung; Tain, You-Lin; Li, Shih-Wen; Yu, Hong-Ren; Chen, Chih-Cheng; Tiao, Miao-Meng; Chen, Yu-Chieh; Huang, Li-Tung

    2016-01-01

    Increasing evidence has shown that many chronic diseases originate from early life, even before birth, through what are termed as fetal programming effects. Glucocorticoids are frequently used prenatally to accelerate the maturation of the lungs of premature infants. High-fat diets are associated with insulin resistance, but the effects of prenatal glucocorticoid exposure plus a postnatal high-fat diet in diabetes mellitus remain unclear. We administered pregnant Sprague-Dawley rats’ intraperitoneal dexamethasone (0.1 mg/kg body weight) or vehicle at gestational days 14–20. Male offspring were administered a normal or high-fat diet starting from weaning. We assessed the effects of prenatal steroid exposure plus postnatal high-fat diet on the liver, pancreas, muscle and fat at postnatal day 120. At 15 and 30 min, sugar levels were higher in the dexamethasone plus high-fat diet (DHF) group than the vehicle plus high-fat diet (VHF) group in the intraperitoneal glucose tolerance test (IPGTT). Serum insulin levels at 15, 30 and 60 min were significantly higher in the VHF group than in the vehicle and normal diet group. Liver insulin receptor and adenosine monophosphate-activated protein kinase mRNA expressions and protein levels were lower in the DHF group. Insulin receptor and insulin receptor substrate-1 mRNA expressions were lower in the epididymal adipose tissue in the VHF and DHF groups. “Programming” of liver or epididymal adipose tissue resulted from prenatal events. Prenatal steroid exposure worsened insulin resistance in animals fed a high-fat diet. PMID:27070590

  19. Programming Effects of Prenatal Glucocorticoid Exposure with a Postnatal High-Fat Diet in Diabetes Mellitus.

    PubMed

    Sheen, Jiunn-Ming; Hsieh, Chih-Sung; Tain, You-Lin; Li, Shih-Wen; Yu, Hong-Ren; Chen, Chih-Cheng; Tiao, Miao-Meng; Chen, Yu-Chieh; Huang, Li-Tung

    2016-04-08

    Increasing evidence has shown that many chronic diseases originate from early life, even before birth, through what are termed as fetal programming effects. Glucocorticoids are frequently used prenatally to accelerate the maturation of the lungs of premature infants. High-fat diets are associated with insulin resistance, but the effects of prenatal glucocorticoid exposure plus a postnatal high-fat diet in diabetes mellitus remain unclear. We administered pregnant Sprague-Dawley rats' intraperitoneal dexamethasone (0.1 mg/kg body weight) or vehicle at gestational days 14-20. Male offspring were administered a normal or high-fat diet starting from weaning. We assessed the effects of prenatal steroid exposure plus postnatal high-fat diet on the liver, pancreas, muscle and fat at postnatal day 120. At 15 and 30 min, sugar levels were higher in the dexamethasone plus high-fat diet (DHF) group than the vehicle plus high-fat diet (VHF) group in the intraperitoneal glucose tolerance test (IPGTT). Serum insulin levels at 15, 30 and 60 min were significantly higher in the VHF group than in the vehicle and normal diet group. Liver insulin receptor and adenosine monophosphate-activated protein kinase mRNA expressions and protein levels were lower in the DHF group. Insulin receptor and insulin receptor substrate-1 mRNA expressions were lower in the epididymal adipose tissue in the VHF and DHF groups. "Programming" of liver or epididymal adipose tissue resulted from prenatal events. Prenatal steroid exposure worsened insulin resistance in animals fed a high-fat diet.

  20. Piracetam prevents memory deficit induced by postnatal propofol exposure in mice.

    PubMed

    Wang, Yuan-Lin; Li, Feng; Chen, Xin

    2016-05-15

    Postnatal propofol exposure impairs hippocampal synaptic development and memory. However, the effective agent to alleviate the impairments was not verified. In this study, piracetam, a positive allosteric modulator of AMPA receptor was administered following a seven-day propofol regime. Two months after propofol administration, hippocampal long-term potentiation (LTP) and long-term memory decreased, while intraperitoneal injection of piracetam at doses of 100mg/kg and 50mg/kg following last propofol exposure reversed the impairments of memory and LTP. Mechanically, piracetam reversed propofol exposure-induced decrease of BDNF and phosphorylation of mTor. Similar as piracetam, BDNF supplementary also ameliorated propofol-induced abnormalities of synaptic plasticity-related protein expressions, hippocampal LTP and long-term memory. These results suggest that piracetam prevents detrimental effects of propofol, likely via activating BDNF synthesis. Copyright © 2016 Elsevier B.V. All rights reserved.

  1. [Children exposure to lead in contaminated sites].

    PubMed

    Flores-Ramírez, Rogelio; Rico-Escobar, Edna; Núñez-Monreal, Jorge E; García-Nieto, Edelmira; Carrizales, Leticia; Ilizaliturri-Hernández, César; Díaz-Barriga, Fernando

    2012-01-01

    To assess the exposure to lead in children living in various types of contaminated sites. The study was conducted from June 2008 to December 2009 at four sites in Mexico: Avalos metallurgical, Chihuahua; Morales metallurgical, San Luis Potosí (SLP); Trinidad pottery area, Tlaxcala and Cedral mine site, SLP. These sites contain different sources of lead. The metal levels were quantified in outdoor dust and in peripheral blood of children. Lead dust concentrations exceed the National Guidelines for residential soils (400 mg/kg) in a range of values for the four sites from 62 to 5 187 mg/kg. Regarding biological monitoring, the studied children showed maximum lead blood levels of 22 µg/dL in Cedral, 31 µg/dL in Morales, 32 µg/dL in Avalos, and 52 µg/dL in Trinidad. It is important to mention that in all the studied sites, a significative positive correlation was found between blood lead levels and the lead concentrations in dust. These sites are an example of the health risks related to lead exposure in Mexico; therefore, there is an urgent need for a national public health program aimed at reducing lead exposure in vulnerable populations.

  2. Prenatal and Postnatal Exposure to Persistent Organic Pollutants and Infant Growth: A Pooled Analysis of Seven European Birth Cohorts

    PubMed Central

    Iszatt, Nina; Stigum, Hein; Verner, Marc-André; White, Richard A.; Govarts, Eva; Murinova, Lubica Palkovicova; Schoeters, Greet; Trnovec, Tomas; Legler, Juliette; Pelé, Fabienne; Botton, Jérémie; Chevrier, Cécile; Wittsiepe, Jürgen; Ranft, Ulrich; Vandentorren, Stéphanie; Kasper-Sonnenberg, Monika; Klümper, Claudia; Weisglas-Kuperus, Nynke; Polder, Anuschka

    2015-01-01

    Background Infant exposure to persistent organic pollutants (POPs) may contribute to obesity. However, many studies so far have been small, focused on transplacental exposure, used an inappropriate measure to assess postnatal exposure through breastfeeding if any, or did not discern between prenatal and postnatal effects. Objectives We investigated prenatal and postnatal exposure to POPs and infant growth (a predictor of obesity). Methods We pooled data from seven European birth cohorts with biomarker concentrations of polychlorinated biphenyl 153 (PCB-153) (n = 2,487), and p,p´-dichlorodiphenyldichloroethylene (p,p´-DDE) (n = 1,864), estimating prenatal and postnatal POPs exposure using a validated pharmacokinetic model. Growth was change in weight-for-age z-score between birth and 24 months. Per compound, multilevel models were fitted with either POPs total exposure from conception to 24 months or prenatal or postnatal exposure. Results We found a significant increase in growth associated with p,p´-DDE, seemingly due to prenatal exposure (per interquartile increase in exposure, adjusted β = 0.12; 95% CI: 0.03, 0.22). Due to heterogeneity across cohorts, this estimate cannot be considered precise, but does indicate that an association with infant growth is present on average. In contrast, a significant decrease in growth was associated with postnatal PCB-153 exposure (β = –0.10; 95% CI: –0.19, –0.01). Conclusion To our knowledge, this is the largest study to date of POPs exposure and infant growth, and it contains state-of-the-art exposure modeling. Prenatal p,p´-DDE was associated with increased infant growth, and postnatal PCB-153 with decreased growth at European exposure levels. Citation Iszatt N, Stigum H, Verner MA, White RA, Govarts E, Palkovicova Murinova L, Schoeters G, Trnovec T, Legler J, Pelé F, Botton J, Chevrier C, Wittsiepe J, Ranft U, Vandentorren S, Kasper-Sonnenberg M, Klümper C, Weisglas-Kuperus N, Polder A, Eggesbø M, OBELIX

  3. Ionizing Radiation Exposure During Pregnancy: Effects on Postnatal Development and Life.

    PubMed

    Sreetharan, Shayenthiran; Thome, Christopher; Tharmalingam, Sujeenthar; Jones, Devon E; Kulesza, Adomas V; Khaper, Neelam; Lees, Simon J; Wilson, Joanna Y; Boreham, Douglas R; Tai, T C

    2017-06-01

    Reliable human data on the effects of prenatal exposure to ionizing radiation are largely based on high-dose exposures. Exposure to low doses may produce effects that are not easily observable at birth, and may persist over the course of the offspring's postnatal life. This is important when considering fetal programing, a phenomenon characterized by changes in offspring phenotype due to a stress experienced in utero. In this review, we briefly summarize the known effects of both high- and low-dose exposure to ionizing radiation during pregnancy in humans. There is a major consensus that the atomic bomb survivors' data shows increased incidence of microcephaly and reductions in IQ of A-bomb survivors, whereas, with diagnostic radiography in utero there is no conclusive evidence of increased cancer risk. Due to the relatively limited data (particularly for low-dose exposures) in humans, animal models have emerged as an important tool to study prenatal effects of radiation. These animal models enable researchers to manipulate various experimental parameters and make it possible to analyze a wider variety of end points. In this review, we discuss the major findings from studies using mouse and rat models to examine prenatal ionizing radiation effects in postnatal development of the offspring. In addition, we broadly categorize trends across studies within three major stages of development: pre-implantation, organogenesis and fetal development. Overall, long-term effects of prenatal radiation exposure (including the possible role on the developmental programing of disease) are important factors to consider when assessing radiation risk, since these effects are of relevance even in the low-dose range.

  4. Postnatal exposure history and airways: oxidant stress responses in airway explants.

    PubMed

    Murphy, Shannon R; Schelegle, Edward S; Edwards, Patricia C; Miller, Lisa A; Hyde, Dallas M; Van Winkle, Laura S

    2012-12-01

    Postnatally, the lung continues to grow and differentiate while interacting with the environment. Exposure to ozone (O(3)) and allergens during postnatal lung development alters structural elements of conducting airways, including innervation and neurokinin abundance. These changes have been linked with development of asthma in a rhesus monkey model. We hypothesized that O(3) exposure resets the ability of the airways to respond to oxidant stress and that this is mediated by changes in the neurokinin-1 receptor (NK-1R). Infant rhesus monkeys received episodic exposure to O(3) biweekly with or without house dust mite antigen (HDMA) from 6 to 12 months of age. Age-matched monkeys were exposed to filtered air (FA). Microdissected airway explants from midlevel airways (intrapulmonary generations 5-8) for four to six animals in each of four groups (FA, O(3), HDMA, and HDMA+O(3)) were tested for NK-1R gene responses to acute oxidant stress using exposure to hydrogen peroxide (1.2 mM), a lipid ozonide (10 μM), or sham treatment for 4 hours in vitro. Airway responses were measured using real-time quantitative RT-PCR of NK-1R and IL-8 gene expression. Basal NK-1R gene expression levels were not different between the exposure groups. Treatment with ozonide or hydrogen peroxide did not change NK-1R gene expression in animals exposed to FA, HDMA, or HDMA+O(3). However, treatment in vitro with lipid ozonide significantly increased NK-1R gene expression in explants from O(3)-exposed animals. We conclude that a history of prior O(3) exposure resets the steady state of the airways to increase the NK-1R response to subsequent acute oxidant stresses.

  5. Physical, behavioral, and cognitive effects of prenatal tobacco and postnatal secondhand smoke exposure.

    PubMed

    Zhou, Sherry; Rosenthal, David G; Sherman, Scott; Zelikoff, Judith; Gordon, Terry; Weitzman, Michael

    2014-09-01

    The purpose of this review is to examine the rapidly expanding literature regarding the effects of prenatal tobacco and postnatal secondhand smoke (SHS) exposure on child health and development. Mechanisms of SHS exposure are reviewed, including critical periods during which exposure to tobacco products appears to be particularly harmful to the developing fetus and child. The biological, biochemical, and neurologic effects of the small fraction of identified components of SHS are described. Research describing these adverse effects of both in utero and childhood exposure is reviewed, including findings from both animal models and humans. The following adverse physical outcomes are discussed: sudden infant death syndrome, low birth weight, decreased head circumference, respiratory infections, otitis media, asthma, childhood cancer, hearing loss, dental caries, and the metabolic syndrome. In addition, the association between the following adverse cognitive and behavioral outcomes and such exposures is described: conduct disorder, attention-deficit/hyperactivity disorder, poor academic achievement, and cognitive impairment. The evidence supporting the adverse effects of SHS exposure is extensive yet rapidly expanding due to improving technology and increased awareness of this profound public health problem. The growing use of alternative tobacco products, such as hookahs (a.k.a. waterpipes), and the scant literature on possible effects from prenatal and secondhand smoke exposure from these products are also discussed. A review of the current knowledge of this important subject has implications for future research as well as public policy and clinical practice. Published by Mosby, Inc.

  6. Pre- and postnatal exposures to pesticides and neurodevelopmental effects in children living in agricultural communities from South-Eastern Spain.

    PubMed

    González-Alzaga, Beatriz; Hernández, Antonio F; Rodríguez-Barranco, Miguel; Gómez, Inmaculada; Aguilar-Garduño, Clemente; López-Flores, Inmaculada; Parrón, Tesifón; Lacasaña, Marina

    2015-12-01

    Childrens exposure to neurotoxic compounds poses a major problem to public health because oftheir actively developing brain that makes them highly vulnerable. However, limited information is available on neuropsychological effects in children associated with pre- and postnatal exposures to pesticides. To evaluate the association between current and pre- and postnatal exposures to pesticides and their effects on neurodevelopment in children aged 6–11 years living in agricultural communities from South-Eastern Spain. An ambispective study was conducted on 305 children aged 6–11 years randomly selected from public schools of the study area. Current exposure to organophosphate pesticides was assessed measuring children's urinary levels of dialkylphosphates (DAPs). Both prenatal and postnatal residential exposure to pesticides was estimated by developing a geographical information system (GIS) technology-based index that integrated distance-weighted measure of agricultural surface, time-series of crop areas per municipality and year, and land-use maps. Neuropsychological performance was evaluated with the Wechsler Intelligence Scale for Children-Fourth Edition (WISC-IV). The association of pre- and postnatal and current pesticide exposure with WISC-IV scale scores was assessed using multivariate linear regression models and generalized estimating equation (GEE) models, respectively. Greater urinary DAP levels were associated with a poorer performance on intelligence quotient and verbal comprehension domain, with effects being more prominent in boys than in girls. The influence of an increase in 10 ha per year in crop surface around the child's residence during the postnatal period was associated with decreased intelligence quotient, processing speed and verbal comprehension scores. As regards prenatal exposure to pesticides, a poor processing speed performance was observed. These effects were also more prominent in boys than in girls. Our results suggest that

  7. Human lead exposure: Some recent research findings

    SciTech Connect

    Saryan, L.A.

    1999-09-01

    One of the practical problems facing industrial hygienists and safety managers in the lead industry is finding new ways to limit or reduce lead intake in order to protect workers from the deleterious effects of this metal. Exposure to lead generally takes place by inhalation of airborne particles and by ingestion. Airborne exposure is comparatively well understood and methods for the control of airborne lead have been developed and put into place in industrial facilities. Both for the general public and for workers, however, it is thought that a significant fraction of the total lead intake occurs by ingestion as opposed to inhalation. Furthermore, factors such as personal hygiene, hand washing, diet, cigarette smoking, alcohol consumption, use of medications, bone injury, existing disease, and others may also have positive or negative effects on lead absorption and blood lead levels. How these variables actually operate in practice for lead-exposed workers is unfortunately not very well understood. As scientific and medical knowledge increases, progress has been made in the understanding of some of the factors affecting blood lead levels. In this article, the author summarizes the findings of a few interesting recent reports that point the way toward future progress in this area.

  8. Neural alterations from lead exposure in zebrafish.

    PubMed

    Roy, Nicole M; DeWolf, Sarah; Schutt, Alexius; Wright, Ashia; Steele, Latina

    2014-01-01

    Lead was used extensively as a gas additive and pesticide, in paints, batteries, lead shot, pipes, canning and toy manufacturing. Although uses of lead have been restricted, lead persists in our environment especially in older homes, and generally in soil and water. Although extensive studies have determined that fetal and childhood exposures to lead have been associated with childhood and adolescent memory impairments and learning disabilities, there are limited studies investigating early neural and morphological effects that may lead to these behavioral and learning abnormalities. Here we utilize the zebrafish vertebrate model system to study early effects of lead exposure on the brain. We treat embryos with 0.2mM lead for 24, 48 and 72 h and analyze neural structures through live imagery and transgenic approaches. We find structural abnormalities in the hindbrain region as well as changes in branchiomotor neuron development and altered neural vasculature. Additionally, we find areas of increased apoptosis. We conclude that lead is developmentally neurotoxic to a specific region of the brain, the hindbrain and is toxic to branchiomotor neurons residing in rhombomeres 2 through 7 of the hindbrain and hindbrain central artery vasculature.

  9. Neurohumoral blood pressure regulation in lead exposure.

    PubMed Central

    Boscolo, P; Carmignani, M

    1988-01-01

    Previous human studies demonstrated that lead exposure may modify the metabolism of catecholamines and of hormones controlled by the hypothalamo-pituitary axis and may affect the kallikrein-kinin system. This paper reports unpublished data on the plasma renin activity of lead-exposed workers; these results are in agreement with those of previous human and experimental studies suggesting that the synthesis or release of renin is increased after short and moderate exposure to inorganic lead and reduced whenever the exposure is prolonged. Previous experimental investigations demonstrated that lead may act on the cardiovascular system, with effects on the renin-angiotensin system, on the reactivity to stimulation of peripheral catecholaminergic receptors, on sympathetic and vagal tone, and on reactivity to the stimulation of baroreceptors. This paper reports the results of a study on male Sprague-Dawley rats that received 0, 15, 30, and 60 micrograms/mL of lead in drinking water for 18 months. Blood pressure was increased in the rats receiving 30 and 60 ppm of lead; cardiac inotropism was augmented only in those receiving the higher dose of the metal, and heart rate was not modified. Cardiovascular responses to agonists indicated that lead exposure affects the renin-angiotensin system and induces sympathetic hyperactivity by acting on central and peripheral sympathetic junctions increasing the responsiveness to stimulation of alpha 2-adrenoreceptors and by increasing the reactivity to stimulation of cardiac and vascular beta-adrenergic and dopaminergic receptors. The cAMP-dependent availability of Ca2+ for contractile mechanisms of the cardiovascular muscle cells was affected by lead. PMID:3060351

  10. Structural changes in the adult rat auditory system induced by brief postnatal noise exposure.

    PubMed

    Ouda, Ladislav; Burianová, Jana; Balogová, Zuzana; Lu, Hui Pin; Syka, Josef

    2016-01-01

    In previous studies (Grécová et al., Eur J Neurosci 29:1921-1930, 2009; Bures et al., Eur J Neurosci 32:155-164, 2010), we demonstrated that after an early postnatal short noise exposure (8 min 125 dB, day 14) changes in the frequency tuning curves as well as changes in the coding of sound intensity are present in the inferior colliculus (IC) of adult rats. In this study, we analyze on the basis of the Golgi-Cox method the morphology of neurons in the IC, the medial geniculate body (MGB) and the auditory cortex (AC) of 3-month-old Long-Evans rats exposed to identical noise at postnatal day 14 and compare the results to littermate controls. In rats exposed to noise as pups, the mean total length of the neuronal tree was found to be larger in the external cortex and the central nucleus of the IC and in the ventral division of the MGB. In addition, the numerical density of dendritic spines was decreased on the branches of neurons in the ventral division of the MGB in noise-exposed animals. In the AC, the mean total length of the apical dendritic segments of pyramidal neurons was significantly shorter in noise-exposed rats, however, only slight differences with respect to controls were observed in the length of basal dendrites of pyramidal cells as well as in the neuronal trees of AC non-pyramidal neurons. The numerical density of dendritic spines on the branches of pyramidal AC neurons was lower in exposed rats than in controls. These findings demonstrate that early postnatal short noise exposure can induce permanent changes in the development of neurons in the central auditory system, which apparently represent morphological correlates of functional plasticity.

  11. Identification of gene expression changes in postnatal rat foreskin after in utero anti-androgen exposure.

    PubMed

    Pike, Jack W; McDowell, Erin; McCahan, Suzanne M; Johnson, Kamin J

    2014-08-01

    In utero human phthalate exposure has been associated with male reproductive disorders in epidemiological studies, but discovering relationships is hindered by the lack of identifying markers. This study identified gene expression changes following in utero dibutyl phthalate (DBP) and flutamide exposures in Sprague-Dawley rat foreskin. Dams were exposed to 100 or 500mg/kg/day dibutyl phthalate or 5mg/kg/day flutamide from gestational days 16-20. Microarray analysis was performed on foreskin tissue from gestational day 20 and postnatal day 5. Expression changes found following DBP exposure were not present following flutamide treatment, indicating that expression changes were specific to DBP exposure and not caused by altered androgen signaling. Genes that were expressed at lower levels in tissue from pups treated with the low dose of DBP were reduced more in pups treated with the high dose of DBP, demonstrating a dose response effect of this compound. Changes in expression of Marcks, Pum1, Nupr1, and Penk caused by in utero phthalate exposure were confirmed by qRT-PCR. Changes in expression of these genes were maintained after birth and consequently their expression could serve as markers of chemical exposure and biological response.

  12. Postnatal Hyperoxia Exposure Durably Impairs Right Ventricular Function and Mitochondrial Biogenesis.

    PubMed

    Goss, Kara N; Kumari, Santosh; Tetri, Laura H; Barton, Greg; Braun, Rudolf K; Hacker, Timothy A; Eldridge, Marlowe W

    2017-05-01

    Prematurity complicates 12% of births, and young adults with a history of prematurity are at risk to develop right ventricular (RV) hypertrophy and impairment. The long-term risk for pulmonary vascular disease, as well as mechanisms of RV dysfunction and ventricular-vascular uncoupling after prematurity, remain poorly defined. Using an established model of prematurity-related lung disease, pups from timed-pregnant Sprague Dawley rats were randomized to normoxia or hyperoxia (fraction of inspired oxygen, 0.85) exposure for the first 14 days of life. After aging to 1 year in standard conditions, rats underwent hemodynamic assessment followed by tissue harvest for biochemical and histological evaluation. Aged hyperoxia-exposed rats developed significantly greater RV hypertrophy, associated with a 40% increase in RV systolic pressures. Although cardiac index was similar, hyperoxia-exposed rats demonstrated a reduced RV ejection fraction and significant RV-pulmonary vascular uncoupling. Hyperoxia-exposed RV cardiomyocytes demonstrated evidence of mitochondrial dysregulation and mitochondrial DNA damage, suggesting potential mitochondrial dysfunction as a cause of RV dysfunction. Aged rats exposed to postnatal hyperoxia recapitulate many features of young adults born prematurely, including increased RV hypertrophy and decreased RV ejection fraction. Our data suggest that postnatal hyperoxia exposure results in mitochondrial dysregulation that persists into adulthood with eventual RV dysfunction. Further evaluation of long-term mitochondrial function is warranted in both animal models of premature lung disease and in human adults who were born preterm.

  13. Early postnatal exposure to endosulfan interferes with the normal development of the male rat mammary gland.

    PubMed

    Altamirano, Gabriela A; Delconte, Melisa B; Gomez, Ayelen L; Alarcón, Ramiro; Bosquiazzo, Verónica L; Luque, Enrique H; Muñoz-de-Toro, Mónica; Kass, Laura

    2017-09-19

    Our aim was to evaluate whether postnatal exposure to endosulfan (ENDO) modifies mammary gland (MG) development in pre- and post-pubertal male rats. From postnatal day 1 (PND1) to PND7, male rats were injected subcutaneously every 48h with either corn oil (vehicle) or 600μg ENDO/kg.bw. On PND21 and PND60, MG and blood samples were collected. Estradiol (E2) and testosterone (T) serum levels, MG histology, collagen fiber organization, proliferation index, and estrogen (ESR1) and androgen receptor (AR) expressions were evaluated. On PND21, E2 and T levels were similar between groups, whereas MG area, perimeter, number of terminal end buds and ESR1 expression were increased in ENDO-exposed rats. These changes were associated with alveolar development and increased organized collagen in the stroma. On PND60, a higher proliferation index in ENDO-exposed rats was correlated with a more developed lobuloalveolar structure. Hyperplastic alveoli and, hyperplastic ducts surrounded by a dense stroma were also observed in this group. T levels and ESR1 expression were similar between groups, whereas E2 levels and AR expression were decreased in ENDO-exposed rats. The exposure to ENDO in the first week of life interferes with the normal development of the MG and induces pre-malignant lesions in post-pubertal male rats. Copyright © 2017 Elsevier B.V. All rights reserved.

  14. Prenatal neuroleptic exposure alters postnatal striatal cholinergic activity in the rat.

    PubMed

    Miller, J C; Friedhoff, A J

    1986-01-01

    Previous studies in our laboratory have shown that prenatal exposure to a neuroleptic during a critical period of gestation in the rat results in a marked deficit in the number of striatal dopamine-binding sites and in a diminution of dopamine agonist-induced stereotyped behavior. In the present studies, we examined the effect of prenatal neuroleptic exposure on biochemical parameters of cholinergic activity to determine whether the balance between striatal dopaminergic and cholinergic activity might be altered. The number of muscarinic cholinergic-binding sites and the specific activity of choline acetyltransferase were found to be significantly increased by prenatal treatment with the neuroleptics haloperidol or (+)-butaclamol. From the present studies and previous observations made in our laboratory, it is concluded that the ability of a neuroleptic to affect the number of muscarinic cholinergic receptors in postnatal life may be a result of the phenotypically undifferentiated state of the developing dopamine-binding site. Our findings of increased striatal cholinergic activity accompanied by a marked decrease in dopaminergic activity may have implications for an increased vulnerability to extrapyramidal motor disturbances during postnatal development.

  15. Lead exposure from aluminum cookware in Cameroon.

    PubMed

    Weidenhamer, Jeffrey D; Kobunski, Peter A; Kuepouo, Gilbert; Corbin, Rebecca W; Gottesfeld, Perry

    2014-10-15

    Blood lead levels have decreased following the removal of lead from gasoline in most of the world. However, numerous recent studies provide evidence that elevated blood lead levels persist in many low and middle-income countries around the world at much higher prevalence than in the more developed countries. One potential source of lead exposure that has not been widely investigated is the leaching of lead from artisanal aluminum cookware, which is commonly used in the developing world. Twenty-nine samples of aluminum cookware and utensils manufactured by local artisans in Cameroon were collected and analyzed for their potential to release lead during cooking. Source materials for this cookware included scrap metal such as engine parts, radiators, cans, and construction materials. The lead content of this cookware is relatively low (<1000 ppm by X-ray fluorescence), however significant amounts of lead, as well as aluminum and cadmium were released from many of the samples using dilute acetic acid extractions at boiling and ambient temperatures. Potential exposures to lead per serving were estimated to be as high as 260 μg, indicating that such cookware can pose a serious health hazard. We conclude that lead, aluminum and cadmium can migrate from this aluminum cookware during cooking and enter food at levels exceeding recommended public health guidelines. Our results support the need to regulate lead content of materials used to manufacture these pots. Artisanal aluminum cookware may be a major contributor to lead poisoning throughout the developing world. Testing of aluminum cookware in other developing countries is warranted.

  16. [Lead exposure among Kaohsiung traffic policemen].

    PubMed

    Chiang, H C; Chang, P Y

    1989-06-01

    In this recent century there has been increasing concern over the possible harmful effects of lead from automobile exhaust on human health. Traffic policemen are heavily exposed to automobile exhaust. In Kaohsiung city because of the increasing number of motor vehicles due to rapid urbanization and heavy traffic transportation from suburbs for export trade, traffic policemen have varied exposure experiences. The automobile exhaust of lead additive gasoline was found to be the major type of exposure for traffic policemen whose duties were in the city, while those who worked in the suburb areas were generally exposed to diesel oil exhaust gas. In this study 98 traffic policemen were studied with 118 students used as a control group. Subjects were evaluated for lead absorption and other metabolic effects. The average value of blood lead for traffic policemen (24.43 +/- 5.31 micrograms/dl) in the city of Kaohsiung was significantly (p less than 0.01) higher than for the control group (20.14 +/- 5.07 micrograms/dl). According to other bioindicators it was also found that the mean values of carboxyhemoglobin, urine lead and urine coproporphyrin were significantly higher in the traffic policemen group. Linear regression between blood lead and the duration of employment was also found in this study (R = -0.2447, p less than 0.05). The most reasonable explanations for these findings are the effects of lead emission from motor vehicles and the employment shifting system that cause this effect.

  17. Lead exposure and radiator repair work

    SciTech Connect

    Lussenhop, D.H.; Parker, D.L.; Barklind, A.; McJilton, C. )

    1989-11-01

    In 1986, the ambient air for lead in radiator repair shops in the Minneapolis-St. Paul metropolitan area exceeded the Occupational Safety and Health Administration (OSHA) action level in nine of 12 shops sampled by Minnesota OSHA. We therefore sought to determine the prevalence of lead exposure/toxicity in this industry. Thirty-five radiator shops were identified, 30 were visited, and 53 workers were studied. The mean blood lead level was 1.53 (range 0.24-2.80). Seventeen individuals had blood lead levels greater than or equal to 1.93 mumol/L (40 micrograms/dl). The mean zinc protoporphyrin level (ZPP) was 0.55 mumol/L (range 0.16-1.43). No single worksite or personal characteristic was a strong determinant of either blood lead or ZPP level.

  18. Lead exposure and radiator repair work.

    PubMed Central

    Lussenhop, D H; Parker, D L; Barklind, A; McJilton, C

    1989-01-01

    In 1986, the ambient air for lead in radiator repair shops in the Minneapolis-St. Paul metropolitan area exceeded the Occupational Safety and Health Administration (OSHA) action level in nine of 12 shops sampled by Minnesota OSHA. We therefore sought to determine the prevalence of lead exposure/toxicity in this industry. Thirty-five radiator shops were identified, 30 were visited, and 53 workers were studied. The mean blood lead level was 1.53 (range 0.24-2.80). Seventeen individuals had blood lead levels greater than or equal to 1.93 mumol/L (40 micrograms/dl). The mean zinc protoporphyrin level (ZPP) was 0.55 mumol/L (range 0.16-1.43). No single worksite or personal characteristic was a strong determinant of either blood lead or ZPP level. PMID:2817174

  19. Lead exposure and radiator repair work.

    PubMed

    Lussenhop, D H; Parker, D L; Barklind, A; McJilton, C

    1989-11-01

    In 1986, the ambient air for lead in radiator repair shops in the Minneapolis-St. Paul metropolitan area exceeded the Occupational Safety and Health Administration (OSHA) action level in nine of 12 shops sampled by Minnesota OSHA. We therefore sought to determine the prevalence of lead exposure/toxicity in this industry. Thirty-five radiator shops were identified, 30 were visited, and 53 workers were studied. The mean blood lead level was 1.53 (range 0.24-2.80). Seventeen individuals had blood lead levels greater than or equal to 1.93 mumol/L (40 micrograms/dl). The mean zinc protoporphyrin level (ZPP) was 0.55 mumol/L (range 0.16-1.43). No single worksite or personal characteristic was a strong determinant of either blood lead or ZPP level.

  20. Prenatal and post-natal exposure to antibiotics and risk of asthma in childhood.

    PubMed

    Metsälä, J; Lundqvist, A; Virta, L J; Kaila, M; Gissler, M; Virtanen, S M

    2015-01-01

    Evidence on the association between post-natal exposure to antibiotics and the development of asthma is extensive, but inconsistent and even less is known about prenatal exposure. The aim of this study was to examine the associations between prenatal and post-natal exposure to different antibiotics and the risk of childhood asthma in a population- and register-based nested case-control study. All children who were born in 1996-2004 in Finland and diagnosed with asthma by 2006 were identified from a national health register. For each case, one matched control was selected. Information on asthma diagnoses, purchased anti-asthmatic drugs and antibiotics as well as putative confounders was obtained from national health registries. The associations were analysed using conditional logistic regression for children diagnosed at the age of 3 years or later (n = 6 690 case-control pairs). Maternal use of any antibiotics during pregnancy was associated with an increased risk of asthma in the offspring [adjusted odds ratio (OR) = 1.31 (95% confidence interval (CI): 1.21-1.42)]. Several maternal specific antibiotics were associated with the risk of asthma, and the strongest association was observed for cephalosporins [OR = 1.46 (95% CI 1.30-1.64)]. Child's use of antibiotics during the first year of life was associated with an increased risk of asthma [OR = 1.60 (95% CI 1.48-1.73)]. Child's use of cephalosporins [OR = 1.79 (95% CI 1.59-2.01)], sulphonamides and trimethoprim [OR = 1.65 (95% CI 1.34-2.02)], macrolides [OR = 1.61 (95% CI 1.46-1.78)] and amoxicillin [OR = 1.46 (95% CI 1.35-1.58)] was associated with an increased risk of asthma. Both prenatal and post-natal exposure to antibiotics was associated with an increased risk of asthma. The potential role of adverse effects of antibiotics on the gut microbiota and the development of asthma should be further explored. © 2014 John Wiley & Sons Ltd.

  1. Lead exposure and growth in the early preschool child: A follow-up report from the Cincinnati Lead Study

    SciTech Connect

    Shukla, R.; Dietrich, K.N.; Bornschein, R.L.; Berger, O.; Hammond, P.B. )

    1991-11-01

    This report is a follow-up of an earlier study of the effects of low to moderate prenatal and postnatal lead exposure on children's growth in stature. Two hundred thirty-five subjects were assessed every 3 months for lead exposure (blood lead level) and stature (recumbent length) up to 33 months of age. Fetal lead exposure was indexed by maternal blood lead level during pregnancy. The adverse effects of lead on growth during the first year of life were reported previously. This analysis covers essentially the second and third years of life. The results indicate that mean blood lead level during this period was negatively associated with attained height at 33 months of age (P = .002). This association was, however, evidenced only among those children who had mean blood lead levels greater than the cohort median (greater than or equal to 10.77 micrograms/dL) during the 3- to 15-month interval. The results also suggest that the effect of lead exposure (both in utero as well as during the first year of life) are transient provided that subsequent exposure to lead is not excessive. It appears that maintaining an average blood lead level of 25 micrograms/dL or more during the second and third year of life was detrimental to the child's attained stature at 33 months of age. Approximately 15% of this cohort experienced these levels of lead exposure. Continued follow-up of this cohort will reveal whether these lead-related deficits persist and whether they continue to be dependent on the level of exposure in an earlier period.

  2. Lead exposure in Mexican radiator repair workers.

    PubMed

    Dykeman, Ronald; Aguilar-Madrid, Guadalupe; Smith, Tom; Juárez-Pérez, Cuauhtemoc Arturo; Piacitelli, Gregory M; Hu, Howard; Hernandez-Avila, Mauricio

    2002-03-01

    Lead exposure was investigated among 73 Mexican radiator repair workers (RRWs), 12 members of their family (4 children and 8 wives), and 36 working controls. RRWs were employed at 4 radiator repair shops in Mexico City and 27 shops in Cuernavaca and surrounding areas. Exposure was assessed directly through the use of personal air sampling and hand wipe samples. In addition, industrial hygiene inspections were performed and detailed questionnaires were administered. Blood lead levels were measured by graphite furnace atomic absorption spectroscopy (AAS). The mean (SD) values for blood lead of the RRWs, 35.5 (13.5) microg/dl, was significantly greater than the same values for the working controls, 13.6 (8.7) microg/dl; P < 001. After excluding a single outlier (247 microg/m(3)), air lead levels ranged from 0 to 99 microg/m(3) with a mean (SD) value of 19 (23) microg/m(3) (median = 7.9 microg/m(3)). In a final multivariate regression model of elevated blood lead levels, the strongest predictors were smoking (vs. non-smoking), the number of radiators repaired per day on average, and the use (vs. non-use) of a uniform while at work, which were associated with blood lead elevations of 11.4 microg/dl, 1.95 microg/dl/radiator/day, and 16.4 microg/dl, respectively (all P <.05). Uniform use was probably a risk factor because they were not laundered regularly and consequently served as reservoir of contamination on which RRWs frequently wiped their hands. Lead exposure is a significant problem of radiator repair work, a small industry that is abundant in Mexico and other developing countries. Copyright 2002 Wiley-Liss, Inc.

  3. Postnatal cerebral infection leading to hemiplegic cerebral palsy: clinical description of 13 children in Stockholm, Sweden.

    PubMed

    Tillberg, Elsa; Radell, Ulrika; Amark, P

    2008-01-01

    The aim of this research was to estimate the prevalence of postnatal cerebral infection leading to hemiplegic cerebral palsy (CP) in Stockholm County and to describe the motor impairments, associated impairments and involvement of the non hemiplegic side. Children with hemiplegic CP subsequent to a cerebral infection in the perinatal period up to the age of seven years were identified. The assessments of child psychologists and speech therapists and EEG-studies, CT-scan or MRI of the brain were extracted from the children's files. Thirteen children, with a mean age of 9.5 years, participated. The prevalence was 0.03/1000. Nine children suffered from mental retardation, seven took antiepileptic drugs and six had bilateral radiological anomalies. The non-hemiplegic side was involved in six of the children. Cerebral infection at an early age can cause hemiplegic CP with a high frequency of associated impairments and with involvement of the non-hemiplegic side. The infectious origin probably gives rise to a more widespread brain injury.

  4. Effect of Lycopersicon esculentum extract on apoptosis in the rat cerebellum, following prenatal and postnatal exposure to an electromagnetic field.

    PubMed

    Köktürk, Sibel; Yardimoglu, Melda; Celikozlu, Saadet D; Dolanbay, Elif Gelenli; Cimbiz, Ali

    2013-07-01

    The expansion of mobile phone technology has raised concerns regarding the effect of 900-MHz electromagnetic field (EMF) exposure on the central nervous system. At present, the developing human brain is regularly exposed to mobile telephones, pre- and postnatally. Several studies have demonstrated the acute effects of EMF exposure during pre- or postnatal periods; however, the chronic effects of EMF exposure are less understood. Thus, the aim of the present study was to determine the chronic effects of EMF on the pre- and postnatal rat cerebellum. The control group was maintained in the same conditions as the experimental groups, without the exposure to EMF. In the EMF1 group, the rats were exposed to EMF during pre- and postnatal periods (until postnatal day 80). In the EMF2 group, the rats were also exposed to EMF pre- and postnatally; in addition, however, they were provided with a daily oral supplementation of Lycopersicon esculentum extract (∼2 g/kg). The number of caspase-3-labeled Purkinje neurons and granule cells present in the rats in the control and experimental groups were then counted. The neurodegenerative changes were studied using cresyl violet staining, and these changes were evaluated. In comparison with the control animals, the EMF1 group demonstrated a significant increase in the number of caspase-3-labeled Purkinje neurons and granule cells present in the cerebellum (P<0.001). However, in comparison with the EMF1 group, the EMF2 group exhibited significantly fewer caspase-3-labeled Purkinje neurons and granule cells in the cerebellum. In the EMF1 group, the Purkinje neurons were revealed to have undergone dark neuron degenerative changes. However, the presence of dark Purkinje neurons was reduced in the EMF2 group, compared with the EMF1 group. The results indicated that apoptosis and neurodegeneration in rats exposed to EMF during pre- and postnatal periods may be reduced with Lycopersicon esculentum extract therapy.

  5. Effect of Lycopersicon esculentum extract on apoptosis in the rat cerebellum, following prenatal and postnatal exposure to an electromagnetic field

    PubMed Central

    KÖKTÜRK, SIBEL; YARDIMOGLU, MELDA; CELIKOZLU, SAADET D.; DOLANBAY, ELIF GELENLI; CIMBIZ, ALI

    2013-01-01

    The expansion of mobile phone technology has raised concerns regarding the effect of 900-MHz electromagnetic field (EMF) exposure on the central nervous system. At present, the developing human brain is regularly exposed to mobile telephones, pre- and postnatally. Several studies have demonstrated the acute effects of EMF exposure during pre- or postnatal periods; however, the chronic effects of EMF exposure are less understood. Thus, the aim of the present study was to determine the chronic effects of EMF on the pre- and postnatal rat cerebellum. The control group was maintained in the same conditions as the experimental groups, without the exposure to EMF. In the EMF1 group, the rats were exposed to EMF during pre- and postnatal periods (until postnatal day 80). In the EMF2 group, the rats were also exposed to EMF pre- and postnatally; in addition, however, they were provided with a daily oral supplementation of Lycopersicon esculentum extract (∼2 g/kg). The number of caspase-3-labeled Purkinje neurons and granule cells present in the rats in the control and experimental groups were then counted. The neurodegenerative changes were studied using cresyl violet staining, and these changes were evaluated. In comparison with the control animals, the EMF1 group demonstrated a significant increase in the number of caspase-3-labeled Purkinje neurons and granule cells present in the cerebellum (P<0.001). However, in comparison with the EMF1 group, the EMF2 group exhibited significantly fewer caspase-3-labeled Purkinje neurons and granule cells in the cerebellum. In the EMF1 group, the Purkinje neurons were revealed to have undergone dark neuron degenerative changes. However, the presence of dark Purkinje neurons was reduced in the EMF2 group, compared with the EMF1 group. The results indicated that apoptosis and neurodegeneration in rats exposed to EMF during pre- and postnatal periods may be reduced with Lycopersicon esculentum extract therapy. PMID:23935717

  6. [Lead exposure of people living in a lead high exposure area from local diet].

    PubMed

    Zhou, Yong; He, Liping; Huang, Xiao; He, Junshan

    2011-11-01

    To study the lead exposure of people living in a lead high exposure area from local diet, and to assess its health risks. Thirty five subjects were selected by random from a mining area and another 30 subjects were selected from a non-polluted area. The exposure of lead was estimated by the content of lead in drinking water and vegetables, and health risks was estimated by the levels of lead in blood and urine. The content of lead in drinking water and vegetables in the mining area was 20.6 microg/L and 1.61mg/kg (geometric mean) respectively, which were higher than that in the unpolluted area (6.0 microg/L and 0.56 mg/kg, geometric mean) (P < 0.01). The daily lead exposure of male and female inhabitants in the mining area from diet was 16.88 microg/kg and 16.09 microg/kg respectively, which was higher than that in the unpolluted area (P < 0.01), but the sex difference was not significant statistically (P > 0.05). Blood lead and urine lead of inhabitants in the mining-area were higher than those in the unpolluted area. The health risks for male and female inhabitants in the mining area were 4.73 and 4.51. The health risks of lead exposure caused by diet (drinking water and food) were relatively high in the mining area.

  7. Prenatal Exposure to Paint Thinner Alters Postnatal Development and Behavior in Mice

    PubMed Central

    Malloul, Hanaa; Mahdani, Ferdaousse M.; Bennis, Mohammed; Ba-M’hamed, Saadia

    2017-01-01

    Occupational exposure and sniffing of volatile organic solvents continue to be a worldwide health problem, raising the risk for teratogenic sequelae of maternal inhalant abuse. Real life exposures usually involve simultaneous exposures to multiple solvents, and almost all the abused solvents contain a mixture of two or more different volatile compounds. However, several studies examined the teratogenicity due to industrial exposure to a single volatile solvent but investigating the teratogenic potential of complex chemical mixture such as thinner remains unexplored. This study was undertaken to evaluate developmental neurotoxicity of paint thinner using a mouse model. Mated female mice (N = 21) were, therefore, exposed to repeated and brief inhalation episodes of 0, 300 or 600 ppm of thinner during the entire period of pregnancy. Females weigh was recorded and their standard fertility and reproductive parameters were assessed. After birth postnatal day 1 (PND1), offspring (N = 88) length and body weight were measured in a daily basis. At PND5, the pups were assessed for their postnatal growth, physical maturation, reflex development, neuromotor abilities, sensory function, activity level, anxiety, depression, learning and memory functions. At adulthood, structural changes of the hippocampus were examined by estimating the total volume of the dentate gyrus. Except one case of thinner induced abortion at the higher dose, our results showed that the prenatal exposure to the solvent did not cause any maternal toxicity or decrease in the viability of the offspring. Therefore, a lower birth weight, decrease in the litter size and delayed reflexes ontogeny were registered in prenatally exposed offspring to both 300 ppm and 600 ppm of thinner. In addition, prenatally exposure to thinner resulted in increased anxiolytic- and depression-like behaviors. In contrast, impaired learning and memory functions and decreased hippocampal dentate gyrus volume were revealed only in the

  8. Neurodevelopment in Early Childhood Affected by Prenatal Lead Exposure and Iron Intake.

    PubMed

    Shah-Kulkarni, Surabhi; Ha, Mina; Kim, Byung-Mi; Kim, Eunjeong; Hong, Yun-Chul; Park, Hyesook; Kim, Yangho; Kim, Bung-Nyun; Chang, Namsoo; Oh, Se-Young; Kim, Young Ju; Kimʼs, Young Ju; Lee, Boeun; Ha, Eun-Hee

    2016-01-01

    No safe threshold level of lead exposure in children has been recognized. Also, the information on shielding effect of maternal dietary iron intake during pregnancy on the adverse effects of prenatal lead exposure on children's postnatal neurocognitive development is very limited. We examined the association of prenatal lead exposure and neurodevelopment in children at 6, 12, 24, and 36 months and the protective action of maternal dietary iron intake against the impact of lead exposure. The study participants comprise 965 pregnant women and their subsequent offspring of the total participants enrolled in the Mothers and Children's environmental health study: a prospective birth cohort study. Generalized linear model and linear mixed model analysis were performed to analyze the effect of prenatal lead exposure and mother's dietary iron intake on children's cognitive development at 6, 12, 24, and 36 months. Maternal late pregnancy lead was marginally associated with deficits in mental development index (MDI) of children at 6 months. Mothers having less than 75th percentile of dietary iron intake during pregnancy showed significant increase in the harmful effect of late pregnancy lead exposure on MDI at 6 months. Linear mixed model analyses showed the significant detrimental effect of prenatal lead exposure in late pregnancy on cognitive development up to 36 months in children of mothers having less dietary iron intake during pregnancy. Thus, our findings imply importance to reduce prenatal lead exposure and have adequate iron intake for better neurodevelopment in children.

  9. Adolescent initiation of licit and illicit substance use: Impact of intrauterine exposures and post-natal exposure to violence.

    PubMed

    Frank, Deborah A; Rose-Jacobs, Ruth; Crooks, Denise; Cabral, Howard J; Gerteis, Jessie; Hacker, Karen A; Martin, Brett; Weinstein, Zohar B; Heeren, Timothy

    2011-01-01

    Whether intrauterine exposures to alcohol, tobacco, marijuana, or cocaine predispose offspring to substance use in adolescence has not been established. We followed a sample of 149 primarily African American/African Caribbean, urban adolescents, recruited at term birth, until age 16 to investigate intrauterine cocaine exposure (IUCE). We found that in Kaplan-Meier analyses higher levels of IUCE were associated with a greater likelihood of initiation of any substance (licit or illicit), as well as marijuana and alcohol specifically. Adolescent initiation of other illicit drugs and cigarettes were analyzed only in the "any" summary variable since they were used too infrequently to analyze as individual outcomes. In Cox proportional hazard models controlling for intrauterine exposure to alcohol, tobacco, and marijuana and demographic and post-natal covariates, those who experienced heavier IUCE had a greater likelihood of initiation of any substance, and those with lighter intrauterine marijuana exposure had a greater likelihood of initiation of any substance as well as of marijuana specifically. Time-dependent higher levels of exposure to violence between ages of 8 and 16 were also robustly associated with initiation of any licit or illicit substance, and of marijuana, and alcohol particularly.

  10. Effects of postnatal alcohol exposure on hippocampal gene expression and learning in adult mice.

    PubMed

    Lee, Dong Hoon; Moon, Jihye; Ryu, Jinhyun; Jeong, Joo Yeon; Roh, Gu Seob; Kim, Hyun Joon; Cho, Gyeong Jae; Choi, Wan Sung; Kang, Sang Soo

    2016-04-28

    Fetal alcohol syndrome (FAS) is a condition resulting from excessive drinking by pregnant women. Symptoms of FAS include abnormal facial features, stunted growth, intellectual deficits and attentional dysfunction. Many studies have investigated FAS, but its underlying mechanisms remain unknown. This study evaluated the relationship between alcohol exposure during the synaptogenesis period in postnatal mice and subsequent cognitive function in adult mice. We delivered two injections, separated by 2 h, of ethanol (3 g/kg, ethanol/saline, 20% v/v) to ICR mice on postnatal day 7. After 10 weeks, we conducted a behavioral test, sacrificed the animals, harvested brain tissue and analyzed hippocampal gene expression using a microarray. In ethanol-treated mice, there was a reduction in brain size and decreased neuronal cell number in the cortex, and also cognitive impairment. cDNA microarray results indicated that 1,548 genes showed a > 2-fold decrease in expression relative to control, whereas 974 genes showed a > 2-fold increase in expression relative to control. Many of these genes were related to signal transduction, synaptogenesis and cell membrane formation, which are highlighted in our findings.

  11. Brief postnatal exposure to phenobarbital impairs passive avoidance learning and sensorimotor gating in rats.

    PubMed

    Gutherz, Samuel B; Kulick, Catherine V; Soper, Colin; Kondratyev, Alexei; Gale, Karen; Forcelli, Patrick A

    2014-08-01

    Phenobarbital is the most commonly utilized drug for the treatment of neonatal seizures. However, mounting preclinical evidence suggests that even brief exposure to phenobarbital in the neonatal period can induce neuronal apoptosis, alterations in synaptic development, and long-lasting changes in behavioral functions. In the present report, we treated neonatal rat pups with phenobarbital and evaluated behavior in adulthood. Pups were treated initially with a loading dose (80 mg/kg) on postnatal day (P)7 and with a lower dose (40 mg/kg) on P8 and P9. We examined sensorimotor gating (prepulse inhibition), passive avoidance, and conditioned place preference for cocaine when the animals reached adulthood. Consistent with our previous reports, we found that three days of neonatal exposure to phenobarbital significantly impaired prepulse inhibition compared with vehicle-exposed control animals. Using a step-though passive avoidance paradigm, we found that animals exposed to phenobarbital as neonates and tested as adults showed significant deficits in passive avoidance retention compared with matched controls, indicating impairment in associative memory and/or recall. Finally, we examined place preference conditioning in response to cocaine. Phenobarbital exposure did not alter the normal conditioned place preference associated with cocaine exposure. Our findings expand the profile of behavioral toxicity induced by phenobarbital. Copyright © 2014 Elsevier Inc. All rights reserved.

  12. Brief postnatal exposure to phenobarbital impairs passive-avoidance learning and sensorimotor gating in rats

    PubMed Central

    Gutherz, Samuel B.; Kulick, Catherine V.; Soper, Colin; Kondratyev, Alexei; Gale, Karen; Forcelli, Patrick A.

    2014-01-01

    Phenobarbital is the most commonly utilized drug for the treatment of neonatal seizures. However, mounting preclinical evidence suggests that even brief exposure to phenobarbital in the neonatal period can induce neuronal apoptosis, alterations in synaptic development, and long-lasting changes in behavioral functions. In the present report, we treated neonatal rat pups with phenobarbital and evaluated behavior in adulthood. Pups were treated initially with a loading dose (80mg/kg) on postnatal day (P)7 and with a lower dose (40 mg/kg) on P8 and P9. We examined sensorimotor gating (prepulse inhibition), passive avoidance, and conditioned place preference to cocaine when the animals reached adulthood. Consistent with our previous reports, we found that three days of neonatal exposure to phenobarbital significantly impaired prepulse inhibition as compared to vehicle-exposed control animals. Using a step-though passive avoidance paradigm, we found that animals exposed to phenobarbital as neonates and tested as adults showed significant deficits in passive avoidance retention as compared to matched controls, indicating impairment in associative memory and/or recall. Finally, we examined place preference conditioning in response to cocaine. Phenobarbital exposure did not alter the normal conditioned place preference associated with cocaine exposure. Our findings expand the profile of behavioral toxicity induced by phenobarbital. PMID:25112558

  13. Exposure to lead exacerbates dental fluorosis.

    PubMed

    Leite, G A S; Sawan, R M M; Teófilo, J M; Porto, I M; Sousa, F B; Gerlach, R F

    2011-07-01

    Our aim was to test the hypothesis that co-exposure to lead and fluoride alter the severity of enamel fluorosis. Wistar rats were allocated in four groups: control, and 3 groups that received water containing 100 ppm of fluoride (F), 30 ppm of lead (Pb), or 100 ppm of F and 30 ppm of Pb (F+Pb) from the beginning of gestation. Enamel analysis and F and Pb determinations in enamel, dentine, and bone were performed in 81-day-old animals. Fluorosis was quantified using a new fluorosis index based on the identification of incisor enamel defects (white bands and white islets, representing hypomineralization, and cavities) weighted according to their severity and quantity. Hypomineralization was validated histopathologically by polarizing microscopy and microradiography. Scores were given by two blinded calibrated examiners (intra and interexaminer kappa values were 0.8 and 0.86, respectively). The control and the Pb groups presented normal enamel. The F+Pb group presented more severe enamel defects compared with the F group (P<0.0001). This study shows that lead exacerbates dental fluorosis in rodents, suggesting that co-exposure to lead may affect the degree of fluorosis. Copyright © 2011 Elsevier Ltd. All rights reserved.

  14. Altered behavioral development in Nrf2 knockout mice following early postnatal exposure to valproic acid

    PubMed Central

    Furnari, Melody A.; Saw, Constance Lay-Lay; Kong, Ah-Ng; Wagner, George C

    2015-01-01

    Early exposure to valproic acid results in autism-like neural and behavioral deficits in humans and other animals through oxidative stress-induced neural damage. In the present study, valproic acid was administered to genetically altered mice lacking the Nrf2 (nuclear factor-erythroid 2 related factor 2) gene on postnatal day 14 (P14). Nrf2 is a transcription factor that induces genes that protect against oxidative stress. It was found that valproic acid-treated Nrf2 knockout mice were less active in open field activity chambers, less successful on the rotorod, and had deficits in learning and memory in the Morris water maze compared to the valproic acid-treated wild type mice. Given these results, it appears that Nrf2 knockout mice were more sensitive to the neural damage caused by valproic acid administered during early development. PMID:25454122

  15. Effect of early postnatal exposure to polychlorinated biphenyls (PCBs) on fertility in male rats

    SciTech Connect

    Sager, D.B.; Shih-Schroeder, W.; Girard, D.

    1987-06-01

    Males exposed to PCBs during lactation exhibited reduced fertility, i.e., reduced incidence of implantation in normal females mated to experimental males. However, a reduced weight gain during the time of treatment in the pups exposed to the higher doses of PCBs was also observed. After treatment, weight gain was comparable or greater in the experimental pups and by the time of mating and autopsy, body weights in all groups were comparable. The present experiments were designed 1) to determine if the early reduced weight gain (previously observed) has any influence on fertility, and 2) to investigate the effect of early postnatal exposure to PCBs on sperm counts and the ability of the sperm to support normal development.

  16. Altered behavioral development in Nrf2 knockout mice following early postnatal exposure to valproic acid.

    PubMed

    Furnari, Melody A; Saw, Constance Lay-Lay; Kong, Ah-Ng; Wagner, George C

    2014-10-01

    Early exposure to valproic acid results in autism-like neural and behavioral deficits in humans and other animals through oxidative stress-induced neural damage. In the present study, valproic acid was administered to genetically altered mice lacking the Nrf2 (nuclear factor-erythroid 2 related factor 2) gene on postnatal day 14 (P14). Nrf2 is a transcription factor that induces genes that protect against oxidative stress. It was found that valproic acid-treated Nrf2 knockout mice were less active in open field activity chambers, less successful on the rotorod, and had deficits in learning and memory in the Morris water maze compared to the valproic acid-treated wild type mice. Given these results, it appears that Nrf2 knockout mice were more sensitive to the neural damage caused by valproic acid administered during early development. Copyright © 2014 Elsevier Inc. All rights reserved.

  17. The Australian Work Exposures Study: Occupational Exposure to Lead and Lead Compounds.

    PubMed

    Driscoll, Timothy R; Carey, Renee N; Peters, Susan; Glass, Deborah C; Benke, Geza; Reid, Alison; Fritschi, Lin

    2016-01-01

    The aims of this study were to produce a population-based estimate of the prevalence of work-related exposure to lead and its compounds, to identify the main circumstances of exposures, and to collect information on the use of workplace control measures designed to decrease those exposures. Data came from the Australian Workplace Exposures Study, a nationwide telephone survey which investigated the current prevalence and circumstances of work-related exposure to 38 known or suspected carcinogens, including lead, among Australian workers aged 18-65 years. Using the web-based tool, OccIDEAS, semi-quantitative information was collected about exposures in the current job held by the respondent. Questions were addressed primarily at tasks undertaken rather than about self-reported exposures. A total of 307 (6.1%) of the 4993 included respondents were identified as probably being exposed to lead in the course of their work. Of these, almost all (96%) were male; about half worked in trades and technician-related occupations, and about half worked in the construction industry. The main tasks associated with probable exposures were, in decreasing order: soldering; sanding and burning off paint while painting old houses, ships, or bridges; plumbing work; cleaning up or sifting through the remains of a fire; radiator-repair work; machining metals or alloys containing lead; mining; welding leaded steel; and working at or using indoor firing ranges. Where information on control measures was available, inconsistent use was reported. Applied to the Australian working population, approximately 6.3% [95% confidence interval (CI) = 5.6-7.0] of all workers (i.e. 631000, 95% CI 566000-704000 workers) were estimated to have probable occupational exposure to lead. Lead remains an important exposure in many different occupational circumstances in Australia and probably other developed countries. This information can be used to support decisions on priorities for intervention and control

  18. Cannabinoid-opioid interactions in drug discrimination and self-administration: effect of maternal, postnatal, adolescent and adult exposure to the drugs.

    PubMed

    Spano, M S; Fadda, P; Fratta, W; Fattore, L

    2010-04-01

    Cannabinoids and opioids are known to strictly interact in many physiological and pathological functions, including addiction. The endogenous opioid system is significantly influenced by maternal or perinatal cannabinoid exposure, major changes concerning operant behaviour in adult animals. Copious data suggests that adolescence is also a particularly sensitive period of life not only for the initiation of abusing illicit drugs, but also for the effects that these drugs exert on the neural circuitries leading to drug dependence. This paper examines the role played by the age of drug exposure in the susceptibility to discriminative and reinforcing effects of both cannabinoids and opioids. We first revisited evidence of alterations in the density and functionality of mu-opioid and CB1 cannabinoid receptors in reward-related brain regions caused by either maternal, postnatal, adolescent or adult exposure to opioids and cannabinoids. Then, we reviewed behavioural evidence of the long-term consequences of exposure to opioids and cannabinoids during gestation, postnatal period, adolescence or adulthood, focusing mostly on drug discrimination and self-administration studies. Overall, evidence confirms a neurobiological convergence of the cannabinoid and opioid systems that is manifest at both receptor and behavioural levels. Although discrepant results have been reported, some data support the gateway hypothesis that adolescent cannabis exposure contributes to greater opioid intake in adulthood. However, it should be kept into consideration that in humans genetic, environmental, and social factors could influence the direct neurobiological effects of early cannabis exposure to the progression to adult drug abuse.

  19. Effect of prenatal and neonatal exposure to lead on gonadotropin receptors and steroidogenesis in rat ovaries

    SciTech Connect

    Wiebe, J.P.; Barr, K.J.; Buckingham, K.D.

    1988-01-01

    Sprague-Dawley rats were treated with lead chloride (20 or 200 ppm) or sodium chloride (controls) in their drinking water, either prior to pregnancy or during pregnancy and lactation, and female offspring were examined at weaning (21 d) or at 150 d. Other female rats were treated from d 21 to 35. Tissue (blood, kidney, bone) lead levels, body, ovary, and uterus weights, ovarian steroidogenesis, and gonadotropin (luteinizing hormone and follicle-stimulating hormone) levels, and gonadotropin-receptor binding were determined. Prenatal and/or postnatal exposure to lead at these levels (20 and 200 ppm) did not affect tissue weights but did cause a significant decrease in gonadotropin-receptor binding in the prepubertal, pubertal and adult females. Conversion of progesterone to androstenedione and dihydrotestosterone was significantly decreased in 21-d-old rats; in 150-d-old females, the prenatal and/or postnatal exposure to lead resulted in significantly increased conversion to the 5-alpha-reduced steroid, normally high during puberty. The results demonstrate that lead exposure prior to mating may affect gonadotropin-receptor binding in the offspring and that lead exposure (in utero, via mother's milk, or post weaning) may significantly alter steroid production and gonadotropin binding in ovaries of the prepubertal, pubertal, and adult female.

  20. Prenatal alcohol exposure increases postnatal acceptability of nicotine odor and taste in adolescent rats.

    PubMed

    Mantella, Nicole M; Youngentob, Steven L

    2014-01-01

    Human studies indicate that alcohol exposure during gestation not only increases the chance for later alcohol abuse, but also nicotine dependence. The flavor attributes of both alcohol and nicotine can be important determinants of their initial acceptance and they both share the component chemosensory qualities of an aversive odor, bitter taste and oral irritation. There is a growing body of evidence demonstrating epigenetic chemosensory mechanisms through which fetal alcohol exposure increases adolescent alcohol acceptance, in part, by decreasing the aversion to alcohol's bitter and oral irritation qualities, as well as its odor. Given that alcohol and nicotine have noteworthy chemosensory qualities in common, we investigated whether fetal exposure to alcohol increased the acceptability of nicotine's odor and taste in adolescent rats. Study rats were alcohol-exposed during fetal development via the dams' liquid diet. Control animals received ad lib access to an iso-caloric, iso-nutritive diet throughout gestation. Odorant-induced innate behavioral responses to nicotine odor (Experiment 1) or orosensory-mediated responses to nicotine solutions (Experiment 2) were obtained, using whole-body plethysmography and brief access lick tests, respectively. Compared to controls, rats exposed to fetal alcohol showed an enhanced nicotine odor response that was paralleled by increased oral acceptability of nicotine. Given the common aversive component qualities imbued in the flavor profiles of both drugs, our findings demonstrate that like postnatal alcohol avidity, fetal alcohol exposure also influences nicotine acceptance, at a minimum, by decreasing the aversion of both its smell and taste. Moreover, they highlight potential chemosensory-based mechanism(s) by which fetal alcohol exposure increases the later initial risk for nicotine use, thereby contributing to the co-morbid expression with enhanced alcohol avidity. Where common chemosensory mechanisms are at play, our

  1. Prenatal Alcohol Exposure Increases Postnatal Acceptability of Nicotine Odor and Taste in Adolescent Rats

    PubMed Central

    Mantella, Nicole M.; Youngentob, Steven L.

    2014-01-01

    Human studies indicate that alcohol exposure during gestation not only increases the chance for later alcohol abuse, but also nicotine dependence. The flavor attributes of both alcohol and nicotine can be important determinants of their initial acceptance and they both share the component chemosensory qualities of an aversive odor, bitter taste and oral irritation. There is a growing body of evidence demonstrating epigenetic chemosensory mechanisms through which fetal alcohol exposure increases adolescent alcohol acceptance, in part, by decreasing the aversion to alcohol's bitter and oral irritation qualities, as well as its odor. Given that alcohol and nicotine have noteworthy chemosensory qualities in common, we investigated whether fetal exposure to alcohol increased the acceptability of nicotine's odor and taste in adolescent rats. Study rats were alcohol-exposed during fetal development via the dams' liquid diet. Control animals received ad lib access to an iso-caloric, iso-nutritive diet throughout gestation. Odorant-induced innate behavioral responses to nicotine odor (Experiment 1) or orosensory-mediated responses to nicotine solutions (Experiment 2) were obtained, using whole-body plethysmography and brief access lick tests, respectively. Compared to controls, rats exposed to fetal alcohol showed an enhanced nicotine odor response that was paralleled by increased oral acceptability of nicotine. Given the common aversive component qualities imbued in the flavor profiles of both drugs, our findings demonstrate that like postnatal alcohol avidity, fetal alcohol exposure also influences nicotine acceptance, at a minimum, by decreasing the aversion of both its smell and taste. Moreover, they highlight potential chemosensory-based mechanism(s) by which fetal alcohol exposure increases the later initial risk for nicotine use, thereby contributing to the co-morbid expression with enhanced alcohol avidity. Where common chemosensory mechanisms are at play, our

  2. Prenatal and postnatal tobacco smoke exposure and development of insulin resistance in 10 year old children.

    PubMed

    Thiering, Elisabeth; Brüske, Irene; Kratzsch, Jürgen; Thiery, Joachim; Sausenthaler, Stefanie; Meisinger, Christa; Koletzko, Sibylle; Bauer, Carl-Peter; Schaaf, Beate; von Berg, Andrea; Berdel, Dietrich; Lehmann, Irina; Herbarth, Olf; Krämer, Ursula; Wichmann, H Erich; Heinrich, Joachim

    2011-09-01

    In this study, we evaluated the association between prenatal and postnatal exposure to environmental tobacco smoke and the development of insulin resistance in 10 year old children. Fasting blood samples were collected from 470 children participating in two prospective birth cohorts. Of those 276 were selected population based and enriched with 194 children exceeding the 85th percentile of body mass index in this age group. Children already having diabetes type 1 or 2 at the age of 10 years were excluded. Fasting blood insulin and glucose levels and calculated HOMA index for insulin resistance assessment were analysed using generalised additive models. Potential confounders were adjusted for. Insulin resistance was increased by 24% in children frequently exposed to environmental tobacco smoke during childhood (MR(adj) = 1.24, p = 0.001), while glucose levels were not. Exclusion of prenatally exposed children did not attenuate the association (MR(adj) = 1.25, p = 0.006). After stratification, the effect sizes were identical within overweight children and the population based sample of children. Insulin resistance and fasting insulin levels were increasing with increasing numbers of cigarettes smoked in children's home. Maternal smoking during the third trimester of pregnancy increased children's insulin levels (MR(adj) = 1.19, p = 0.037), and even more so, if children were exclusively breastfed after birth (MR(adj) = 1.31, p = 0.016). Increased mean ratios were found for smoking of a third person in addition to maternal smoking. Positive dose-dependent associations and independent effects of postnatal exposure suggest involvement of environmental tobacco smoke in the risk for development of insulin resistance in children.

  3. Effects of low level lead exposure on associative learning and memory in the rat: Influences of sex and developmental timing of exposure.

    PubMed

    Anderson, D W; Mettil, W; Schneider, J S

    2016-03-30

    Lead (Pb) exposure during development impairs a variety of cognitive, behavioral and neurochemical processes resulting in deficits in learning, memory, attention, impulsivity and executive function. Numerous studies have attempted to model this effect of Pb in rodents, with the majority of studies focusing on hippocampus-associated spatial learning and memory processes. Using a different paradigm, trace fear conditioning, a process requiring coordinated integration of both the medial prefrontal cortex and the hippocampus, we have assessed the effects of Pb exposure on associative learning and memory. The present study examined both female and male long evans rats exposed to three environmentally relevant levels of Pb (150 ppm, 375 ppm and 750 ppm) during different developmental periods: perinatal (PERI; gestation-postnatal day 21), early postnatal (EPN; postnatal days 1-21) and late postnatal (LPN; postnatal days 1-55). Testing began at postnatal day 55 and consisted of a single day of acquisition training, and three post training time points (1, 2 and 10 days) to assess memory consolidation and recall. All animals, regardless of sex, developmental window or level of Pb-exposure, successfully acquired conditioned-unconditioned stimulus association during training. However, there were significant effects of Pb-exposure on consolidation and memory recall at days 1-10 post training. In females, EPN and LPN exposure to 150 ppm Pb (but not PERI exposure) significantly impaired recall. In contrast, only PERI 150 ppm and 750 ppm-exposed males had significant recall deficits. These data suggest a complex interaction between sex, developmental window of exposure and Pb-exposure level on consolidation and recall of associative memories. Copyright © 2016 Elsevier Ireland Ltd. All rights reserved.

  4. Monitoring wild bird populations for lead exposure

    SciTech Connect

    Scheuhammer, A.M. )

    1989-07-01

    Delta-aminolevulinic acid dehydratase (ALA-d), an enzyme in the heme biosynthetic pathway is extremely sensitive to inhibition by lead (Pb). I evaluated the erythrocyte ALA-d activity ratio (the ratio between the fully restored enzyme activity and that measured without removing any inhibitory influence that might be present) as an indicator of Pb exposure in free-living birds. In the absence of elevated Pb exposure, birds, had comparable ALA-d activity ratios regardless of species, geographical location, or time of year sampled. The normal range of ratios for free-living species was similar to that for aviary-raised birds (1.0-1.3). Individuals with enzyme inhibition were readily identified. In blood collected from free-living mallards (Anas platyrhynchos), ALA-d activity ratios were better correlated with blood-Pb than were blood-protoporphyrin (PP) concentrations. At least 9.5% of mallards with blood-Pb>80 {mu}g/dL did not have elevated PP levels. Underestimation of Pb exposure did not occur using the ALA-d activity ratio method. The ALA-d activity ratio was as accurate as blood-Pb measurements for monitoring the relative degree of recent Pb exposure in the wild bird populations studied. Unlike blood-Pb analyses, ALA-d determinations do not require exposure in the wild bird populations studied. Unlike blood-Pb analyses, ALA-d determinations do not require exposure in the wild bird populations studied. Unlike blood-Pb analyses, ALA-d determinations do not require sophisticated and expensive instrumentation, and assays can be performed efficiently with minimal training.

  5. Early postnatal rat ventricle resection leads to long‐term preserved cardiac function despite tissue hypoperfusion

    PubMed Central

    Zogbi, Camila; Saturi de Carvalho, Ana E. T.; Nakamuta, Juliana S.; Caceres, Viviane de M.; Prando, Silvana; Giorgi, Maria C. P.; Rochitte, Carlos E.; Meneghetti, Jose C.; Krieger, Jose E.

    2014-01-01

    Abstract One‐day‐old mice display a brief capacity for heart regeneration after apex resection. We sought to examine this response in a different model and to determine the impact of this early process on long‐term tissue perfusion and overall cardiac function in response to stress. Apical resection of postnatal rats at day 1 (P1) and 7 (P7) rendered 18 ± 1.0% and 16 ± 1.3% loss of cardiac area estimated by magnetic resonance imaging (MRI), respectively (P > 0.05). P1 was associated with evidence of cardiac neoformation as indicated by Troponin I and Connexin 43 expression at 21 days postresection, while in the P7 group mainly scar tissue replacement ensued. Interestingly, there was an apparent lack of uniform alignment of newly formed cells in P1, and we detected cardiac tissue hypoperfusion for both groups at 21 and 60 days postresection using SPECT scanning. Direct basal cardiac function at 60 days, when the early lesion is undetectable, was preserved in all groups, whereas under hemodynamic stress the degree of change on LVDEP, Stroke Volume and Stroke Work indicated diminished overall cardiac function in P7 (P < 0.05). Furthermore, the End‐Diastolic Pressure–Volume relationship and increased interstitial collagen deposition in P7 is consistent with increased chamber stiffness. Taken together, we provide evidence that early cardiac repair response to apex resection in rats also leads to cardiomyocyte neoformation and is associated to long‐term preservation of cardiac function despite tissue hypoperfusion. PMID:25168870

  6. Effect of pre- and postnatal exposure to urban air pollution on myocardial lipid peroxidation levels in adult mice.

    PubMed

    Damaceno-Rodrigues, Nilsa Regina; Veras, Mariana Matera; Negri, Elnara Márcia; Zanchi, Ana Claudia Tedesco; Rhoden, Claudia Ramos; Saldiva, Paulo Hilário Nascimento; Dolhnikoff, Marisa; Caldini, Elia Garcia

    2009-11-01

    Exposure to air pollution can elicit cardiovascular health effects. Children and unborn fetuses appear to be particularly vulnerable. However, the mechanisms involved in cardiovascular damage are poorly understood. It has been suggested that the oxidative stress generated by air pollution exposure triggers tissue injury. To investigate whether prenatal exposure can enhance oxidative stress in myocardium of adult animals, mice were placed in a clean chamber (CC, filtered urban air) and in a polluted chamber (PC, São Paulo city) during the gestational period and/or for 3 mo after birth, according to 4 protocols: control group-prenatal and postnatal life in CC; prenatal group-prenatal in PC and postnatal life in CC; postnatal group-prenatal in CC and postnatal life in PC; and pre-post group-prenatal and postnatal life in PC. As an indicator of oxidative stress, levels of lipid peroxidation in hearts were measured by malondialdehyde (MDA) quantification and by quantification of the myocardial immunoreactivity for 15-F2t-isoprostane. Ultrastructural studies were performed to detect cellular alterations related to oxidative stress. Concentration of MDA was significantly increased in postnatal (2.45 +/- 0.84 nmol/mg) and pre-post groups (3.84 +/- 1.39 nmol/mg) compared to the control group (0.31 +/- 0.10 nmol/mg) (p < .01). MDA values in the pre-post group were significantly increased compared to the prenatal group (0.71 +/- 0.15 nmol/mg) (p = .017). Myocardial isoprostane area fraction in the pre-post group was increased compared to other groups (p < or = .01). Results show that ambient levels of air pollution elicit cardiac oxidative stress in adult mice, and that gestational exposure may enhance this effect.

  7. The effect of gestational ethanol exposure on voluntary ethanol intake in early postnatal and adult rats.

    PubMed

    Youngentob, Steven L; Molina, Juan C; Spear, Norman E; Youngentob, Lisa M

    2007-12-01

    Clinical and epidemiological studies provide strong data for a relationship between prenatal ethanol exposure and the risk for abuse in adolescent and young adult humans. However, drug-acceptance results in response to fetal exposure have differed by study, age at evaluation, and experimental animal. In the present study, the authors tested whether voluntary ethanol intake was enhanced in both the infantile and adult rat (15 and 90 days of age, respectively), as a consequence of chronic fetal drug experience. Experimental rats were exposed in utero by administering ethanol to a pregnant dam in a liquid diet during gestational Days 6-20. Compared with those for isocaloric pair-fed and ad lib chow control animals, the results for experimental animals demonstrated that fetal exposure significantly increased infantile affinity for ethanol ingestion without affecting intake patterns of an alternative fluid (water). Heightened affinity for ethanol was absent in adulthood. Moreover, the results argue against malnutrition as a principal factor underlying the infantile phenomenon. These data add to a growing literature indicative of heightened early postnatal acceptance patterns resulting from maternal use or abuse of ethanol during pregnancy.

  8. Postnatal development of rat pups is altered by prenatal methamphetamine exposure.

    PubMed

    Slamberová, Romana; Pometlová, Marie; Charousová, Petra

    2006-01-01

    There are studies showing that drug abuse during pregnancy may have impairing effect on progeny of drug-abusing mothers. Methamphetamine (MA) is one of the most common illicit drugs throughout the world. The purpose of the present study was to assess the effect of prenatal MA exposure on postnatal development of rat pups before the time of separation from their mothers. Female rats were injected with MA (5 mg/kg daily) for the duration of their pregnancy. Pups were then tested throughout the lactation period. They were weighed daily and the ano-genital distance was measured on postnatal day (PD) 1. Development of postural motor reaction was tested by righting reflex on surface between PD 1 and 12, and righting reflex in mid-air after PD 12 until successfully accomplished. On PD 15 homing test was examined as a test of pup acute learning. On PD 23 sensory-motor coordination was examined using the rotarod and bar-holding tests. Additionally, the markers of physical maturation, such as eye opening, testes descent in males and vaginal opening in females were also recorded. The birth weight in prenatally MA-exposed pups was lower than in controls or saline-exposed pups regardless of sex. There were no changes induced by prenatal MA exposure in weight gain or in sexual maturation. In righting reflexes, we demonstrated that pups exposed prenatally to MA were slower in righting reflex on surface and that they accomplished the test of righting reflex in mid-air later than controls or saline-exposed pups. The performance of homing test was not affected by prenatal drug exposure. The sensory-motor coordination was impaired in prenatally MA-exposed pups when testing in the rotarod test. Also, the number of falls in the bar-holding test was higher in MA-exposed pups than in controls. There were no sex differences in any measures. Thus, the present study demonstrated that prenatal MA exposure impairs development of postural motor movements of rat pups during the first 3 weeks

  9. Early Postnatal Manganese Exposure Causes Lasting Impairment of Selective and Focused Attention and Arousal Regulation in Adult Rats

    PubMed Central

    Beaudin, Stephane A.; Strupp, Barbara J.; Strawderman, Myla; Smith, Donald R.

    2016-01-01

    Background: Studies in children and adolescents have associated early developmental manganese (Mn) exposure with inattention, impulsivity, hyperactivity, and oppositional behaviors, but causal inferences are precluded by the correlational nature of the data and generally limited control for potential confounders. Objectives: To determine whether early postnatal oral Mn exposure causes lasting attentional and impulse control deficits in adulthood, and whether continued lifelong Mn exposure exacerbates these effects, using a rat model of environmental Mn exposure. Methods: Neonates were exposed orally to 0, 25 or 50 mg Mn/kg/day during early postnatal life (PND 1–21) or throughout life from PND 1 until the end of the study. In adulthood, the animals were tested on a series of learning and attention tasks using the five-choice serial reaction time task. Results: Early postnatal Mn exposure caused lasting attentional dysfunction due to impairments in attentional preparedness, selective attention, and arousal regulation, whereas associative ability (learning) and impulse control were spared. The presence and severity of these deficits varied with the dose and duration of Mn exposure. Conclusions: This study is the first to show that developmental Mn exposure can cause lasting impairments in focused and selective attention and arousal regulation, and to identify the specific nature of the impairments. Given the importance of attention and arousal regulation in cognitive functioning, these findings substantiate concerns about the adverse effects of developmental Mn exposure in humans. Citation: Beaudin SA, Strupp BJ, Strawderman M, Smith DR. 2017. Early postnatal manganese exposure causes lasting impairment of selective and focused attention and arousal regulation in adult rats. Environ Health Perspect 125:230–237; http://dx.doi.org/10.1289/EHP258 PMID:27384154

  10. Evaluating the Effectiveness of Fish Consumption Advisories: Modeling Prenatal, Postnatal, and Childhood Exposures to Persistent Organic Pollutants

    PubMed Central

    Binnington, Matthew J.; Quinn, Cristina L.; McLachlan, Michael S.

    2013-01-01

    Background: Because human exposure to persistent organic pollutants (POPs) occurs mainly through ingestion of contaminated food, regulatory bodies issue dietary consumption advisories to describe safe intake levels for food items of concern, particularly fish. Objectives: Our study goal was to estimate the effectiveness of fish consumption advisories in reducing exposure of infants and children to POPs. Methods: We used the time-variant mechanistic model CoZMoMAN to estimate and compare prenatal, postnatal, and childhood exposure to polychlorinated biphenyl congener PCB-153 under different scenarios of maternal guideline adherence for both hypothetical constant and realistic time-variant chemical emissions. The scenarios differed in terms of length of compliance (1 vs. 5 years), extent of fish substitution (all vs. half), and replacement diet (uncontaminated produce vs. beef). We also estimated potential exposure reductions for a range of theoretical chemicals to explore how guideline effectiveness varies with a chemical’s partitioning and degradation properties. Results: When assuming realistic time periods of advisory compliance, our findings suggest that temporarily eliminating or reducing maternal fish consumption is largely ineffective in reducing pre- and postnatal exposure to substances with long elimination half-lives in humans, especially during periods of decreasing environmental emissions. Substituting fish with beef may actually result in higher exposure to certain groups of environmental contaminants. On the other hand, advisories may be highly effective in reducing exposure to substances with elimination half-lives in humans shorter than the length of compliance. Conclusions: Our model estimates suggest that fish consumption advisories are unlikely to be effective in reducing prenatal, postnatal, and childhood exposures to compounds with long elimination half-lives in humans. Citation: Binnington MJ, Quinn CL, McLachlan MS, Wania F. 2014. Evaluating

  11. Behavioral Effects of Pre- and Postnatal Exposure to Smoking, Alcohol, and Caffeine in 5-Month-Old Infants.

    ERIC Educational Resources Information Center

    Dowler, Jeffrey K.; Jacobson, Sandra W.

    This study examined the behavioral effects of prenatal and postnatal exposure to smoking, alcohol, and caffeinated beverages on 5-month-old infants. The sample consisted of 179 Caucasian infants and their mothers. All mothers were 19 years of age or older and had at least a tenth-grade education. Mental and motor portions of the Bayley Scales of…

  12. Behavioral Effects of Pre- and Postnatal Exposure to Smoking, Alcohol, and Caffeine in 5-Month-Old Infants.

    ERIC Educational Resources Information Center

    Dowler, Jeffrey K.; Jacobson, Sandra W.

    This study examined the behavioral effects of prenatal and postnatal exposure to smoking, alcohol, and caffeinated beverages on 5-month-old infants. The sample consisted of 179 Caucasian infants and their mothers. All mothers were 19 years of age or older and had at least a tenth-grade education. Mental and motor portions of the Bayley Scales of…

  13. The Relationship between Prenatal and Postnatal Exposure to Polychlorinated Biphenyls (PCBs) and Cognitive, Neuropsychological, and Behavioral Deficits: A Critical Appraisal

    ERIC Educational Resources Information Center

    Cicchetti, Domenic V.; Kaufman, Alan S.; Sparrow, Sara S.

    2004-01-01

    Our purpose in this report is to evaluate scientifically that body of literature relating the effects of prenatal and postnatal exposure to polychlorinated biphenyls (PCBs) upon neurobehavioral, health-related, and cognitive deficits in neonates, developing infants, children, and adults. The data derive from seven cohorts: six cohorts of mothers…

  14. The Relationship between Prenatal and Postnatal Exposure to Polychlorinated Biphenyls (PCBs) and Cognitive, Neuropsychological, and Behavioral Deficits: A Critical Appraisal

    ERIC Educational Resources Information Center

    Cicchetti, Domenic V.; Kaufman, Alan S.; Sparrow, Sara S.

    2004-01-01

    Our purpose in this report is to evaluate scientifically that body of literature relating the effects of prenatal and postnatal exposure to polychlorinated biphenyls (PCBs) upon neurobehavioral, health-related, and cognitive deficits in neonates, developing infants, children, and adults. The data derive from seven cohorts: six cohorts of mothers…

  15. Early chronic lead exposure reduces exploratory activity in young C57BL/6J mice.

    PubMed

    Flores-Montoya, Mayra Gisel; Sobin, Christina

    2015-07-01

    Research has suggested that chronic low-level lead exposure diminishes neurocognitive function in children. Tests that are sensitive to behavioral effects at lowest levels of lead exposure are needed for the development of animal models. In this study we investigated the effects of chronic low-level lead exposure on exploratory activity (unbaited nose poke task), exploratory ambulation (open field task) and motor coordination (Rotarod task) in pre-adolescent mice. C57BL/6J pups were exposed to 0 ppm (controls), 30 ppm (low-dose) or 230 ppm (high-dose) lead acetate via dams' drinking water administered from birth to postnatal day 28, to achieve a range of blood lead levels (BLLs) from not detectable to 14.84 µg dl(-1) ). At postnatal day 28, mice completed behavioral testing and were killed (n = 61). BLLs were determined by inductively coupled plasma mass spectrometry. The effects of lead exposure on behavior were tested using generalized linear mixed model analyses with BLL, sex and the interaction as fixed effects, and litter as the random effect. BLL predicted decreased exploratory activity and no threshold of effect was apparent. As BLL increased, nose pokes decreased. The C57BL/6J mouse is a useful model for examining effects of early chronic low-level lead exposure on behavior. In the C57BL/6J mouse, the unbaited nose poke task is sensitive to the effects of early chronic low-level lead exposure. This is the first animal study to show behavioral effects in pre-adolescent lead-exposed mice with BLL below 5 µg dl(-1).

  16. Association of prenatal maternal or postnatal child environmental tobacco smoke exposure and neurodevelopmental and behavioral problems in children.

    PubMed Central

    Eskenazi, B; Castorina, R

    1999-01-01

    We review the potential neurodevelopmental and behavioral effects of children's prenatal and/or postnatal exposure to environmental tobacco smoke (ETS). Children's exposure to ETS has been assessed in epidemiologic studies as a risk factor for a variety of behavioral and neurodevelopmental problems including reduced general intellectual ability, skills in language and auditory tasks, and academic achievement, and behavioral problems such as hyperactivity and decreased attention spans. We review 17 epidemiologic studies that have attempted to separate the effects of maternal active smoking during pregnancy from passive ETS smoke exposure by the pregnant mother or the child. Based on the available data, we found that ETS exposure could cause subtle changes in children's neurodevelopment and behavior. However, studies to date are difficult to interpret because of the unknown influence of uncontrolled confounding factors, imprecision in measurements of smoking exposure, and collinearity of pre- and postnatal maternal smoking. Although some evidence suggests that maternal smoking during pregnancy may be associated with deficits in intellectual ability and behavioral problems in children, the impact of prenatal or postnatal ETS exposure remains less clear. PMID:10585903

  17. Influence of antibiotic exposure in the early postnatal period on the development of intestinal microbiota.

    PubMed

    Tanaka, Shigemitsu; Kobayashi, Takako; Songjinda, Prapa; Tateyama, Atsushi; Tsubouchi, Mina; Kiyohara, Chikako; Shirakawa, Taro; Sonomoto, Kenji; Nakayama, Jiro

    2009-06-01

    The influence of antibiotic exposure in the early postnatal period on the development of intestinal microbiota was monitored in 26 infants including five antibiotic-treated (AT) subjects orally administered a broad-spectrum antibiotic for the first 4 days of life and three caesarean-delivered (CD) subjects whose mothers were intravenously injected by the similar type of antibiotics in the same period. The faecal bacterial composition was analysed daily for the first 5 days and monthly for the first 2 months. Terminal restriction fragment length polymorphisms in the AT subjects showed less diversity with the attenuation of the colonization of some bacterial groups, especially in Bifidobacterium and unusual colonization of Enterococcus in the first week than the control antibiotic-free infants (AF, n=18). Quantitative real-time PCR showed overgrowth of enterococci (day 3, P=0.01; day 5, P=0.003; month 1, P=0.01) and arrested growth of Bifidobacterium (day 3, P=0.03) in the AT group. Furthermore, after 1 month, the Enterobacteriaceae population was markedly higher in the AT group than in the AF group (month 1, P=0.02; month 2, P=0.02). CD infants sustained similar, although relatively weaker, alteration in the developing microbiota. These results indicate that antibiotic exposure at the beginning of life greatly influences the development of neonatal intestinal microbiota.

  18. The consequences of prenatal and/or postnatal methamphetamine exposure on neonatal development and behaviour in rat offspring.

    PubMed

    McDonnell-Dowling, Kate; Kelly, John P

    2015-12-01

    Methamphetamine (MA) has become a popular drug of abuse in recent years not only in the general population but also amongst pregnant women. Although there is a growing body of preclinical investigations of MA exposure during pregnancy, there has been little investigation of the consequences of such exposure via the breast milk during the neonatal period. Therefore, the aim of this study was to determine the consequences of MA exposure during pregnancy and lactation on neurodevelopment and behaviour in the rat offspring. Pregnant Sprague-Dawley dams received MA (3.75 mg/kg) or control (distilled water) once daily via oral gavage from gestation day 7-21, postnatal day 1-21 or gestation day 7- postnatal day 21. A range of well-recognised neurodevelopmental parameters were examined in the offspring. Prenatal MA significantly reduced maternal weight gain, with a concomitant reduction in food intake. A significant increase in neonatal pup mortality was observed, being most marked in the prenatal/postnatal MA group. Significant impairments in neurodevelopmental parameters were also evident in all MA treatment groups including somatic development (e.g. pinna unfolding, fur appearance, eye opening) and behavioural development (e.g. surface righting, inclined plane test, forelimb grip). In conclusion, this study demonstrates that exposure to MA during any of these exposure periods (prenatal and/or postnatal) can have a profound effect on neonatal outcome, suggesting that regardless of the exposure period MA is associated with detrimental consequences in the offspring. These results indicate that in the clinical scenario, exposure during lactation needs to be considered when assessing the potential harmful effects of MA on offspring development.

  19. Olivary Climbing Fiber Alterations in PN40 Rat Cerebellum Following Postnatal Ethanol Exposure

    PubMed Central

    Pierce, Dwight R.; Hayar, Abdallah; Williams, D. Keith; Light, Kim Edward

    2011-01-01

    Developmental ethanol exposure in rats during postnatal days (PN) 4–6 is known to cause significant loss of cerebellar Purkinje cells. It is not known what happens to the surviving neurons as they continue to develop. This study was designed to quantify the interactions between the olivary climbing fibers and the Purkinje cells when the cerebellar circuits have matured. Rat pups were treated with a daily dose of ethanol (4.5 g/kg body weight) delivered by intragastric intubation on PN4, PN4-6, or PN7-9. The interactions between climbing fibers and Purkinje cells were examined on PN40 using confocal microscopy. Mid-vermal cerebellar sections were stained with antibodies to calbindin-D28k (to visualize Purkinje cells) and vesicular glutamate transporter 2 (VGluT2, to visualize climbing fibers). Confocal z-stack images were obtained from Lobule 1 and analyzed with Imaris software to quantify the staining of the two antibodies. The VGluT2 immunostaining was significantly reduced and this was associated with alterations in the synaptic integrity, and synaptic number per Purkinje cell with only a single exposure on PN4 enough to cause the alterations. Previously, we demonstrated similar deficits in climbing fiber innervation when analyzed on PN14 (Pierce, Hayar, Williams, and Light, 2010). The present study confirms that these alterations are sustained and further identifies the decreased synaptic density as well as alterations to the general morphology of the molecular layer of the cerebellar cortex that are the result of the binge ethanol exposure. PMID:21241681

  20. Gestational naltrexone ameliorates fetal ethanol exposures enhancing effect on the postnatal behavioral and neural response to ethanol.

    PubMed

    Youngentob, Steven L; Kent, Paul F; Youngentob, Lisa M

    2012-10-01

    The association between gestational exposure to ethanol and adolescent ethanol abuse is well established. Recent animal studies support the role of fetal ethanol experience-induced chemosensory plasticity as contributing to this observation. Previously, we established that fetal ethanol exposure, delivered through a dam's diet throughout gestation, tuned the neural response of the peripheral olfactory system of early postnatal rats to the odor of ethanol. This occurred in conjunction with a loss of responsiveness to other odorants. The instinctive behavioral response to the odor of ethanol was also enhanced. Importantly, there was a significant contributory link between the altered response to the odor of ethanol and increased ethanol avidity when assessed in the same animals. Here, we tested whether the neural and behavioral olfactory plasticity, and their relationship to enhanced ethanol intake, is a result of the mere exposure to ethanol or whether it requires the animal to associate ethanol's reinforcing properties with its odor attributes. In this later respect, the opioid system is important in the mediation (or modulation) of the reinforcing aspects of ethanol. To block endogenous opiates during prenatal life, pregnant rats received daily intraperitoneal administration of the opiate antagonist naltrexone from gestational day 6-21 jointly with ethanol delivered via diet. Relative to control progeny, we found that gestational exposure to naltrexone ameliorated the enhanced postnatal behavioral response to the odor of ethanol and postnatal drug avidity. Our findings support the proposition that in utero ethanol-induced olfactory plasticity (and its relationship to postnatal intake) requires, at least in part, the associative pairing between ethanol's odor quality and its reinforcing aspects. We also found suggestive evidence that fetal naltrexone ameliorated the untoward effects of gestational ethanol exposure on the neural response to non-fetal-exposure

  1. Gestational naltrexone ameliorates fetal ethanol exposures enhancing effect on the postnatal behavioral and neural response to ethanol

    PubMed Central

    Youngentob, Steven L; Kent, Paul F; Youngentob, Lisa M

    2012-01-01

    The association between gestational exposure to ethanol and adolescent ethanol abuse is well established. Recent animal studies support the role of fetal ethanol experience-induced chemosensory plasticity as contributing to this observation. Previously, we established that fetal ethanol exposure, delivered through a dam’s diet throughout gestation, tuned the neural response of the peripheral olfactory system of early postnatal rats to the odor of ethanol. This occurred in conjunction with a loss of responsiveness to other odorants. The instinctive behavioral response to the odor of ethanol was also enhanced. Importantly, there was a significant contributory link between the altered response to the odor of ethanol and increased ethanol avidity when assessed in the same animals. Here, we tested whether the neural and behavioral olfactory plasticity, and their relationship to enhanced ethanol intake, is a result of the mere exposure to ethanol or whether it requires the animal to associate ethanol’s reinforcing properties with its odor attributes. In this later respect, the opioid system is important in the mediation (or modulation) of the reinforcing aspects of ethanol. To block endogenous opiates during prenatal life, pregnant rats received daily intraperitoneal administration of the opiate antagonist naltrexone from gestational day 6–21 jointly with ethanol delivered via diet. Relative to control progeny, we found that gestational exposure to naltrexone ameliorated the enhanced postnatal behavioral response to the odor of ethanol and postnatal drug avidity. Our findings support the proposition that in utero ethanol-induced olfactory plasticity (and its relationship to postnatal intake) requires, at least in part, the associative pairing between ethanol’s odor quality and its reinforcing aspects. We also found suggestive evidence that fetal naltrexone ameliorated the untoward effects of gestational ethanol exposure on the neural response to non-fetal-exposure

  2. Risk of Learning and Behavioral Disorders Following Prenatal and Early Postnatal Exposure to Tetrachloroethylene (PCE)-contaminated Drinking Water

    PubMed Central

    Janulewicz, Patricia A; White, Roberta F; Winter, Michael R; Weinberg, Janice M; Gallagher, Lisa E; Vieira, Veronica; Webster, Thomas F; Aschengrau, Ann

    2008-01-01

    This population-based retrospective cohort study examined the association between developmental disorders of learning, attention and behavior and prenatal and early postnatal drinking water exposure to tetrachloroethylene (PCE) on Cape Cod, Massachusetts. Subjects were identified through birth records from 1969 through 1983. Exposure was modeled using information from town water departments, a PCE leaching and transport algorithm, EPANet water flow modeling software, and a Geographic Information System (GIS). Mothers completed a questionnaire on disorders of attention, learning and behavior in their children and on potential confounding variables. The final cohort consisted of 2,086 children. Results of crude and multivariate analyses showed no association between prenatal exposure and receiving tutoring for reading or math, being placed on an Individual Education Plan, or repeating a school grade (adjusted Odds Ratios (OR)=1.0–1.2). There was also no consistent pattern of increased risk for receiving a diagnosis of Attention Deficit Disorder (ADD) or Hyperactive Disorder (HD), special class placement for academic or behavioral problems, or lower educational attainment. Modest associations were observed for the latter outcomes only in the low exposure group (e.g., adjusted ORs for ADD were 1.4 and 1.0 for low and high exposure, respectively). (All ORs are based on an unexposed referent group.) Results for postnatal exposure through age five years were similar to those for prenatal exposure. We conclude that prenatal and early postnatal PCE exposure is not associated with disorders of attention, learning and behavior identified on the basis of questionnaire responses and at the exposure levels experienced by this population. PMID:18353612

  3. Prenatal amphetamine exposure effects on dopaminergic receptors and transporter in postnatal rats.

    PubMed

    Flores, Gonzalo; de Jesús Gómez-Villalobos, María; Rodríguez-Sosa, Leonardo

    2011-10-01

    We investigated the influence of prenatal amphetamine exposure (PAE) on dopamine (DA) receptors, and dopamine transporter (DAT) in various striatal and limbic subregions and locomotor activity induced by novel environmental conditions and amphetamine at two postnatal ages, 35 days old (prepubertal) and 60 days old (postpubertal). Experiments were carried out on pregnant female Sprague-Dawley rats, which were daily injected with either d-amphetamine sulfate (1 mg/kg) or saline solution (0.9%) for 11 days, from gestation day 11-21. In PAE rats compared to control we found the following: at pre-pubertal age, an enhancement of DA D1 in the dorsolateral area of the caudate-putamen (CPu), CPu-ventral and shell of the nucleus accumbens (NAcc) with a decrement of the DA D3 receptors in NAcc, olfactory tubercle (OT), and the islands of Calleja (IoC); whereas at postpubertal age, an increase in the levels of DAT in the NAcc and fundus of the CPu, and OT along with a decrease in the expression of DA D2 receptors only in the NAcc shell were found in PAE rats compared to control. In addition, amphetamine induces a marked decrease in locomotor activity at postpubertal age in rats with PAE. These results suggest a differential effect of amphetamines on the DAT mechanism of the nervous system during embryonic development of animals with implications in behavior and drug addictions at adulthood age.

  4. Altering the trajectory of early postnatal cortical development can lead to structural and behavioural features of autism

    PubMed Central

    2010-01-01

    Background Autism is a behaviourally defined neurodevelopmental disorder with unknown etiology. Recent studies in autistic children consistently point to neuropathological and functional abnormalities in the temporal association cortex (TeA) and its associated structures. It has been proposed that the trajectory of postnatal development in these regions may undergo accelerated maturational alterations that predominantly affect sensory recognition and social interaction. Indeed, the temporal association regions that are important for sensory recognition and social interaction are one of the last regions to mature suggesting a potential vulnerability to early maturation. However, direct evaluation of the emerging hypothesis that an altered time course of early postnatal development can lead to an ASD phenotype remains lacking. Results We used electrophysiological, histological, and behavioural techniques to investigate if the known neuronal maturational promoter valproate, similar to that in culture systems, can influence the normal developmental trajectory of TeA in vivo. Brain sections obtained from postnatal rat pups treated with VPA in vivo revealed that almost 40% of cortical cells in TeA prematurely exhibited adult-like intrinsic electrophysiological properties and that this was often associated with gross cortical hypertrophy and a reduced predisposition for social play behaviour. Conclusions The co-manifestation of these functional, structural and behavioural features suggests that alteration of the developmental time course in certain high-order cortical networks may play an important role in the neurophysiological basis of autism. PMID:20723245

  5. Pain reactivity in 2-month-old infants after prenatal and postnatal serotonin reuptake inhibitor medication exposure.

    PubMed

    Oberlander, Tim F; Grunau, Ruth Eckstein; Fitzgerald, Colleen; Papsdorf, Michael; Rurak, Dan; Riggs, Wayne

    2005-02-01

    In this prospective study, we examined biobehavioral responses to acute procedural pain at 2 months of age in infants with prenatal and postnatal selective serotonin reuptake inhibitor (SSRI) medication exposure. Based on previous findings showing reduced pain responses in newborns after prenatal exposure, we hypothesized that altered pain reactivity would also be found at 2 months of age. Facial action (Neonatal Facial Coding System) and cardiac autonomic reactivity derived from the respiratory activity and heart rate variability (HRV) responses to a painful event (heel-lance) were compared between 3 groups of infants: (1) infants with prenatal SSRI exposure alone (n = 11; fluoxetine, n = 2; paroxetine, n = 9); (2) infants with prenatal and postnatal SSRI (via breast milk) exposure (total n = 30; fluoxetine, n = 6; paroxetine, n = 20; sertraline, n = 4); and (3) control infants (n = 22; nonexposed) during baseline, lance, and recovery periods. Measures of maternal mood and drug levels were also obtained, and Bayley Scales of Infant Development-II were administered at ages 2 and 8 months. Facial action increased in all groups immediately after the lance but was significantly lower in the pSE group during the lance period. HR among infants in the pSE and ppSE groups was significantly lower during recovery. Using measures of HRV and the transfer relationship between heart rate and respiration, exposed infants had a greater return of parasympathetic cardiac modulation in the recovery period, whereas a sustained sympathetic response continued in control infants. Although postnatal exposure via breast milk was extremely low when infant drug levels could be detected in ppSE infants, changes in HR and HRV from lance to recovery were greater compared among infants with levels too low to be quantified. Neither maternal mood nor the presence of clonazepam influenced pain responses. Blunted facial-action responses were observed among infants with prenatal SSRI exposure alone

  6. Fetal lead exposure at each stage of pregnancy as a predictor of infant mental development.

    PubMed

    Hu, Howard; Téllez-Rojo, Martha María; Bellinger, David; Smith, Donald; Ettinger, Adrienne S; Lamadrid-Figueroa, Héctor; Schwartz, Joel; Schnaas, Lourdes; Mercado-García, Adriana; Hernández-Avila, Mauricio

    2006-11-01

    The impact of prenatal lead exposure on neurodevelopment remains unclear in terms of consistency, the trimester of greatest vulnerability, and the best method for estimating fetal lead exposure. We studied prenatal lead exposure's impact on neurodevelopment using repeated measures of fetal dose as reflected by maternal whole blood and plasma lead levels. We measured lead in maternal plasma and whole blood during each trimester in 146 pregnant women in Mexico City. We then measured umbilical cord blood lead at delivery and, when offspring were 12 and 24 months of age, measured blood lead and administered the Bayley Scales of Infant Development. We used multivariate regression, adjusting for covariates and 24-month blood lead, to compare the impacts of our pregnancy measures of fetal lead dose. Maternal lead levels were moderately high with a first-trimester blood lead mean (+/- SD) value of 7.1 +/- 5.1 microg/dL and 14% of values >or=10 microg/dL. Both maternal plasma and whole blood lead during the first trimester (but not in the second or third trimester) were significant predictors (p < 0.05) of poorer Mental Development Index (MDI) scores. In models combining all three trimester measures and using standardized coefficients, the effect of first-trimester maternal plasma lead was somewhat greater than the effect of first-trimester maternal whole blood lead and substantially greater than the effects of second- or third-trimester plasma lead, and values averaged over all three trimesters. A 1-SD change in first-trimester plasma lead was associated with a reduction in MDI score of 3.5 points. Postnatal blood lead levels in the offspring were less strongly correlated with MDI scores. Fetal lead exposure has an adverse effect on neurodevelopment, with an effect that may be most pronounced during the first trimester and best captured by measuring lead in either maternal plasma or whole blood.

  7. Prenatal and postnatal exposure to DDT by breast milk analysis in Canary Islands.

    PubMed

    Vall, Oriol; Gomez-Culebras, Mario; Puig, Carme; Rodriguez-Carrasco, Ernesto; Gomez Baltazar, Arelis; Canchucaja, Lizzeth; Joya, Xavier; Garcia-Algar, Oscar

    2014-01-01

    The use of p,p'-dichlorodiphenyltrichloroethane (DDT) has been banned since the late 1970s due to its toxicity. However, its long half-life makes it persistent in the environment and, consequently, almost everyone has DDT residues in the body. Human milk constitutes an ideal non-conventional matrix to investigate environmental chronic exposure to organochlorine compounds (OCs) residues. The study aimed to identify potential population risk factors of exposure to DDT due to the proximity to countries where it is still used. Seventy-two consecutive lactating women were prospectively included in Tenerife, Canary Islands (Spain). A validated questionnaire was used to obtain socioeconomic, demographics data, and daily habits during pregnancy. DDT levels in breast milk were measured by gas chromatography with-electron capture detector (GC-ECD). Anthropometrics measurements in newborns were obtained. Thirty-four out of 72 (47.2%) of the analysed milk samples presented detectable levels of DDT (mean: 0.92 ng/g), ranging between 0.08 to 16.96 ng/g. The socio-demographic variables did not significantly differ between detectable DDT and non-detectable DDT groups. We found positive association between DDT levels and vegetables (OR (95%CI): 1.23 (1.01-1.50)) and poultry meat (OR (95%CI): 2.05 (1.16-3.60)) consumption, and also between the presence of DDT in breast milk and gestational age (OR (95%CI): 0.59 (0.40-0.90)). DDT is present in breast milk of women at the time of delivery. Residual levels and the spread from countries still using DDT explain DDT detection from vegetables and from animal origin food. The presence of this compound in breast milk represents a pre- and postnatal exposure hazard for foetuses and infants due to chronic bioaccumulation and poor elimination, with possible deleterious effects on health. This data should be used to raise awareness of the risks of OCs exposure and to help establish health policies in order to avoid its use worldwide and thus, to

  8. Prenatal and Postnatal Exposure to DDT by Breast Milk Analysis in Canary Islands

    PubMed Central

    Vall, Oriol; Gomez-Culebras, Mario; Puig, Carme; Rodriguez-Carrasco, Ernesto; Gomez Baltazar, Arelis; Canchucaja, Lizzeth; Joya, Xavier; Garcia-Algar, Oscar

    2014-01-01

    Introduction The use of p,p′-dichlorodiphenyltrichloroethane (DDT) has been banned since the late 1970s due to its toxicity. However, its long half-life makes it persistent in the environment and, consequently, almost everyone has DDT residues in the body. Human milk constitutes an ideal non-conventional matrix to investigate environmental chronic exposure to organochlorine compounds (OCs) residues. The study aimed to identify potential population risk factors of exposure to DDT due to the proximity to countries where it is still used. Methods Seventy-two consecutive lactating women were prospectively included in Tenerife, Canary Islands (Spain). A validated questionnaire was used to obtain socioeconomic, demographics data, and daily habits during pregnancy. DDT levels in breast milk were measured by gas chromatography with-electron capture detector (GC-ECD). Anthropometrics measurements in newborns were obtained. Results Thirty-four out of 72 (47.2%) of the analysed milk samples presented detectable levels of DDT (mean: 0.92 ng/g), ranging between 0.08 to 16.96 ng/g. The socio-demographic variables did not significantly differ between detectable DDT and non-detectable DDT groups. We found positive association between DDT levels and vegetables (OR (95%CI): 1.23 (1.01–1.50)) and poultry meat (OR (95%CI): 2.05 (1.16–3.60)) consumption, and also between the presence of DDT in breast milk and gestational age (OR (95%CI): 0.59 (0.40–0.90)). Conclusions DDT is present in breast milk of women at the time of delivery. Residual levels and the spread from countries still using DDT explain DDT detection from vegetables and from animal origin food. The presence of this compound in breast milk represents a pre- and postnatal exposure hazard for foetuses and infants due to chronic bioaccumulation and poor elimination, with possible deleterious effects on health. This data should be used to raise awareness of the risks of OCs exposure and to help establish health policies

  9. Deletion of Rbpj from postnatal endothelium leads to abnormal arteriovenous shunting in mice

    PubMed Central

    Nielsen, Corinne M.; Cuervo, Henar; Ding, Vivianne W.; Kong, Yupeng; Huang, Eric J.; Wang, Rong A.

    2014-01-01

    Arteriovenous malformations (AVMs) are tortuous vessels characterized by arteriovenous (AV) shunts, which displace capillaries and shunt blood directly from artery to vein. Notch signaling regulates embryonic AV specification by promoting arterial, as opposed to venous, endothelial cell (EC) fate. To understand the essential role of endothelial Notch signaling in postnatal AV organization, we used inducible Cre-loxP recombination to delete Rbpj, a mediator of canonical Notch signaling, from postnatal ECs in mice. Deletion of endothelial Rbpj from birth resulted in features of AVMs by P14, including abnormal AV shunting and tortuous vessels in the brain, intestine and heart. We further analyzed brain AVMs, as they pose particular health risks. Consistent with AVM pathology, we found cerebral hemorrhage, hypoxia and necrosis, and neurological deficits. AV shunts originated from capillaries (and possibly venules), with the earliest detectable morphological abnormalities in AV connections by P8. Prior to AV shunt formation, alterations in EC gene expression were detected, including decreased Efnb2 and increased Pai1, which encodes a downstream effector of TGFβ signaling. After AV shunts had formed, whole-mount immunostaining showed decreased Efnb2 and increased Ephb4 expression within AV shunts, suggesting that ECs were reprogrammed from arterial to venous identity. Deletion of Rbpj from adult ECs led to tortuosities in gastrointestinal, uterine and skin vascular beds, but had mild effects in the brain. Our results demonstrate a temporal requirement for Rbpj in postnatal ECs to maintain proper artery, capillary and vein organization and to prevent abnormal AV shunting and AVM pathogenesis. PMID:25209249

  10. Exposure to maternal pre- and postnatal depression and anxiety symptoms: risk for major depression, anxiety disorders, and conduct disorder in adolescent offspring.

    PubMed

    Glasheen, Cristie; Richardson, Gale A; Kim, Kevin H; Larkby, Cynthia A; Swartz, Holly A; Day, Nancy L

    2013-11-01

    This study evaluated whether exposure to maternal pre- or postnatal depression or anxiety symptoms predicted psychopathology in adolescent offspring. Growth mixture modeling was used to identify trajectories of pre- and postnatal depression and anxiety symptoms in 577 women of low socioeconomic status selected from a prenatal clinic. Logistic regression models indicated that maternal pre- and postnatal depression trajectory exposure was not associated with offspring major depression, anxiety, or conduct disorder, but exposure to the high depression trajectory was associated with lower anxiety symptoms in males. Exposure to medium and high pre- and postnatal anxiety was associated with the risk of conduct disorder among offspring. Male offspring exposed to medium and high pre- and postnatal anxiety had higher odds of conduct disorder than did males with low exposure levels. Females exposed to medium or high pre- and postnatal anxiety were less likely to meet conduct disorder criteria than were females with lower exposure. To the best of our knowledge, this is the first study to examine the effect of pre- and postnatal anxiety trajectories on the risk of conduct disorder in offspring. These results suggest new directions for investigating the etiology of conduct disorder with a novel target for intervention.

  11. Exposure to Maternal Pre- and Postnatal Depression and Anxiety Symptoms: Risk for Major Depression, Anxiety Disorders, and Conduct Disorder in Adolescent Offspring

    PubMed Central

    Glasheen, Cristie; Richardson, Gale A.; Kim, Kevin H.; Larkby, Cynthia A.; Swartz, Holly A.; Day, Nancy L.

    2015-01-01

    This study evaluated whether exposure to maternal pre- or postnatal depression or anxiety symptoms predicted psychopathology in adolescent offspring. Growth mixture modeling was used to identify trajectories of pre- and postnatal depression and anxiety symptoms in 577 women of low socioeconomic status selected from a prenatal clinic. Logistic regression models indicated that maternal pre- and postnatal depression trajectory exposure was not associated with offspring major depression, anxiety, or conduct disorder but exposure to the high depression trajectory was associated with lower anxiety symptoms in males. Exposure to medium and high pre- and postnatal anxiety was associated with the risk of conduct disorder among offspring. Male offspring exposed to medium and high pre- and postnatal anxiety had higher odds of conduct disorder than males with low exposure levels. Females exposed to medium or high pre- and postnatal anxiety were less likely to meet conduct disorder criteria than females with lower exposure. To the best of our knowledge, this is the first study to examine the effect of pre- and postnatal anxiety trajectories on the risk of conduct disorder in offspring. These results suggest new directions for investigating the etiology of conduct disorder with a novel target for intervention. PMID:24229548

  12. Effects of postnatal exposure to methamphetamine on the development of the rat retina.

    PubMed

    Rodrigues, Lorena G; Melo, Pedro; Silva, M Carolina; Tavares, Maria Amélia

    2006-08-01

    Since the development of different cell types in the retina occurs at different rates, it is possible that exposure to an exogenous substance may produce effects during one time period, but not during another. This study aims to analyze the effects of methamphetamine (METH) in the growth pattern of an experimental model as well as neurochemical and immunohistochemical parameters of the dopaminergic system of the rat retina. The three development stages chosen in this study are key markers in rat eye development. Rats were given 15 mg/kg body weight per day of METH as subcutaneous injections in 0.9% saline (3 mL/kg weight/day) from the day after birth PND 1 to PND 6, PND 13, and PND 29. Each daily dose was split into two. The control group was injected subcutaneously with saline. Both the schedule and volume for injecting saline in the control group were the same as for the METH-treated group. There were no significant differences in the total number of offspring per litter among treatment groups. All offspring had similar body weight at birth. Analysis of body weight on PND 1, showed that animals treated with METH had similar body weights to control-treated animals and females had smaller weights than males. For growth evolution, only litters with a sex ratio of four males and four females were used. Animals treated with METH had smaller body weights than the control-treated animals for all ages studied (PND 7, 14, and 30). Within the control group at PND 30, a significant difference was found in the body weight of females, which was lower when compared with males. For the postnatal model, 7 deaths occurred for the METH-exposed group. No deaths occurred in the control group in a total of 16 saline-injected litters comprising 186 pups. Although the levels of dopamine (DA) was within normal values for the postnatally exposed METH group when compared with its respective control group at PND 7 and 30, at PND 14 this was not the case: in this experimental group, the

  13. Problematic Substance Use in Urban Adolescents: Role of Intrauterine Exposures to Cocaine and Marijuana and Post-Natal Environment

    PubMed Central

    Frank, Deborah A.; Kuranz, Seth; Appugliese, Danielle; Cabral, Howard; Chen, Clara; Crooks, Denise; Heeren, Timothy; Liebschutz, Jane; Richardson, Mark; Rose-Jacobs, Ruth

    2014-01-01

    Background Linkages between intrauterine exposures to cocaine and marijuana and adolescents’ problematic substance use have not been fully delineated. Methods Prospective longitudinal study with assessors unaware of intrauterine exposure history followed 157 urban participants from birth until late adolescence. Level of intrauterine exposures was identified by mother's report and infant’s meconium. Problematic substance use, identified by the Voice Diagnostic Interview Schedule for Children (V-DISC) or the Audio Computer Assisted Self-Interview (ACASI) and urine assay, was a composite encompassing DSM-IV indication of tolerance, abuse, and dependence on alcohol, marijuana, and tobacco and any use of cocaine, glue, or opiates. Results Twenty percent (32/157) of the sample experienced problematic substance use by age 18 years, of whom the majority (22/157) acknowledged abuse, tolerance or dependence on marijuana with or without other substances. Structural equation models examining direct and indirect pathways linking a Cox survival model for early substance initiation to a logistic regression models found effects of post-natal factors including childhood exposure to violence and household substance use, early youth substance initiation, and ongoing youth violence exposure contributing to adolescent problematic substance use. Conclusion We did not identify direct relationships between intrauterine cocaine or marijuana exposure and problematic substance use, but did find potentially modifiable post-natal risk factors also noted to be associated with problematic substance use in the general population including earlier substance initiation, exposure to violence and to household substance use. PMID:24999059

  14. Structural equation modeling and nested ANOVA: Effects of lead exposure on maternal and fetal growth in rats

    SciTech Connect

    Hamilton, J.D. ); O'Flaherty, E.J.; Shukla, R.; Gartside, P.S. ); Ross, R. )

    1994-01-01

    This study provided an assessment of the effects of lead on early growth in rats based on structural equation modeling and nested analysis of variance (ANOVA). Structural equation modeling showed that lead in drinking water (250, 500, or 1000 ppm) had a direct negative effect on body weight and tail length (i.e., growth) in female rats during the first week of exposure. During the following 2 weeks of exposure, high correlation between growth measurements taken over time resulted in reduced early postnatal growth. By the fourth week of exposure, reduced growth was not evident. Mating began after 8 weeks of exposure, and exposure continued during gestation. Decreased fetal body weight was detected when the effects of litter size, intrauterine position, and sex were controlled in a nested ANOVA. Lead exposure did not appear to affect fetal skeletal development, possibly because lead did not alter maternal serum calcium and phosphorus levels. The effect of lead on individual fetal body weight suggests that additional studies are needed to examine the effect of maternal lead exposure on fetal development and early postnatal growth. 24 refs., 4 figs., 6 tabs.

  15. Postnatal methylmercury exposure induces hyperlocomotor activity and cerebellar oxidative stress in mice: dependence on the neurodevelopmental period.

    PubMed

    Stringari, James; Meotti, Flávia C; Souza, Diogo O; Santos, Adair R S; Farina, Marcelo

    2006-04-01

    During the early postnatal period the central nervous system (CNS) is extremely sensitive to external agents. The present study aims at the investigation of critical phases where methylmercury (MeHg) induces cerebellar toxicity during the suckling period in mice. Animals were treated with daily subcutaneous injections of MeHg (7 mg/kg of body weight) during four different periods (5 days each) at the early postnatal period: postnatal day (PND) 1-5, PND 6-10, PND 11-15, or PND 16-20. A control group was treated with daily subcutaneous injections of a 150 mM NaCl solution (10 ml/kg of body weight). Subjects exposed to MeHg at different postnatal periods were littermate. At PND 35, behavioral tests were performed to evaluate spontaneous locomotor activity in the open field and motor performance in the rotarod task. Biochemical parameters related to oxidative stress (levels of glutathione and thiobarbituric acid reactive substances, as well as glutathione peroxidase and glutathione reductase activity) were evaluated in cerebellum. Hyperlocomotor activity and high levels of cerebellar thiobarbituric acid reactive substances were observed in animals exposed to MeHg during the PND 11-15 or PND 16-20 periods. Cerebellar glutathione reductase activity decreased in MeHg-exposed animals. Cerebellar glutathione peroxidase activity was also decreased after MeHg exposure and the lowest enzymatic activity was found in animals exposed to MeHg during the later days of the suckling period. In addition, low levels of cerebellar glutathione were found in animals exposed to MeHg during the PND 16-20 period. The present results show that the postnatal exposure to MeHg during the second half of the suckling period causes hyperlocomotor activity in mice and point to this phase as a critical developmental stage where mouse cerebellum is a vulnerable target for the neurotoxic and pro-oxidative effects of MeHg.

  16. SOURCES AND PATHWAYS OF LEAD EXPOSURE

    EPA Science Inventory

    Exposure is defined here as the amount of a substance that comes into contact with an absorbing surface during a specified period of time. The normal units of exposure are expressed as micrograms per day. The two components of exposure are the concentration of the substance in ...

  17. SOURCES AND PATHWAYS OF LEAD EXPOSURE

    EPA Science Inventory

    Exposure is defined here as the amount of a substance that comes into contact with an absorbing surface during a specified period of time. The normal units of exposure are expressed as micrograms per day. The two components of exposure are the concentration of the substance in ...

  18. Effects of Gestational and Postnatal Exposure to Chronic Intermittent Hypoxia on Diaphragm Muscle Contractile Function in the Rat

    PubMed Central

    McDonald, Fiona B.; Dempsey, Eugene M.; O'Halloran, Ken D.

    2016-01-01

    Alterations to the supply of oxygen during early life presents a profound stressor to physiological systems with aberrant remodeling that is often long-lasting. Chronic intermittent hypoxia (CIH) is a feature of apnea of prematurity, chronic lung disease, and sleep apnea. CIH affects respiratory control but there is a dearth of information concerning the effects of CIH on respiratory muscles, including the diaphragm—the major pump muscle of breathing. We investigated the effects of exposure to gestational CIH (gCIH) and postnatal CIH (pCIH) on diaphragm muscle function in male and female rats. CIH consisted of exposure in environmental chambers to 90 s of hypoxia reaching 5% O2 at nadir, once every 5 min, 8 h a day. Exposure to gCIH started within 24 h of identification of a copulation plug and continued until day 20 of gestation; animals were studied on postnatal day 22 or 42. For pCIH, pups were born in normoxia and within 24 h of delivery were exposed with dams to CIH for 3 weeks; animals were studied on postnatal day 22 or 42. Sham groups were exposed to normoxia in parallel. Following gas exposures, diaphragm muscle contractile, and endurance properties were examined ex vivo. Neither gCIH nor pCIH exposure had effects on diaphragm muscle force-generating capacity or endurance in either sex. Similarly, early life exposure to CIH did not affect muscle tolerance of severe hypoxic stress determined ex vivo. The findings contrast with our recent observation of upper airway dilator muscle weakness following exposure to pCIH. Thus, the present study suggests a relative resilience to hypoxic stress in diaphragm muscle. Co-ordinated activity of thoracic pump and upper airway dilator muscles is required for optimal control of upper airway caliber. A mismatch in the force-generating capacity of the complementary muscle groups could have adverse consequences for the control of airway patency and respiratory homeostasis. PMID:27462274

  19. Inactivation of Fam20B in Joint Cartilage Leads to Chondrosarcoma and Postnatal Ossification Defects

    PubMed Central

    Ma, Pan; Yan, Wenjuan; Tian, Ye; Wang, Jingya; Feng, Jian Q.; Qin, Chunlin; Cheng, Yi-Shing Lisa; Wang, Xiaofang

    2016-01-01

    During endochondral ossification, chondrocytes embed themselves in a proteoglycan-rich matrix during the proliferation-maturation transition. Accumulating evidence shows that proteoglycans are essential components for chondrocyte proliferation and differentiation. When we conditionally inactivated FAM20B (Family with sequence similarity 20 member-B), which is a newly identified xylose kinase essential for glycosaminoglycan (GAG) formation on the protein core of proteoglycans, from the dental mesenchyme using Osr2-Cre, which is also strongly expressed in joint cartilage, we found chondrosarcoma in the knee joint and remarkable defects of postnatal ossification in the long bones. Mechanistic analysis revealed that the defects were associated with gain of function in multiple signaling pathways in the epiphyseal chondrocytes, such as those derived by WNT, BMP, and PTHrP/IHH molecules, suggesting that the FAM20B-catalyzed proteoglycans are critical mediators for a signaling balance in the regulatory network controlling chondrocyte differentiation and proliferation. In particular, we demonstrated that the WNT inhibitor was able to rescue part of the bone defects in Osr2-Cre;Fam20Bfl/fl mice, indicating that FAM20B-catalyzed proteoglycans regulate postnatal endochondral ossification partially through the mediation of WNT signaling. PMID:27405802

  20. Burden of higher lead exposure in African-Americans starts in utero and persists into childhood.

    PubMed

    Cassidy-Bushrow, Andrea E; Sitarik, Alexandra R; Havstad, Suzanne; Park, Sung Kyun; Bielak, Lawrence F; Austin, Christine; Johnson, Christine Cole; Arora, Manish

    2017-09-05

    Recent public health lead crises in urban areas emphasize the need to better understand exposure to environmental toxicants, particularly in higher risk groups. Although African-American children have the highest prevalence of elevated blood lead levels in the United States, little is known about when this trajectory of disproportionate burden of lead exposure first emerges. Using tooth-matrix biomarkers that directly measure fetal and early childhood metal levels, the primary goal of this study was to determine if there were racial disparities in lead levels during fetal development and early childhood. Manganese, an essential nutrient that modifies the neurotoxic effects of lead, was also measured. Pregnant women served by the Henry Ford Health System and living in a predefined geographic area in and around Detroit, Michigan, were recruited during the second trimester or later into the Wayne County Health, Environment, Allergy and Asthma Longitudinal Study (WHEALS), a population-based birth cohort. Offspring born between September 2003 and December 2007 were studied in childhood. Child race was parent-reported. Lead and manganese during the second and third trimesters, early postnatal life (birth through age 1year) and early childhood (age 1 through time of tooth shedding, which ranges from 6 to 12years) were measured via high-resolution microspatial mapping of dentin growth rings, a validated biomarker for prenatal and childhood metal exposure. African-American children (N=71) had 2.2 times higher lead levels in the second and third trimesters (both p<0.001) and 1.9 times higher lead levels postnatally in the first year of life (p=0.003) compared to white children (N=51). Lead levels in African-American children were also higher during childhood, but this effect was only marginally significant (p=0.066) and was attenuated after covariate adjustment. Additionally, we observed that African-American children had lower tooth‑manganese levels during the third

  1. Lead exposure in US worksites: A literature review and development of an occupational lead exposure database from the published literature

    PubMed Central

    Koh, Dong-Hee; Locke, Sarah J.; Chen, Yu-Cheng; Purdue, Mark P.; Friesen, Melissa C.

    2016-01-01

    Background Retrospective exposure assessment of occupational lead exposure in population-based studies requires historical exposure information from many occupations and industries. Methods We reviewed published US exposure monitoring studies to identify lead exposure measurement data. We developed an occupational lead exposure database from the 175 identified papers containing 1,111 sets of lead concentration summary statistics (21% area air, 47% personal air, 32% blood). We also extracted ancillary exposure-related information, including job, industry, task/location, year collected, sampling strategy, control measures in place, and sampling and analytical methods. Results Measurements were published between 1940 and 2010 and represented 27 2-digit standardized industry classification codes. The majority of the measurements were related to lead-based paint work, joining or cutting metal using heat, primary and secondary metal manufacturing, and lead acid battery manufacturing. Conclusions This database can be used in future statistical analyses to characterize differences in lead exposure across time, jobs, and industries. PMID:25968240

  2. Biological tests of lead absorption following a brief massive exposure

    SciTech Connect

    Williams, M.K.

    1984-07-01

    A contractor's man suffered a brief, massive exposure to lead fume by contaminating and then smoking hand-rolled cigarettes. His blood lead concentration rose very rapidly to very high levels, but zinc erythrocyte protoporphyrin, urinary lead, and urinary coproporphyrin did not. It is possible that only the blood lead concentration is of value in detecting brief massive exposure.

  3. Pre- and postnatal arsenic exposure and child development at 18 months of age: a cohort study in rural Bangladesh.

    PubMed

    Hamadani, Jena D; Grantham-McGregor, Sally M; Tofail, Fahmida; Nermell, Barbro; Fängström, Britta; Huda, Syed N; Yesmin, Sakila; Rahman, Mahfuzar; Vera-Hernández, Marcos; Arifeen, Shams E; Vahter, Marie

    2010-10-01

    Exposure to arsenic through drinking water has been associated with impaired cognitive function in school-aged children in cross-sectional studies; however, there are few longitudinal studies and little information on effects of exposure in early life when the brain is generally most vulnerable. A longitudinal cohort study beginning in early pregnancy was conducted in rural Bangladesh, where arsenic concentrations in well water vary considerably. We assessed the effects of pre- and postnatal arsenic exposure on development of 2112 children at 18 months of age with Bayley Scales of Infant Development-II (mental and psychomotor development indices), Wolke's Behavior Rating Scale and maternal report of language. We related the measures of child development to arsenic concentrations in maternal urine in gestational weeks 9 and 30 and child's urinary arsenic at 18 months of age. Details of socio-economic background, home stimulation and anthropometric measurements of mothers and children were also available. Median maternal urinary arsenic concentration averaged over early and late gestation was 96 µg/l, whereas children's urine contained 35 µg/l of arsenic. There was no significant effect of any of the arsenic exposure measures on any of the child development measures after controlling for social and economic confounders, child's age and sex. Contrary to expectations, we found no indications of adverse effects of pre- or postnatal arsenic exposure on child development at 18 months. It remains possible that duration of exposure is critical and that effects will become apparent later in childhood.

  4. Fetal Lead Exposure at Each Stage of Pregnancy as a Predictor of Infant Mental Development

    PubMed Central

    Hu, Howard; Téllez-Rojo, Martha María; Bellinger, David; Smith, Donald; Ettinger, Adrienne S.; Lamadrid-Figueroa, Héctor; Schwartz, Joel; Schnaas, Lourdes; Mercado-García, Adriana; Hernández-Avila, Mauricio

    2006-01-01

    Background The impact of prenatal lead exposure on neurodevelopment remains unclear in terms of consistency, the trimester of greatest vulnerability, and the best method for estimating fetal lead exposure. Objective We studied prenatal lead exposure’s impact on neurodevelopment using repeated measures of fetal dose as reflected by maternal whole blood and plasma lead levels. Methods We measured lead in maternal plasma and whole blood during each trimester in 146 pregnant women in Mexico City. We then measured umbilical cord blood lead at delivery and, when offspring were 12 and 24 months of age, measured blood lead and administered the Bayley Scales of Infant Development. We used multivariate regression, adjusting for covariates and 24-month blood lead, to compare the impacts of our pregnancy measures of fetal lead dose. Results Maternal lead levels were moderately high with a first-trimester blood lead mean (± SD) value of 7.1 ± 5.1 μg/dL and 14% of values ≥10 μg/dL. Both maternal plasma and whole blood lead during the first trimester (but not in the second or third trimester) were significant predictors (p < 0.05) of poorer Mental Development Index (MDI) scores. In models combining all three trimester measures and using standardized coefficients, the effect of first-trimester maternal plasma lead was somewhat greater than the effect of first-trimester maternal whole blood lead and substantially greater than the effects of second- or third-trimester plasma lead, and values averaged over all three trimesters. A 1-SD change in first-trimester plasma lead was associated with a reduction in MDI score of 3.5 points. Postnatal blood lead levels in the offspring were less strongly correlated with MDI scores. Conclusions Fetal lead exposure has an adverse effect on neurodevelopment, with an effect that may be most pronounced during the first trimester and best captured by measuring lead in either maternal plasma or whole blood. PMID:17107860

  5. Early Postnatal Secondhand Smoke Exposure Disrupts Bacterial Clearance and Abolishes Immune Responses in Muco-Obstructive Lung Disease.

    PubMed

    Lewis, Brandon W; Sultana, Razia; Sharma, Rahul; Noël, Alexandra; Langohr, Ingeborg; Patial, Sonika; Penn, Arthur L; Saini, Yogesh

    2017-08-01

    Secondhand smoke (SHS) exposure has been linked to the worsening of ongoing lung diseases. However, whether SHS exposure affects the manifestation and natural history of imminent pediatric muco-obstructive airway diseases such as cystic fibrosis remains unclear. To address these questions, we exposed Scnn1b transgenic (Scnn1b-Tg(+)) mice to SHS from postnatal day (PND) 3-21 and lung phenotypes were examined at PND22. Although a majority of filtered air (FA)-exposed Scnn1b-Tg(+) (FA-Tg(+)) mice successfully cleared spontaneous bacterial infections by PND22, the SHS-exposed Scnn1b-Tg(+) (SHS-Tg(+)) mice failed to resolve these infections. This defect was associated with suppressed antibacterial defenses, i.e., phagocyte recruitment, IgA secretion, and Muc5b expression. Whereas the FA-Tg(+) mice exhibited marked mucus obstruction and Th2 responses, SHS-Tg(+) mice displayed a dramatic suppression of these responses. Mechanistically, downregulated expression of IL-33, a stimulator of type II innate lymphoid cells, in lung epithelial cells was associated with suppression of neutrophil recruitment, IgA secretions, Th2 responses, and delayed bacterial clearance in SHS-Tg(+) mice. Cessation of SHS exposure for 21 d restored previously suppressed responses, including phagocyte recruitment, IgA secretion, and mucous cell metaplasia. However, in contrast with FA-Tg(+) mice, the SHS-Tg(+) mice had pronounced epithelial necrosis, alveolar space consolidation, and lymphoid hyperplasia; indicating lagged unfavorable effects of early postnatal SHS exposure in later life. Collectively, our data show that early postnatal SHS exposure reversibly suppresses IL-33 levels in airspaces which, in turn, results in reduced neutrophil recruitment and diminished Th2 response. Our data indicate that household smoking may predispose neonates with muco-obstructive lung disease to bacterial exacerbations. Copyright © 2017 by The American Association of Immunologists, Inc.

  6. Lead, mercury, and cadmium exposure and attention deficit hyperactivity disorder in children

    SciTech Connect

    Kim, Stephani; Arora, Monica; Fernandez, Cristina; Landero, Julio; Caruso, Joseph; Chen, Aimin

    2013-10-15

    Background: There is limited research examining the relationship between lead (Pb) exposure and medically diagnosed attention deficit hyperactivity disorder (ADHD) in children. The role of mercury (Hg) and cadmium (Cd) exposures in ADHD development is even less clear. Objectives: To examine the relationship between Pb, Hg, and Cd and ADHD in children living inside and outside a Lead Investigation Area (LIA) of a former lead refinery in Omaha, NE. Methods: We carried out a case-control study with 71 currently medically diagnosed ADHD cases and 58 controls from a psychiatric clinic and a pediatric clinic inside and outside of the LIA. The participants were matched on age group (5–8, 9–12 years), sex, race (African American or Caucasians and others), and location (inside or outside LIA). We measured whole blood Pb, total Hg, and Cd using inductively coupled plasma mass spectrometry. Results: Inside the LIA, the 27 cases had blood Pb geometric mean (GM) 1.89 µg/dL and the 41 controls had 1.51 µg/dL. Outside the LIA, the 44 cases had blood Pb GM 1.02 µg/dL while the 17 controls had 0.97 µg/dL. After adjustment for matching variables and maternal smoking, socioeconomic status, and environmental tobacco exposure, each natural log unit blood Pb had an odds ratio of 2.52 with 95% confidence interval of 1.07–5.92. Stratification by the LIA indicated similar point estimate but wider CIs. No associations were observed for Hg or Cd. Conclusions: Postnatal Pb exposure may be associated with higher risk of clinical ADHD, but not the postnatal exposure to Hg or Cd. -- Highlights: • Blood Pb levels are associated with ADHD diagnosis in children. • No association was found between blood Cd or Hg levels and ADHD. • Children living close to hazardous waste site need to reduce metal exposure.

  7. Prenatal exposure of a novel antipsychotic aripiprazole: impact on maternal, fetal and postnatal body weight modulation in rats.

    PubMed

    Singh, K P; Tripathi, Nidhi

    2014-03-01

    Nearly all atypical antipsychotic drugs (AAPDs) of second- generation are associated with body weight gain in adults with prolonged exposure; but reports on third-generation AAPDs like Aripiprazole (ARI) and weight gain are scanty and ambiguous. This may be attributed to some unknown mechanism of action, the study of which is essential to investigate gestational exposure of equivalent therapeutic doses of ARI on maternal and fetal weight gain and its longlasting impact on postnatal development and growth of offspring in rodent model. 30 pregnant Wistar rats were exposed to selected doses (2mg, 3mg and 5mg/kg BW) of ARI from GD3-21 orally, with control subjects. Half of the pregnant subjects of each group were sacrificed at GD22 and rest dams were allowed to deliver normally and pups were reared postnatally up to 10 weeks of age. In ARI treated groups, there was no substantial alteration of body weight gain and food intake in pregnant subjects while significant reduction was found in fetal and postnatal (pre-and post weaning) body weight gain. ARI was found neutral for substantial weight gain in pregnant rats but may induce significant weight loss in fetuses, creating long-lasting negative impact on offspring growth (in weight) till PND70. Therefore, ARI could be a good alternative of second- generation AAPDs for adult females but may not be safe for developing fetuses and offspring.

  8. Racial differences in Urban children's environmental exposures to lead.

    PubMed Central

    Lanphear, B P; Weitzman, M; Eberly, S

    1996-01-01

    OBJECTIVES: This study explored whether differences in environmental lead exposures explain the racial disparity in children's blood lead levels. METHODS: Environmental sources of lead were identified for a random sample of 172 urban children. RESULTS: Blood lead levels were significantly higher among Black children. Lead-contamination of dust was higher in Black children's homes, and the condition of floors and interior paint was generally poorer. White children were more likely to put soil in their mouths and to suck their fingers, whereas Black children were more likely to put their mouths on window sills and to use a bottle. Major contributors to blood lead were interior lead exposures for Black children and exterior lead exposures for White children. CONCLUSIONS: Differences in housing conditions and exposures to lead-contaminated house dust contribute strongly to the racial disparity in urban children's blood lead levels. PMID:8876521

  9. Developmental lead exposure impairs contextual fear conditioning and reduces adult hippocampal neurogenesis in the rat brain.

    PubMed

    Jaako-Movits, Külli; Zharkovsky, Tamara; Romantchik, Olga; Jurgenson, Monika; Merisalu, Eda; Heidmets, Lenne-Triin; Zharkovsky, Alexander

    2005-11-01

    The effects of developmental lead exposure on the emotional reactivity, contextual fear conditioning and neurogenesis in the dentate gyrus of 60-80 days-old rats were studied. Wistar rat pups were exposed to 0.2% lead acetate via their dams' drinking water from postnatal day (PND) 1 to PND 21 and directly via drinking water from weaning until PND 30. At PND 60 and 80 the level of anxiety and contextual fear conditioning were studied, respectively. At PND 80 all animals received injections of BrdU to determine the effects of Pb on the generation of new cells in the dentate gyrus of hippocampus and on their survival and differentiation patterns. The results of the present study demonstrate that developmental lead exposure induces persistent increase in the level of anxiety and inhibition of contextual fear conditioning. Developmental lead exposure reduced generation of new cells in the dentate gyrus and altered the pattern of differentiation of BrdU-positive cells into mature neurons. A lower proportion of BrdU-positive cells co-expressed with the marker for mature neurons, calbindin. In contrast, the proportions of young not fully differentiated neurons and proportions of astroglial cells, generated from newly born cells, were increased in lead-exposed animals. Our results demonstrate that developmental lead exposure induces persistent inhibition of neurogenesis and alters the pattern of differentiation of newly born cells in the dentate gyrus of rat hippocampus, which could, at least partly, contribute to behavioral and cognitive impairments observed in adulthood.

  10. Lead exposure in Canada geese of the Eastern Prairie Population

    USGS Publications Warehouse

    DeStefano, S.; Brand, C.J.; Rusch, D.H.; Finley, Daniel L.; Gillespie, M.M.

    1991-01-01

    We monitored lead exposure in Eastern Prairie Population Canada geese during summer-winter, 1986-1987 and 1987-1988 at 5 areas. Blood lead concentrations in geese trapped during summer at Cape Churchill Manitoba were below levels indicative of recent lead exposure (0.18 ppm). Geese exposed to lead (≥0.18 ppm blood lead) increased to 7.6% at Oak Hammock Wildlife Management Area (WMA), southern Manitoba, where lead shot was still in use, and to 10.0% at Roseau River WMA, northern Minnesota, when fall-staging geese were close to a source of lead shot in Manitoba. Proportion of birds exposed to lead dropped to <2% at Lac Qui Parle WMA, Minnesota, a steel shot zone since 1980. On the wintering grounds at Swan Lake National Wildlife Refuge in Missouri, 4.9% of all geese showed exposure to lead before the hunting season. Lead exposure rose to 10.0% after hunting ended and then decreased to 5.2% in late winter. Incidence of lead shot in gizzards and concentrations of lead in livers supported blood assay data. Soil samples indicated that lead shot continues to be available to geese at Swan Lake, even though the area was established as a non-toxic shot zone in 1978. Steel shot zones have reduced lead exposure in the Eastern Prairie Population, but lead shot persists in the environment and continues to account for lead exposure and mortality in Eastern Prairie Population Canada geese.

  11. Changes in adrenoceptors and monoamine metabolism in neonatal and adult rat brain after postnatal exposure to the antihypertensive labetalol.

    PubMed Central

    Erdtsieck-Ernste, E. B.; Feenstra, M. G.; Botterblom, M. H.; De Barrios, J.; Boer, G. J.

    1992-01-01

    1. The purpose of the present study was to investigate the acute (single injection), direct (chronic treatment) and the long-lasting effects after exposure to the alpha 1/beta-adrenoceptor antagonist labetalol during rat brain development on adrenoceptors and monoamine metabolism. 2. In 10-day-old rat pups, subcutaneously administered labetalol (10 mg kg-1) passed the blood-brain barrier, reaching a level of 2.1 micrograms g-1 tissue in the brain 90 min after injection. 3. Chronic labetalol treatment (10 mg kg-1, s.c., twice daily) during the first 10 days of life significantly increased alpha 1-adrenoceptor binding in the hypothalamus (+39%), but not in the occipital cortex. 4. This chronic postnatal labetalol treatment did not result in long-lasting changes in alpha 1- and beta-receptors measured on day 60. 5. A single labetalol injection (10 mg kg-1, s.c.) on postnatal day 10 significantly increased noradrenaline (NA) metabolism in all brain regions tested (+25 to 105%), but had no effects on 5-hydroxytryptamine (5-HT) or dopamine metabolism. 6. Chronic labetalol treatment between postnatal (PN) days 1 and 10 also increased NA metabolism on PN 10 (3-methoxy-4-hydroxyphenylglycol (MHPG)/NA, +20 to 100%), suggesting that tolerance to the acute effect of labetalol did not occur. A slight increase in 5-HT metabolism (20%) was induced by the chronic labetalol treatment in the hippocampus and meso-limbic system. 7. In general, long-lasting effects on NA metabolism could not be detected on day 60 more than one month after the treatment. However, 5-HT metabolism was significantly increased in all four brain regions measured (+20 to 70%). 8. We conclude that chronic labetalol exposure during early postnatal rat brain development does not cause long-lasting changes in beta-receptor number or NA metabolism, but appears to be critical for the rate of 5-HT metabolism in later life. PMID:1596689

  12. Adverse Associations of both Prenatal and Postnatal Exposure to Organophosphorous Pesticides with Infant Neurodevelopment in an Agricultural Area of Jiangsu Province, China.

    PubMed

    Liu, Ping; Wu, Chunhua; Chang, Xiuli; Qi, Xiaojuan; Zheng, Minglan; Zhou, Zhijun

    2016-10-01

    Prenatal exposure to organophosphorous (OP) pesticides has been found to be associated with adverse effects on child neurodevelopment, but evidence on potential effects induced by both prenatal and postnatal OP exposure in infants is limited. Our aim was to investigate the associations of both prenatal and postnatal OP exposure with birth outcomes and infant neurodevelopment. Exposure to OP in 310 mother-infant pairs was assessed by measuring dimethylphosphate (DM), diethylphosphate (DE), and total dialkylphosphate (DAP) metabolites in urines from pregnant women and their children at 2 years of age. The Gesell Developmental Schedules was administered to examine neurodevelopment of 2-year-old children. Based on the Gesell Developmental Schedules, the proportions of children with developmental delays were < 6%. Adverse associations between head circumference at birth and prenatal OP exposure were demonstrated. Both prenatal and postnatal OP exposure was significantly associated with increased risk of being developmentally delayed. Specifically, odds ratio (OR) value for prenatal DEs was 9.75 (95% CI: 1.28, 73.98, p = 0.028) in the adaptive area, whereas in the social area, OR values for postnatal DEs and DAPs were 9.56 (95% CI: 1.59, 57.57, p = 0.014) and 12.00 (95% CI: 1.23, 117.37, p = 0.033), respectively. Adverse associations were observed only in boys, not in girls. Both prenatal and postnatal OP exposure may adversely affect the neurodevelopment of infants living in the agricultural area. The present study adds to the accumulating evidence on associations of prenatal and postnatal OP exposure with infant neurodevelopment. Liu P, Wu C, Chang X, Qi X, Zheng M, Zhou Z. 2016. Adverse associations of both prenatal and postnatal exposure to organophosphorous pesticides with infant neurodevelopment in an agricultural area of Jiangsu Province, China. Environ Health Perspect 124:1637-1643; http://dx.doi.org/10.1289/EHP196.

  13. Adverse Associations of both Prenatal and Postnatal Exposure to Organophosphorous Pesticides with Infant Neurodevelopment in an Agricultural Area of Jiangsu Province, China

    PubMed Central

    Liu, Ping; Wu, Chunhua; Chang, Xiuli; Qi, Xiaojuan; Zheng, Minglan; Zhou, Zhijun

    2016-01-01

    Background: Prenatal exposure to organophosphorous (OP) pesticides has been found to be associated with adverse effects on child neurodevelopment, but evidence on potential effects induced by both prenatal and postnatal OP exposure in infants is limited. Objectives: Our aim was to investigate the associations of both prenatal and postnatal OP exposure with birth outcomes and infant neurodevelopment. Methods: Exposure to OP in 310 mother–infant pairs was assessed by measuring dimethylphosphate (DM), diethylphosphate (DE), and total dialkylphosphate (DAP) metabolites in urines from pregnant women and their children at 2 years of age. The Gesell Developmental Schedules was administered to examine neurodevelopment of 2-year-old children. Results: Based on the Gesell Developmental Schedules, the proportions of children with developmental delays were < 6%. Adverse associations between head circumference at birth and prenatal OP exposure were demonstrated. Both prenatal and postnatal OP exposure was significantly associated with increased risk of being developmentally delayed. Specifically, odds ratio (OR) value for prenatal DEs was 9.75 (95% CI: 1.28, 73.98, p = 0.028) in the adaptive area, whereas in the social area, OR values for postnatal DEs and DAPs were 9.56 (95% CI: 1.59, 57.57, p = 0.014) and 12.00 (95% CI: 1.23, 117.37, p = 0.033), respectively. Adverse associations were observed only in boys, not in girls. Conclusions: Both prenatal and postnatal OP exposure may adversely affect the neurodevelopment of infants living in the agricultural area. The present study adds to the accumulating evidence on associations of prenatal and postnatal OP exposure with infant neurodevelopment. Citation: Liu P, Wu C, Chang X, Qi X, Zheng M, Zhou Z. 2016. Adverse associations of both prenatal and postnatal exposure to organophosphorous pesticides with infant neurodevelopment in an agricultural area of Jiangsu Province, China. Environ Health Perspect 124:1637–1643; http

  14. Prenatal and Early Postnatal Odorant Exposure Heightens Odor-Evoked Mitral Cell Responses in the Mouse Olfactory Bulb

    PubMed Central

    2017-01-01

    Abstract Early sensory experience shapes the anatomy and function of sensory circuits. In the mouse olfactory bulb (OB), prenatal and early postnatal odorant exposure through odorized food (food/odorant pairing) not only increases the volume of activated glomeruli but also increases the number of mitral and tufted cells (M/TCs) connected to activated glomeruli. Given the importance of M/TCs in OB output and in mediating lateral inhibitory networks, increasing the number of M/TCs connected to a single glomerulus may significantly change odorant representation by increasing the total output of that glomerulus and/or by increasing the strength of lateral inhibition mediated by cells connected to the affected glomerulus. Here, we seek to understand the functional impact of this long-term odorant exposure paradigm on the population activity of mitral cells (MCs). We use viral expression of GCaMP6s to examine odor-evoked responses of MCs following prenatal and early postnatal odorant exposure to two dissimilar odorants, methyl salicylate (MS) and hexanal, which are both strong activators of glomeruli on the dorsal OB surface. Previous work suggests that odor familiarity may decrease odor-evoked MC response in rodents. However, we find that early food-based odorant exposure significantly changes MC responses in an unexpected way, resulting in broad increases in the amplitude, number, and reliability of excitatory MC responses across the dorsal OB. PMID:28955723

  15. Prenatal and Early Postnatal Odorant Exposure Heightens Odor-Evoked Mitral Cell Responses in the Mouse Olfactory Bulb.

    PubMed

    Liu, Annie; Urban, Nathaniel N

    2017-01-01

    Early sensory experience shapes the anatomy and function of sensory circuits. In the mouse olfactory bulb (OB), prenatal and early postnatal odorant exposure through odorized food (food/odorant pairing) not only increases the volume of activated glomeruli but also increases the number of mitral and tufted cells (M/TCs) connected to activated glomeruli. Given the importance of M/TCs in OB output and in mediating lateral inhibitory networks, increasing the number of M/TCs connected to a single glomerulus may significantly change odorant representation by increasing the total output of that glomerulus and/or by increasing the strength of lateral inhibition mediated by cells connected to the affected glomerulus. Here, we seek to understand the functional impact of this long-term odorant exposure paradigm on the population activity of mitral cells (MCs). We use viral expression of GCaMP6s to examine odor-evoked responses of MCs following prenatal and early postnatal odorant exposure to two dissimilar odorants, methyl salicylate (MS) and hexanal, which are both strong activators of glomeruli on the dorsal OB surface. Previous work suggests that odor familiarity may decrease odor-evoked MC response in rodents. However, we find that early food-based odorant exposure significantly changes MC responses in an unexpected way, resulting in broad increases in the amplitude, number, and reliability of excitatory MC responses across the dorsal OB.

  16. Fetal nicotine exposure produces postnatal up-regulation of adenylate cyclase activity in peripheral tissues

    SciTech Connect

    Slotkin, T.A.; Navarro, H.A.; McCook, E.C.; Seidler, F.J. )

    1990-01-01

    Gestational exposure to nicotine has been shown to affect development of noradrenergic activity in both the central and peripheral nervous systems. In the current study, pregnant rats received nicotine infusions of 6 mg/kg/day throughout gestation, administered by osmotic minipump implants. After birth, offspring of the nicotine-infused dams exhibited marked increases in basal adenylate cyclase activity in membranes prepared from kidney and heart, as well as supersensitivity to stimulation by either a {beta}-adrenergic agonist, isoproterenol, or by forskolin. The altered responses were not accompanied by up-regulation of {beta}-adrenergic receptors: in fact, ({sup 125}I)pindolol binding was significantly decreased in the nicotine group. These results indicate that fetal nicotine exposure affects enzymes involved in membrane receptor signal transduction, leading to altered responsiveness independently of changes at the receptor level.

  17. Occupational and environmental human lead exposure in Brazil

    SciTech Connect

    Paoliello, M.M.B. . E-mail: monibas@sercomtel.com.br; De Capitani, E.M.

    2007-02-15

    The purpose of this paper is to present a review of data on assessment of exposure and adverse effects due to environmental and occupational lead exposure in Brazil. Epidemiological investigations on children lead exposure around industrial and mining areas have shown that lead contamination is an actual source of concern. Lead in gasoline has been phasing out since the 1980s, and it is now completely discontinued. The last lead mining and lead refining plant was closed in 1995, leaving residual environmental lead contamination which has recently been investigated using a multidisciplinary approach. Moreover, there are hundreds of small battery recycling plants and secondary smelting facilities all over the country, which produce focal urban areas of lead contamination. Current regulatory limits for workplace lead exposure have shown to be inadequate as safety limits according to a few studies carried out lately.

  18. Effects of prenatal cocaine exposure on early postnatal rodent brain structure and diffusion properties.

    PubMed

    McMurray, Matthew S; Oguz, Ipek; Rumple, Ashley M; Paniagua, Beatriz; Styner, Martin A; Johns, Josephine M

    2015-01-01

    Prenatal cocaine exposure has been associated with numerous behavioral phenotypes in clinical populations, including impulsivity, reduced attention, alterations in social behaviors, and delayed language and sensory-motor development. Detecting associated changes in brain structure in these populations has proven difficult, and results have been inconclusive and inconsistent. Due to their more controlled designs, animal models may shed light on the neuroanatomical changes caused by prenatal cocaine; however, to maximize clinical relevance, data must be carefully collected using translational methods. The goal of this study was two-fold: (1) to determine if prenatal cocaine alters developmental neuroanatomy using methods that are available to human researchers, specifically structural MRI and diffusion tensor imaging, and (2) to determine the feasibility of rodent in vivo neuroimaging for usage in longitudinal studies of developmental disorders. Cocaine-exposed (prenatal days 1-20, 30mg/kg/day) rat pups were sedated and imaged live using diffusion tensor imaging and postmortem (fixed) using magnetic resonance histology on postnatal day 14. Volume and diffusion properties in whole brain as well as specific regions of interest were then assessed from the resulting images. Whole brain analyses revealed that cocaine-exposed animals showed no change in whole brain volume. Additionally, we found alterations in fractional anisotropy across regions associated with reward processing and emotional regulation, especially in the thalamus and globus pallidus, as well as sex-dependent effects of cocaine in the right cortex. Reductions in fractional anisotropy were paired with reductions only in axial diffusivity, which preliminarily suggests that the changes observed here may be due to axonal damage, as opposed to reductions in myelination of the affected regions/pathways. Our data indicate that prenatal cocaine may target a number of developing brain structures but does not

  19. Binge ethanol exposure in late gestation induces ethanol aversion in the dam but enhances ethanol intake in the offspring and affects their postnatal learning about ethanol

    PubMed Central

    Chotro, M. Gabriela; Arias, Carlos; Spear, Norman E.

    2009-01-01

    Previous studies show that exposure to 1 or 2 g/kg ethanol during the last days of gestation increases ethanol acceptance in infant rats. We tested whether prenatal exposure to 3 g/kg, a relatively high ethanol dose, generates an aversion to ethanol in both the dam and offspring, and whether this prenatal experience affects the expression of learning derived from ethanol exposure postnatally. The answer was uncertain, since postnatal administration of a 3 g/kg ethanol dose induces an aversion to ethanol after postnatal day 10 but increases ethanol acceptance when administered during the first postnatal week. In the present study pregnant rats received intragastric administrations of water or ethanol (3 g/kg) on gestation days 17-20. On postnatal days 7-8 or 10-11 the offspring were administered water or ethanol (3 g/kg). Intake of ethanol and water, locomotor activity in an open-field and ethanol odor preference were evaluated in the pups, while the mothers were evaluated in terms of ethanol intake. Results indicated an aversion to ethanol in dams that had been administered ethanol during gestation, despite a general increase in ethanol intake observed in their pups relative to controls. The prenatal ethanol exposure also potentiated the increase in ethanol intake observed after intoxication on postnatal days 7-8. Ethanol intoxication on postnatal days 10-11 reduced ethanol consumption; this ethanol aversion was still evident in infant rats exposed prenatally to ethanol despite their general increase in ethanol intake. No effects of prenatal ethanol exposure were observed in terms of motor activity or odor preference. It is concluded that prenatal exposure to ethanol, even in a dose that induces ethanol aversion in the gestating dam, increases ethanol intake in infant rats and that this experience modulates age-related differences in subsequent postnatal learning about ethanol. PMID:19801275

  20. Lead, mercury, and cadmium exposure and attention deficit hyperactivity disorder in children.

    PubMed

    Kim, Stephani; Arora, Monica; Fernandez, Cristina; Landero, Julio; Caruso, Joseph; Chen, Aimin

    2013-10-01

    There is limited research examining the relationship between lead (Pb) exposure and medically diagnosed attention deficit hyperactivity disorder (ADHD) in children. The role of mercury (Hg) and cadmium (Cd) exposures in ADHD development is even less clear. To examine the relationship between Pb, Hg, and Cd and ADHD in children living inside and outside a Lead Investigation Area (LIA) of a former lead refinery in Omaha, NE. We carried out a case-control study with 71 currently medically diagnosed ADHD cases and 58 controls from a psychiatric clinic and a pediatric clinic inside and outside of the LIA. The participants were matched on age group (5-8, 9-12 years), sex, race (African American or Caucasians and others), and location (inside or outside LIA). We measured whole blood Pb, total Hg, and Cd using inductively coupled plasma mass spectrometry. Inside the LIA, the 27 cases had blood Pb geometric mean (GM) 1.89 µg/dL and the 41 controls had 1.51 µg/dL. Outside the LIA, the 44 cases had blood Pb GM 1.02 µg/dL while the 17 controls had 0.97 µg/dL. After adjustment for matching variables and maternal smoking, socioeconomic status, and environmental tobacco exposure, each natural log unit blood Pb had an odds ratio of 2.52 with 95% confidence interval of 1.07-5.92. Stratification by the LIA indicated similar point estimate but wider CIs. No associations were observed for Hg or Cd. Postnatal Pb exposure may be associated with higher risk of clinical ADHD, but not the postnatal exposure to Hg or Cd. © 2013 Published by Elsevier Inc.

  1. Effects of low level exposure to lead on neurophysiological functions among lead battery workers.

    PubMed

    Kovala, T; Matikainen, E; Mannelin, T; Erkkilä, J; Riihimäki, V; Hänninen, H; Aitio, A

    1997-07-01

    Assessment of neurophysiological functions in workers with low level exposure to lead and evaluation of the efficacy of bone lead measurements in the prediction of effects of lead. Exposure to lead of 60 workers from a lead battery battery factory was estimated from historical blood lead measurements and analysis of lead in the tibial and calcaneal bones with x ray fluorescence. Peripheral and central nervous system functions were assessed by measuring conduction velocities, sensory distal latencies, sensory amplitudes, and vibration thresholds as well as by quantitative measurement of the absolute and relative powers and mean frequencies of different electroencephalograph (EEG) channels. Sensory amplitudes, and to a smaller degree sensory or motor conduction velocities, showed a negative correlation with long term exposure to lead, most clearly with integrated blood lead concentration and exposure time. Vibration thresholds measured in the arm were related to recent exposure to lead, those measured in the leg to long term exposure. The alpha and beta activities of the EEG were more abundant in subjects with higher long term exposure to lead. Calcaneal lead content reflected short term exposure, tibial lead content reflected long term exposure. Blood lead history showed a closer relation with effects of lead than the tibial or calcaneal lead concentrations. Vibratory thresholds, quantitative EEG, and to a smaller extent the sensory amplitude, provide sensitive measures of effects of lead in occupationally exposed adults. Most accurate estimates of health risks induced by lead can be obtained from a good history of blood lead measurements. If such a history of blood lead concentrations is not available, analysis of bone lead may be used for the assessment of health risks.

  2. Effects of lead exposure on dendrite and spine development in hippocampal dentate gyrus areas of rats.

    PubMed

    Hu, Fan; Ge, Meng-Meng; Chen, Wei-Heng

    2016-03-01

    Lead exposure has been implicated in the impairment of synaptic plasticity in the hippocampal dentate gyrus (DG) areas of rats. However, whether the degradation of physiological properties is based on the morphological alteration of granule neurons in DG areas remains elusive. Here, we examined the dendritic branch extension and spine formation of granule neurons after lead exposure during development in rats. Dendritic morphology was studied using Golgi-Cox stain method, which was followed by Sholl analysis at postnatal days 14 and 21. Our results indicated that, for both ages, lead exposure significantly decreased the total dendritic length and spine density of granule neurons in the DG of the rat hippocampus. Further branch order analysis revealed that the decrease of dendritic length was observed only at the second branch order. Moreover, there were obvious deficits in the proportion and size of mushroom-type spines. These deficits in spine formation and maturity were accompanied by a decrease in Arc/Arg3.1 expression. Our present findings are the first to show that developmental lead exposure disturbs branch and spine formation in hippocampal DG areas. Arc/Arg3.1 may have a critical role in the disruption of neuronal morphology and synaptic plasticity in lead-exposed rats.

  3. Soil is an important pathway of human lead exposure.

    PubMed Central

    Mielke, H W; Reagan, P L

    1998-01-01

    This review shows the equal or greater importance of leaded gasoline-contaminated dust compared to lead-based paint to the child lead problem, and that soil lead, resulting from leaded gasoline and pulverized lead-based paint, is at least or more important than lead-based paint (intact and not pulverized) as a pathway of human lead exposure. Because lead-based paint is a high-dose source, the biologically relevant dosage is similar to lead in soil. Both lead-based paint and soil lead are associated with severe lead poisoning. Leaded gasoline and lead in food, but not lead-based paint, are strongly associated with population blood lead levels in both young children and adults. Soil lead and house dust, but not lead-based paint, are associated with population blood lead levels in children. Most soil lead and house dust are associated with leaded gasoline. Lead-based paint dust is associated with cases of renovation of either exterior or interior environments in which the paint was pulverized. Based upon the limited data to date, abatement of soil lead is more effective than abatement of lead-based paint in reducing blood lead levels of young children. About equal numbers of children under 7 years of age are exposed to soil lead and lead-based paint. Seasonality studies point to soil lead as the main source of population blood lead levels. Soil lead is a greater risk factor than lead-based paint to children engaged in hand-to-mouth and pica behavior. In summary, soil lead is important for addressing the population of children at risk of lead poisoning. When soil lead is acknowledged by regulators and the public health community as an important pathway of human lead exposure, then more effective opportunities for improving primary lead prevention can become a reality. Images Figure 1 PMID:9539015

  4. Influence of developmental lead exposure on expression of DNA methyltransferases and methyl cytosine-binding proteins in hippocampus.

    PubMed

    Schneider, J S; Kidd, S K; Anderson, D W

    2013-02-13

    Developmental exposure to lead (Pb) has adverse effects on cognitive functioning and behavior that can persist into adulthood. Exposures that occur during fetal or early life periods may produce changes in brain related to physiological re-programming from an epigenetic influence such as altered DNA methylation status. Since DNA methylation is regulated by DNA methyltransferases and methyl cytosine-binding proteins, this study assessed the extent to which developmental Pb exposure might affect expression of these proteins in the hippocampus. Long Evans dams were fed chow with or without added Pb acetate (0, 150, 375, 750 ppm) prior to breeding and remained on the same diet through weaning (perinatal exposure group). Other animals were exposed to the same doses of Pb but exposure started on postnatal day 1 and continued through weaning (early postnatal exposure group). All animals were euthanized on day 55 and hippocampi were removed. Western blot analyses showed significant effects of Pb exposure on DNMT1, DNMT3a, and MeCP2 expression, with effects often seen at the lowest level of exposure and modified by sex and developmental window of Pb exposure. These data suggest potential epigenetic effects of developmental Pb exposure on DNA methylation mediated at least in part through dysregulation of methyltransferases. Copyright © 2012 Elsevier Ireland Ltd. All rights reserved.

  5. Neonatal withdrawal following pre- and postnatal exposure to methadone in the rat.

    PubMed

    Barr, G A; Zmitrovich, A; Hamowy, A S; Liu, P Y; Wang, S; Hutchings, D E

    1998-05-01

    Recent evidence has shown that infant rats undergo precipitated withdrawal following chronic postnatal injection of morphine. In this study we examined whether or not infants exposed to methadone prenatally via the placental blood supply and postnatally via the dam's milk would also experience precipitated withdrawal. Dam's were implanted on gestational day 14 with osmotic minipumps containing one of two concentrations of methadone to supply the opiate throughout gestation and the first postnatal week. Nontreated and pair-fed controls were used. On postnatal day 7, pups were injected with naltrexone and their locomotor activity and ultrasonic vocalizations measured. Methadone exposed pups were more active and vocalized more when injected with naltrexone than with saline. The controls did not show these behavioral changes. The milk of methadone-exposed dams apparently contains sufficient quantities of the opiate for dependence to develop. The results are consistent with other data that demonstrate that very young rat pups can experience an opiate abstinence syndrome that includes increased behavioral activation.

  6. Role of Neurotrophins on Postnatal Neurogenesis in the Thalamus: Prenatal Exposure to Ethanol

    PubMed Central

    Mooney, Sandra M.; Miller, Michael W.

    2011-01-01

    A second wave of neuronal generation occurs in the ventrobasal nucleus of the rat thalamus (VB) during the first three postnatal weeks. The present study tested the hypotheses (1) that postnatal neurogenesis in the VB is neurotrophin-regulated and (2) that ethanol-induced changes in this proliferation are mediated by neurotrophins. The first studies examined the effects of neurotrophins on the numbers of cycling cells in ex vivo preparations of the VB from three-day-old rats. The proportion of cycling (Ki-67-positive) VB cells was higher in cultured thalamic slices treated with neurotrophins than in controls. Interestingly, this increase occurred with nerve growth factor (NGF) alone or with a combination of NGF and brain-derived neurotrophic factor (BDNF), but not with BDNF alone. Based on these data, the VBs from young offspring of pregnant rats fed an ethanol-containing or an isocaloric non-alcoholic liquid diet were examined between postnatal day (P) 1 and P31. Studies used enzyme-linked immunosorbent assays and immunoblots to explore the effects of ethanol on the expression of neurotrophins, their receptors, and representative signaling proteins. Ethanol altered the expression of neurotrophins and receptors throughout the first postnatal month. Expression of NGF increased, but there was no change in the expression of BDNF. The high affinity receptors (TrkA and TrkB) were unchanged but ethanol decreased expression of the low affinity receptor, p75. One downstream signaling protein, extracellular signal-regulated kinase (ERK), decreased but Akt expression was unchanged. Thus, postnatal cell proliferation in the VB of young rat pups is neurotrophin-responsive and is affected by ethanol. PMID:21277941

  7. Lead Exposure and Cardiovascular Disease—A Systematic Review

    PubMed Central

    Navas-Acien, Ana; Guallar, Eliseo; Silbergeld, Ellen K.; Rothenberg, Stephen J.

    2007-01-01

    Objective This systematic review evaluates the evidence on the association between lead exposure and cardiovascular end points in human populations. Methods We reviewed all observational studies from database searches and citations regarding lead and cardiovascular end points. Results A positive association of lead exposure with blood pressure has been identified in numerous studies in different settings, including prospective studies and in relatively homogeneous socioeconomic status groups. Several studies have identified a dose–response relationship. Although the magnitude of this association is modest, it may be underestimated by measurement error. The hypertensive effects of lead have been confirmed in experimental models. Beyond hypertension, studies in general populations have identified a positive association of lead exposure with clinical cardiovascular outcomes (cardiovascular, coronary heart disease, and stroke mortality; and peripheral arterial disease), but the number of studies is small. In some studies these associations were observed at blood lead levels < 5 μg/dL. Conclusions We conclude that the evidence is sufficient to infer a causal relationship of lead exposure with hypertension. We conclude that the evidence is suggestive but not sufficient to infer a causal relationship of lead exposure with clinical cardiovascular outcomes. There is also suggestive but insufficient evidence to infer a causal relationship of lead exposure with heart rate variability. Public Health Implications These findings have immediate public health implications. Current occupational safety standards for blood lead must be lowered and a criterion for screening elevated lead exposure needs to be established in adults. Risk assessment and economic analyses of lead exposure impact must include the cardiovascular effects of lead. Finally, regulatory and public health interventions must be developed and implemented to further prevent and reduce lead exposure. PMID:17431501

  8. Chronic exposure of adult, postnatal and in utero rat models to low-dose 137Cesium: impact on circulating biomarkers

    PubMed Central

    Manens, Line; Grison, Stéphane; Bertho, Jean-Marc; Lestaevel, Philippe; Guéguen, Yann; Benderitter, Marc; Aigueperse, Jocelyne; Souidi, Maâmar

    2016-01-01

    The presence of 137Cesium (137Cs) in the environment after nuclear accidents at Chernobyl and more recently Fukushima Daiichi raises many health issues for the surrounding populations chronically exposed through the food chain. To mimic different exposure situations, we set up a male rat model of exposure by chronic ingestion of a 137Cs concentration likely to be ingested daily by residents of contaminated areas (6500 Bq.l−1) and tested contaminations lasting 9 months for adult, neonatal and fetal rats. We tested plasma and serum biochemistry to identify disturbances in general indicators (lipids, proteins, carbohydrates and electrolytes) and in biomarkers of thyroid, heart, brain, bone, kidney, liver and testis functions. Analysis of the general indicators showed increased levels of cholesterol (+26%), HDL cholesterol (+31%), phospholipids B (+15%) and phosphorus (+100%) in the postnatal group only. Thyroid, heart, brain, bone and kidney functions showed no blood changes in any model. The liver function evaluation showed changes in total bilirubin (+67%) and alkaline phosphatase (–11%) levels, but only for the rats exposed to 137Cs intake in adulthood. Large changes in 17β-estradiol (–69%) and corticosterone (+36%) levels affected steroidogenesis, but only in the adult model. This study showed that response profiles differed according to age at exposure: lipid metabolism was most radiosensitive in the postnatal model, and steroid hormone metabolism was most radiosensitive in rats exposed in adulthood. There was no evidence of deleterious effects suggesting a potential impact on fertility or procreation. PMID:27466399

  9. Measuring Lead Exposure in Infants, Children, and Other Sensitive Populations.

    ERIC Educational Resources Information Center

    National Academy of Sciences - National Research Council, Washington, DC.

    Adverse health effects from exposure to lead are now recognized to be among industrialized society's most important health problems. This report, prepared by the National Research Council's Committee on Measuring Lead Exposure in Critical Populations, concurs with new findings issued by the Centers for Disease Control which state that lead…

  10. Lead exposures in the human environment. Final report

    SciTech Connect

    Elias, R.W.

    1985-01-01

    Humans consume lead by inhaling air, drinking beverages, eating food and ingesting dust. The natural source of this lead is primarily soil. Anthropogenic sources are lead in gasoline, fossil fuels and industrial products and processes. Lead is ubiquitous in the human environment, and pinpointing the primary sources of lead in any particular environmental component is difficult. Nevertheless, our purpose is to describe the total exposure of humans to environmental lead and to determine the sources of lead contributing to this exposure. The total exposure is the total amount of lead consumed by ingestion and inhalation. Excluding lead exposure from choice or circumstance, a baseline level of potential human exposure can be defined for a normal individual eating a typical diet and living in a non-urban community remote from industrial sources of lead in a house without lead-based paints. Beyond this level, additive exposure factors can be determined for other environments (e.g. urban, occupational and smelter communities) and for certain habits and activities (e.g. pica, smoking, drinking and hobbies), with variation for age, sex or socioeconomic status.

  11. Trends in occupational lead exposure since the 1978 OSHA lead standard.

    PubMed

    Okun, Andrea; Cooper, Gregory; Bailer, A John; Bena, James; Stayner, Leslie

    2004-06-01

    The purpose of the study was to evaluate trends in occupational lead exposures throughout U.S. industry after the establishment of the general industry lead standard in 1978 and the construction industry standard in 1993. Lead exposure measurements collected by the Occupational Safety and Health Administration (OSHA) under their compliance and consultation programs were analyzed. Time trends in the distributions of exposure levels were evaluated graphically. Trends in the proportion of exposures above the OSHA permissible exposure limit (PEL) were analyzed using logistic regression models. The distribution of lead exposure levels declined over the study time period for general industry, but not for construction. The median exposure levels for general industry facilities decreased five- to tenfold. Logistic regression models reveal statistically significant declines in the odds of a lead exposure exceeding the PEL. This study provides evidence for relatively large decreases in lead exposure levels in general industry facilities over time. The study does not provide similar evidence for the construction industry. Given the limited number of years of data available since the implementation of the revised construction standard for lead, re-analysis of lead exposure levels within this industry would be worthwhile when more data become available.

  12. Lead exposure from battery recycling in Indonesia.

    PubMed

    Haryanto, Budi

    2016-03-01

    In Indonesia, more than 200 illegal used lead acid battery (ULAB) smelters are currently operating. Only a few health studies support the finding of lead-related symptoms and diseases among populations living near the smelters. To assess the blood lead levels (BLLs) and potential health impacts among the population surrounding ULAB recycling smelters, we evaluated health effects reported from 2003 to 2013, conducted focus group discussions with lead smelter owner/workers and a group of 35 female partners of smelter owners or workers not actively engaged in smelter work, and retook and measured BLLs. It was found that many children in the areas were having difficulty achieving high grades at school and having stunting or other problems with physical development. The average mean of BLLs increased by almost double in 2015, compared with in 2011. The risk of having hypertension, interference in the ability to make red blood cells in females occurred among 24% of respondents; Elevated blood pressure, hearing loss, and interference in the ability to make red bloods cell occurred in 20% of males; Kidney damage, infertility in male, nerve problems, including decreased sensation and decreased ability to move quickly occurred in 13%; Decreased ability to make red blood cells (20%), and; Frank anemia, decreased life-span, coma/seizures were experienced by 22%. The populations living in areas surrounding ULAB smelters are experiencing severe chronic health problems. It is recommended that the smelters must be moved and placed far away from the municipality.

  13. Determinants of childhood lead exposure in the postleaded petrol era: The Tooth Fairy cohort from Newcastle upon Tyne.

    PubMed

    Hodgson, Susan; Manmee, Charuwan; Dirks, Wendy; Shepherd, Thomas; Pless-Mulloli, Tanja

    2015-01-01

    Lead is an environmental contaminant causing irreversible health effects in children. We used dentine lead levels as a measure of early-life lead exposure and explored determinants of lead exposure in children living in Newcastle upon Tyne, a historically industrialised UK city, in a cohort born since legislation was introduced to remove lead from petrol, paint and water pipes. The "Tooth Fairy study" cohort comprised 69 children aged 5-8 years. We collected upper deciduous incisors from children and questionnaire data from their parents in 2005. We measured lead levels in pre- and postnatal enamel and dentine using laser ablation inductively coupled plasma mass spectrometry, and assessed associations between dentine lead levels and residential, dietary, lifestyle and socio-economic characteristics. Dentine lead levels were low (mean 0.26 μg/g, range 0.06-0.77); however, we observed considerable variability in dentine lead levels within and between children suggestive of differing exposure levels and/or exposure sources across this population. Variables earlier documented to be associated with childhood lead levels were not found to be significant determinants of dentine lead levels in this study. Exposure pathways should continue to be investigated to enable targeted interventions and prevention of lead-induced health impacts in vulnerable populations.

  14. Postnatal exposure to trichloroethylene alters glutathione redox homeostasis, methylation potential, and neurotrophin expression in the mouse hippocampus

    PubMed Central

    Blossom, Sarah J.; Melnyk, Stepan; Cooney, Craig A.; Gilbert, Kathleen M.; James, S. Jill

    2012-01-01

    Previous studies have shown that continuous exposure throughout gestation until the juvenile period to environmentally-relevant doses of trichloroethylene (TCE) in the drinking water of MRL+/+ mice promoted adverse behavior associated with glutathione depletion in the cerebellum indicating increased sensitivity to oxidative stress. The purpose of this study was to extend our findings and further characterize the impact of TCE exposure on redox homeostasis and biomarkers of oxidative stress in the hippocampus, a brain region prone to oxidative stress. Instead of a continuous exposure, the mice were exposed to water only or two environmentally relevant doses of TCE in the drinking water postnatally from birth until 6 weeks of age. Biomarkers of plasma metabolites in the transsulfuration pathway and the transmethylation pathway of the methionine cycle were also examined. Gene expression of neurotrophins was examined to investigate a possible relationship between oxidative stress, redox imbalance and neurotrophic factor expression with TCE exposure. Our results show that hippocampi isolated from male mice exposed to TCE showed altered glutathione redox homeostasis indicating a more oxidized state. Also observed was a significant, dose dependent increase in glutathione precursors. Plasma from the TCE treated mice showed alterations in metabolites in the transsulfuration and transmethylation pathways indicating redox imbalance and altered methylation capacity. 3-Nitrotyrosine, a biomarker of protein oxidative stress, was also significantly higher in plasma and hippocampus of TCE-exposed mice compared to controls. In contrast, expression of key neurotrophic factors in the hippocampus (BDNF, NGF, and NT-3) was significantly reduced compared to controls. Our results demonstrate that low-level postnatal and early life TCE exposure modulates neurotrophin gene expression in the mouse hippocampus and may provide a mechanism for TCE-mediated neurotoxicity. PMID:22421312

  15. Pre and post-natal antigen exposure can program the stress axis of adult zebra finches: evidence for environment matching

    PubMed Central

    Merrill, Loren; Grindstaff, Jennifer L.

    2014-01-01

    Both maternal exposure to stressors and exposure of offspring to stressors during early life can have lifelong effects on the physiology and behavior of offspring. Stress exposure can permanently shape an individual’s phenotype by influencing the development of the hypothalamic-pituitary-adrenal (HPA) axis, which is responsible for the production and regulation of glucocorticoids such as corticosterone (CORT). In this study we used captive zebra finches (Taeniopygia guttata) to examine the effects of matching and mismatching maternal and early post-natal exposure to one of two types of antigens or a control on HPA axis reactivity in adult offspring. Prior to breeding, adult females were injected with lipopolysaccharide (LPS), keyhole limpet hemocyanin (KLH) or a control. Offspring of females in each of the three treatments were themselves exposed to LPS, KLH or a control injection at 5 and 28 days post-hatch. When offspring were at least 18 months of age, standardized capture and restraint stress tests were conducted to determine the impact of the treatments on adult stress responsiveness. We found significant interaction effects between maternal and offspring treatments on stress-induced CORT levels, and evidence in support of the environment matching hypothesis for KLH-treated birds not LPS-treated birds. KLH-treated offspring of KLH-treated mothers exhibited reduced stress-induced CORT levels, whereas LPS-treated or control offspring of KLH-treated mothers exhibited elevated stress-induced CORT levels. Although the treatment effects on baseline CORT were non-significant, the overall pattern was similar to the effects observed on stress-induced CORT levels. Our results highlight the complex nature of HPA axis programming, and to our knowledge, provide the first evidence that a match or mismatch between pre and post-natal antigen exposure can have life-long consequences for HPA axis function. PMID:25535860

  16. Neurotoxicity and biomarkers of lead exposure: a review.

    PubMed

    Liu, Kang-sheng; Hao, Jia-hu; Zeng, Yu; Dai, Fan-chun; Gu, Ping-qing

    2013-09-01

    Appropriate selection and measurement of lead biomarkers of exposure are critically important for health care management purposes, public health decision making, and primary prevention synthesis. Lead is one of the neurotoxicants that seems to be involved in the etiology of psychologies. Biomarkers are generally classified into three groups: biomarkers of exposure, effect, and susceptibility.The main body compartments that store lead are the blood, soft tissues, and bone; the half-life of lead in these tissues is measured in weeks for blood, months for soft tissues, and years for bone. Within the brain, lead-induced damage in the prefrontal cerebral cortex, hippocampus, and cerebellum can lead to a variety of neurological disorders, such as brain damage, mental retardation, behavioral problems, nerve damage, and possibly Alzheimer's disease, Parkinsons disease, and schizophrenia. This paper presents an overview of biomarkers of lead exposure and discusses the neurotoxic effects of lead with regard to children and adults.

  17. Modifications of inhibitory transmission onto pyramidal neurons by postnatal exposure to MK-801: Effects of enriched environment.

    PubMed

    Shojaei, Amir; Anaraki, Afsaneh Kamali; Mirnajafi-Zadeh, Javad; Atapour, Nafiseh

    2017-04-01

    Early enriched environment (EE) prevents several deficits associated with postnatal MK-801 [N-Methyl-d-Aspartate (NMDA) receptor antagonist] treatment such as cognitive and locomotor deficits. We sought physiological correlates to such changes by looking at inhibitory synaptic inputs onto pyramidal cells in a prefrontal cortex slice preparation. Pharmacologically isolated γ-amino-butyric acid A (GABAA) receptor-mediated currents were measured using whole-cell patch clamp recordings. Wistar rats were raised in standard or EE from birth up to the time of experiments and were injected with saline or MK-801 (1mg/kg) on postnatal days (P) 6-10. We recorded miniature inhibitory post-synaptic currents (mIPSCs) of pyramidal cells in layer II/III of prefrontal cortex and measured their frequency, amplitude and kinetics. In control animals, the amplitude and frequency of mIPSCs increased strikingly during development from P21 to P28. MK-801 accelerated the development of mIPSCs frequency but caused a significant decrease in the amplitude of mIPSCs on P28 suggesting a significant reduction of inhibition onto pyramidal cells. EE per se led to a significant increase in both frequency and amplitude of mIPSCs, but its application to MK-801-treated rats resulted in moderate rescue of GABAergic transmission on P28. We conclude that postnatal MK-801 leads to reduced inhibitory transmission onto pyramidal cells of prefrontal cortex at adolescence which may underlie behavioural and morphological differences detected in vivo in rats. EE presentation from birth rather prevents GABAergic alterations associated with postnatal MK-801 treatment at adolescence.

  18. Effects of prenatal exposure to diesel exhaust particles on postnatal development, behavior, genotoxicity and inflammation in mice

    PubMed Central

    Hougaard, Karin S; Jensen, Keld A; Nordly, Pernille; Taxvig, Camilla; Vogel, Ulla; Saber, Anne T; Wallin, Håkan

    2008-01-01

    Background Results from epidemiological studies indicate that particulate air pollution constitutes a hazard for human health. Recent studies suggest that diesel exhaust possesses endocrine activity and therefore may affect reproductive outcome. This study in mice aimed to investigate whether exposure to diesel exhaust particles (DEP; NIST 2975) would affect gestation, postnatal development, activity, learning and memory, and biomarkers of transplacental toxicity. Pregnant mice (C57BL/6; BomTac) were exposed to 19 mg/m3 DEP (~1·106 particles/cm3; mass median diameter ≅ 240 nm) on gestational days 9–19, for 1 h/day. Results Gestational parameters were similar in control and diesel groups. Shortly after birth, body weights of DEP offspring were slightly lower than in controls. This difference increased during lactation, so by weaning the DEP exposed offspring weighed significantly less than the control progeny. Only slight effects of exposure were observed on cognitive function in female DEP offspring and on biomarkers of exposure to particles or genotoxic substances. Conclusion In utero exposure to DEP decreased weight gain during lactation. Cognitive function and levels of biomarkers of exposure to particles or to genotoxic substances were generally similar in exposed and control offspring. The particle size and chemical composition of the DEP and differences in exposure methods (fresh, whole exhaust versus aged, resuspended DEP) may play a significant role on the biological effects observed in this compared to other studies. PMID:18331653

  19. Prenatal exposure to anti-tubercular drugs and postnatal effect on growth, development and cognitive ability in rats.

    PubMed

    Bharathi, K N; Natesh, T S; Ashwitha Reddy, A

    2012-04-27

    The effect of prenatal exposure to antitubercular drugs in therapeutic and double therapeutic doses on postnatal developments was studied in albino rats of Wistar strain. Seven groups with six female rats each were taken for the study and were allowed to mate with male in the ratio of (2:1). The drugs isoniazid 27 and 54mg/kg b.w. p.o., ethambutol 144 and 288mg/kg b.w. p.o., rifampin 54 and 108mg/kg b.w. p.o. were administered to each group from the day of pregnancy till parturition. Control group was administered with distilled water (1ml/kg). Litters of the respective groups were studied for litter size; body weight; physical development i.e. eye opening, pinna detachment, incisor eruption; behavioral development i.e. righting reflex, negative geotaxis, ascending wire mesh; motor development i.e. rotarod and cognitive function i.e. elevated plus maze, Hebb-William maze and step-down (passive avoidance). The results obtained indicate that the prenatal exposure to therapeutic dose of rifampin and double therapeutic dose of rifampin, isoniazid and ethambutol affect the postnatal growth, development and cognitive ability. Hence, the study suggests that potential benefit risk ratios to be considered for their use in pregnancy.

  20. Worker lead exposures during renovation of homes with lead-based paint

    SciTech Connect

    Sussell, A.; Gittleman, J.; Singal, M.

    1998-11-01

    The authors evaluated lead exposures among full-time home renovators and part-time volunteers working primarily in pre-1960 homes with lead-based paint. Potentially hazardous lead exposures were measured during two tasks: exterior dry scraping and wet scraping. Maximum exposures were 120 and 63 {micro}g/m{sup 3}, respectively. Exposures during other tasks, including general repair, weatherization, exterior scraping/painting, window replacement, demolition, and plumbing, were low, as were all 13 full-shift personal exposures. Blood lead levels for full-time workers ranged up to 17.5 {micro}g/dl, with a GM of 5.2 {micro}g/dl; the GM for volunteers was 3.2 {micro}g/dl. All of the paint samples collected from work surfaces had detectable amounts of lead, with 65% of the work surfaces tested having an average lead concentration of >0.5%.

  1. Lead exposure increases blood pressure by increasing angiotensinogen expression.

    PubMed

    Jiao, Jiandong; Wang, Miaomiao; Wang, Yiqing; Sun, Na; Li, Chunping

    2016-01-01

    Lead exposure can induce increased blood pressure. Several mechanisms have been proposed to explain lead-induced hypertension. Changes in angiotensinogen (AGT) expression levels or gene variants may also influence blood pressure. In this study, we hypothesized that AGT expression levels or gene variants contribute to lead-induced hypertension. A preliminary HEK293 cell model experiment was performed to analyze the association between AGT expression and lead exposure. In a population-based study, serum AGT level was measured in both lead-exposed and control populations. To further detect the influence of AGT gene single nucleotide polymorphisms (SNPs) in lead-induced hypertension, two SNPs (rs699 and rs4762) were genotyped in a case-control study including 219 lead-exposed subjects and 393 controls. Lead exposure caused an increase in AGT expression level in HEK 293 cell models (P < 0.001) compared to lead-free cells, and individuals exposed to lead had higher systolic and diastolic blood pressure (P < 0.001). Lead-exposed individuals had higher serum AGT levels compared to controls (P < 0.001). However, no association was found between AGT gene SNPs (rs699 and rs4762) and lead exposure. Nevertheless, the change in AGT expression level may play an important role in the development of lead-induced hypertension.

  2. Foetal and postnatal exposure to high temperatures alter growth pattern but do not modify reproductive function in male rabbits.

    PubMed

    Marco-Jiménez, Francisco; Naturil-Alfonso, Carmen; Jiménez-Trigos, Estrella; García-Diego, Fernando; Lavara, Raquel; Vicente, Jose S

    2014-03-01

    The 'foetal origin hypothesis' postulates that a number of organ structures and associated functions undergo programming during embryonic and foetal life and the neonatal period, which determines the set point of physiological and metabolic responses that carry into adulthood. We evaluate the relationship between high environmental temperatures and the reproductive function of male offspring to determine whether pregnant mammals and their infants are potentially vulnerable to the effects of climate change. Rabbit pups were exposed to high temperatures during gestation and lactation. Foetal and postnatal exposure to high temperatures did not alter semen characteristics and was associated with a similar fertility rate and number of pups born. Moreover, males showed reduced rate of maturing and carcass traits at adulthood. Our findings suggest that male exposure during the foetal period to high temperatures did not affect sperm quality but permitted an adaptive phenotypic plasticity of growth in adulthood.

  3. The management of lead exposure in pediatric populations

    SciTech Connect

    Barker, P.O.; Lewis, D.A. )

    1990-12-01

    Chronically elevated lead levels are a common problem affecting children. Although this problem occurs most frequently in the inner city, no community is safe from excessive pediatric lead exposure. Screening by erythrocyte protoporphyrin is a sensitive early indicator of rising lead levels. A Centers for Disease Control report recommends that all children be screened starting at 9 to 12 months. A classification system of various lead levels helps determine proper treatment. Health care practitioners need to be well-informed about lead exposure and how it occurs in order to educate parents. 10 refs.

  4. Gestational and Early Postnatal Exposure to an Environmentally Relevant Mixture of Brominated Flame Retardants: General Toxicity and Skeletal Variations.

    PubMed

    Tung, Emily W Y; Yan, Han; Lefèvre, Pavine L C; Berger, Robert G; Rawn, Dorothea F K; Gaertner, Dean W; Kawata, Alice; Rigden, Marc; Robaire, Bernard; Hales, Barbara F; Wade, Michael G

    2016-06-01

    Brominated flame retardants (BFRs) are stable environmental contaminants known to exert endocrine-disrupting effects. Developmental exposure to polybrominated diphenyl ethers (PBDEs) is correlated with impaired thyroid hormone signaling, as well as estrogenic and anti-androgenic effects. As previous studies have focused on a single congener or technical mixture, the purpose of the current study was to examine the effects of gestational and early postnatal exposure to an environmentally relevant mixture of BFRs designed to reflect house dust levels of PBDEs and hexabromocyclododecane on postnatal developmental outcomes. Pregnant Sprague-Dawley rats were exposed to the PBDE mixture from preconception to weaning (PND 21) through the diet containing 0, 0.75, 250, and 750 mg mixture/kg diet. BFR exposure induced transient reductions in body weight at PND 35 in male and from PND 30-45 in female offspring (250 and 750 mg/kg). Liver weights (PND 21) and xenobiotic metabolizing enzyme activities (PND 21 and 46) were increased in both male and female offspring exposed to 250 and 750 mg/kg diets. Furthermore, serum T4 levels were reduced at PND 21 in both,male and female offspring (250 and 750 mg/kg). At PND 21, Serum alkaline phosphatase (ALP) was decreased in males exposed to 750 mg/kg dietat, and females exposed to 250 and 750 mg/kg diets. At PND 46 ALP was significantly elevated in males (250 and 750 mg/kg). Variations in the cervical vertebrae and phalanges were observed in pups at PND 4 (250 and 750 mg/kg). Therefore, BFR exposure during gestation through to weaning alters developmental programming in the offspring. The persistence of BFRs in the environment remains a cause for concern with regards to developmental toxicity.

  5. Dietary exposure to lead of adults in Shenzhen city, China.

    PubMed

    Pan, Liubo; Wang, Zhou; Peng, Zhaoqiong; Liu, Guihua; Zhang, Huimin; Zhang, Jinzhou; Jiang, Jie; Pathiraja, Nimal; Xiao, Ying; Jiao, Rui; Huang, Wei

    2016-07-01

    Lead, a ubiquitous heavy metal, can be found in the environment and food. The present study is the first to estimate the lead dietary exposure of Shenzhen adults (≥ 20 years old) in various age-gender subgroups, and to assess the associated health risk. Food samples that represented the Shenzhen people's dietary pattern were collected and prepared for analysis. Lead was determined in 13 food groups using 276 individual cooked samples by inductively coupled plasma-mass spectrometry (ICP-MS). Dietary exposures were estimated by combining the analytical results with the local food consumption data of Shenzhen adults. The mean and 95th percentile lead exposure of Shenzhen adults were 0.59-0.73 and 0.75-0.94 μg kg(-1) bw day(-1), respectively. In all food groups, the highest lead exposure was from 'Eggs and their products' (42.4-51.6% of the total exposure); preserved eggs being the main contributor. The other major contributors to lead exposure of Shenzhen adults were 'Fish and seafood, and their products' (14.3-16.7% of the total exposure) and 'Vegetables and their products' (15.5-16.2% of the total exposure). The margin of exposure (MOE) approach was used for the risk assessment of lead, and the results showed that the risk was considered to be low in all age-gender groups for Shenzhen adults. However, having considered a number of toxic effects of lead, it is suggested that more efforts should be made to reduce the lead levels in foodstuff for Shenzhen adults.

  6. DIETARY EXPOSURE OF CHILDREN IN LEAD-LADEN ENVIRONMENTS

    EPA Science Inventory

    Children are the most susceptible population to lead exposure because of three interacting factors; they have more opportunity for contact with lead sources due to their activities, lead absorption occurs more readily in a child compared to an adult, and the child's development i...

  7. DIETARY EXPOSURE OF CHILDREN LIVING IN LEAD-LADEN ENVIRONMENTS

    EPA Science Inventory

    Children are the most susceptible population to lead exposure because of three interacting factors: they have more opportunity for contact with lead sources due to their activities; lead absorption occurs more readily in a child as compared to an adult; and the child's developmen...

  8. DIETARY EXPOSURE OF CHILDREN IN LEAD-LADEN ENVIRONMENTS

    EPA Science Inventory

    Children are the most susceptible population to lead exposure because of three interacting factors; they have more opportunity for contact with lead sources due to their activities, lead absorption occurs more readily in a child compared to an adult, and the child's development i...

  9. DIETARY EXPOSURE OF CHILDREN LIVING IN LEAD-LADEN ENVIRONMENTS

    EPA Science Inventory

    Children are the most susceptible population to lead exposure because of three interacting factors: they have more opportunity for contact with lead sources due to their activities; lead absorption occurs more readily in a child as compared to an adult; and the child's developmen...

  10. Lead exposure and the central auditory processing abilities and cognitive development of urban children: the Cincinnati Lead Study cohort at age 5 years

    SciTech Connect

    Dietrich, K.N.; Succop, P.A.; Berger, O.G.; Keith, R.W. )

    1992-01-01

    This analysis examined the relationship between lead exposure as registered in whole blood (PbB) and the central auditory processing abilities and cognitive developmental status of the Cincinnati cohort (N = 259) at age 5 years. Although the effects were small, higher prenatal, neonatal, and postnatal PbB levels were associated with poorer central auditory processing abilities on the Filtered Word Subtest of the SCAN (a screening test for auditory processing disorders). Higher postnatal PbB levels were associated with poorer performance on all cognitive developmental subscales of the Kaufman Assessment Battery for Children (K-ABC). However, following adjustment for measures of the home environment and maternal intelligence, few statistically or near statistically significant associations remained. Our findings are discussed in the context of the related issues of confounding and the detection of weak associations in high risk populations.

  11. Biological monitoring of child lead exposure in the Czech Republic.

    PubMed Central

    Cikrt, M; Smerhovsky, Z; Blaha, K; Nerudova, J; Sediva, V; Fornuskova, H; Knotkova, J; Roth, Z; Kodl, M; Fitzgerald, E

    1997-01-01

    The area around the Pribram lead smelter has been recognized to be heavily contaminated by lead (Pb). In the early 1970s, several episodes of livestock lead intoxication were reported in this area; thereafter, several epidemiological and ecological studies focused on exposure of children. In contrast to earlier studies, the recent investigation (1992-1994) revealed significantly lower exposure to lead. From 1986-1990, recorded average blood lead levels were about 37.2 micrograms lead (Pb)/100 ml in an elementary school population living in a neighborhood close to the smelter (within 3 km of the plant). The present study, however, has found mean blood lead levels of 11.35 micrograms/100 ml (95% CI = 9.32; 13.82) among a comparable group of children. In addition to blood lead, tooth lead was used to assess exposure among children. Statistically significant differences (p < 0.05) were observed between the geometric mean tooth lead level of 6.44 micrograms Pb/g (n = 13; 95% CI = 3.95; 10.50) in the most contaminated zone and 1.43 micrograms Pb/g (n = 35; 95% CI = 1.11; 1.84) in zones farther away from the point source. Both biomarkers, blood and tooth lead levels, reflect a similar pattern of lead exposure in children. This study has attempted a quantitative assessment of risk factors associated with elevated lead exposure in the Czech Republic. Content of lead in soil, residential distance from the smelter, consumption of locally grown vegetables or fruits, drinking water from local wells, the mother's educational level, cigarette consumption among family members, and the number of children in the family were factors positively related (p < 0.05) to blood lead levels. The resulting blood lead level was found to be inversely proportional to the child's age. Images Figure 1. PMID:9189705

  12. Chronic lead exposure reduces junctional resistance at an electrical synapse.

    PubMed

    Audesirk, G; Audesirk, T

    1984-01-01

    Both acute and chronic lead exposure have been found to inhibit transmission at chemical synapses, possibly by interfering with inward calcium current. We have found that chronic lead exposure slightly reduces input resistance and greatly reduces the junctional resistance between two strongly electrically coupled neurons in the pond snail Lymnaea stagnalis. The net effect is to increase the strength of electrical coupling. A reduction in gap junctional resistance would also be expected to increase the flow of small molecules between cells. However, Lucifer Yellow injections did not reveal dye-coupling between the cells. Lead exposure also increases the capacitance of the neurons.

  13. Effect of exposure to lead on reproduction in male rats

    SciTech Connect

    Piasek, M.; Kostial, K.

    1987-09-01

    The objective of present study was to determine the effect of chronic oral exposure to different levels of lead on male reproductive performance since oral exposure data are more relevant to human environmental exposure. Additionally, most previous results have been obtained after parenteral administration of lead. These experiments were performed on rats by using the incidence of pregnancy to assess male fertility and litter size and pup weight as indicators of the lead effect on perinatal development. Similar parameters were used in reproduction studies by other authors.

  14. Epigenetics, obesity and early-life cadmium or lead exposure.

    PubMed

    Park, Sarah S; Skaar, David A; Jirtle, Randy L; Hoyo, Cathrine

    2017-01-01

    Obesity is a complex and multifactorial disease, which likely comprises multiple subtypes. Emerging data have linked chemical exposures to obesity. As organismal response to environmental exposures includes altered gene expression, identifying the regulatory epigenetic changes involved would be key to understanding the path from exposure to phenotype and provide new tools for exposure detection and risk assessment. In this report, we summarize published data linking early-life exposure to the heavy metals, cadmium and lead, to obesity. We also discuss potential mechanisms, as well as the need for complete coverage in epigenetic screening to fully identify alterations. The keys to understanding how metal exposure contributes to obesity are improved assessment of exposure and comprehensive establishment of epigenetic profiles that may serve as markers for exposures.

  15. Environmental exposure to lead (Pb) and variations in its susceptibility.

    PubMed

    Kim, Jina; Lee, Youngeun; Yang, Mihi

    2014-01-01

    Based on exposure frequency and intrinsic toxicity, lead (Pb) ranks one of the highest priority toxic materials. Continuous regulation of environmental Pb exposure has contributed to dramatically diminished exposure levels of Pb, for example, blood level of Pb. However, the safety level of Pb is not established, as low-level exposure to Pb still shows severe toxicity in high susceptible population and late onset of some diseases from early exposure. In the present study, we focused on food-borne Pb exposure and found broad variations in Pb exposure levels via food among countries. In addition, there are genetic or ethnical variations in Pb-targeted and protective genes. Moreover, various epigenetic alterations were induced by Pb poisoning. Therefore, we suggest a systemic approach including governmental (public) and individual prevention from Pb exposure with continuous biological monitoring and genetic or epigenetic consideration.

  16. Postnatal exposure to a progestin does not prevent uterine adenogenesis in domestic dogs

    PubMed Central

    Ponchon, Tamara; Lopez Merlo, Mariana; Faya, Marcela; Priotto, Marcelo; Barbeito, Claudio

    2016-01-01

    To assess the effects of a single supraphysiological postnatal administration of a progestogen on uterine glands in dogs, 10 females were randomly assigned to a medroxyprogesterone acetate 35 mg (MPA; n = 6) or placebo (n = 4) group within the first 24 h of birth. The safety of the treatment was also evaluated. A transient mild clitoris enlargement appeared in MPA-treated females. Microscopic postpubertal uterine assessment revealed the presence of uterine glands in all cases without significant differences in the area occupied by the glands per µm2 of endometrium nor in the height of the uterine epithelium. PMID:27051347

  17. Childhood Lead Exposure from Battery Recycling in Vietnam.

    PubMed

    Daniell, William E; Van Tung, Lo; Wallace, Ryan M; Havens, Deborah J; Karr, Catherine J; Bich Diep, Nguyen; Croteau, Gerry A; Beaudet, Nancy J; Duy Bao, Nguyen

    2015-01-01

    Battery recycling facilities in developing countries can cause community lead exposure. To evaluate child lead exposure in a Vietnam battery recycling craft village after efforts to shift home-based recycling outside the village. This cross-sectional study evaluated 109 children in Dong Mai village, using blood lead level (BLL) measurement, parent interview, and household observation. Blood samples were analyzed with a LeadCare II field instrument; highest BLLs (≥45 μg/dL) were retested by laboratory analysis. Surface and soil lead were measured at 11 households and a school with X-ray fluorescence analyzer. All children had high BLLs; 28% had BLL ≥45 μg/dL. Younger age, family recycling, and outside brick surfaces were associated with higher BLL. Surface and soil lead levels were high at all tested homes, even with no recycling history. Laboratory BLLs were lower than LeadCare BLLs, in 24 retested children. In spite of improvements, lead exposure was still substantial and probably associated with continued home-based recycling, legacy contamination, and workplace take-home exposure pathways. There is a need for effective strategies to manage lead exposure from battery recycling in craft villages. These reported BLL values should be interpreted cautiously, although the observed field-laboratory discordance may reflect bias in laboratory results.

  18. Childhood Lead Exposure from Battery Recycling in Vietnam

    PubMed Central

    Van Tung, Lo; Wallace, Ryan M.; Havens, Deborah J.; Karr, Catherine J.; Bich Diep, Nguyen; Croteau, Gerry A.; Beaudet, Nancy J.; Duy Bao, Nguyen

    2015-01-01

    Background. Battery recycling facilities in developing countries can cause community lead exposure. Objective. To evaluate child lead exposure in a Vietnam battery recycling craft village after efforts to shift home-based recycling outside the village. Methods. This cross-sectional study evaluated 109 children in Dong Mai village, using blood lead level (BLL) measurement, parent interview, and household observation. Blood samples were analyzed with a LeadCare II field instrument; highest BLLs (≥45 μg/dL) were retested by laboratory analysis. Surface and soil lead were measured at 11 households and a school with X-ray fluorescence analyzer. Results. All children had high BLLs; 28% had BLL ≥45 μg/dL. Younger age, family recycling, and outside brick surfaces were associated with higher BLL. Surface and soil lead levels were high at all tested homes, even with no recycling history. Laboratory BLLs were lower than LeadCare BLLs, in 24 retested children. Discussion. In spite of improvements, lead exposure was still substantial and probably associated with continued home-based recycling, legacy contamination, and workplace take-home exposure pathways. There is a need for effective strategies to manage lead exposure from battery recycling in craft villages. These reported BLL values should be interpreted cautiously, although the observed field-laboratory discordance may reflect bias in laboratory results. PMID:26587532

  19. Immunological effects of occupational exposure to lead (Review).

    PubMed

    Fenga, Concettina; Gangemi, Silvia; Di Salvatore, Valentina; Falzone, Luca; Libra, Massimo

    2017-05-01

    It is well-known that occupational and environmental exposure to several factors, including benzene, heavy metals, chemicals and mineral fibers, is associated with the risk of developing a great number of diseases. Numerous studies have been carried out in order to investigate the mechanisms of toxicity of these substances, with particular regard to the possible toxic effects on the immune system. However, little is known about the influence of heavy metals, such as lead, on the immune system in human populations. Lead is a heavy metal still used in many industrial activities. Human exposure to lead can induce various biological effects depending upon the level and duration of exposure, such as toxic effects on haematological, cardiovascular, nervous and reproductive systems. Several studies demonstrated that exposure to lead is associated to toxic effects also on the immune system, thus increasing the incidence of allergy, infectious disease, autoimmunity or cancer. However, the effects of lead exposure on the human immune system are not conclusive, mostly in occupationally exposed subjects; nevertheless some immunotoxic abnormalities induced by lead have been suggested. In particular, in vivo, in vitro and ex vivo lead is able to improve T helper 2 (Th2) cell development affecting Th1 cell proliferation. Further studies are required to better understand the mechanisms of lead immunotoxicity and the ability of lead to affect preferentially one type of immune response.

  20. The Yugoslavia Prospective Study of environmental lead exposure.

    PubMed Central

    Factor-Litvak, P; Wasserman, G; Kline, J K; Graziano, J

    1999-01-01

    The Yugoslavia Prospective Study of environmental lead exposure has studied the associations between exposure to lead and pregnancy outcomes; childhood neuropsychological, behavioral, and physical development; and hematologic, renal, and cardiovascular function. The cohort comprises 577 children born to women recruited at midpregnancy in two towns in Kosovo, Yugoslavia; one town is the site of a lead smelter, refinery, and battery plant and the other is 25 miles away and relatively unexposed. A sample of these children has been followed at 6-month intervals through 7.5 years of age. Blood lead concentrations ranged from 1 to 70 microg/dl. Exposure to lead was not associated with adverse pregnancy outcomes. Exposure was associated with modest decrements in intelligence, small increases in blood pressure, higher risks of proteinuria, small increases in behavior problems, and perturbed hematopoiesis. Only at low level exposures (i.e., <16 microg/dl) were small associations with decreased height found. We discuss methodological problems that may hinder causal interpretation of these data, namely, use of blood lead concentration as an exposure measure, confounding, and town-specific associations. We conclude that while reported associations are small, collectively they lend support to the notion that lead is a toxicant with numerous adverse health effects. Images Figure 1 PMID:9872712

  1. Association between Prenatal Lead Exposure and Blood Pressure in Children

    PubMed Central

    Zhang, Aimin; Sánchez, Brisa N.; Ettinger, Adrienne S.; Park, Sung Kyun; Cantonwine, David; Schnaas, Lourdes; Wright, Robert O.; Lamadrid-Figueroa, Hector; Tellez-Rojo, Martha Maria

    2011-01-01

    Background: Lead exposure in adults is associated with hypertension. Altered prenatal nutrition is associated with subsequent risks of adult hypertension, but little is known about whether prenatal exposure to toxicants, such as lead, may also confer such risks. Objectives: We investigated the relationship of prenatal lead exposure and blood pressure (BP) in 7- to 15-year-old boys and girls. Methods: We evaluated 457 mother–child pairs, originally recruited for an environmental birth cohort study between 1994 and 2003 in Mexico City, at a follow-up visit in 2008–2010. Prenatal lead exposure was assessed by measurement of maternal tibia and patella lead using in vivo K-shell X-ray fluorescence and cord blood lead using atomic absorption spectrometry. BP was measured by mercury sphygmomanometer with appropriate-size cuffs. Results: Adjusting for relevant covariates, maternal tibia lead was significantly associated with increases in systolic BP (SBP) and diastolic BP (DBP) in girls but not in boys (p-interaction with sex = 0.025 and 0.007 for SBP and DBP, respectively). Among girls, an interquartile range increase in tibia lead (13 μg/g) was associated with 2.11-mmHg [95% confidence interval (CI): 0.69, 3.52] and 1.60-mmHg (95% CI: 0.28, 2.91) increases in SBP and DBP, respectively. Neither patella nor cord lead was associated with child BP. Conclusions: Maternal tibia lead, which reflects cumulative environmental lead exposure and a source of exposure to the fetus, is a predisposing factor to higher BP in girls but not boys. Sex-specific adaptive responses to lead toxicity during early-life development may explain these differences. PMID:21947582

  2. Biomarkers of lead exposure and DNA methylation within retrotransposons.

    PubMed

    Wright, Robert O; Schwartz, Joel; Wright, Rosalind J; Bollati, Valentina; Tarantini, Letizia; Park, Sung Kyun; Hu, Howard; Sparrow, David; Vokonas, Pantel; Baccarelli, Andrea

    2010-06-01

    DNA methylation is an epigenetic mark that regulates gene expression. Changes in DNA methylation within white blood cells may result from cumulative exposure to environmental metals such as lead. Bone lead, a marker of cumulative exposure, may therefore better predict DNA methylation than does blood lead. In this study we compared associations between lead biomarkers and DNA methylation. We measured global methylation in participants of the Normative Aging Study (all men) who had archived DNA samples. We measured patella and tibia lead levels by K-X-Ray fluorescence and blood lead by atomic absorption spectrophotometry. DNA samples from blood were used to determine global methylation averages within CpG islands of long interspersed nuclear elements-1 (LINE-1) and Alu retrotransposons. A mixed-effects model using repeated measures of Alu or LINE-1 as the dependent variable and blood/bone lead (tibia or patella in separate models) as the primary exposure marker was fit to the data. Overall mean global methylation (+/- SD) was 26.3 +/- 1.0 as measured by Alu and 76.8 +/- 1.9 as measured by LINE-1. In the mixed-effects model, patella lead levels were inversely associated with LINE-1 (beta = -0.25; p < 0.01) but not Alu (beta = -0.03; p = 0.4). Tibia lead and blood lead did not predict global methylation for either Alu or LINE-1. Patella lead levels predicted reduced global DNA methylation within LINE-1 elements. The association between lead exposure and LINE-1 DNA methylation may have implications for the mechanisms of action of lead on health outcomes, and also suggests that changes in DNA methylation may represent a biomarker of past lead exposure.

  3. Effect of prenatal and postnatal exposure to therapeutic doses of chlorimipramine on emotionality in the rat.

    PubMed

    Rodríguez Echandía, E L; Broitman, S T

    1983-01-01

    Prenatal administration of high doses of tricyclic antidepressants have been reported to produce teratogenic and behavioral effects in rat offspring. In the present work, behavioral abnormalities are described in offspring of rats treated with therapeutic doses of chlorimipramine (CIM) during pregnancy (CIM-P), lactation (CIM-L) and during the whole pregnancy-lactation period (CIM-PL). CIM-P treatment did not produce teratogenic effects, did not affect number or body weight of pups at birth and did not induce neonatal mortality. At 2 months of age, the CIM-P males showed a significant increase in digging and grooming (familiar environment test), a decrease in "exploration" (novel environment test) and a decrease in active social interactions (social behavior test). Females were more resistant than males to the prenatal CIM treatment. The results suggest increased emotionality in CIM-P pups. Some behavioral abnormalities were also observed in the tests performed at 4 months of age. CIM-L treatment had minor effects on litter behavior. CIM-PL treatment potentiated the effects of the CIM-P treatment. In the CIM-PL males, impairment of exploration of a novel environment still remained in the tests performed at 4 months of age. It is speculated that when prenatal brain development is altered by CIM, further postnatal treatment may impair compensatory processes occurring in early postnatal life.

  4. Chronic exposure of adult, postnatal and in utero rat models to low-dose 137Cesium: impact on circulating biomarkers.

    PubMed

    Manens, Line; Grison, Stéphane; Bertho, Jean-Marc; Lestaevel, Philippe; Guéguen, Yann; Benderitter, Marc; Aigueperse, Jocelyne; Souidi, Maâmar

    2016-11-01

    The presence of (137)Cesium ((137)Cs) in the environment after nuclear accidents at Chernobyl and more recently Fukushima Daiichi raises many health issues for the surrounding populations chronically exposed through the food chain. To mimic different exposure situations, we set up a male rat model of exposure by chronic ingestion of a (137)Cs concentration likely to be ingested daily by residents of contaminated areas (6500 Bq.l(-1)) and tested contaminations lasting 9 months for adult, neonatal and fetal rats. We tested plasma and serum biochemistry to identify disturbances in general indicators (lipids, proteins, carbohydrates and electrolytes) and in biomarkers of thyroid, heart, brain, bone, kidney, liver and testis functions. Analysis of the general indicators showed increased levels of cholesterol (+26%), HDL cholesterol (+31%), phospholipids B (+15%) and phosphorus (+100%) in the postnatal group only. Thyroid, heart, brain, bone and kidney functions showed no blood changes in any model. The liver function evaluation showed changes in total bilirubin (+67%) and alkaline phosphatase (-11%) levels, but only for the rats exposed to (137)Cs intake in adulthood. Large changes in 17β-estradiol (-69%) and corticosterone (+36%) levels affected steroidogenesis, but only in the adult model. This study showed that response profiles differed according to age at exposure: lipid metabolism was most radiosensitive in the postnatal model, and steroid hormone metabolism was most radiosensitive in rats exposed in adulthood. There was no evidence of deleterious effects suggesting a potential impact on fertility or procreation. © The Author 2016. Published by Oxford University Press on behalf of The Japan Radiation Research Society and Japanese Society for Radiation Oncology.

  5. The identification of lead ammunition as a source of lead exposure in First Nations: the use of lead isotope ratios.

    PubMed

    Tsuji, Leonard J S; Wainman, Bruce C; Martin, Ian D; Sutherland, Celine; Weber, Jean-Philippe; Dumas, Pierre; Nieboer, Evert

    2008-04-15

    The use of lead shotshell to hunt water birds has been associated with lead-contamination in game meat. However, evidence illustrating that lead shotshell is a source of lead exposure in subsistence hunting groups cannot be deemed definitive. This study seeks to determine whether lead shotshell constitutes a source of lead exposure using lead isotope ratios. We examined stable lead isotope ratios for lichens, lead shotshell and bullets, and blood from residents of Fort Albany and Kashechewan First Nations, and the City of Hamilton, Ontario, Canada. Data were analyzed using ANOVA and regression analyses. ANOVA of isotope ratios for blood revealed significant differences with respect to location, but not sex. Hamilton differed from both Kashechewan and Fort Albany; however, the First Nations did not differ from each other. ANOVA of the isotope ratios for lead ammunition and lichens revealed no significant differences between lichen groups (north and south) and for the lead ammunition sources (pellets and bullets). A plot of (206)Pb/(204)Pb and (206)Pb/(207)Pb values illustrated that lichens and lead ammunition were distinct groupings and only the 95% confidence ellipse of the First Nations group overlapped that of lead ammunition. In addition, partial correlations between blood-lead levels (adjusted for age) and isotope ratios revealed significant (p<0.05) positive correlations for (206)Pb/(204)Pb and (206)Pb/(207)Pb, and a significant negative correlation for (208)Pb/(206)Pb, as predicted if leaded ammunition were the source of lead exposure. In conclusion, lead ammunition was identified as a source of lead exposure for First Nations people; however, the isotope ratios for lead shotshell pellets and bullets were indistinguishable. Thus, lead-contaminated meat from game harvested with lead bullets may also be contributing to the lead body burden.

  6. Prenatal and early postnatal exposure to high-saturated-fat diet represses Wnt signaling and myogenic genes in offspring rats.

    PubMed

    Yang, Ke-Feng; Shen, Xiu-Hua; Cai, Wei

    2012-08-01

    The prenatal and early postnatal period is a key developmental window for nutrition status, and high-fat exposure in this period has been shown to be associated with type 2 diabetes, obesity and other features of metabolic disorders later in life. The present study was designed to investigate the underlying molecular mechanisms and role of relative genes involved in this process. We investigated the impact of prenatal and early postnatal exposure to a high-saturated-fat diet on the regulation of the Wnt signaling pathway and myogenic genes in skeletal muscle of rat offspring as well as the serum and muscle physiological outcomes. Timed-pregnant Sprague-Dawley rats were fed either a control (C, 16% kcal fat) or high-saturated-fat diet (HF, 45% kcal fat) throughout gestation and lactation. After weaning, female offspring were fed a control diet to generate two offspring groups: control diet-fed offspring of control diet-fed dams (C/C) and control diet-fed offspring of HF diet-fed dams (HF/C). The serum glucose of the HF/C offspring (5.58 ± 0.26 mmol/L) was significantly higher than that of C/C offspring (4.97 ± 0.28 mmol/L), and the Homeostasis Model Assessment-Insulin Resistance of HF/C offspring (2.00 ± 0.11) was also significantly higher when compared with C/C (1.84 ± 0.09). Furthermore, HF/C offspring presented excessive intramuscular fat accumulation (1.8-fold, P < 0.05) and decreased muscle glycogen (1.3-fold, P < 0.05), as well as impairment of muscle development at the age of 12 weeks. Meanwhile, we observed the repression of Wnt/β-catenin signaling and myogenic genes in HF/C offspring. The present study indicates that prenatal and early postnatal exposure to a high-saturated-fat diet suppresses the development of skeletal muscle and myogenic genes via Wnt/β-catenin signaling, and the inappropriate muscle development could potentially contribute to the predisposition of offspring to develop metabolic-syndrome-like phenotype in adulthood.

  7. The effects of postnatal alcohol exposure and galantamine on the context pre-exposure facilitation effect and acetylcholine efflux using in vivo microdialysis.

    PubMed

    Perkins, Amy E; Fadel, Jim R; Kelly, Sandra J

    2015-05-01

    Fetal alcohol spectrum disorders (FASD) are characterized by damage to multiple brain regions, including the hippocampus, which is involved in learning and memory. The acetylcholine neurotransmitter system provides major input to the hippocampus and is a possible target of developmental alcohol exposure. Alcohol (3.0 g/kg/day) was administered via intubation to male rat pups (postnatal day [PD] 2-10; ethanol-treated [ET]). Controls received a sham intubation (IC) or no treatment (NC). Acetylcholine efflux was measured using in vivo microdialysis (PD 32-35). ET animals were not different at baseline, but had decreased K(+)/Ca(2+)-induced acetylcholine efflux compared to NC animals and an enhanced acetylcholine response to galantamine (acetylcholinesterase inhibitor; 2.0 mg/kg) compared to both control groups. A separate cohort of animals was tested in the context pre-exposure facilitation effect task (CPFE; PD 30-32) following postnatal alcohol exposure and administration of galantamine (2.0 mg/kg; PD 11-30). Neither chronic galantamine nor postnatal alcohol exposure influenced performance in the CPFE task. Using immunohistochemistry, we found that neither alcohol exposure nor behavioral testing significantly altered the density of vesicular acetylcholine transporter or alpha7 nicotinic acetylcholine receptor in the ventral hippocampus (CA1). In the medial septum, the average number of choline acetyltransferase (ChAT+) cells was increased in ET animals that displayed the context-shock association; there were no changes in IC and NC animals that learned the context-shock association or in any animals that were in the control task that entailed no learning. Taken together, these results indicate that the hippocampal acetylcholine system is significantly disrupted under conditions of pharmacological manipulations (e.g., galantamine) in alcohol-exposed animals. Furthermore, ChAT was up‑regulated in ET animals that learned the CPFE, which may account for their ability

  8. Control of excessive lead exposure in radiator repair workers

    SciTech Connect

    Not Available

    1991-03-01

    In 1988, 83 automotive repair workers with blood lead levels (BLLs) greater than 25 micrograms/dL were reported to state health departments in the seven states that collaborated with CDC's National Institute for Occupational Safety and Health (NIOSH) in maintaining registries of elevated BLLs in adults. In 18 (22%) of these 83 persons, BLLs were greater than 50 micrograms/dL. Among automotive repair workers for whom a job category was specified, radiator repair work was the principal source of lead exposure. The major sources of exposure for radiator repair workers are lead fumes generated during soldering and lead dust produced during radiator cleaning. This report summarizes current BLL surveillance data for radiator repair workers and describes three control technologies that are effective in reducing lead exposures in radiator repair shops.

  9. Control of excessive lead exposure in radiator repair workers.

    PubMed

    1991-03-01

    In 1988, 83 automotive repair workers with blood lead levels (BLLs) greater than 25 micrograms/dL were reported to state health departments in the seven states that collaborated with CDC's National Institute for Occupational Safety and Health (NIOSH) in maintaining registries of elevated BLLs in adults. In 18 (22%) of these 83 persons, BLLs were greater than 50 micrograms/dL. Among automotive repair workers for whom a job category was specified, radiator repair work was the principal source of lead exposure. The major sources of exposure for radiator repair workers are lead fumes generated during soldering and lead dust produced during radiator cleaning. This report summarizes current BLL surveillance data for radiator repair workers and describes three control technologies that are effective in reducing lead exposures in radiator repair shops.

  10. Exposure to lead in stained glass work. An environmental evaluation.

    PubMed

    Pant, B C; Harrison, J R; Long, G W; Gupta, S

    1994-01-25

    An environmental evaluation was conducted to determine lead exposure in a group of crafts people who produce stained glass and Tiffany glass. The environmental evaluation consisted of air sampling for potential lead emissions from solder and of work area dusts. In addition, the completion of a questionnaire, observation of work practices and noting of other details relevant to hazardous exposures were carried out. Lead concentrations in air were found to be well below the ACGIH TLV-TWA of 150 micrograms/m3. High lead concentrations were found in the work area dust samples. Exposure to high concentrations of lead could occur by ingestion as a result of neglect of basic hygiene precautions.

  11. Prenatal and lactational lead exposure enhanced oxidative stress and altered apoptosis status in offspring rats' hippocampus.

    PubMed

    Lu, Xiaobo; Jin, Cuihong; Yang, Jinghua; Liu, Qiufang; Wu, Shengwen; Li, Dandan; Guan, Yangyang; Cai, Yuan

    2013-01-01

    Oxidative stress and apoptosis facilitation in the developing central nervous system (CNS) have been inferred as two mechanisms related to lead's neurotoxicity, and excessive reactive oxygen species (ROS) can promote oxidative stress and apoptosis facilitation. Few studies systematically investigated the potential relationship among oxidative stress, ROS generation, and apoptosis facilitation after lead exposure in earlier life as a whole. To better understand the adverse effect on the developing central nervous system (CNS) after lead exposure during pregnancy and lactation, the indexes of oxidative stress, apoptosis status, and Bax and Bcl-2 expression of offspring rats' hippocampus were determined. Pregnant rats were randomly divided into four groups and given free access to drinking water which contained 0 %, 0.05 %, 0.1 %, and 0.2 % Pb(AC)(2) respectively from gestation day 0 to postnatal day 21 (PND21). Results showed that ROS and malondialdehyde level of either PND7 or PND21 pups' hippocampus were significantly raised; reduced glutathione level and superoxide dismutase activity were obviously decreased following the increase of blood and brain lead level. Similar to apoptotic indexes, Bax/Bcl-2 ratio increased after 0.1 % and 0.2 % Pb(AC)(2) exposure, especially for the pups on PND7. Comparing with cortex, the hippocampus seemed much more sensitive to damage induced by lead. We concluded that the disruption of pro-oxidant and antioxidant balance and apoptosis facilitation could be associated with the mechanisms of neurotoxicity after lead exposure in earlier life.

  12. Study and models of total lead exposures of battery workers.

    PubMed

    Chavalitnitikul, C; Levin, L; Chen, L C

    1984-12-01

    In an attempt to establish a more realistic and reliable model for relating environmental exposure measurements to the biological indices of exposure, a study was undertaken to quantify the total sources of lead exposure among lead storage battery workers. In addition to the usual personal and area lead air sampling, quantitative and repeatable measurements of removable lead from work surfaces and the workers' hands and faces were obtained daily for ten consecutive work days in the pasting and battery assembly departments. Mathematical correlations of blood lead and zinc protoporphyrin (ZPP) levels as the dependent variable with the lead exposure sources were derived and demonstrated most strongly as log-log relationships. Statistical analyses by computer programming indicated that the airborne, hand, facial and work surface levels have a high degree of inter-correlation with a very significant positive individual correlation with blood lead levels and a somewhat lower correlation with ZPP. The results suggest that contaminated personal and work surfaces may play a more significant role in toxic occupational and environmental exposures, generally, than had heretofore been demonstrated or suspected.

  13. Port Pirie Cohort Study: environmental exposure to lead and children's abilities at the age of four years

    SciTech Connect

    McMichael, A.J.; Baghurst, P.A.; Wigg, N.R.; Vimpani, G.V.; Robertson, E.F.; Roberts, R.J.

    1988-08-25

    We studied the effect of environmental exposure to lead on children's abilities at the age of four years in a cohort of 537 children born during 1979 to 1982 to women living in a community situated near a lead smelter. Samples for measuring blood lead levels were obtained from the mothers antenatally, at delivery from the mothers and umbilical cords, and at the ages of 6, 15, and 24 months and then annually from the children. Concurrently, the mothers were interviewed about personal, family, medical, and environmental factors. Maternal intelligence, the home environment, and the children's mental development (as evaluated with use of the McCarthy Scales of Children's Abilities) were formally assessed. The mean blood lead concentration varied from 0.44 mumol per liter in midpregnancy to a peak of 1.03 mumol per liter at the age of two years. The blood lead concentration at each age, particularly at two and three years, and the integrated postnatal average concentration were inversely related to development at the age of four. Multivariate analysis incorporating many factors in the children's lives indicated that the subjects with an average postnatal blood lead concentration of 1.50 mumol per liter had a general cognitive score 7.2 points lower (95 percent confidence interval, 0.3 to 13.2; mean score, 107.1) than those with an average concentration of 0.50 mumol per liter. Similar deficits occurred in the perceptual-performance and memory scores. Within the range of exposure studied, no threshold dose for an effect of lead was evident. We conclude that postnatal blood lead concentration is inversely related to cognitive development in children, although one must be circumspect in making causal inferences from studies of this relation, because of the difficulties in defining and controlling confounding effects.

  14. A new neurobehavioral model of autism in mice: pre- and postnatal exposure to sodium valproate.

    PubMed

    Wagner, George C; Reuhl, Kenneth R; Cheh, Michelle; McRae, Paulette; Halladay, Alycia K

    2006-08-01

    Autism symptoms, including impairments in language development, social interactions, and motor skills, have been difficult to model in rodents. Since children exposed in utero to sodium valproate (VPA) demonstrate behavioral and neuroanatomical abnormalities similar to those seen in autism, the neurodevelopmental effects of this antiepileptic agent were examined in mice following its pre- or postnatal administration. Exposed pups were evaluated in a battery of neurodevelopmental procedures designed to assess VPA-induced retardation (wherein a behavior fails to mature on schedule), regression (wherein a behavior does mature on time but then deteriorates), or intrusions (wherein normal behaviors are overshadowed by stereotypic or self-injurious behaviors). The resulting observations were interpreted in the context of this new strategy to model autism.

  15. Postnatal exposure to flutamide affects CDH1 and CTNNB1 gene expression in adult pig epididymis and prostate and alters metabolism of testosterone.

    PubMed

    Gorowska, E; Zarzycka, M; Chojnacka, K; Bilinska, B; Hejmej, A

    2014-03-01

    In both epididymis and prostate the dynamic cross-talk between the cells is hormonally regulated and, in part, through direct cell-to-cell interactions. Functionality of the male reproductive organs may be affected by exposure to specific chemicals, so-called 'reprotoxicants'. In this study we tested whether early postnatal and prepubertal exposure to anti-androgen flutamide altered the expression of adherens junction genes encoding E-cadherin (CDH1) and β-catenin (CTNNB1) in adult pig epididymis and prostate. In addition, the expression of mRNAs and proteins for 5α-reductase (ST5AR2) and aromatase (CYP19A1) were examined to show whether flutamide alters metabolism of testosterone. Thus, flutamide was injected into male piglets between Days 2 and 10 and between Days 90 and 98 postnatally (PD2 and PD90; 50 mg/kg bw), tissues that were obtained on postnatal Day 270. To assess the expression of the genes and proteins, real-time RT-PCR and Western blot were performed respectively. Moreover, adherens junction proteins were localized by immunohistochemistry. In response to flutamide, CDH1 and CTNNB1 expressions were down-regulated along the epididymis, mostly in PD2 group (p < 0.001, p < 0.01). In the prostate, CDH1 mRNA and protein expressions were significantly down-regulated (p < 0.01), whereas CTNNB1 mRNA was slightly up-regulated in both flutamide-treated groups. CTNNB1 protein level was markedly elevated in both PD2 (p < 0.001) and PD90 (p < 0.01) groups. In the epididymis, the expression of ST5AR2 and CYP19A1 was down- and up-regulated, respectively (p < 0.05), whereas in the prostate evident decrease in CYP19A1 expression (p < 0.001, p < 0.01, p < 0.05) was demonstrated. In both tissues, membranous immunolocalization of CTNNB1 suggests its involvement in cell-cell adhesion. Overall, flutamide administration resulted in suppression of androgen action in the epididymis and prostate leading to deregulation of CDH1 and CTNNB1 gene expressions which is probably

  16. Site-specific lead exposure from lead pellet ingestion in sentinel mallards

    USGS Publications Warehouse

    Rocke, T.E.; Brand, C.J.; Mensik, John G.

    1997-01-01

    We monitored lead poisoning from the ingestion of spent lead pellets in sentinel mallards (Anas platyhrynchos) at the Sacramento National Wildlife Refuge (SNWR), Willows, California for 4 years (1986-89) after the conversion to steel shot for waterfowl hunting on refuges in 1986. Sentinel mallards were held in 1.6-ha enclosures in 1 hunted (P8) and 2 non-hunted (T19 and TF) wetlands. We compared site-specific rates of lead exposure, as determined by periodic measurement of blood lead concentrations, and lead poisoning mortality between wetlands with different lead pellet densities, between seasons, and between male and female sentinels. In 1986, the estimated 2-week rate of lead exposure was significantly higher (P < 0.005) in P8 (43.8%), the wetland with the highest density of spent lead pellets (>2,000,000 pellets/ha), than in those with lower densities of lead pellets, T19 (18.1%; 173,200 pellets/ha) and TF (0.9%; 15,750 pellets/ha). The probability of mortality from lead poisoning was also significantly higher (P < 0.01) in sentinel mallards enclosed in P8 (0.25) than T19 (0) and TF (0) in 1986 and remained significantly higher (P < 0.001) during the 4-year study. Both lead exposure and the probability of lead poisoning mortality in P8 were significantly higher (P < 0.001) in the fall of 1986 (43.8%; 0.25), before hunting season, than in the spring of 1987 (21.6%; 0.04), after hunting season. We found no significant differences in the rates of lead exposure or lead poisoning mortality between male and female sentinel mallards. The results of this study demonstrate that in some locations, lead exposure and lead poisoning in waterfowl will continue to occur despite the conversion to steel shot for waterfowl hunting.

  17. Site-specific lead exposure from lead pellet ingestion in sentinel mallards

    USGS Publications Warehouse

    Rocke, T.E.; Brand, C.J.; Mensik, John G.

    1997-01-01

    We monitored lead poisoning from the ingestion of spent lead pellets in sentinel mallards (Anas platyhrynchos) at the Sacramento National Wildlife Refuge (SNWR), Willows, California for 4 years (1986-89) after the conversion to steel shot for waterfowl hunting on refuges in 1986. Sentinel mallards were held in 1.6-ha enclosures in 1 hunted (P8) and 2 non-hunted (T19 and TF) wetlands. We compared site-specific rates of lead exposure, as determined by periodic measurement of blood lead concentrations, and lead poisoning mortality between wetlands with different lead pellet densities, between seasons, and between male and female sentinels. In 1986, the estimated 2-week rate of lead exposure was significantly higher (P < 0.005) in P8 (43.8%), the wetland with the highest density of spent lead pellets (>2,000,000 pellets/ha), than in those with lower densities of lead pellets, T19 (18.1%; 173,200 pellets/ha) and TF (0.9%; 15,750 pellets/ha). The probability of mortality from lead poisoning was also significantly higher (P < 0.01) in sentinel mallards enclosed in P8 (0.25) than T19 (0) and TF (0) in 1986 and remained significantly higher (P < 0.001) during the 4-year study. Both lead exposure and the probability of lead poisoning mortality in P8 were significantly higher (P < 0.001) in the fall of 1986 (43.8%; 0.25), before hunting season, than in the spring of 1987 (21.6%; 0.04), after hunting season. We found no significant differences in the rates of lead exposure or lead poisoning mortality between male and female sentinel mallards. The results of this study demonstrate that in some locations, lead exposure and lead poisoning in waterfowl will continue to occur despite the conversion to steel shot for waterfowl hunting.

  18. Association of Cumulative Lead Exposure with Parkinson’s Disease

    PubMed Central

    Weisskopf, Marc G.; Weuve, Jennifer; Nie, Huiling; Saint-Hilaire, Marie-Helene; Sudarsky, Lewis; Simon, David K.; Hersh, Bonnie; Schwartz, Joel; Wright, Robert O.; Hu, Howard

    2010-01-01

    Background Research using reconstructed exposure histories has suggested an association between heavy metal exposures, including lead, and Parkinson’s disease (PD), but the only study that used bone lead, a biomarker of cumulative lead exposure, found a nonsignificant increase in risk of PD with increasing bone lead. Objectives We sought to assess the association between bone lead and PD. Methods Bone lead concentrations were measured using 109Cd excited K-shell X-ray fluorescence from 330 PD patients (216 men, 114 women) and 308 controls (172 men, 136 women) recruited from four clinics for movement disorders and general-community cohorts. Adjusted odds ratios (ORs) for PD were calculated using logistic regression. Results The average age of cases and controls at bone lead measurement was 67 (SD = 10) and 69 (SD = 9) years of age, respectively. In primary analyses of cases and controls recruited from the same groups, compared with the lowest quartile of tibia lead, the OR for PD in the highest quartile was 3.21 [95% confidence interval (CI), 1.17–8.83]. Results were similar but slightly weaker in analyses restricted to cases and controls recruited from the movement disorders clinics only (fourth-quartile OR = 2.57; 95% CI, 1.11–5.93) or when we included controls recruited from sites that did not also contribute cases (fourth-quartile OR = 1.91; 95% CI, 1.01–3.60). We found no association with patella bone lead. Conclusions These findings, using an objective biological marker of cumulative lead exposure among typical PD patients seen in our movement disorders clinics, strengthen the evidence that cumulative exposure to lead increases the risk of PD. PMID:20807691

  19. Association of cumulative lead exposure with Parkinson's disease.

    PubMed

    Weisskopf, Marc G; Weuve, Jennifer; Nie, Huiling; Saint-Hilaire, Marie-Helene; Sudarsky, Lewis; Simon, David K; Hersh, Bonnie; Schwartz, Joel; Wright, Robert O; Hu, Howard

    2010-11-01

    Research using reconstructed exposure histories has suggested an association between heavy metal exposures, including lead, and Parkinson's disease (PD), but the only study that used bone lead, a biomarker of cumulative lead exposure, found a nonsignificant increase in risk of PD with increasing bone lead. We sought to assess the association between bone lead and PD. Bone lead concentrations were measured using 109Cd excited K-shell X-ray fluorescence from 330 PD patients (216 men, 114 women) and 308 controls (172 men, 136 women) recruited from four clinics for movement disorders and general-community cohorts. Adjusted odds ratios (ORs) for PD were calculated using logistic regression. The average age of cases and controls at bone lead measurement was 67 (SD = 10) and 69 (SD = 9) years of age, respectively. In primary analyses of cases and controls recruited from the same groups, compared with the lowest quartile of tibia lead, the OR for PD in the highest quartile was 3.21 [95% confidence interval (CI), 1.17-8.83]. Results were similar but slightly weaker in analyses restricted to cases and controls recruited from the movement disorders clinics only (fourth-quartile OR = 2.57; 95% CI, 1.11-5.93) or when we included controls recruited from sites that did not also contribute cases (fourth-quartile OR = 1.91; 95% CI, 1.01-3.60). We found no association with patella bone lead. These findings, using an objective biological marker of cumulative lead exposure among typical PD patients seen in our movement disorders clinics, strengthen the evidence that cumulative exposure to lead increases the risk of PD.

  20. Parental occupational lead exposure and lead concentration of newborn cord blood

    SciTech Connect

    Wang, J.D.; Shy, W.Y.; Chen, J.S.; Yang, K.H.; Hwang, Y.H.

    1989-01-01

    The purpose of this study was to determine the influence of parental occupational lead exposure on the lead levels of newborn cord blood in the Taipei area. From September 1984 to June 1985, 5,000 pregnant women voluntarily participated in the study at the Taipei Municipal Maternal and Child Hospital. Each woman was interviewed regarding her and her husband's occupational exposures; 2,948 successfully delivered healthy newborns, and cord blood samples were obtained using Terumo Venoject, and 242 samples were analyzed by graphite furnace atomic absorption spectrometry using an Instrumentation Laboratory 251 instrument. Nine cord blood samples were from newborns with both parents exposed, 26 samples had maternal exposure only, 105 samples had paternal exposure only, and 102 were nonexposed. The results showed that the average lead level of cord blood with both parents exposed was 8.9 +/- 2.9 micrograms%, maternal exposure 9.0 +/- 3.8 micrograms%, paternal exposure 8.3 +/- 3.4 micrograms%, and 6.9 +/- 3.2 micrograms% in the nonexposed group. There were significant differences between the nonexposed and the maternal exposure groups, and also between the nonexposed and paternal exposure groups. All 26 maternal exposures were from lead soldering operations. Multivariate analysis revealed that, after control of father's exposure status, newborn cord blood lead level increased 0.27 micrograms% for each hour the mother spent on lead soldering during a normal working day, thus suggesting that soldering during pregnancy may be hazardous to newborns. Paternal contribution to the cord blood lead levels seemed to be through either working at home with the pregnant mother also at home or bringing work clothes home for laundering.

  1. Early childhood lead exposure and exceptionality designations for students.

    PubMed

    Miranda, Marie Lynn; Maxson, Pamela; Kim, Dohyeong

    2010-01-01

    The achievement gap continues to be an important educational issue, with disadvantaged groups exhibiting poorer school performance. Recently, literature has shown that even very low levels of early lead exposure affect cognitive and academic performance. As individuals at the lower end of the socioeconomic spectrum are more likely to be exposed to lead, this exposure may be an important contributor to the achievement gap. In this paper, we explore whether early childhood blood lead levels are associated with membership in exceptionality designation groups. In addition, we examine the racial and socioeconomic composition of these exceptional groups. Data from the North Carolina Childhood Lead Poisoning Prevention Program surveillance registry were linked at the individual child level to educational outcomes available through the North Carolina Education Research Data Center. Designation into exceptionality groups was obtained from the end-of-grade (EOG) data. Both standard bivariate and multivariate analyses were employed. Bivariate analyses indicate that blood lead levels and reading EOG scores differ by exceptionality, as well as by race and enrollment in free/reduced lunch. Logistic regression confirmed the relationship between blood lead levels and likelihood of exceptionality. Contextual factors - enrollment in the free/reduced lunch program, race, and parental education - are also significant with regard to exceptionality. This study demonstrates that early childhood lead exposure significantly influences the likelihood of being designated exceptional. These results provide additional evidence that early childhood lead exposure is a significant explanator of the achievement gap.

  2. Artificial Christmas trees: how real are the lead exposure risks?

    PubMed

    Maas, Richard P; Patch, Steven C; Pandolfo, Tamara J

    2004-12-01

    Exposure to lead has long been recognized as a major public health issue in the United States and other industrialized nations. The health risks associated with low lead levels mean that consumer products (such as those made from polyvinyl chloride [PVC] plastic, which often incorporates lead as a stabilizer) with even moderate lead exposure risks could be dangerous. The purpose of the experiments reported in this article was to test for lead exposure from artificial Christmas trees made of PVC, which are now present in an estimated 50 million U.S. households. The first phase of experimentation tested artificial Christmas trees in the laboratory for lead content in branches, lead transfer from hand contact, and lead dust levels under the tree. The second phase was based on a field-testing survey of households with artificial Christmas trees. Results from these experiments show that, while the average artificial Christmas tree does not present a significant exposure risk, in the worst-case scenarios a substantial health risk to young children is quite possible.

  3. Prenatal and postnatal tobacco exposure and behavioral problems in 10-year-old children: results from the GINI-plus prospective birth cohort study.

    PubMed

    Rückinger, Simon; Rzehak, Peter; Chen, Chih-Mei; Sausenthaler, Stefanie; Koletzko, Sibylle; Bauer, Carl-Peter; Hoffmann, Ute; Kramer, Ursula; Berdel, Dietrich; von Berg, Andrea; Bayer, Otmar; Wichmann, H-Erich; von Kries, Rüdiger; Heinrich, Joachim

    2010-01-01

    Prenatal and postnatal tobacco exposure have been reported to be associated with behavioral problems. However, the magnitude of the association with tobacco exposure at specific periods of exposure is unclear. We assessed the relative risk of behavioral problems in children who had been exposed to tobacco smoke in utero and postnatally. We analyzed data from a prospective birth cohort study in two cities in Germany: the German Infant Nutrition Intervention. Our sample included 5,991 children born between 1995 and 1998 as well as their parents. We measured behavioral problems using the Strength and Difficulties Questionnaire (SDQ) at follow-up 10 years after birth. According to prespecified SDQ cutoff values, children were classified as "normal," "borderline," or "abnormal" according to the subscales "emotional symptoms," "conduct problems," "hyperactivity/inattention," "peer-relationship problems," and a total difficulties score. Smoke exposure and further covariates were assessed using parent questionnaires. Compared with children not exposed to tobacco smoke, children exposed both pre- and postnatally to tobacco smoke had twice the estimated risk [95% confidence interval (CI), 1.4-3.1] of being classified as abnormal according to the total difficulties score of the SDQ at 10 years of age. Children who were only prenatally exposed had a 90% higher relative risk (95% CI, 0.9-4.0), whereas children who were only postnatally exposed had a 30% higher relative risk (95% CI, 0.9-1.9). These results could not be explained by confounding by parental education, father's employment, child's time spent in front of computer or television screen, being a single father or mother, or mother's age. Prenatal exposure to tobacco smoke is associated with behavioral problems in school-age children. Although our findings do not preclude the influence of postnatal exposure, prenatal exposure seems to be more important.

  4. Endogenous Opioids as Substrates for Ethanol Intake in the Neonatal Rat: The impact of prenatal ethanol exposure on the opioid family in the early postnatal period

    PubMed Central

    Bordner, Kelly; Deak, Terrence

    2015-01-01

    Background Despite considerable knowledge that prenatal ethanol exposure can lead to devastating effects on the developing fetus, alcohol consumption by pregnant women remains strikingly prevalent. Both clinical and basic research has suggested that, in addition to possible physical, behavioral, and cognitive deficits, gestational exposure to alcohol may lead to an increased risk for the development of later alcohol-related use and abuse disorders. The current work sought to characterize alterations in endogenous opioid signaling peptides and gene expression produced by ethanol exposure during the last days of gestation. Methods Experimental subjects were 4-, 8-, and 12-day old infant rats obtained from pregnant females that were given daily intubations of 0, 1, or 2 g/kg ethanol during the last few days of gestation (GD17-20). Using real-time RT-PCR, western blotting analysis, and enzyme immunoassays, we examined mRNA and protein for three opioid receptors and ligands in the nucleus accumbens, ventral tegmental area, and hypothalamus. Results Three main trends emerged - (1) mRNA for the majority of factors were found to upregulate across each of the three postnatal ages assessed, indicative of escalating ontogenetic expression of opioid-related genes; (2) prenatal ethanol significantly reduced many opioid peptides, suggesting a possible mechanism by which prenatal exposure can affect future responsiveness towards ethanol; and (3) the nucleus accumbens emerged as a key site for ethanol-dependent effects, suggesting a potential target for additional assessment and intervention towards understanding the ethanol's ability to program the developing brain. Conclusion We provide a global assessment of relatively long-term changes in both opioid gene expression and protein following exposure to only moderate amounts of ethanol during a relatively short window in the prenatal period. These results suggest that, while continuing to undergo ontogenetic changes, the infant

  5. Multimedia lead exposure and associated risk assessment in Dhaka, Bangladesh

    SciTech Connect

    Sarwar, M.

    1998-12-31

    Motor vehicles consume the largest amount of leaded gasoline in Bangladesh. The number of vehicles and fuel consumption have increased significantly in recent years. These vehicles, which are believed to be the major sources of lead emissions in Dhaka, may cause an excessive level of lead exposure in children. The paper describes the results of a study conducted to determine risk associated with the multimedia lead exposure for children in Dhaka. Specifically, data related to lead content in air and soil in Dhaka were collected and used to estimate the blood lead levels in children. The Integrated Exposure Uptake Biokinetics Model, developed by the United States Environmental Protection Agency (USEPA), was used. Bangladesh is yet to adopt any blood lead standards. The results of the study indicated that the model predicted geometric blood lead levels in children in Dhaka are significantly below the blood lead standard recommended by the World Health Organization (WHO). It was also found that children in Dhaka are not expected to contain blood lead levels higher than the WHO recommended standard.

  6. Biochemical diagnosis of occupational exposure to lead toxicity

    SciTech Connect

    Somashekaraiah, B.V.; Venkaiah, B.; Prasad, A.R.K. )

    1990-02-01

    Lead has been shown to interfere with the biosynthesis of heme in a number of in vitro systems and in experimental animals as well as in human beings. Several steps of the heme biosynthetic chain are subject to the toxic effects of lead. ALA- dehydratase and Ferrochelatase, in particular, are two enzymes which are strongly inhibited by lead, leading to decreased heme synthesis, a constituent of hemoglobin. The inhibition of ALA dehydratase in the red blood cells by lead is generally recognized as the most sensitive index of the individuals exposure to this environmental chemical. Earlier reports show that the determination of blood lead content (Pb-B), zinc protoporphyrin levels and erythrocyte Aminolevulinic acid dehydratase (ALA.D) are widely used as biological indicators for lead toxicity. Hence, the aim of the present study was to screen for occupational exposure to lead in the workers of three different occupations and correlate their blood lead levels with erythrocyte ALA.D and total blood porphyrin content as biochemical indicators of lead exposure.

  7. Maternal lead exposure and the secondary sex ratio.

    PubMed

    Jarrell, John F; Weisskopf, Marc G; Weuve, Jennifer; Téllez-Rojo, Maria Martha; Hu, Howard; Hernández-Avila, Mauricio

    2006-07-01

    A reduction in the secondary sex ratio may be associated with exposure to environmental toxicants. Little data exists relating this outcome to lead exposure, a well-known reproductive toxicant. We studied 1980 women having singleton births from 1994 to 1995 and from 1997 to 2001 who participated in a cohort study of lead exposure and infant outcomes in Mexico City. Levels of lead were measured in maternal and cord blood using graphite furnace atomic absorption spectroscopy, and levels of lead in maternal patella and tibia bone (a reflection of cumulative exposure) were measured using noninvasive K-X-ray fluorescence measurements. Using logistic regression models, we evaluated the relations of these measures to secondary sex ratio in the offspring, adjusting for maternal age, parity and year of infants' birth. We found no consistent association between any of the lead measures and secondary sex ratio. Results were unchanged when we adjusted for infants' year of birth, maternal age and parity. Despite a large sample size and the use of sensitive biomarkers, we did not find evidence that maternal and fetal lead exposure is associated with a lower secondary sex ratio among newborns.

  8. Environmental lead exposure: a public health problem of global dimensions.

    PubMed Central

    Tong, S.; von Schirnding, Y. E.; Prapamontol, T.

    2000-01-01

    Lead is the most abundant of the heavy metals in the Earth's crust. It has been used since prehistoric times, and has become widely distributed and mobilized in the environment. Exposure to and uptake of this non-essential element have consequently increased. Both occupational and environmental exposures to lead remain a serious problem in many developing and industrializing countries, as well as in some developed countries. In most developed countries, however, introduction of lead into the human environment has decreased in recent years, largely due to public health campaigns and a decline in its commercial usage, particularly in petrol. Acute lead poisoning has become rare in such countries, but chronic exposure to low levels of the metal is still a public health issue, especially among some minorities and socioeconomically disadvantaged groups. In developing countries, awareness of the public health impact of exposure to lead is growing but relatively few of these countries have introduced policies and regulations for significantly combating the problem. This article reviews the nature and importance of environmental exposure to lead in developing and developed countries, outlining past actions, and indicating requirements for future policy responses and interventions. PMID:11019456

  9. A discriminant analysis of neuropsychological effect of low lead exposure.

    PubMed

    Boey, K W; Jeyaratnam, J

    1988-05-01

    The purpose of this study is to determine the contribution of psychological tests in discriminating neuropsychological effects of low lead exposure. The sample consists of 49 workers occupationally exposed to lead and a control group of 36 non-exposed workers. Their performance on various neuropsychological measures was subject to a discriminant analysis using the SPSS DISCRIMINANT subprogramme. The results indicate that simple reaction time, Digit Symbol (WAIS) and Trail-Making Test (Part A) provide the best combination of tests for the detection of neurotoxic effect of low lead exposure.

  10. Environmental lead exposure to toll booth workers in Hong Kong

    SciTech Connect

    Tan, T.C.; Wong, L.T.L.; Lam, C.W.K.

    1988-01-01

    A survey of workers in the Lion Rock Tunnel toll booths was conducted, as they were regarded as a high risk group in lead exposure due to high density of vehicular traffic. The exposure of the workers to lead was determined by continuous sapling of air around the breathing zone of workers inside the booths. Blood lead concentration of 50 workers showed a mean of 0.65 {mu}mol/L and the mean urine lead concentration was 0.14 {mu}mol/L. Other tests, such as urinary amino-levulinic acid (ALA), erythrocyte zinc protoporphyrin (ZnPP) and hemoglobin concentration (Hb), were also preformed. The blood lead concentrations and other biological parameters of the toll-booth workers were acceptable and may be attributed to the recent legislation to lower the lead content in petrol and to the good preventive measures taken by the management.

  11. Reassessment of lead exposure in New Jersey using GIS technology.

    PubMed

    Guthe, W G; Tucker, R K; Murphy, E A; England, R; Stevenson, E; Luckhardt, J C

    1992-12-01

    In order to prevent children's exposure to lead, a variety of sources must be controlled. The New Jersey Department of Environmental Protection and Energy (NJDEPE) is using its Geographic Information System to identify areas within Newark, East Orange, and Irvington, New Jersey, where there may be greater environmental exposure to lead. Sensitive populations are identified through the U.S. Bureau of the Census information. Blood screening data provided by the New Jersey Department of Health (NJDOH) provide reported patterns of elevated blood lead in the study area. Comparisons of these spatial patterns will assist the NJDEPE in its soil sampling activities and lead exposure research, will provide information for public education, and will provide valuable information on sections of the study area where further screening and public education may be needed.

  12. Lead uptake and lead loss in the fresh water field crab, Barytelphusa guerini, on exposure to organic and inorganic lead

    SciTech Connect

    Tulasi, S.J.; Yasmeen, R.; Reddy, C.P.; Rao, J.V.R.

    1987-07-01

    Lead is a heavy metal which is widely used in paint industry, pigments, dyes, electrical components and electronics, plastic chemicals and in various other things. Since some of the lead salts are soluble in water, lead presents a potential threat to aquatic organisms. Studies dealing with invertebrates include those on mortality, growth and lead uptake in Lymnaea palustris and bioaccumulation of heavy metals in oysters and mussels. Little information exists regarding the effect of lead on the fresh water crustaceans. Hence the present investigation has been undertaken to study the uptake and loss of lead on exposure to subtoxic levels or organic and inorganic lead.

  13. Environmental urban lead exposure and blood lead levels in children of Mexico City.

    PubMed Central

    Romieu, I; Carreon, T; Lopez, L; Palazuelos, E; Rios, C; Manuel, Y; Hernandez-Avila, M

    1995-01-01

    Lead contamination is now a leading public health problem in Mexico. However, there are few data on the lead content of various environmental sources, and little is known about the contribution of these sources to the total lead exposure in the population of children residing in Mexico City. We conducted a cross-sectional study in a random sample of 200 children younger than 5 years of age who lived in one of two areas of Mexico City. Environmental samples of floor, window, and street dust, paint, soil, water, and glazed ceramics were obtained from the participants' households, as well as blood samples and dirt from the hands of the children. Blood lead levels ranged from 1 to 31 micrograms/dl with a mean of 9.9 micrograms/dl (SD 5.8 micrograms/dl). Forty-four percent of the children 18 months of age or older had blood lead levels exceeding 10 micrograms/dl. The lead content of environmental samples was low, except in glazed ceramic. The major predictors of blood lead levels were the lead content of the glazed ceramics used to prepare children's food, exposure to airborne lead due to vehicular emission, and the lead content of the dirt from the children's hands. We conclude that the major sources of lead exposure in Mexico City could be controlled by adequate public health programs to reinforce the use of unleaded gasoline and to encourage production and use of unleaded cookware instead of lead-glazed ceramics. PMID:8605853

  14. Environmental urban lead exposure and blood lead levels in children of Mexico City.

    PubMed

    Romieu, I; Carreon, T; Lopez, L; Palazuelos, E; Rios, C; Manuel, Y; Hernandez-Avila, M

    1995-11-01

    Lead contamination is now a leading public health problem in Mexico. However, there are few data on the lead content of various environmental sources, and little is known about the contribution of these sources to the total lead exposure in the population of children residing in Mexico City. We conducted a cross-sectional study in a random sample of 200 children younger than 5 years of age who lived in one of two areas of Mexico City. Environmental samples of floor, window, and street dust, paint, soil, water, and glazed ceramics were obtained from the participants' households, as well as blood samples and dirt from the hands of the children. Blood lead levels ranged from 1 to 31 micrograms/dl with a mean of 9.9 micrograms/dl (SD 5.8 micrograms/dl). Forty-four percent of the children 18 months of age or older had blood lead levels exceeding 10 micrograms/dl. The lead content of environmental samples was low, except in glazed ceramic. The major predictors of blood lead levels were the lead content of the glazed ceramics used to prepare children's food, exposure to airborne lead due to vehicular emission, and the lead content of the dirt from the children's hands. We conclude that the major sources of lead exposure in Mexico City could be controlled by adequate public health programs to reinforce the use of unleaded gasoline and to encourage production and use of unleaded cookware instead of lead-glazed ceramics.

  15. Prenatal lead exposure and childhood blood pressure and kidney function.

    PubMed

    Skröder, Helena; Hawkesworth, Sophie; Moore, Sophie E; Wagatsuma, Yukiko; Kippler, Maria; Vahter, Marie

    2016-11-01

    Exposure to lead, a common environmental pollutant, is known to cause cardiovascular and nephrotoxic effects in adults. Potential effects of early-life lead exposure on these functions are, however, less well characterized. To assess blood pressure and kidney function in preschool-aged children in relation to prenatal lead exposure. This prospective study in rural Bangladesh measured children's systolic and diastolic blood pressure in triplicate at the follow-up at 4.5±0.11 years. Their kidney function was assessed by the estimated glomerular filtration rate (eGFR), calculated based on serum cystatin C concentrations, and by kidney volume, measured by sonography. Exposure to lead was assessed by concentrations in the mothers' blood (erythrocyte fraction; Ery-Pb) in gestational weeks (GW) 14 and 30, the effects of which were evaluated separately in multivariable-adjusted linear regression analyses. We found no associations between maternal exposure to lead [n~1500 for GW14 and 700 for GW30] and children's blood pressure or eGFR. However, we found an inverse association between late gestation lead and kidney volume, although the sample size was limited (n=117), but not with early gestation lead (n=573). An increase of 85µg/kg in Ery-Pb (median concentration at GW30) was associated with a 6.0cm(3)/m(2) decrease in kidney volume (=0.4SD; p=0.041). After stratifying on gender, there seemed to be a somewhat stronger association in girls. Prenatal lead exposure may cause long-lasting effects on the kidney. This warrants follow-up studies in older children, as well as additional studies in other populations. Copyright © 2016. Published by Elsevier Inc.

  16. Immune and airway effects of house dust mite aeroallergen exposures during postnatal development of the infant rhesus monkey.

    PubMed

    Miller, L A; Plopper, C G; Hyde, D M; Gerriets, J E; Pieczarka, E M; Tyler, N K; Evans, M J; Gershwin, L J; Schelegle, E S; Van Winkle, L S

    2003-12-01

    The effect of chronic environmental aeroallergen exposure on the immune system and airways has not been experimentally defined in very young children. The purpose of this study was to determine the immunophenotype of peripheral blood and airway leucocytes in the newborn rhesus macaque monkey, following recurrent aerosol exposure to house dust mite (HDM) (Dermatophagoides farinae). A regimen of HDM aerosolization was initiated for 2 h per day, three times per week, starting when rhesus macaque monkeys were 1 week of age. All monkeys were inoculated with diptheria, tetanus, and acellular pertussis vaccine at 5 weeks of age to simulate human infant vaccination schedules. Following 8 weeks of HDM aeroallergen exposure, infant monkeys exhibited a significant reduction in the total peripheral blood lymphocyte numbers and a decreased frequency of peripheral blood CD4+ T lymphocytes with a CD45RA-'memory' immunophenotype. Lavage CD4+ T lymphocytes from HDM-exposed monkeys showed elevated expression of CD25, as well as an increase in CD45RA-/CD62L-/CD11ahigh immunophenotype. Eosinophils were more abundant within airways of HDM-exposed monkeys, accumulating maximally within the trachea. These data demonstrate the development of immunological responses following chronic inhalation of a common environmental allergen during postnatal maturation in the non-human primate.

  17. Intrauterine exposure to 17β-oestradiol (E2) impairs postnatal development in both female and male prostate in gerbil.

    PubMed

    Sanches, Bruno D A; Santos, Juliana M; Zani, Bruno C; Biancardi, Manoel F; Santos, Fernanda C A; Góes, Rejane M; Vilamaior, Patricia S L; Taboga, Sebastião R

    2017-07-30

    We employed histological techniques to assess the effects of intrauterine exposure to different dosages of E2 on male and female Mongolian gerbils on the postnatal development of the prostate. E2 promotes alterations this gland branches in the female, but not in males, even at low dosage, at higher dosages, acini of altered aspect are verified in the male and female prostate, as well as a decrease in branching number, reduced cell proliferation and staining for FGF10, simultaneously to the increased labelling for TGFβ1, which may account for alterations on branching of the prostate. The sensitivity of the female prostate to intrauterine exposure to E2, which can reflect the E2 dependence of female prostate development. This becomes alarming in view of the occurrence of prostate in female of several mammals and including women, and the possibility that low E2 dosage exposures considered safe to males provoke developmental alterations in female prostate. Copyright © 2017. Published by Elsevier Inc.

  18. Toddler temperament and prenatal exposure to lead and maternal depression.

    PubMed

    Stroustrup, Annemarie; Hsu, Hsiao-Hsien; Svensson, Katherine; Schnaas, Lourdes; Cantoral, Alejandra; Solano González, Maritsa; Torres-Calapiz, Mariana; Amarasiriwardena, Chitra; Bellinger, David C; Coull, Brent A; Téllez-Rojo, Martha M; Wright, Robert O; Wright, Rosalind J

    2016-06-16

    Temperament is a psychological construct that reflects both personality and an infant's reaction to social stimuli. It can be assessed early in life and is stable over time Temperament predicts many later life behaviors and illnesses, including impulsivity, emotional regulation and obesity. Early life exposure to neurotoxicants often results in developmental deficits in attention, social function, and IQ, but environmental predictors of infant temperament are largely unknown. We propose that prenatal exposure to both chemical and non-chemical environmental toxicants impacts the development of temperament, which can itself be used as a marker of risk for maladaptive neurobehavior in later life. In this study, we assessed associations among prenatal and early life exposure to lead, mercury, poverty, maternal depression and toddler temperament. A prospective cohort of women living in the Mexico City area were followed longitudinally beginning in the second trimester of pregnancy. Prenatal exposure to lead (blood, bone), mercury, and maternal depression were assessed repeatedly and the Toddler Temperament Scale (TTS) was completed when the child was 24 months old. The association between each measure of prenatal exposure and performance on individual TTS subscales was evaluated by multivariable linear regression. Latent profile analysis was used to classify subjects by TTS performance. Multinomial regression models were used to estimate the prospective association between prenatal exposures and TTS performance. 500 mother-child pairs completed the TTS and had complete data on exposures and covariates. Three latent profiles were identified and categorized as predominantly difficult, intermediate, or easy temperament. Prenatal exposure to maternal depression predicted increasing probability of difficult toddler temperament. Maternal bone lead, a marker of cumulative exposure, also predicted difficult temperament. Prenatal lead exposure modified this association

  19. Brainstem auditory evoked potentials in children with lead exposure.

    PubMed

    Alvarenga, Katia de Freitas; Morata, Thais Catalani; Lopes, Andrea Cintra; Feniman, Mariza Ribeiro; Corteletti, Lilian Cassia Bornia Jacob

    2015-01-01

    Earlier studies have demonstrated an auditory effect of lead exposure in children, but information on the effects of low chronic exposures needs to be further elucidated. To investigate the effect of low chronic exposures of the auditory system in children with a history of low blood lead levels, using an auditory electrophysiological test. Contemporary cross-sectional cohort. Study participants underwent tympanometry, pure tone and speech audiometry, transient evoked otoacoustic emissions, and brainstem auditory evoked potentials, with blood lead monitoring over a period of 35.5 months. The study included 130 children, with ages ranging from 18 months to 14 years, 5 months (mean age 6 years, 8 months ± 3 years, 2 months). The mean time-integrated cumulative blood lead index was 12 μg/dL (SD ± 5.7, range: 2.433). All participants had hearing thresholds equal to or below 20 dBHL and normal amplitudes of transient evoked otoacoustic emissions. No association was found between the absolute latencies of waves I, III, and V, the interpeak latencies I-III, III-V, and I-V, and the cumulative lead values. No evidence of toxic effects from chronic low lead exposures was observed on the auditory function of children living in a lead contaminated area. Copyright © 2014 Associação Brasileira de Otorrinolaringologia e Cirurgia Cérvico-Facial. Published by Elsevier Editora Ltda. All rights reserved.

  20. The intersection of aggregate-level lead exposure and crime.

    PubMed

    Boutwell, Brian B; Nelson, Erik J; Emo, Brett; Vaughn, Michael G; Schootman, Mario; Rosenfeld, Richard; Lewis, Roger

    2016-07-01

    Childhood lead exposure has been associated with criminal behavior later in life. The current study aimed to analyze the association between elevated blood lead levels (n=59,645) and crime occurrence (n=90,433) across census tracts within St. Louis, Missouri. Longitudinal ecological study. Saint Louis, Missouri. Blood lead levels. Violent, Non-violent, and total crime at the census tract level. Spatial statistical models were used to account for the spatial autocorrelation of the data. Greater lead exposure at the census-tract level was associated with increased violent, non-violent, and total crime. In addition, we examined whether non-additive effects existed in the data by testing for an interaction between lead exposure and concentrated disadvantage. Some evidence of a negative interaction emerged, however, it failed to reach traditional levels of statistical significance (supplementary models, however, revealed a similar negative interaction that was significant). More precise measurements of lead exposure in the aggregate, produced additional evidence that lead is a potent predictor of criminal outcomes. Copyright © 2016 Elsevier Inc. All rights reserved.

  1. Exposure of migrant bald eagles to lead in prairie Canada.

    PubMed

    Miller, M J; Wayland, M E; Bortolotti, G R

    2001-01-01

    The prevalence of elevated exposure to lead was assessed in a migrant population of bald eagles (Haliaeetus leucocephalus) at a waterfowl staging area in the southern portion of the Canadian prairies, from September to November, 1992-1995. Of 103 eagles, 8% exhibited blood lead (PbB) concentrations suggestive of elevated exposure to lead (> or = 0.200 microgram ml-1 wet wt.). PbB concentrations in eagles from the study area ranged from < 0.01 to 0.585 microgram ml-1, while those of nestling eagles from a reference site indicated normal or background exposure (< 0.01 microgram ml-1). No differences in the prevalence of elevated exposure were detected among genders or age classes (0.5- and > or = 1.5-year-old birds) (P > 0.05). The prevalence of elevated exposure was significantly greater in November than in October (21.7 vs. 3.8%) (all years: chi 2Y = 5.75, P = 0.017). Eagles with shotshell pellets in the digestive tract did not have accompanying high PbB concentrations. The prevalence of elevated lead exposure in this study was low in comparison to other areas in North America. Potential biases in the trapping technique as they relate to interpreting the results are addressed.

  2. Exposure to lead and human health in the Czech Republic.

    PubMed

    Bláha, K; Bencko, V; Cikrt, M

    1996-12-01

    The aim of presented review is to address the most relevant issues related to the health effects caused by the human exposure to lead, as they have been recognized in Czech Republic in the period of 1992-1994 within the framework of the National Integrated Programme on Environment and Health (NIPEH) approved in 1992 and supported by WHO-European Centre for Environment and Health (WHO-ECEH), Bilthoven, The Netherlands and by the Government of the Netherlands. Basic sources of environment exposure to lead are identified and the fate of lead in the individual compartments of the environment is discussed. Relevant methods used for the exposure evaluation are summarized and the highest-risk group of population is defined. Attention is being paid to the effects of the long-term exposure to low lead levels, while other exposure settings are intentionally omitted. Interventional measures developed in the Czech Republic in attempt to reduce the environmental exposure are introduced. Instead of presenting specific data, current state-of-art and general trends are presented; list of references tries to combine the internationally recognized studies with those coming from national sources.

  3. Window renovation and exposure to lead--an observational study.

    PubMed

    Mason, Howard; Gallagher, Frank; Sen, Dil

    2005-12-01

    Renovation of windows in old houses has recently established itself as an industry. A recognizable occupational lead exposure exists, which has not been studied previously. To compare lead exposure amongst window renovators with other groups of lead-exposed workers. Using blood lead results measured at the Health and Safety Laboratory (HSL), Sheffield, comparisons were made between three cohorts: window renovation workers, all male workers monitored by HSL during the period 1999-2001 and 63 male subjects involved in chemical paint-stripping of wood. Both the window renovation and the wood-stripping cohorts show significantly higher blood lead distributions than the 'all workers' cohort (P < 0.001). A similar pattern was also found for comparison of the prevalence of subjects above the UK suspension level of 60 microg/dl (2.89 microM) (window renovation, P < 0.001; wood-stripping, P < 0.0001). Blood lead results at or above the suspension level in wood-strippers were significantly higher compared to window renovators (P = 0.034). Window renovation is shown to present a potential for significant lead exposure, and suspension from work under The Control of Lead at Work Regulations 2002. Two groups of risk factors predominate: the well-documented potential for release of lead from old paint, and the peripatetic nature of the work.

  4. Occupational exposure to airborne lead in Brazilian police officers.

    PubMed

    Rocha, Ernesto Díaz; Sarkis, Jorge E Souza; Carvalho, Maria de Fátima H; Santos, Gerson Vechio Dos; Canesso, Claudemir

    2014-07-01

    Shooting with lead-containing ammunition in indoor firing ranges is a known source of lead exposure in adults. Police officers may be at risk of lead intoxication when regular training shooting exercises are yearly mandatory to law enforcement officers. Effects on health must be documented, even when low-level elemental (inorganic) lead exposure is detected. Forty police officers (nineteen cadets and twenty-one instructors) responded to a questionnaire about health, shooting habits, and potential lead exposure before a training curse. Blood samples were collected and analyzed for blood lead level (BLL) before and after a three days training curse. The mean BLL for the instructors' group was 5.5 μg/dL ± 0.6. The mean BLL for the cadets' group before the training was 3.3 μg/dL ± 0.15 and after the training the main BLL was 18.2 μg/d L± 1.5. Samples were analyzed by Inductively Coupled Plasma Mass Spectrometer (ICP-MS). All the participants in the training curse had significantly increased BLL (mean increment about 15 μg/dL) after the three days indoor shooting season. In conclusion, occupational lead exposure in indoor firing ranges is a source of lead exposure in Brazilian police officers, and appears to be a health risk, especially when heavy weapons with lead-containing ammunition are used in indoor environments during the firing training seasons. Copyright © 2013 Elsevier GmbH. All rights reserved.

  5. Lead Exposure during Early Human Development and DNA Methylation of Imprinted Gene Regulatory Elements in Adulthood

    SciTech Connect

    Li, Yue; Xie, Changchun; Murphy, Susan K.; Skaar, David; Nye, Monica; Vidal, Adriana C.; Cecil, Kim M.; Dietrich, Kim N.; Puga, Alvaro; Jirtle, Randy L.; Hoyo, Cathrine

    2015-06-26

    Here, lead exposure during early development causes neurodevelopmental disorders by unknown mechanisms. Epidemiologic studies have focused recently on determining associations between lead exposure and global DNA methylation; however, such approaches preclude the identification of loci that may alter human disease risk. The objective of this study was to determine whether maternal, postnatal, and early childhood lead exposure can alter the differentially methylated regions (DMRs) that control the monoallelic expression of imprinted genes involved in metabolism, growth, and development. Questionnaire data and serial blood lead levels were obtained from 105 participants (64 females, 41 males) of the Cincinnati Lead Study from birth to 78 months. When participants were adults, we used Sequenom EpiTYPER assays to test peripheral blood DNA to quantify CpG methylation in peripheral blood leukocytes at DMRs of 22 human imprinted genes. Statistical analyses were conducted using linear regression. Mean blood lead concentration from birth to 78 months was associated with a significant decrease in PEG3 DMR methylation (β = –0.0014; 95% CI: –0.0023, –0.0005, p = 0.002), stronger in males (β = –0.0024; 95% CI: –0.0038, –0.0009, p = 0.003) than in females (β = –0.0009; 95% CI: –0.0020, 0.0003, p = 0.1). Elevated mean childhood blood lead concentration was also associated with a significant decrease in IGF2/H19 (β = –0.0013; 95% CI: –0.0023, –0.0003, p = 0.01) DMR methylation, but primarily in females, (β = –0.0017; 95% CI: –0.0029, –0.0006, p = 0.005) rather than in males, (β = –0.0004; 95% CI: –0.0023, 0.0015, p = 0.7). Elevated blood lead concentration during the neonatal period was associated with higher PLAGL1/HYMAI DMR methylation regardless of sex (β = 0.0075; 95% CI: 0.0018, 0.0132, p = 0.01). The magnitude of associations between cumulative lead exposure and CpG methylation remained unaltered from 30 to 78 months. Our findings

  6. Lead Exposure during Early Human Development and DNA Methylation of Imprinted Gene Regulatory Elements in Adulthood

    DOE PAGES

    Li, Yue; Xie, Changchun; Murphy, Susan K.; ...

    2015-06-26

    Here, lead exposure during early development causes neurodevelopmental disorders by unknown mechanisms. Epidemiologic studies have focused recently on determining associations between lead exposure and global DNA methylation; however, such approaches preclude the identification of loci that may alter human disease risk. The objective of this study was to determine whether maternal, postnatal, and early childhood lead exposure can alter the differentially methylated regions (DMRs) that control the monoallelic expression of imprinted genes involved in metabolism, growth, and development. Questionnaire data and serial blood lead levels were obtained from 105 participants (64 females, 41 males) of the Cincinnati Lead Study frommore » birth to 78 months. When participants were adults, we used Sequenom EpiTYPER assays to test peripheral blood DNA to quantify CpG methylation in peripheral blood leukocytes at DMRs of 22 human imprinted genes. Statistical analyses were conducted using linear regression. Mean blood lead concentration from birth to 78 months was associated with a significant decrease in PEG3 DMR methylation (β = –0.0014; 95% CI: –0.0023, –0.0005, p = 0.002), stronger in males (β = –0.0024; 95% CI: –0.0038, –0.0009, p = 0.003) than in females (β = –0.0009; 95% CI: –0.0020, 0.0003, p = 0.1). Elevated mean childhood blood lead concentration was also associated with a significant decrease in IGF2/H19 (β = –0.0013; 95% CI: –0.0023, –0.0003, p = 0.01) DMR methylation, but primarily in females, (β = –0.0017; 95% CI: –0.0029, –0.0006, p = 0.005) rather than in males, (β = –0.0004; 95% CI: –0.0023, 0.0015, p = 0.7). Elevated blood lead concentration during the neonatal period was associated with higher PLAGL1/HYMAI DMR methylation regardless of sex (β = 0.0075; 95% CI: 0.0018, 0.0132, p = 0.01). The magnitude of associations between cumulative lead exposure and CpG methylation remained unaltered from 30 to 78 months. Our

  7. Take home lead exposure in children of oil field workers.

    PubMed

    Khan, Fahad

    2011-06-01

    Childhood lead poisoning is a major, preventable environmental health problem. While residential lead-based paint and lead contaminated dust and soil are the most common sources of childhood lead poisoning, children can also be at risk if they live with an adult with a job or hobby that involves exposure to lead. Currently, the Oklahoma Childhood Lead Poisoning Prevention Program (OCLPPP) has a small number of cases of "take home" lead exposure in children of oil field workers. These workers may come in contact with a threading compound, "pipe dope" that can contain large amounts of lead. Workers handling this product may be exposed to lead by not following safety instructions. Additionally workers may not be provided the facilities to shower and change out of the contaminated clothing before leaving the work location. The OCLPPP recommends employers and worksites should consider effective alternative options like lead free biodegradable pipe dopes or dope free connections to prevent workers and their families from adverse health effects associated with lead.

  8. Influences of pre- and postnatal nutritional exposures on vascular/endocrine systems in animals.

    PubMed Central

    Hoet, J J; Ozanne, S; Reusens, B

    2000-01-01

    Human epidemiological and animal studies have revealed the long-term effects of malnutrition during gestation and early life on the health of the offspring. The aim of the current review is to survey the different means of achieving fetal malnutrition and its consequences, mainly in animals, and to identify key areas in which to direct future research. We address the impact of various models of a maternal protein-restricted diet and global maternal caloric restriction (either through the reduction of nutrient supply or through mechanic devices), the influence of maternal diabetes, and other maternal causes of fetal damage (maternal infections and toxic food components). More specifically, we enumerate data on how the different insults at different prenatal and early postnatal periods affect and program the development and the function of organs involved in diabetes, hypertension, and cardiovascular disease. Particular emphasis is given to the endocrine pancreas, but insulin-sensitive tissues, kidneys, and vasculature are also analyzed. Where available, the protective effects of maternal food supplementation for fetal organ development and function are discussed. Specific attention is paid to the amino acids profile, and the preventive role of taurine is discussed. Tentative indications about critical time windows for fetal development under different deleterious conditions are presented whenever possible. We also discuss future research and intervention. PMID:10852855

  9. PRE- AND POSTNATAL EXPOSURE TO KYNURENINE CAUSES COGNITIVE DEFICITS IN ADULTHOOD

    PubMed Central

    Pocivavsek, Ana; Wu, Hui-Qiu; Elmer, Greg I.; Bruno, John P.; Schwarcz, Robert

    2013-01-01

    Levels of kynurenic acid (KYNA), an endogenous product of tryptophan degradation, are elevated in the brain and cerebrospinal fluid of individuals with schizophrenia (SZ). This increase has been implicated in the cognitive dysfunctions seen in the disease since KYNA is an antagonist of the α7 nicotinic acetylcholine receptor and the NMDA receptor, both of which are critically involved in cognitive processes and in a defining neurodevelopmental period in the pathophysiology of SZ. We tested the hypothesis that early developmental increases in brain KYNA synthesis might cause biochemical and functional impairments in adulthood. To this end, we stimulated KYNA formation by adding the KYNA precursor kynurenine (100 mg/day) to the chow fed to rat dams from gestational day 15 to postnatal day 21 (PD 21). This treatment raised brain KYNA levels in the offspring by 341% on PD 2 and 210% on PD 21. Rats were then fed normal chow until adulthood (PD 56-PD 80). In the adult animals, basal levels of extracellular KYNA, measured in the hippocampus by in vivo microdialysis, were elevated (+12%), whereas extracellular glutamate levels were significantly reduced (−13%). In separate adult animals, early kynurenine treatment was shown to impair performance in two behavioral tasks linked to hippocampal function, the passive avoidance test and the Morris water maze test. Collectively, these studies introduce a novel, naturalistic rat model of SZ and also suggest that increases in brain KYNA during a vulnerable period in brain development may play a significant role in the pathophysiology of the disease. PMID:22515201

  10. Lead exposure from backyard chicken eggs: a public health risk?

    PubMed

    Bautista, Adrienne C; Puschner, Birgit; Poppenga, Robert H

    2014-09-01

    Although the USA has made significant strides in reducing lead exposure, new and emerging sources are raising cause for public concern. Recent reports of finding lead in eggs from chickens raised in urban gardens has highlighted the need to consider the potential health risks of consuming eggs from backyard chickens. Following the detection of 0.33 μg/g lead in the edible portion of eggs submitted for lead analysis from a backyard chicken owner, further investigation was conducted to determine the source and extent of lead exposure in the flock. Several birds, almost two dozen eggs, and environmental samples were submitted to the California Animal Health and Food Safety Laboratory for further testing. Lead was detected in the blood, liver, kidney, and bone at varying concentrations in all birds but was not detected in the muscle tissue. All egg shells contained detectable amounts of lead, while only a little over half of the edible portion of the eggs contained lead. The detected concentrations in the edible portion approached or exceeded the recommended threshold of lead consumption per day that should not be exceeded by young children if a child consumed one average-sized egg. Peeling paint from a wooded structure adjacent to the flock's coop was the likely lead source containing 3,700 μg/g lead. Thus, removal of the chickens from the source and periodic testing of eggs for lead were recommended. This case illustrates the need for consumers and health care workers to be aware of potential sources for lead exposure such as backyard chickens.

  11. Risk of postnatal exposure to Sarcocystis neurona and Neospora hughesi in horses.

    PubMed

    Duarte, Paulo C; Conrad, Patricia A; Wilson, W David; Ferraro, Gregory L; Packham, Andrea E; Bowers-Lepore, Jeanne; Carpenter, Tim E; Gardner, Ian A

    2004-08-01

    To estimate risk of exposure and age at first exposure to Sarcocystis neurona and Neospora hughesi and time to maternal antibody decay in foals. 484 Thoroughbred and Warmblood foals from 4 farms in California. Serum was collected before and after colostrum ingestion and at 3-month intervals thereafter. Samples were tested by use of the indirect fluorescent antibody test; cutoff titers were > or = 40 and > or = 160 for S neurona and N hughesi, respectively. Risk of exposure to S neurona and N hughesi during the study were 8.2% and 3.1%, respectively. Annual rate of exposure was 3.1% for S neurona and 1.7% for N hughesi. There was a significant difference in the risk of exposure to S neurona among farms but not in the risk of exposure to N hughesi. Median age at first exposure was 1.2 years for S neurona and 0.8 years for N hughesi. Highest prevalence of antibodies against S neurona and N hughesi was 6% and 2.1 %, respectively, at a mean age of 1.7 and 1.4 years, respectively. Median time to maternal antibody decay was 96 days for S neurona and 91 days for N hughesi. There were no clinical cases of equine protozoal myeloenchaphlitis (EPM). Exposure to S neurona and N hughesi was low in foals between birth and 2.5 years of age. Maternally acquired antibodies may cause false-positive results for 3 or 4 months after birth, and EPM was a rare clinical disease in horses < or = 2.5 years of age.

  12. Prenatal and Postnatal PCB-153 and p,p'-DDE Exposures and Behavior Scores at 5-9 Years of Age among Children in Greenland and Ukraine.

    PubMed

    Rosenquist, Aske Hess; Høyer, Birgit Bjerre; Julvez, Jordi; Sunyer, Jordi; Pedersen, Henning Sloth; Lenters, Virissa; Jönsson, Bo A G; Bonde, Jens Peter; Toft, Gunnar

    2017-10-03

    Studies have reported some evidence of adverse effects of organochlorine exposures on child development, but the results have been inconsistent, and few studies have evaluated associations with child behavior. We investigated the association between prenatal and early-life exposures to 2,2',4,4',5,5'-hexachlorobiphenyl (PCB-153) and 1,1-dichloro-2,2-bis(p-chlorophenyl)-ethylene (p,p'-DDE) and behaviors in children between 5 and 9 y of age. In the Biopersistent organochlorines in diet and human fertility: Epidemiologic studies of time to pregnancy and semen quality in Inuit and European populations (INUENDO) cohort, consisting of mother-child pairs from Greenland and Ukraine (n=1,018), maternal serum PCB-153 and p,p'-DDE concentrations were measured during pregnancy, and cumulative postnatal exposures during the first 12 months after delivery were estimated using a pharmacokinetic model. Parents completed the Strengths and Difficulties Questionnaire (SDQ), and children's behaviors were dichotomized as abnormal (high) versus normal/borderline for five SDQ subscales and the total difficulties score. The total difficulties score, an overall measure of abnormal behavior, was not clearly associated with pre- or postnatal exposures to PCB-153 or to p,p'-DDE. However, pooled adjusted odds ratios (ORs) for high conduct problem scores with a doubling of exposure were 1.19 (95% CI: 0.99, 1.42) and 1.16 (95% CI: 0.96, 1.41) for pre- and postnatal PCB-153, respectively, and 1.25 (95% CI: 1.04, 1.51) and 1.24 (95% CI: 1.01, 1.51) for pre- and postnatal p,p'-DDE, respectively. Corresponding ORs for high hyperactivity scores were 1.24 (95% CI: 0.94, 1.62) and 1.08 (95% CI: 0.81, 1.45) for pre- and postnatal PCB-153, respectively, and 1.43 (95% CI: 1.06, 1.92) and 1.27 (95% CI: 0.93, 1.73) for pre- and postnatal p,p'-DDE, respectively. Prenatal and early postnatal exposures to p,p'-DDE and PCB-153 were associated with a higher prevalence of abnormal scores for conduct and

  13. Sertraline exposure leads to small left heart syndrome in adult mice.

    PubMed

    Haskell, Sarah E; Hermann, Gregory M; Reinking, Benjamin E; Volk, Kenneth A; Peotta, Veronica A; Zhu, Vivian; Roghair, Robert D

    2013-03-01

    Sertraline, a selective serotonin reuptake inhibitor (SSRI), is the most commonly prescribed therapy for maternal depression. Epidemiologic studies have linked SSRI exposure with decreased fetal growth, altered autonomic regulation, and cardiac malformations. We hypothesized that SSRI exposure decreases left-ventricular (LV) volumes and increases adult sympathetic nervous system activation, resulting in increased adult heart rates. C57BL/6 mice received saline or sertraline (5 or 15 mg/kg/day i.p.) on postnatal days 1-14. Adult phenotypes were assessed at 5 mo. Sertraline-exposed mice had smaller LV internal diameters in diastole (control 4.0 ± 0.1 mm, SSRI 3.7 ± 0.1 mm, P < 0.05), decreased stroke volumes (control 46 ± 2.6 µl, SSRI 37 ± 2.3 µl, P < 0.05), higher heart rates (control 530 ± 13 beats per minute (bpm), SSRI 567 ± 6 bpm, P <0.05), and increased urinary excretion of noradrenaline (control 174 ± 29.4 ng/ml, SSRI 276 ± 35.1 ng/ml, P < 0.05). These changes were associated with increased cerebral serotonin transporter (5-HTT) expression. Neonatal sertraline exposure causes long-term changes in cardiac morphology and physiology. We speculate that early-life SSRI exposure impairs cardiomyocyte growth and central serotonin signaling, leading to a small left heart syndrome in adult mice.

  14. Sertraline exposure leads to small left heart syndrome in adult mice

    PubMed Central

    Haskell, Sarah E.; Hermann, Gregory M.; Reinking, Benjamin E.; Volk, Kenneth A.; Peotta, Veronica A.; Zhu, Vivian; Roghair, Robert D.

    2013-01-01

    Background Sertraline, a selective serotonin reuptake inhibitor (SSRI), is the most commonly prescribed therapy for maternal depression. Epidemiologic studies have linked SSRI exposure with decreased fetal growth, altered autonomic regulation, and cardiac malformations. We hypothesized SSRI exposure decreases left ventricular volumes and increases adult sympathetic nervous system activation, resulting in increased adult heart rates. Methods C57BL/6 mice received saline or sertraline (5 or 15 mg/kg/day i.p.) on postnatal days 1–14. Adult phenotypes were assessed at 5 months. Results Sertraline-exposed mice had smaller left ventricular internal diameters in diastole (control 4.0 ± 0.1 mm, SSRI 3.7 ± 0.1 mm, p < 0.05), decreased stroke volumes (control 46 ± 2.6 μL, SSRI 37 ± 2.3 μL, p < 0.05), higher heart rates (control 530 ± 13 beats per minute (bpm), SSRI 567 ± 6 bpm, p <0.05) and increased urinary excretion of noradrenaline (control 174 ± 29.4 ng/mL, SSRI 276 ± 35.1 ng/mL, p<0.05). These changes were associated with increased cerebral serotonin transporter (5-HTT) expression. Conclusion Neonatal sertraline exposure causes long term changes in cardiac morphology and physiology. We speculate that early life SSRI exposure impairs cardiomyocyte growth and central serotonin signaling, leading to a small left heart syndrome in adult mice. PMID:23232669

  15. The cultural parameters of lead poisoning: A medical anthropologist's view of intervention in environmental lead exposure

    SciTech Connect

    Trotter, R.T. II )

    1990-11-01

    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.

  16. The cultural parameters of lead poisoning: a medical anthropologist's view of intervention in environmental lead exposure.

    PubMed Central

    Trotter, R T

    1990-01-01

    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. PMID:2088759

  17. Lead exposure in firearms instructors of the Italian State Police.

    PubMed

    Di Lorenzo, L; Borraccia, V; Corfiati, Marisa; Mantineo, G A; Caciari, Tiziana; Marino, Marina; Soleo, L

    2010-01-01

    Several studies evaluated exposure to lead in relatively small groups of firearms instructors and shooters, mainly operating at indoor ranges. To assess the levels of lead exposure in a large sample of firearms instructors of the Italian State Police (SP) operating at either indoor or outdoor ranges. A crosssectional study was conducted in firearms instructors working in indoor (No. 188) and outdoor (No. 188) ranges compared with 170 foodplant workers. The personal and work characteristics and current blood lead (Pb-B) levels were evaluated The concentrations of environmental lead (Pb-E) were measured using personal samplers in 6 indoor and 6 outdoor firing ranges. The Pb-B levels in the two groups of firearms instructors were well below the ACGIH BEI, but significantly higher than in food plant workers. In the entire study sample the Pb-B level was seen to be influenced by age and job group. An excess risk of having Pb-B >100 microg/l was found in indoor range instructors and in those with greater job seniority. Pb-E <25 pg/m3 was measured in all the firing ranges examined. The low Pb-B and Pb-E levels assessed are the result of primary and secondary prevention interventions carried out over the years by the Italian State Police. The current Pb-B levels also seemed to be poorly influenced by higher past environmental and/or occupational lead exposure. In fact a certain number of firearms instructors, mainly operating at indoor ranges and with greater job seniority, had Pb-B levels consistent with occupational exposure to lead. Environmental and biological monitoring of lead exposure and specific health surveillance are therefore still necessary in this job group topreventpossible adverse health effects of lead even at low doses.

  18. 1H magnetic resonance spectroscopy metabolite profiles of neonatal rat hippocampus and brainstem regions following early postnatal exposure to intermittent hypoxia

    NASA Astrophysics Data System (ADS)

    Darnall, Robert A.; Chen, Xi; Nemani, Krishnamurthy V.; Sirieix, Chrystelle M.; Gimi, Barjor

    2017-03-01

    Most premature infants born at less than 30 weeks gestation are exposed to periods of mild intermittent hypoxia (IH) associated with apnea of prematurity and periodic breathing. In adults, IH associated with sleep apnea causes neurochemical and structural alterations in the brain. However, it is unknown whether IH in the premature infant leads to neurodevelopmental impairment. Quantification of biochemical markers that can precisely identify infants at risk of adverse neurodevelopmental outcome is essential. In vivo 1H magnetic resonance spectroscopy (1H MRS) facilitates the quantification of metabolites from distinct regions of the developing brain. We report the changes in metabolite profiles in the brainstem and hippocampal regions of developing rat brains, resulting from exposure to IH. Rat pups were chosen for study because there is rapid postnatal hippocampal development that occurs during the first 4 weeks in the developing rat brain, which corresponds to the first 2-3 postnatal years of development in humans. The brainstem was examined because of our interest in respiratory control disorders in the newborn and because of brainstem gliosis described in infants who succumb to Sudden Infant Death Syndrome (SIDS). Metabolite profiles were compared between hypoxia treated rat pups (n = 9) and normoxic controls (n = 6). Metabolite profiles were acquired using the Point-RESolved spectroscopy (PRESS) MRS sequence and were quantified using the TARQUIN software. There was a significant difference in the concentrations of creatine (p = 0.031), total creatine (creatine + phosphocreatine) (p = 0.028), and total choline (p = 0.001) in the brainstem, and glycine (p = 0.031) in the hippocampal region. The changes are consistent with altered cellular bioenergetics and metabolism associated with hypoxic insult.

  19. Tremor secondary to neurotoxic exposure: mercury, lead, solvents, pesticides.

    PubMed

    Lucchini, Roberto G; Hashim, Dana

    2015-01-01

    Lead, mercury, solvents, and pesticide exposures are common in certain occupations and may cause nervous system dysfunction. Tremors may be the herald manifestation among a constellation of acute toxicity signs and symptoms. However, since tremors may also be the only sign on clinical presentation and since tremors also occur in other diseases, relating tremors to a specific occupational exposure can be challenging. Diagnosis of tremor etiology must be based on other findings on physical exam, laboratory results, and/or imaging. Discerning whether the tremor resulted from the occupational environment versus other etiologies requires knowledge of potential exposure sources, additional detail in history taking, and support of other health and industrial professionals. Reduction or removal from the exposure source remains the key first step in treating patients suffering from tremor that had resulted from occupational exposure toxicity.

  20. Pediatric lead exposure from imported Indian spices and cultural powders.

    PubMed

    Lin, Cristiane Gurgel; Schaider, Laurel Anne; Brabander, Daniel Joseph; Woolf, Alan David

    2010-04-01

    Significant lead poisoning has been associated with imported nonpaint products. To describe cases of pediatric lead intoxication from imported Indian spices and cultural powders, determine lead concentrations in these products, and predict effects of ingestion on pediatric blood lead levels (BLLs). Cases and case-study information were obtained from patients followed by the Pediatric Environmental Health Center (Children's Hospital Boston). Imported spices (n = 86) and cultural powders (n = 71) were analyzed for lead by using x-ray fluorescence spectroscopy. The simple bioaccessibility extraction test was used to estimate oral bioavailability. The integrated exposure uptake biokinetic model for lead in children was used to predict population-wide geometric mean BLLs and the probability of elevated BLLs (>10 microg/dL). Four cases of pediatric lead poisoning from Indian spices or cultural powders are described. Twenty-two of 86 spices and foodstuff products contained >1 microg/g lead (for these 22 samples, mean: 2.6 microg/g [95% confidence interval: 1.9-3.3]; maximum: 7.6 microg/g). Forty-six of 71 cultural products contained >1 microg/g lead (for 43 of these samples, mean: 8.0 microg/g [95% confidence interval: 5.2-10.8]; maximum: 41.4 microg/g). Three sindoor products contained >47% lead. With a fixed ingestion of 5 microg/day and 50% bioavailability, predicted geometric mean BLLs for children aged 0 to 4 years increased from 3.2 to 4.1 microg/dL, and predicted prevalence of children with a BLL of >10 microg/dL increased more than threefold (0.8%-2.8%). Chronic exposure to spices and cultural powders may cause elevated BLLs. A majority of cultural products contained >1 microg/g lead, and some sindoor contained extremely high bioaccessible lead levels. Clinicians should routinely screen for exposure to these products.

  1. Environmental contamination and human exposure to lead in Brazil.

    PubMed

    Paoliello, Monica M B; De Capitani, Eduardo M

    2005-01-01

    Adverse effects caused by environmental lead pollution are well recognized. Being a widespread agent in the environment and a major harmful element to organic systems, mostly to children, lead has been investigated all over the world, aiming to improve measures regarding its control. The purpose of this chapter is to present a review of the situation of production, uses, assessment of exposure, and adverse effects from environmental lead contamination in Brazil. It also presents aspects of Brazilian legislation setting up maximum permissible levels of lead in several environmental compartments such as surface and drinking water, soils, sediment, urban air, and also in commercially sold food, vegetables, fish, and meat, in an effort to control industrial emissions. Epidemiological investigations on children's lead exposure around industrial and mining areas are revised, showing that many situations where lead contamination is potentially present still need to be addressed by governmental agencies. In Brazil, lead was withdrawn from gasoline by the end of the 1980s, and the last lead mining and primary smelting plant was closed in 1995, leaving residual environmental lead contamination, which has recently been investigated using a multidisciplinary approach. Nevertheless, there are hundreds of small secondary battery recycling plants all over the country, running smelting facilities that produce local urban areas of lead contamination.

  2. Assessment of soil lead exposure in children in Shenyang, China.

    PubMed

    Ren, H M; Wang, J D; Zhang, X L

    2006-11-01

    Soil lead pollution is serious in Shenyang, China. The paper brings together the soil work, the bioaccessibility, and the blood lead data to assess the soil lead exposure in children in Shenyang, China. Approximately 15.25% of the samples were above China Environment Protection Agency guideline concentration for soil Pb to protect human from health risk (350 mgkg(-1)). Pb concentrations varied among use scenarios. The main lead contamination sources are industry emission and automobile exhaust. Bioaccessibility also varied among use scenarios. Children, who ingested soil from industrial area, public parks, kindergarten playground, and commercial area, are more susceptible to soil lead toxicity. The industrial area soil samples presented higher bioaccessibility compared to the other use scenario soil samples contaminated by automobile exhaust. The result also suggested a most significant linear relationship between the level of Pb contamination and the amount of Pb mobilized from soil into ingestion juice. Soil pH seemed to have insignificant influence on bioaccessibility in the present study. Bioaccessibility was mainly controlled by other factors that are not investigated in this study. A linear relationship between children blood lead and soil intestinal bioaccessibility was present in the study. Children who are 4-5 years old are more likely to demonstrate the significant relationship between soil lead bioaccessibility and blood lead as their behaviors place them at greatest risk of soil lead toxicity, and their blood lead levels are more likely to represent recent exposure.

  3. Exposure of pregnant rats to uranium and restraint stress: effects on postnatal development and behavior of the offspring.

    PubMed

    Sánchez, Domènec J; Bellés, Montserrat; Albina, Maria L; Gómez, Mercedes; Linares, Victoria; Domingo, José L

    2006-12-07

    The effects on postnatal development and behavior were assessed in the offspring of female rats concurrently exposed to uranium (U) and restraint stress. Adult female rats were administered uranyl acetate dihydrate (UAD) in the drinking water at doses of 0, 40 and 80 mg/(kg day) for 4 weeks before mating with untreated males, as well as during pregnancy and lactation. One-half of female rats in each group were concurrently subjected to restraint (2h/day). On gestation day 14, one-half of restrained and unrestrained rats were sacrificed in order to evaluate maternal toxicity and gestational parameters. Pups were evaluated for physical development, neuromotor maturation, and behavior. Uranium concentrations were also determined in various tissues of dams and fetuses. In all uranium-treated groups, the highest concentrations of this element were found in kidney and bone, being considerably higher than those in brain. Uranium levels in tissues of dam or fetuses were not significantly affected by restraint. No significant interactions between uranium and restraint could be observed in maternal toxicity. Moreover, no relevant effects of uranium, maternal restraint, or their combination were noted on developmental landmarks in the offspring. In the passive avoidance test, at 40 and 80 mg UAD/(kg day) restraint significantly modified passive avoidance acquisition (T1) and retention time (T2) 24h later. However, no significant differences were observed on the Morris water maze test. The results of the present study indicate that, in general terms, exposure of female rats to UAD before mating with untreated males, as well as during gestation and lactation, did not cause relevant dose-related adverse effects on postnatal development and behavior of the offspring. The influence of stress was very limited.

  4. OSHA lead in construction compliance directive: Exposure assessment

    SciTech Connect

    Vernon, L.S.

    1994-07-01

    This article is the second in a series that reviews the Occupational Health and Safety Administration (OSHA) Instruction CPL 2-2.58, a compliance directive for 29 CFR 1926.62, Lead Exposure in Construction. The OSHA document is intended to provide guidance to those charged with field enforcement of the lead regulation; however, it also provides vital information to those in industry who must comply with the regulation. This month, the requirements for compliance with 29 CFR 1926.62 (d) Exposure Assessment are discussed.

  5. Prenatal and postnatal polybrominated diphenyl ether exposure and visual spatial abilities in children.

    PubMed

    Vuong, Ann M; Braun, Joseph M; Yolton, Kimberly; Xie, Changchun; Webster, Glenys M; Sjödin, Andreas; Dietrich, Kim N; Lanphear, Bruce P; Chen, Aimin

    2017-02-01

    Polybrominated diphenyl ethers (PBDEs) are associated with impaired visual spatial abilities in toxicological studies, but no epidemiologic study has investigated PBDEs and visual spatial abilities in children. The Health Outcomes and Measures of the Environment Study, a prospective birth cohort (2003-2006, Cincinnati, OH), was used to examine prenatal and childhood PBDEs and visual spatial abilities in 199 children. PBDEs were measured at 16±3 weeks gestation and at 1, 2, 3, 5, and 8 years using gas chromatography/isotope dilution high-resolution mass spectrometry. We used the Virtual Morris Water Maze to measure visual spatial abilities at 8 years. In covariate-adjusted models, 10-fold increases in BDE-47, -99, and -100 at 5 years were associated with shorter completion times by 5.2s (95% Confidence Interval [CI] -9.3, -1.1), 4.5s (95% CI -8.1, -0.9), and 4.7s (95% CI -9.0, -0.3), respectively. However, children with higher BDE-153 at 3 years had longer completion times (β=5.4s, 95% CI -0.3, 11.1). Prenatal PBDEs were associated with improved visual spatial memory retention, with children spending a higher percentage of their search path in the correct quadrant. Child sex modified some associations between PBDEs and visual spatial learning. Longer path lengths were observed among males with increased BDE-47 at 2 and 3 years, while females had shorter paths. In conclusion, prenatal and postnatal BDE-28, -47, -99, and -100 at 5 and 8 years were associated with improved visual spatial abilities, whereas a pattern of impairments in visual spatial learning was noted with early childhood BDE-153 concentrations.

  6. CSU-FDA collaborative radiological health laboratory annual report, 1980: health effects of prenatal and postnatal whole-body exposure to ionizing radiation in the beagle dog

    SciTech Connect

    Benjamin, S.A.

    1982-01-01

    A long-term study of the mortality, morbidity, and physiopathology of beagles exposed to a single dose of ionizing radiation during one of six stages of either prenatal or postnatal development. The results of this study will provide insight into the lifetime risks associated with prenatal and postnatal exposure to low levels of ionizing radiation. This annual report describes the long-term study and the short-term experiments being performed to evaluate spontaneous and radiation-induced problems, as well as the computer storage and retrieval system and its uses in the study.

  7. Environmental and biological monitoring for lead exposure in California workplaces.

    PubMed Central

    Rudolph, L; Sharp, D S; Samuels, S; Perkins, C; Rosenberg, J

    1990-01-01

    Patterns of environmental and biological monitoring for lead exposure were surveyed in lead-using industries in California. Employer self-reporting indicates a large proportion of potentially lead-exposed workers have never participated in a monitoring program. Only 2.6 percent of facilities have done environmental monitoring for lead, and only 1.4 percent have routine biological monitoring programs. Monitoring practices vary by size of facility, with higher proportions in industries in which larger facilities predominate. Almost 80 percent of battery manufacturing employees work in job classifications which have been monitored, versus only 1 percent of radiator-repair workers. These findings suggest that laboratory-based surveillance for occupational lead poisoning may seriously underestimate the true number of lead poisoned workers and raise serious questions regarding compliance with key elements of the OSHA Lead Standard. PMID:2368850

  8. Effects of limited postnatal ethanol exposure on the development of myelin and nerve fibers in rat optic nerve.

    PubMed

    Phillips, D E

    1989-01-01

    This study was designed to morphologically evaluate the effects of limited postnatal alcohol exposure on the development of myelin and axons in the rat optic nerve. Rat pups were artificially reared on Days 5-18 with a supplemented milk diet fed via a chronic gastrostomy tube. Experimental animals received 4% ethanol in their diet on Days 5-9, otherwise the experimental and control animals received identical diets in identical volumes. Optic nerve tissues were prepared for electron microscopy on Days 10, 16, 22, 29, and 90. The cross-sectional areas of optic nerves were smaller, there were fewer myelinated nerve fibers per unit area, and the progress of myelination was slowed on Day 10 in the ethanol-exposed animals. All of these effects were compensated for at later times. The ratio of myelin thickness to axon diameter was similar in experimental and control animals, indicating that the interaction between axon size and myelin formation was not affected by alcohol. The general distribution of axon sizes was unaffected by ethanol except at 10 days when the largest fibers were smaller. There was no evidence of alcohol-induced degeneration of axons, myelin, or glial structures. Thus, alcohol exposure during myelin development causes a delay in myelin acquisition that is later compensated for.

  9. Effects of in utero or suckling exposure to cerium (citrate) on the postnatal developmental of the mouse

    SciTech Connect

    D'Agostino, R.B.; Lown, B.A.; Morganti, J.B.; Massaro, E.J.

    1982-09-01

    Gravid female mice received either a single subcutaneous dose of cerium citrate (80 mg Ce/kg) or an equivalent (in citrate) dose of sodium citrate on day 7 or 12 of gestation or on day 2 postpartum. To separate effects of prenatal and postnatal exposure, a cross-fostering design was employed. The weight and gross activity of the neonates were assessed on day 8 or 13 postpartum. Open-field behavioral parameters, accelerating rotarod performance, and passive avoidance learning were assessed on day 60-65 postpartum. Maternal offspring retrival latency was measured on day 3 postpartum. Maternal offspring retrieval latency was measured on day 3 postpartum. Analyses revealed that neonatal weight was reduced both in offspring exposed to Ce in utero and in the offspring of mothers receiving Ce during lactation/suckling. Ce also appeared to affect maternal/offspring interaction: pups exposed prenatally to Ce were retrieved in less time than control pups. Except for an increased frequency of rearings in the open field of adult offspring exposed to Ce in utero, Ce exposure had no apparent effect on behavioral parameters, either in neonatal or adult offspring.

  10. Effects of Early Postnatal Alcohol Exposure on the Developing Retinogeniculate Projections in C57BL/6 Mice

    PubMed Central

    Dursun, İlknur; Jakubowska-Doğru, Ewa; Birsen, Elibol-Can; van der List, Deborah; Chapman, Barbara; Qi, Lihong; Berman, Robert F.

    2013-01-01

    Previous studies on the adverse effects of perinatal exposure to ethanol on the developing visual system mainly focused on retinal and optic nerve morphology. The aim of the present study was to investigate whether earlier reported retinal and optic nerve changes are accompanied by anomalies in eye-specific fiber segregation in the dorsal lateral geniculate nucleus (dLGN). C57BL/6 mice pups were exposed to ethanol by intragastric intubation at either 3 or 4 g/kg from postnatal days (PD) 3-10, the third trimester equivalent to human gestation. Control (C) and intubation control (IC) groups not exposed to ethanol were included. On PD9 retinogeniculate projections, were labeled by intraocular microinjections of cholera toxin-β (CTB) either conjugated to Alexa 488 (green) or 594 (red) administrated to the left and right eye, respectively. Pups were sacrificed 24 h after the last CTB injection. The results showed that ethanol exposure decreased the total number of dLGN neurons and significantly reduced the total dLGN projection as well as the contralateral and ipsilateral projection areas. PMID:23402901

  11. Chronic lead exposure in children living in Miskolc Hungary, on the basis of teeth lead levels

    SciTech Connect

    Selypes, A.; Banfalvi, S.; Bokros, F.

    1997-03-01

    The lead pollution of the environment is a global problem. The major part of lead pollution can derive from the traffic, from exhausted gases of vehicles. Adverse health effects of lead exposure in childhood are well documented. Blood lead (Pb) levels are indicis of absorption during the previous 21- 30 days, whereas measurements of Pb in bone and in teeth reflect cumulative lead exposure. On the basis of that knowledge, we wanted to determine the tooth lead levels of children living in Miskolc, Hungary. The city of Miskolc is situated on the North-East part of Hungary, and can be characterized by urban-industrial air pollution. The population of the city is about 200,000. 10 refs., 1 fig., 3 tabs.

  12. Neurotoxic Effects and Biomarkers of Lead Exposure: A Review

    PubMed Central

    Sanders, Talia; Liu, Yiming; Buchner, Virginia; Tchounwou, Paul B.

    2010-01-01

    Biological monitoring techniques are useful for risk assessment of toxic agents in the field of environmental health. Lead, a systemic toxicant affecting virtually every organ system, primarily affects the central nervous system, particularly the developing brain. Consequently, children are at a greater risk than adults of suffering from the neurotoxic effects of lead. The ability of lead to pass through the blood-brain barrier is due in large part to its ability to substitute for calcium ions. Within the brain, lead-induced damage in the prefrontal cerebral cortex, hippocampus, and cerebellum can lead to a variety of neurological disorders, such as brain damage, mental retardation, behavioral problems, nerve damage, and possibly Alzheimer’s disease, Parkinson’s disease, and schizophrenia. At the molecular level, lead interferes with the regulatory action of calcium on cell functions and disrupts many intracellular biological activities. Experimental studies have also shown that lead exposure may have genotoxic effects, especially in the brain, bone marrow, liver, and lung cells. This paper presents an overview of biomarkers of lead exposure and discusses the neurotoxic effects of lead with regard to children, adults, and experimental animals, updated to January 2009. PMID:19476290

  13. Influence of social factors on lead exposure and child development.

    PubMed Central

    Bornschein, R L

    1985-01-01

    A brief overview of current views of child development is provided, with particular attention given to the role the child's physical and social environment plays in influencing the developmental process. Examples from the recent literature are used to illustrate how these factors can influence lead exposure and most importantly how they might interact with lead to ameliorate or exacerbate possible lead effects. An example is provided which demonstrates that failure to control adequately and to adjust the data statistically to correct for the influence of these factors can lead one erroneously to attribute cognitive and behavioral changes to lead. Finally, data from the Cincinnati Prospective Lead Study are presented to illustrate the application of structural equation modeling as a means for unraveling the complex web of sociodemographic, environmental and behavioral influences on childhood lead exposure. The latter analysis indicates that for children less than 24 months of age, lead-containing dust in the home and on the children's hands are important determinates of their blood lead levels. This relationship is influenced by the amount of maternal involvement with their child and other indices of interaction between the child and primary caregiver. PMID:2417831

  14. Neurobehavioral Development following Exposure of Male Mice to Polybrominated Diphenyl Ether 47 on Postnatal Day 10

    EPA Science Inventory

    Polybrominated diphenyl ethers (PBDEs) are commonly used as commercial flame retardants in a variety of products including plastics and textiles. Previous studies in our laboratory and in the literature have shown that exposure to a specific PBDE congener, PBDE 47, during a crit...

  15. Neurobehavioral Development following Exposure of Male Mice to Polybrominated Diphenyl Ether 47 on Postnatal Day 10

    EPA Science Inventory

    Polybrominated diphenyl ethers (PBDEs) are commonly used as commercial flame retardants in a variety of products including plastics and textiles. Previous studies in our laboratory and in the literature have shown that exposure to a specific PBDE congener, PBDE 47, during a crit...

  16. Early postnatal nicotine exposure causes hippocampus-dependent memory impairments in adolescent mice: Association with altered nicotinic cholinergic modulation of LTP, but not impaired LTP.

    PubMed

    Nakauchi, Sakura; Malvaez, Melissa; Su, Hailing; Kleeman, Elise; Dang, Richard; Wood, Marcelo A; Sumikawa, Katumi

    2015-02-01

    Fetal nicotine exposure from smoking during pregnancy causes long-lasting cognitive impairments in offspring, yet little is known about the mechanisms that underlie this effect. Here we demonstrate that early postnatal exposure of mouse pups to nicotine via maternal milk impairs long-term, but not short-term, hippocampus-dependent memory during adolescence. At the Schaffer collateral (SC) pathway, the most widely studied synapses for a cellular correlate of hippocampus-dependent memory, the induction of N-methyl-D-aspartate receptor-dependent transient long-term potentiation (LTP) and protein synthesis-dependent long-lasting LTP are not diminished by nicotine exposure, but rather unexpectedly the threshold for LTP induction becomes lower after nicotine treatment. Using voltage sensitive dye to visualize hippocampal activity, we found that early postnatal nicotine exposure also results in enhanced CA1 depolarization and hyperpolarization after SC stimulation. Furthermore, we show that postnatal nicotine exposure induces pervasive changes to the nicotinic modulation of CA1 activity: activation of nicotinic receptors no longer increases CA1 network depolarization, acute nicotine inhibits rather than facilitates the induction of LTP at the SC pathway by recruiting an additional nicotinic receptor subtype, and acute nicotine no longer blocks LTP induction at the temporoammonic pathway. These findings reflect the pervasive impact of nicotine exposure during hippocampal development, and demonstrate an association of hippocampal memory impairments with altered nicotinic cholinergic modulation of LTP, but not impaired LTP. The implication of our results is that nicotinic cholinergic-dependent plasticity is required for long-term memory formation and that postnatal nicotine exposure disrupts this form of plasticity.

  17. Lead exposure and behavioral changes: comparisons of four occupational groups with different levels of lead absorption.

    PubMed

    Valciukas, J A; Lilis, R; Singer, R; Fischbein, A; Anderson, H A; Glickman, L

    1980-01-01

    The association between lead absorption and objective psychological performance tests in five groups with different levels of lead absorption was studied in the following groups: (1) a control, non-lead-exposed group; (2) cable splicers, (3) cable manufactures, and (4) secondary lead smelter workers. The following performance tests were used: Block Design, Digit Symbol, and Embedded Figures. Age-corrected performance test scores and the average of three test scores (INDEX) were used throughout. A significant association between performance tests scores and increased lead absorption was found. Zinc protoporphyrin level was a more "powerful" (in the statistical sense) indicator of lead-induced CNS effects than blood lead levels. This study provides additional evidence that neurotoxic effects associated with occupational exposure to lead can be demonstrated by means of performance tests. It has been known and widely accepted that increased lead absorption is associated with "non-specific" subjective symptoms: tiredness, sleep disturbance, irritability, etc. Psychometric techniques (including an appropriate statistical analysis strategy) are highly sensitive for the early detection of CNS neurotoxicity, such as metal toxicity. Moreover, even in lead-exposed but asymptomatic individuals, a significant correlation (negative) between test scores and levels of lead absorption could be detected. It is concluded that workers exposed to lead at levels considered "safe" might be at risk of developing brain dysfunction with long term exposure.

  18. Lead

    MedlinePlus

    ... EPA United States Environmental Protection Agency Search Search Lead Contact Us Share Lead Poisoning is Preventable If your home was built ... to protect people from harmful lead exposures. Less Lead in Drinking Water = Better Health Learn about the ...

  19. Hypertension`s lead connection: Does low-level exposure to lead cause high blood pressure?

    SciTech Connect

    Fackelmann, K.

    1996-06-15

    {open_quotes}Paying for the sins of the past.{close_quotes} is how researcher Howard Hu describes a proposed disease process in which lead stored for decades in the skeleton puts people at risk of high blood pressure. Previous research has linked this silvery white, poisonous metal to a host of ill effects in children, including learning disabilities, behavior problems, and brain damage. Now, Hu`s study indicates that past exposure may be causing today`s high blood pressure. If he`s right, the public health impact would be significant. {open_quotes}Tens of millions of Americans have been exposed over the years to lead,{close_quotes} says Philip J. Landrigan of Mount Sinai Medical Center in New York. {open_quotes}Adults today grew up at a time when we were still putting several hundred thousand tons of lead into gasoline each year.{close_quotes} Indeed, the men who developed high blood pressure during the recent study had in their bones lead concentrations, or lead burdens, that came from decades of everyday exposure. Such exposures resulted principally from breathing in fumes from leaded gasoline, drinking tap water from lead pipes or pipes soldered with lead, and inhaling or ingesting lead-laced paint dust or chips. This article goes on to discuss other studies and questions which still need to be answered.

  20. Developmental lead exposure has mixed effects on butterfly cognitive processes.

    PubMed

    Philips, Kinsey H; Kobiela, Megan E; Snell-Rood, Emilie C

    2017-01-01

    While the effects of lead pollution have been well studied in vertebrates, it is unclear to what extent lead may negatively affect insect cognition. Lead pollution in soils can elevate lead in plant tissues, suggesting it could negatively affect neural development of insect herbivores. We used the cabbage white butterfly (Pieris rapae) as a model system to study the effect of lead pollution on insect cognitive processes, which play an important role in how insects locate and handle resources. Cabbage white butterfly larvae were reared on a 4-ppm lead diet, a concentration representative of vegetation in polluted sites; we measured eye size and performance on a foraging assay in adults. Relative to controls, lead-reared butterflies did not differ in time or ability to search for a food reward associated with a less preferred color. Indeed, lead-treated butterflies were more likely to participate in the behavioral assay itself. Lead exposure did not negatively affect survival or body size, and it actually sped up development time. The effects of lead on relative eye size varied with sex: lead tended to reduce eye size in males, but increase eye size in females. These results suggest that low levels of lead pollution may have mixed effects on butterfly vision, but only minimal impacts on performance in foraging tasks, although follow-up work is needed to test whether this result is specific to cabbage whites, which are often associated with disturbed areas.

  1. Environmental exposure to lead and children's intelligence at the age of seven years. The Port Pirie Cohort Study

    SciTech Connect

    Baghurst, P.A.; McMichael, A.J.; Wigg, N.R.; Vimpani, G.V.; Robertson, E.F.; Roberts, R.J.; Tong, S.L. )

    1992-10-29

    Exposure to lead in early childhood is thought to result in delayed neuropsychological development. As yet there is little longitudinal evidence to establish whether these effects persist into later childhood. The authors measured IQ scores in 494 seven-year-old children from the lead-smelting community of Port Pirie, Australia, in whom developmental deficits associated with elevated blood lead concentrations had already been reported at the ages of two and four years. Exposure to lead was estimated from the lead concentrations in maternal blood samples drawn antenatally and at delivery and from blood samples drawn from the children at birth (umbilical-cord blood), at the ages of 6 and 15 months and 2 years, and annually thereafter. Data relating to known covariates of child development were collected systematically for each child throughout the first seven years of life. The authors found inverse relations between IQ at the age of seven years and both antenatal and postnatal blood lead concentrations. After adjustment by multiple regression for sex, parents' level of education, maternal age at delivery, parents' smoking status, socioeconomic status, quality of the home environment, maternal IQ, birth weight, birth order, feeding method (breast, bottle, or both), duration of breast-feeding, and whether the child's natural parents were living together, the relation with lead exposure was still evident for postnatal blood samples, particularly within the age range of 15 months to 4 years. For an increase in blood lead concentration from 10 micrograms per deciliter (0.48 mumol per liter) to 30 micrograms per deciliter (1.45 mumol per liter), expressed as the average of the concentrations at 15 months and 2, 3, and 4 years, the estimated reduction in the IQ of the children was in the range of 4.4 points (95 percent confidence interval, 2.2 to 6.6) to 5.3 points (95 percent confidence interval, 2.8 to 7.8).

  2. Cardiotoxicity and hypertension in rats after oral lead exposure.

    PubMed

    Lal, B; Murthy, R C; Anand, M; Chandra, S V; Kumar, R; Tripathi, O; Srimal, R C

    1991-01-01

    The rats were exposed to lead (0.25, 0.5 and 1.0 per cent lead acetate through drinking water) for 90 days to study its effect on some physiological and morphological parameters of the cardiovascular system. Blood lead levels increased in a dose dependent manner but heart tissue showed rise at only two higher doses in exposed animals. The two higher doses of lead resulted in an increased arterial blood pressure and calcium influx in atrial trabeculae and papillary muscles. No marked pathological or histochemical changes were observed in heart tissue excepting congestion and slightly reduced activity of succinic dehydrogenase in the highest dosed group. It was concluded that lead exposure through drinking water may produce increased arterial blood pressure and minor changes in the myocardium. Whether these changes are mediated through the effect of lead on the calcium transport needs further investigation.

  3. Public health. Childhood lead exposure in Wisconsin in 1990

    SciTech Connect

    Schirmer, J.; Anderson, H.; Peterson, D.E. )

    1991-01-01

    It will take the cooperation of many people to address the issue of lead poisoning. The recent death has dramatized the problem of high dose exposures. But a larger challenge is posed by the fact that most preschool children in Wisconsin are not screened for lead and as a result many asymptomatic children without signs of pica behavior will experience subtle neurological damage as a result of low to moderate elevations of lead in blood. Because many of these cases occur in children without recognized pica behavior, doctors need to expand screening, especially during well child visits, to identify children with elevated blood lead levels. Additionally, the public health community and property owners need to evaluate and control sources of lead. Major efforts are needed to address the lead hazards which now impair hundreds of Wisconsin children each year.

  4. CHRONIC DEVELOPMENTAL LEAD EXPOSURE REDUCES NEUROGENESIS IN ADULT HIPPOCAMPUS.

    EPA Science Inventory

    CHRONIC DEVELOPMENTAL LEAD EXPOSURE REDUCES NEUROGENESIS IN ADULT HIPPOCAMPUS. ME Gilbert1, ME Kelly2, S. Salant3, T Shafer1, J Goodman3 1Neurotoxicology Div, US EPA, RTP, NC, 27711, 2Children's Hospital, Philadelphia, PA, 19104, 3Helen Hayes Hospital, Haverstraw, NY, 10993.
    ...

  5. CHRONIC DEVELOPMENTAL LEAD EXPOSURE REDUCES NEUROGENESIS IN ADULT HIPPOCAMPUS.

    EPA Science Inventory

    CHRONIC DEVELOPMENTAL LEAD EXPOSURE REDUCES NEUROGENESIS IN ADULT HIPPOCAMPUS. ME Gilbert1, ME Kelly2, S. Salant3, T Shafer1, J Goodman3 1Neurotoxicology Div, US EPA, RTP, NC, 27711, 2Children's Hospital, Philadelphia, PA, 19104, 3Helen Hayes Hospital, Haverstraw, NY, 10993.
    ...

  6. Developmental lead exposure alters methamphetamine self-administration in the male rat: acquisition and reinstatement.

    PubMed

    Rocha, Angelica; Valles, Rodrigo; Bratton, Gerald R; Nation, Jack R

    2008-05-01

    The rate of acquisition of drug self-administration and the return to drug seeking are important elements of the overall drug profile, and are essential factors in understanding risks associated with drug abuse. Experiment 1 examined the effects of perinatal (gestation/lactation) lead exposure on adult rates of acquisition of intravenous (i.v.) methamphetamine self-administration. Experiment 2 investigated the effects of perinatal lead exposure on drug-maintained responding in a reinstatement (relapse) paradigm. In Experiment 1, female rats were gavaged daily with 0 or 16 mg lead for 30 days prior to breeding with nonexposed males. Lead exposure continued through gestation and lactation and was discontinued at weaning (postnatal day [PND] 21). Male rats born to control or lead-exposed dams were tested daily as adults in an acquisition paradigm that incorporated both Pavlovian and operant components. An initial 3-h autoshaping period preceded a 3-h self-administration period. For 35 daily training sessions i.v. methamphetamine infusions [inf] (0.02 mg/kg) were paired with the extension and retraction of a lever (autoshaping), while inf occurred during self-administration only when a lever press was executed (FR-1). In Experiment 2 animals developmentally exposed to lead were trained on an FR-2 to self-administer methamphetamine (0.04 mg/kg/inf) and then placed on an extinction schedule prior to receiving intraperitoneal (i.p.) priming injections of saline, 0.50, 1.00, or 1.50 mg/kg methamphetamine. The findings from Experiment 1 showed that acquisition was delayed in rats born to lead-exposed dams gavaged daily with 16 mg lead throughout gestation and lactation when a 0.02-mg/kg/inf of methamphetamine served as the reinforcement outcome. Additional data from Experiment 2 indicated priming cues (injections of methamphetamine [i.p.]) administered after extinction were less likely to occasion a return to drug seeking (relapse) in the 16-mg group relative to the 0-mg

  7. Potential reproductive and postnatal morbidity from exposure to polychlorinated biphenyls: epidemiologic considerations.

    PubMed Central

    Rogan, W J; Gladen, B C; Wilcox, A J

    1985-01-01

    There is both laboratory and epidemiologic evidence that PCBs are toxic to several phases of reproduction. Workplace exposure is an important but small part of the exposure to these compounds, since most of the population has detectable levels in blood or fat. Studies in the general population on PCBs and reproduction have not been done. Some studies in workers are under way, and in epidemic PCB poisonings, small babies with a distinct clinical syndrome are seen. We review some of the laboratory and epidemiologic data and the methods available for study of reproduction in humans; study of any highly exposed group should be done and studies of spontaneous abortion, birth weight and certain congenital anomalies should look for an effect of PCBs. PMID:3928349

  8. Neurodevelopment of Amazonian Infants: Antenatal and Postnatal Exposure to Methyl- and Ethylmercury

    PubMed Central

    Dórea, José G.; Marques, Rejane C.; Isejima, Cintya

    2012-01-01

    Neurodevelopment as Gesell development scores (GDSs) in relation to mercury exposure in infants (<6 months of age) of one urban center and two rural villages, respectively, of fisherman and cassiterite miners. Mean total hair-Hg (HHg) concentrations of infants from Itapuã (3.95 ± 1.8 ppm) were statistically (P = 0.0001) different from those of infants from Porto Velho (3.84 ± 5.5 ppm) and Bom Futuro (1.85 ± 0.9 ppm). Differences in vaccine coverage among these populations resulted in significantly higher (P = 0.0001) mean ethylmercury (EtHg) exposure in urban infants (150 μg) than in infants from either village (41.67 μg, Itapuã; 42.39 μg, Bom Futuro). There was an inverse significant (Spearman r = −0.2300; P = 0.0376) correlation between HHg and GDS for infants from Porto Velho, but not for the rural infants from Bom Futuro (Spearman r = 0.1336; P = 0.0862) and Itapuã (Spearman r = 0.1666; P = 0.5182). Logistic regression applied to variables above or below the median GDS showed that EtHg exposure (estimated probability = −0.0157; P = 0.0070) and breastfeeding score (estimated probability = −0.0066; P = 0.0536) score were significantly associated with GDS. Conclusion. In nurslings whose mothers are exposed to different levels of fish-MeHg (HHg), a higher score of neurological development at six months was negatively associated with exposure to additional TCV-EtHg. Results should be interpreted with caution because of unaccounted variables. PMID:22619491

  9. Neurodevelopment of Amazonian infants: antenatal and postnatal exposure to methyl- and ethylmercury.

    PubMed

    Dórea, José G; Marques, Rejane C; Isejima, Cintya

    2012-01-01

    Neurodevelopment as Gesell development scores (GDSs) in relation to mercury exposure in infants (<6 months of age) of one urban center and two rural villages, respectively, of fisherman and cassiterite miners. Mean total hair-Hg (HHg) concentrations of infants from Itapuã (3.95 ± 1.8 ppm) were statistically (P = 0.0001) different from those of infants from Porto Velho (3.84 ± 5.5 ppm) and Bom Futuro (1.85 ± 0.9 ppm). Differences in vaccine coverage among these populations resulted in significantly higher (P = 0.0001) mean ethylmercury (EtHg) exposure in urban infants (150 μg) than in infants from either village (41.67 μg, Itapuã; 42.39 μg, Bom Futuro). There was an inverse significant (Spearman r = -0.2300; P = 0.0376) correlation between HHg and GDS for infants from Porto Velho, but not for the rural infants from Bom Futuro (Spearman r = 0.1336; P = 0.0862) and Itapuã (Spearman r = 0.1666; P = 0.5182). Logistic regression applied to variables above or below the median GDS showed that EtHg exposure (estimated probability = -0.0157; P = 0.0070) and breastfeeding score (estimated probability = -0.0066; P = 0.0536) score were significantly associated with GDS. Conclusion. In nurslings whose mothers are exposed to different levels of fish-MeHg (HHg), a higher score of neurological development at six months was negatively associated with exposure to additional TCV-EtHg. Results should be interpreted with caution because of unaccounted variables.

  10. Prenatal and postnatal exposure to polycyclic aromatic hydrocarbons and allergy symptoms in city children.

    PubMed

    Jerzynska, J; Podlecka, D; Polanska, K; Hanke, W; Stelmach, I; Stelmach, W

    Studies indicate that exposure to polycyclic aromatic hydrocarbons (PAH) is associated with adverse respiratory and allergy outcomes. Exposure to PAH may impair the immune function of the foetus and, subsequently, be responsible for an increased susceptibility of children to allergic diseases. The aim of the present study was to assess the association between mother's exposure to PAH during pregnancy and allergy diseases in their infants. We also assessed the above associations using measured PAH exposure in children's urine during the first two years of life. The current analysis was restricted to 455 mothers and their children from Lodz district. The women were interviewed three times during the pregnancy in order to collect demographic, socio-economic and medical history data. Children's health status was assessed at the age of 10-18 months and repeated at two years of age. The associations between dependent dichotomous variables and urine concentrations of 1-hydroxypyrene (1-HP) were analysed using logistic regression. We showed that higher urine concentrations of 1-HP in mothers at 20-24 weeks of pregnancy increased the risk of more frequent respiratory infections (p=0.02) in children during their first year of life. Higher 1-HP concentrations in children's urine increased the risk of food allergy (p=0.002) in children during their first two years of life. This study suggests awareness of environmental factors, which may affect children's health since PAH showed to be a risk factor for airway infections and food allergy in children after adjustment for other risk factors. Copyright © 2016 SEICAP. Published by Elsevier España, S.L.U. All rights reserved.

  11. Changes in Dam and Pup Behavior Following Repeated Postnatal Exposure to a Predator Odor (TMT): A Preliminary Investigation in Long-Evans Rats

    PubMed Central

    Ayers, Luke W.; Asok, Arun; Blaze, Jennifer; Roth, Tania L.; Rosen, Jeffrey B.

    2016-01-01

    The present study investigated whether repeated early postnatal exposure to the predator odor 2,5-dihydro-2,4,5-trimethylthiazoline (TMT) alters behavioral responses to the stimulus later in life, at postnatal day (PN30). Long-Evans rat pups with their mothers were exposed for 20 min daily to TMT, water, or a noxious odor, butyric acid (BTA), during the first three weeks of life. Mothers exposed to TMT displayed more crouching and nursing behavior than those exposed to BTA, and TMT exposed pups emitted more ultrasonic vocalizations than BTA exposed pups. At PN30, rats were tested for freezing to TMT, water, or BTA. Rats exposed to TMT during the postnatal period displayed less freezing to TMT than rats exposed postnatally to water or BTA. Our data indicate that early-life experience with a predator cue has a significant impact on later fear responses to that same cue, highlighting the programming capacity of the postnatal environment on the development of behavior. PMID:26394891

  12. Changes in dam and pup behavior following repeated postnatal exposure to a predator odor (TMT): A preliminary investigation in Long-Evans rats.

    PubMed

    Ayers, Luke W; Asok, Arun; Blaze, Jennifer; Roth, Tania L; Rosen, Jeffrey B

    2016-03-01

    The present study investigated whether repeated early postnatal exposure to the predator odor 2,5-dihydro-2,4,5-trimethylthiazoline (TMT) alters behavioral responses to the stimulus later in life, at postnatal day (PN30). Long-Evans rat pups with their mothers were exposed for 20 min daily to TMT, water, or a noxious odor, butyric acid (BTA), during the first three weeks of life. Mothers exposed to TMT displayed more crouching and nursing behavior than those exposed to BTA, and TMT exposed pups emitted more ultrasonic vocalizations than BTA exposed pups. At PN30, rats were tested for freezing to TMT, water, or BTA. Rats exposed to TMT during the postnatal period displayed less freezing to TMT than rats exposed postnatally to water or BTA. Our data indicate that early-life experience with a predator cue has a significant impact on later fear responses to that same cue, highlighting the programming capacity of the postnatal environment on the development of behavior.

  13. Lead exposure and educational proficiency: moderate lead exposure and educational proficiency on end-of-grade examinations.

    PubMed

    Amato, Michael S; Moore, Colleen F; Magzamen, Sheryl; Imm, Pamela; Havlena, Jeffrey A; Anderson, Henry A; Kanarek, Marty S

    2012-10-01

    To investigate and quantify the impact of moderate lead exposure on students' ability to score at the "proficient" level on end-of-grade standardized tests. We compared the scores of 3757 fourth grade students from Milwaukee, Wisconsin, on the Wisconsin Knowledge and Concepts Exam (WKCE). The sample consisted of children with a blood lead test before age 3 years that was either unquantifiable at the time of testing (<5 μg/dL) or in the range of moderate exposure (10-19 μg/dL). After controlling for gender, poverty, English language learner status, race/ethnicity, school disciplinary actions, and attendance percentage, results showed a significant negative effect of moderate lead exposure on academic achievement for all 5 subtests of the WKCE. Test score deficits owing to lead exposure were equal to 22% of the interval between student categorization at the "proficient" or "basic" levels in Reading, and 42% of the interval in Mathematics. Children exposed to amounts of lead before age 3 years that are insufficient to trigger intervention under current policies in many states are nonetheless at a considerable educational disadvantage compared with their unexposed peers 7 to 8 years later. Exposed students are at greater risk of scoring below the proficient level, an outcome with serious negative consequences for both the student and the school. Copyright © 2012 Elsevier Inc. All rights reserved.

  14. Leaded crystal as a source of dietary lead: An exposure assessment

    SciTech Connect

    Shorten, C.V.; Glowacki, M.L.

    1995-12-31

    Lead is a potent systemic toxic with many environmental sources. It can enter the body through a number of pathways, the most significant is ingestion. While many investigators of lead ingestion have focused on paint and dust sources, the authors examined food contaminated with lead from crystal ware. The rates and amounts of lead leached into vinegar stored in leaded crystal cruets were measured over the course of a 42-day laboratory study. Replicate lead oxide (PbO, 24%) crystal cruets (N = 13) were filled with vinegar, and sample aliquots were periodically removed for analysis. Lead leaching rates were determined by fitting a two-stage, non-linear model to the data, and observed rate coefficients were 0.066 hr{sup {minus}1} and 0.0019{sup {minus}1} for the first and second stages of leaching, respectively (R{sup 2} = 0.9680). Average lead concentrations in the stored vinegar range from 118 {micro}g/L at 8 parameters (ingestion rate, exposure frequency and duration, body weight, and averaging time) was generated to characterize the realm of potential intake estimates. Lead concentrations were input using the fitted model. Results indicated that a worst case lead intake estimate from this source could be as high as 420 {micro}g/kg/yr for a child. Crystal ware can be considered to be a potentially significant dietary source of lead, and risk characterizations cannot ignore this potential avenue when combining risks across all exposure pathways.

  15. Changes in orexinergic immunoreactivity of the piglet hypothalamus and pons after exposure to chronic postnatal nicotine and intermittent hypercapnic hypoxia.

    PubMed

    Hunt, Nicholas J; Russell, Benjamin; Du, Man K; Waters, Karen A; Machaalani, Rita

    2016-06-01

    We recently showed that orexin expression in sudden infant death syndrome (SIDS) infants was reduced by 21% in the hypothalamus and by 40-50% in the pons as compared with controls. Orexin maintains wakefulness/sleeping states, arousal, and rapid eye movement sleep, abnormalities of which have been reported in SIDS. This study examined the effects of two prominent risk factors for SIDS, intermittent hypercapnic hypoxia (IHH) (prone-sleeping) and chronic nicotine exposure (cigarette-smoking), on orexin A (OxA) and orexin B (OxB) expression in piglets. Piglets were randomly assigned to five groups: saline control (n = 7), air control (n = 7), nicotine [2 mg/kg per day (14 days)] (n = 7), IHH (6 min of 7% O2 /8% CO2 alternating with 6-min periods of breathing air, for four cycles) (n = 7), and the combination of nicotine and IHH (N + IHH) (n = 7). OxA/OxB expression was quantified in the central tuberal hypothalamus [dorsal medial hypothalamus (DMH), perifornical area (PeF), and lateral hypothalamus], and the dorsal raphe, locus coeruleus of the pons. Nicotine and N + IHH exposures significantly increased: (i) orexin expression in the hypothalamus and pons; and (ii) the total number of neurons in the DMH and PeF. IHH decreased orexin expression in the hypothalamus and pons without changing neuronal numbers. Linear relationships existed between the percentage of orexin-positive neurons and the area of pontine orexin immunoreactivity of control and exposure piglets. These results demonstrate that postnatal nicotine exposure increases the proportion of orexin-positive neurons in the hypothalamus and fibre expression in the pons, and that IHH exposure does not prevent the nicotine-induced increase. Thus, although both nicotine and IHH are risk factors for SIDS, it appears they have opposing effects on OxA and OxB expression, with the IHH exposure closely mimicking what we recently found in SIDS. © 2016 Federation of European Neuroscience Societies and John

  16. Postnatal development and behavior effects of in-utero exposure of rats to radiofrequency waves emitted from conventional WiFi devices.

    PubMed

    Othman, Haifa; Ammari, Mohamed; Rtibi, Kaïs; Bensaid, Noura; Sakly, Mohsen; Abdelmelek, Hafedh

    2017-06-01

    The present work investigated the effects of prenatal exposure to radiofrequency waves of conventional WiFi devices on postnatal development and behavior of rat offspring. Ten Wistar albino pregnant rats were randomly assigned to two groups (n=5). The experimental group was exposed to a 2.45GHz WiFi signal for 2h a day throughout gestation period. Control females were subjected to the same conditions as treated group without applying WiFi radiations. After delivery, the offspring was tested for physical and neurodevelopment during its 17 postnatal days (PND), then for anxiety (PND 28) and motricity (PND 40-43), as well as for cerebral oxidative stress response and cholinesterase activity in brain and serum (PND 28 and 43). Our main results showed that the in-utero WiFi exposure impaired offspring neurodevelopment during the first seventeen postnatal days without altering emotional and motor behavior at adult age. Besides, prenatal WiFi exposure induced cerebral oxidative stress imbalance (increase in malondialdehyde level (MDA) and hydrogen peroxide (H2O2) levels and decrease in catalase (CAT) and superoxide dismutase (SOD) activities) at 28 but not 43days old, also the exposure affected acethylcolinesterase activity at both cerebral and seric levels. Thus, the current study revealed that maternal exposure to WiFi radiofrequencies led to various adverse neurological effects in the offspring by affecting neurodevelopment, cerebral stress equilibrium and cholinesterase activity. Copyright © 2017 Elsevier B.V. All rights reserved.

  17. Neural stem cell apoptosis after low-methylmercury exposures in postnatal hippocampus produce persistent cell loss and adolescent memory deficits.

    PubMed

    Sokolowski, Katie; Obiorah, Maryann; Robinson, Kelsey; McCandlish, Elizabeth; Buckley, Brian; DiCicco-Bloom, Emanuel

    2013-12-01

    The developing brain is particularly sensitive to exposures to environmental contaminants. In contrast to the adult, the developing brain contains large numbers of dividing neuronal precursors, suggesting that they may be vulnerable targets. The postnatal day 7 (P7) rat hippocampus has populations of both mature neurons in the CA1-3 region as well as neural stem cells (NSC) in the dentate gyrus (DG) hilus, which actively produce new neurons that migrate to the granule cell layer (GCL). Using this well-characterized NSC population, we examined the impact of low levels of methylmercury (MeHg) on proliferation, neurogenesis, and subsequent adolescent learning and memory behavior. Assessing a range of exposures, we found that a single subcutaneous injection of 0.6 µg/g MeHg in P7 rats induced caspase activation in proliferating NSC of the hilus and GCL. This acute NSC death had lasting impact on the DG at P21, reducing cell numbers in the hilus by 22% and the GCL by 27%, as well as reductions in neural precursor proliferation by 25%. In contrast, non-proliferative CA1-3 pyramidal neuron cell number was unchanged. Furthermore, animals exposed to P7 MeHg exhibited an adolescent spatial memory deficit as assessed by Morris water maze. These results suggest that environmentally relevant levels of MeHg exposure may decrease NSC populations and, despite ongoing neurogenesis, the brain may not restore the hippocampal cell deficits, which may contribute to hippocampal-dependent memory deficits during adolescence. Copyright © 2013 Wiley Periodicals, Inc.

  18. Estimation of desvenlafaxine transfer into milk and infant exposure during its use in lactating women with postnatal depression.

    PubMed

    Rampono, Jonathan; Teoh, Stephanie; Hackett, L Peter; Kohan, Rolland; Ilett, Kenneth F

    2011-02-01

    This study characterises the extent of desvenlafaxine transfer into milk and provides data on infant exposure to desvenlafaxine via breast milk in ten women with postnatal depression and their breastfed infants. Desvenlafaxine concentration in milk and plasma was measured chromatographically in milk and in maternal and infant plasma collected at steady state. Theoretic and relative infant doses via milk were estimated and the per cent drug in infant versus mother's plasma was calculated. Theoretic infant dose via milk was 85 (53-117) μg kg(-1) day(-1) (mean and 95% confidence interval) and relative infant dose was 6.8% (5.5-8.1%). The ratio of drug in infant/maternal plasma also gave an infant exposure estimate of 4.8% (3.5-6.2%) for all ten infants and 5.3% (4.2-5.7%) in the eight infants who were exclusively breastfed. No adverse effects were seen in the infants. The relative infant dose was similar to that for previous studies using venlafaxine and was supported by a separate exposure measure using the ratio of drug in the infant's plasma relative to that in the mother's plasma. The theoretic infant dose of desvenlafaxine was 41-45% of that for venlafaxine and its metabolite desvenlafaxine in previous studies, reflecting the lower recommended maternal dose for desvenlafaxine. Although our data for desvenlafaxine use in lactation are encouraging and there are supporting data from venlafaxine studies, more patients and their infants need to be studied before the safety of desvenlafaxine as a single therapeutic agent can be fully assessed.

  19. Genistein exposure during the early postnatal period favors the development of obesity in female, but not male rats.

    PubMed

    Strakovsky, Rita S; Lezmi, Stéphane; Flaws, Jodi A; Schantz, Susan L; Pan, Yuan-Xiang; Helferich, William G

    2014-03-01

    Genistein (Gen), the primary isoflavone in soy, has been shown to adversely affect various endocrine-mediated endpoints in rodents and humans. Soy formula intake by human infants has been associated with early age at menarche and decreased female-typical behavior in girls. Adipose deposition and expansion are also hormonally regulated and Gen has been shown to alter these processes. However, little is known about the impact of early-life soy intake on metabolic homeostasis in adulthood. The current study examined the impact of early-life Gen exposure on adulthood body composition (by magnetic resonance imaging) and the molecular signals mediating adipose expansion. From postnatal day (PND) 1 to 22, rat pups were daily orally dosed with 50mg/kg Gen to mimic blood Gen levels in human infants fed soy formula. Female but not male Gen-exposed rats had increased fat/lean mass ratio, fat mass, adipocyte size and number, and decreased muscle fiber perimeter. PND22 Gen-exposed females, but not males, had increased expression of adipogenic factors, including CCAAT/enhancer binding protein alpha (Cebpα), CCAAT/enhancer binding protein beta (Cebpβ), and peroxisome proliferator-activated receptor gamma (Pparγ). Furthermore, Wingless-related MMTV integration site 10b (Wnt10b), a critical regulator of adipogenic cell fate determination, was hypermethylated and had decreased expression in adipose of PND22 Gen-exposed females. These data suggest that developmental Gen exposure in rats has gender-specific effects on adiposity that closely parallel the effects of a postweaning high-fat diet and underscore the importance of considering timing of exposure and gender when establishing safety recommendations for early-life dietary Gen intake.

  20. Low level exposures to lead and neurobehavioral development: the Sydney lead study

    SciTech Connect

    Cooney, G.H.; Bell, A.; McBride, W.; Carter, C.

    1988-01-01

    The Sydney lead study is a prospective five year study investigating the relationship between low level lead exposures and neurobehavioral development during the first five years of life. From an initial cohort of 318 children, 207 remained at the end of the fourth year. Average blood lead levels at 42 and 48 months were 10.6 ug/dL and 10.1 ug/dL respectively, with only a minority of the observations exceeding 15 ug/dL. The series of regression analyses reported in this paper support earlier findings from the study, that exposures to lead which give rise to the range of blood lead levels found in this cohort of children are not associated with cognitive or motor deficits in the preschool years.

  1. Anemia risk in relation to lead exposure in lead-related manufacturing.

    PubMed

    Hsieh, Nan-Hung; Chung, Shun-Hui; Chen, Szu-Chieh; Chen, Wei-Yu; Cheng, Yi-Hsien; Lin, Yi-Jun; You, Su-Han; Liao, Chung-Min

    2017-05-05

    Lead-exposed workers may suffer adverse health effects under the currently regulated blood lead (BPb) levels. However, a probabilistic assessment about lead exposure-associated anemia risk is lacking. The goal of this study was to examine the association between lead exposure and anemia risk among factory workers in Taiwan. We first collated BPb and indicators of hematopoietic function data via health examination records that included 533 male and 218 female lead-exposed workers between 2012 and 2014. We used benchmark dose (BMD) modeling to estimate the critical effect doses for detection of abnormal indicators. A risk-based probabilistic model was used to characterize the potential hazard of lead poisoning for job-specific workers by hazard index (HI). We applied Bayesian decision analysis to determine whether BMD could be implicated as a suitable BPb standard. Our results indicated that HI for total lead-exposed workers was 0.78 (95% confidence interval: 0.50-1.26) with risk occurrence probability of 11.1%. The abnormal risk of anemia indicators for male and female workers could be reduced, respectively, by 67-77% and 86-95% by adopting the suggested BPb standards of 25 and 15 μg/dL. We conclude that cumulative exposure to lead in the workplace was significantly associated with anemia risk. This study suggests that current BPb standard needs to be better understood for the application of lead-exposed population protection in different scenarios to provide a novel standard for health management. Low-level lead exposure risk is an occupational and public health problem that should be paid more attention.

  2. [Association between low blood lead exposure and nervous system symptoms].

    PubMed

    Dou, Qianru; Wang, Yan; Cai, Chang; Li, Jimeng; Tan, Hongzhuan

    2015-05-01

    To explore the association between low blood lead exposure and nervous system symptoms among the workers exposed to oil paint. Through cluster sampling, workers with occupational oil paint exposure in 2 factories were selected to conduct a questionnaire survey, biochemical detection and health examination. χ2 test and unconditional logistic regression analysis were performed for the determinants analysis. A total of 525 oil paint workers completed the survey, in whom, 55 (10.5%) were blood lead positive, the mean of blood lead concentration was (0.0884±0.0539) mg/L, 278 (52.95%) had nervous system like symptoms and 69 (13.14%) had peripheral neuropathy symptoms. Multinomial logistic regression analysis showed that working age (OR=1.827), drinking (OR=1.607), health status (OR=3.862), blood lead (OR=1.983) were risk factors for nervous system like symptoms. Working age (OR=2.282), and drinking (OR=2.704) were risk factors for peripheral neuropathy. Low blood lead exposure might be associated with nervous system like symptoms.

  3. Behavioral effects of low level neonatal lead exposure.

    PubMed

    Hastings, L; Cooper, G P; Bornschein, R L; Michaelson, I A

    1977-07-01

    Rats exposed to lead via maternal milk were tested at various stages of development on a number of behavioral tasks. Beginning at paturition, the dams were given either tap water, 0.02%, or 0.10% lead acetate in the drinking water. Pups from all three groups were weaned to normal chow and tap water at 21 days of age. The mean lead concentration of the dam's blood and of neonatal (20 days of age) brain and blood were all below 50 microgram/100 ml. No significant differences were found between the high lead-exposed group and controls in general as measured by wheel running over a 21 day period beginning at 30 days of age. However, there was a significant difference in wheel running behavior during the first three hr of testing. Both lead-exposed groups were found to display significantly less aggressive behavior as measured by the shock-elicited aggression test. Low level lead exposure had no discernable effect on the acquisition and subsequent reversal of a successive brightness discrimination task. Lead exposure under these conditions appears to affect some aspects of emotional behavior, while having little effect on general activity or cognitive function.

  4. Excess perigestational folic acid exposure induces metabolic dysfunction in post-natal life.

    PubMed

    Keating, Elisa; Correia-Branco, Ana; Araújo, João R; Meireles, Manuela; Fernandes, Rita; Guardão, Luísa; Guimarães, João T; Martel, Fátima; Calhau, Conceição

    2015-03-01

    The aim of this study was to understand whether high folic acid (HFA) exposure during the perigestational period induces metabolic dysfunction in the offspring, later in life. To do this, female Sprague-Dawley rats (G0) were administered a dose of folic acid (FA) recommended for pregnancy (control, C, 2 mg FA/kg of diet, n=5) or a high dose of FA (HFA, 40 mg FA/kg of diet, n=5). Supplementation began at mating and lasted throughout pregnancy and lactation. Body weight and food and fluid intake were monitored in G0 and their offspring (G1) till G1 were 13 months of age. Metabolic blood profiles were assessed in G1 at 3 and 13 months of age (3M and 13M respectively). Both G0 and G1 HFA females had increased body weight gain when compared with controls, particularly 22 (G0) and 10 (G1) weeks after FA supplementation had been stopped. G1 female offspring of HFA mothers had increased glycemia at 3M, and both female and male G1 offspring of HFA mothers had decreased glucose tolerance at 13M, when compared with matched controls. At 13M, G1 female offspring of HFA mothers had increased insulin and decreased adiponectin levels, and G1 male offspring of HFA mothers had increased levels of leptin, when compared with matched controls. In addition, feeding of fructose to adult offspring revealed that perigestational exposure to HFA renders female progeny more susceptible to developing metabolic unbalance upon such a challenge. The results of this work indicate that perigestational HFA exposure the affects long-term metabolic phenotype of the offspring, predisposing them to an insulin-resistant state. © 2015 Society for Endocrinology.

  5. Prenatal exposure to androgen excess increases LH pulse amplitude during postnatal life in male sheep.

    PubMed

    Recabarren, S E; Recabarren, M; Rojas-Garcia, P P; Cordero, M; Reyes, C; Sir-Petermann, T

    2012-09-01

    Prenatal exposure to excess testosterone has a profound impact on reproductive and metabolic functions in young and adult female sheep. Nevertheless, few studies have addressed the impact of prenatal exposure to an excess of androgens on reproductive and metabolic functions in males. The aim of the present study was to assess the impact of prenatal exposure to an excess of testosterone or dihydrotestosterone on the luteinizing hormone (LH) pulse characteristics during sexual development in male sheep. Control male sheep (C-males) and males born to mothers exposed to twice weekly injections of 30 mg testosterone or dihydrotestosterone from day 30-90 and 40 mg from day 90-120 of gestation (T-males, DHT-males) were studied at 5, 10, and 20 weeks of age, ages that represent infancy, early prepubertal, and late prepubertal stages of sexual development in this species, respectively. Patterns of LH pulsatility showed that T- and DHT-males exhibited a higher secretion of LH during the 6-h study and a higher amplitude of the LH pulses compared with C-males. Moreover, nadir of the pulses was higher in T- and DHT-males compared with C-males. Frequency of LH pulses, however, was not different within ages or between groups. These results show that males can be responsive to prenatal androgenization and suggest that treatment transiently alters the amplitude of LH pulses probably as the result of defects in the pituitary responsiveness pattern or in the gonadotropin-releasing hormone (GnRH) release pattern.

  6. Responses of estrogen sensitive tissues in female Wistar rats to pre- and postnatal isoflavone exposure.

    PubMed

    Hertrampf, T; Ledwig, C; Kulling, S; Molzberger, A; Möller, F J; Zierau, O; Vollmer, G; Moors, S; Degen, G H; Diel, P

    2009-12-15

    Effects of isoflavones on estrogen sensitive tissues are discussed controversially. This study was designed to investigate tissue specific effects of an isoflavone exposure through different periods of life in female Wistar rats and to compare the effects of genistein (GEN) to those of mixed dietary isoflavones, GEN and daidzein (DAI). One group received an isoflavone-free diet (IDD), another was fed an isoflavone-rich diet (IRD) and the third group an IDD supplemented with GEN (GEN(d)) prior to mating, throughout pregnancy and up to weaning. The offspring were kept on the respective diets during growth, puberty and adulthood. The weight of the uterus, the height of the uterine and vaginal epithelium, the bone mineral density of the tibia, and the expression of the estrogen sensitive gene CaBP9K in the liver were determined. At d21, the uterine weight, the uterine epithelium and the expression of CaBP9K in the liver were significantly stimulated in GEN(d) animals compared to IDD and IRD. Interestingly, bone mineral density was increased in GEN(d) and in IRD animals. Around puberty (d50) neither uterine wet weights nor trabecular bone density differed significantly among the isoflavone groups and the IDD control. At d80 no significant differences in uterine weight were observed among IDD, GEN(d) and IRD animals. However, bone mineral density was increased in GEN(d) and IRD animals. In summary, our results demonstrate that lifelong dietary exposure to isoflavones can affect estrogen sensitive tissues, apparently in a tissue selective manner. With respect to health risk and benefit our data indicate that an increased bone mineral density can be achieved by lifelong exposure to an IRD, which, in contrast to GEN supplementation, does not seem to stimulate the proliferation of the uterine epithelium.

  7. Maternal administration of melatonin prevents spatial learning and memory deficits induced by developmental ethanol and lead co-exposure.

    PubMed

    Soleimani, Elham; Goudarzi, Iran; Abrari, Kataneh; Lashkarbolouki, Taghi

    2017-05-01

    Melatonin is a radical scavenger with the ability to remove reactive oxidant species. There is report that co-exposure to lead and ethanol during developmental stages induces learning and memory deficits and oxidative stress. Here, we studied the effect of melatonin, with strong antioxidant properties, on memory deficits induced by lead and ethanol co-exposure and oxidative stress in hippocampus. Pregnant rats in lead and ethanol co-exposure group received lead acetate of 0.2% in distilled drinking water and ethanol (4g/kg) by oral gavages once daily from the 5th day of gestation until weaning. Rats received 10mg/kg melatonin by oral gavages. On postnatal days (PD) 30, rats trained with six trials per day for 6 consecutive days in the water maze. On day 37, a probe test was done and oxidative stress markers in the hippocampus were evaluated. Results demonstrated lead and ethanol co-exposed rats exhibited higher escape latency during training trials and reduced time spent in target quadrant, higher escape location latency in probe trial test and had significantly higher malondialdehyde (MDA) levels, significantly lower superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) activities in the hippocampus. Melatonin treatment could improve memory deficits, antioxidants activity and reduced MDA levels in the hippocampus. We conclude, co-exposure to lead and ethanol impair memory and melatonin can prevent from it by oxidative stress modulation. Copyright © 2017 Elsevier Inc. All rights reserved.

  8. Environmental and Occupational Lead Exposure Among Children in Cairo, Egypt

    PubMed Central

    Moawad, Eman Mohamed Ibraheim; Badawy, Nashwa Mostafa; Manawill, Marie

    2016-01-01

    Abstract The aim of this study was to assess childhood lead exposure in a representative sample of Cairo, and to investigate the possible risk factors and sources of exposure. This cross-sectional study was conducted from November 2014 through April 2015. The target population was children aged 6 to 18 years, recruited into 4 groups, garbage city, moderate-living standard area, urban and suburban schools, and workshops in the city of Cairo. Blood lead levels (BLLs) and hemoglobin (Hb) concentrations were measured. Also, potential local environmental sources were assessed for hazardous lead contamination. Analysis on 400 participants has been carried out. A total of 113 children had BLLs in the range 10 to 20 μg/dL. Smoking fathers, housing conditions, playing outdoors, and exposure to lead in residential areas were significantly correlated with high BLLs. The mean values of hemoglobin were inversely correlated with BLLs. Children involved in pottery workshops had the highest BLLs and the lowest Hb values with a mean of (43.3 μg/dL and 8.6 g/dL, respectively). The mean value of environmental lead in workshop areas exceeded the recommended levels. Also, those values measured in dust and paint samples of garbage city were significantly high. Moreover, the mean lead levels in the soil samples were significantly higher in urban schools (P = 0.03) than the suburban ones. Childhood lead poisoning accounts for a substantial burden in Egypt, which could be preventable. Development of national prevention programs including universal screening program should be designed to reduce incidence of lead toxicity among children. PMID:26945415

  9. Perinatal exposure to lead (Pb) induces ultrastructural and molecular alterations in synapses of rat offspring.

    PubMed

    Gąssowska, Magdalena; Baranowska-Bosiacka, Irena; Moczydłowska, Joanna; Frontczak-Baniewicz, Małgorzata; Gewartowska, Magdalena; Strużyńska, Lidia; Gutowska, Izabela; Chlubek, Dariusz; Adamczyk, Agata

    2016-12-12

    Lead (Pb), environmentally abundant heavy-metal pollutant, is a strong toxicant for the developing central nervous system. Pb intoxication in children, even at low doses, is found to affect learning and memorizing, with devastating effects on cognitive function and intellectual development. However, the precise mechanism by which Pb impairs synaptic plasticity is not fully elucidated. The purpose of this study was to investigate the effect of pre- and neonatal exposure to low dose of Pb (with Pb concentrations in whole blood below 10μg/dL) on the synaptic structure and the pre- and postsynaptic proteins expression in the developing rat brain. Furthermore, the level of brain-derived neurotrophic factor (BDNF) was analyzed. Pregnant female Wistar rats received 0.1% lead acetate (PbAc) in drinking water from the first day of gestation until weaning of the offspring, while the control animals received drinking water. During the feeding of pups, mothers from the Pb-group were continuously receiving PbAc. Pups of both groups were weaned at postnatal day 21 and then until postnatal day 28 received only drinking water. 28-day old pups were sacrificed and the ultrastructural changes as well as expression of presynaptic (VAMP1/2, synaptophysin, synaptotagmin-1, SNAP25, syntaxin-1) and postsynaptic (PSD-95) proteins were analyzed in: forebrain cortex, cerebellum and hippocampus. Our data revealed that pre- and neonatal exposure to low dose of Pb promotes pathological changes in synapses, including nerve endings swelling, blurred and thickened synaptic cleft structure as well as enhanced density of synaptic vesicles in the presynaptic area. Moreover, synaptic mitochondria were elongated, swollen or shrunken in Pb-treated animals. These structural abnormalities were accompanied by decrease in the level of key synaptic proteins: synaptotagmin-1 in cerebellum, SNAP25 in hippocampus and syntaxin-1 in cerebellum and hippocampus. In turn, increased level of synaptophysin was

  10. Perinatal exposure to lead (Pb) induces ultrastructural and molecular alterations in synapses of rat offspring.

    PubMed

    Gąssowska, Magdalena; Baranowska-Bosiacka, Irena; Moczydłowska, Joanna; Frontczak-Baniewicz, Małgorzata; Gewartowska, Magdalena; Strużyńska, Lidia; Gutowska, Izabela; Chlubek, Dariusz; Adamczyk, Agata

    2016-10-29

    Lead (Pb), environmentally abundant heavy-metal pollutant, is a strong toxicant for the developing central nervous system. Pb intoxication in children, even at low doses, is found to affect learning and memorizing, with devastating effects on cognitive function and intellectual development. However, the precise mechanism by which Pb impairs synaptic plasticity is not fully elucidated. The purpose of this study was to investigate the effect of pre- and neonatal exposure to low dose of Pb (with Pb concentrations in whole blood below 10μg/dL) on the synaptic structure and the pre- and postsynaptic proteins expression in the developing rat brain. Furthermore, the level of brain-derived neurotrophic factor (BDNF) was analyzed. Pregnant female Wistar rats received 0.1% lead acetate (PbAc) in drinking water from the first day of gestation until weaning of the offspring, while the control animals received drinking water. During the feeding of pups, mothers from the Pb-group were continuously receiving PbAc. Pups of both groups were weaned at postnatal day 21 and then until postnatal day 28 received only drinking water. 28-Day old pups were sacrificed and the ultrastructural changes as well as expression of presynaptic (VAMP1/2, synaptophysin, synaptotagmin-1, SNAP25, syntaxin-1) and postsynaptic (PSD-95) proteins were analyzed in: forebrain cortex, cerebellum and hippocampus. Our data revealed that pre- and neonatal exposure to low dose of Pb promotes pathological changes in synapses, including nerve endings swelling, blurred and thickened synaptic cleft structure as well as enhanced density of synaptic vesicles in the presynaptic area. Moreover, synaptic mitochondria were elongated, swollen or shrunken in Pb-treated animals. These structural abnormalities were accompanied by decrease in the level of key synaptic proteins: synaptotagmin-1 in cerebellum, SNAP25 in hippocampus and syntaxin-1 in cerebellum and hippocampus. In turn, increased level of synaptophysin was

  11. Occupational exposure to lead: effects on renal function

    SciTech Connect

    Hong, C.D.; Hanenson, I.B.; Lerner, S.; Hammond, P.B.; Pesce, A.J.; Pollak, V.E.

    1980-10-01

    Although nephrotoxicity is common following exposure to lead, the dose-response relationship in adults with occupational exposure is not well understood because information is lacking on early nephrotoxic effects. By the time serum urea nitrogen and creatinine levels are elevated, renal damage may be advanced and not fully reversible. Detailed investigations of renal glomerular and tubular function were performed in six adults with occupational exposure to lead. In all patients, the serum creatinine and urea nitrogen concentrations were within the normal range. GFR was decreased in all but two. Glucose reabsorptive capacity (TmG) was decreased in all, and this decrease was disproportionately greater than expected from the reduced GFR in all but one. Normal values for renal plasma flow (RFP) were observed in four of the six, and for rho-aminohippurate (PAH) secretory capacity (TmPAh) in all but one. Bicarbonate reabsorptive capacity (TmHCO3) and urinary excretion of beta2-microglobulin were normal in all. Routine clinical laboratory tests are insensitive for the detection of early renal effects of heavy metal exposure. Measurements of renal tubular reabsorptive capacity for glucose appears to be a sensitive method for the early detection of renal effect of lead.

  12. Gestational lead exposure selectively decreases retinal dopamine amacrine cells and dopamine content in adult mice

    SciTech Connect

    Fox, Donald A.; Hamilton, W. Ryan; Johnson, Jerry E.; Xiao, Weimin; Chaney, Shawntay; Mukherjee, Shradha; Miller, Diane B.; O'Callaghan, James P.

    2011-11-15

    Gestational lead exposure (GLE) produces supernormal scotopic electroretinograms (ERG) in children, monkeys and rats, and a novel retinal phenotype characterized by an increased number of rod photoreceptors and bipolar cells in adult mice and rats. Since the loss of dopaminergic amacrine cells (DA ACs) in GLE monkeys and rats contributes to supernormal ERGs, the retinal DA system was analyzed in mice following GLE. C57BL/6 female mice were exposed to low (27 ppm), moderate (55 ppm) or high (109 ppm) lead throughout gestation and until postnatal day 10 (PN10). Blood [Pb] in control, low-, moderate- and high-dose GLE was {<=} 1, {<=} 10, {approx} 25 and {approx} 40 {mu}g/dL, respectively, on PN10 and by PN30 all were {<=} 1 {mu}g/dL. At PN60, confocal-stereology studies used vertical sections and wholemounts to characterize tyrosine hydroxylase (TH) expression and the number of DA and other ACs. GLE dose-dependently and selectively decreased the number of TH-immunoreactive (IR) DA ACs and their synaptic plexus without affecting GABAergic, glycinergic or cholinergic ACs. Immunoblots and confocal revealed dose-dependent decreases in retinal TH protein expression and content, although monoamine oxidase-A protein and gene expression were unchanged. High-pressure liquid chromatography showed that GLE dose-dependently decreased retinal DA content, its metabolites and DA utilization/release. The mechanism of DA selective vulnerability is unknown. However, a GLE-induced loss/dysfunction of DA ACs during development could increase the number of rods and bipolar cells since DA helps regulate neuronal proliferation, whereas during adulthood it could produce ERG supernormality as well as altered circadian rhythms, dark/light adaptation and spatial contrast sensitivity. -- Highlights: Black-Right-Pointing-Pointer Peak [BPb] in control, low-, moderate- and high-dose newborn mice with gestational lead exposure: {<=} 1, {<=} 10, 25 and 40 {mu}g/dL Black

  13. Effect of postnatal exposure to caffeine on the pattern of adenosine A1 receptor distribution in respiration-related nuclei of the rat brainstem.

    PubMed

    Gaytan, S P; Saadani-Makki, F; Bodineau, L; Frugière, A; Larnicol, N; Pásaro, R

    2006-06-30

    Caffeine, which belongs to the methylxantine family of compounds, is commonly ingested in a range of beverages such as coffee, tea, and cola drinks. It is also used therapeutically and is frequently employed in the treatment of respiratory disturbances in human neonates. The aim of the present work has been to examine the ontogeny of the adenosine A1 receptor system in the brainstem of the newborn rat following postnatal treatment with caffeine to mimic the therapeutic administration of caffeine to premature human infants. The effect of this postnatal exposure to caffeine on the gradual appearance of adenosine A1 receptors was analysed by determining immunohistochemically the distribution of the receptors. The main difference between control animals and animals exposed to caffeine was the transient increase (only at postnatal day 6) in the number of immunopositive neurons in two brainstem areas, the ventrolateral medulla and the rostral dorsolateral pons, in caffeine-treated rat pups, or more specifically, the parabrachial and Kölliker-Fuse nuclei, both of which are classically associated with respiratory control. With previous research highlighting the important role played by the rostral pons in respiratory modulation by the adenosine A1 receptor system, it is thus possible that postnatal exposure to caffeine modulates the ontogeny of the adenosine A1 receptor network. This could imply that the role of caffeine to decrease the incidence of neonatal respiratory disturbances may be due to the earlier than normal development of the adenosinergic system in the brain.

  14. [Lead exposure in pregnant women and newborns: a screening update].

    PubMed

    Yazbeck, C; Cheymol, J; Dandres, A-M; Barbéry-Courcoux, A-L

    2007-01-01

    Human lead exposure has many sources. Relative importance of these sources varies widely according to geographic regions and human lifestyle. The impact of lead exposure on health has been well studied and public health interventions have been conducted. The aim of this study was to evaluate current prevalence of lead burden in neonates, and seek for sources of maternal and fetal intoxication. A prospective multicentre study was conducted by the "Réseau périnatal 92" on a population of pregnant women attending 3 maternal wards in the north of 'Hauts-de-Seine' department in France. Between December 2003 and May 2004, a total of 1021 pregnant women were included. All patients signed an informed consent before participating in the study. Cord blood samples were collected at delivery for lead measurements. The mean cord blood lead concentration was 23.2 microg/l. Eighteen neonates over 1021 (1.8%) had lead levels above 100 microg/l. An environmental query was conducted by the social and public health office of the department (DDASS), and data were collected regarding the state of the housing and the lifestyle of the concerned family. Main sources of lead intoxication were 'tagine' food plates in 83.3% of cases, 'khôl' powder (used as eyeliner) in 88.9% of cases and substandard housings in 22.2% of cases. A specialized paediatric follow-up for the 18 neonates was performed. With the exception of substandard housing (old lead painting), other sources of lead intoxication were discovered: 'tagine' plates and 'khôl' powder. Almost all of these products came from Morocco. A public health intervention would be able to inform the population about these yet unknown sources of lead intoxication.

  15. Effects of pre- and postnatal exposure to chromium picolinate or picolinic acid on neurological development in CD-1 mice.

    PubMed

    Bailey, Melissa M; Boohaker, Jonathan G; Jernigan, Peter L; Townsend, Megan B; Sturdivant, John; Rasco, Jane F; Vincent, John B; Hood, Ronald D

    2008-07-01

    Chromium picolinate, Cr(pic)3, a popular dietary supplement marketed as an aid in fat loss and lean muscle gain, has also been suggested as a therapy for women with gestational diabetes. The current study investigated the effects of maternal exposure to Cr(pic)3 and picolinic acid during gestation and lactation on neurological development of the offspring. Mated female CD-1 mice were fed diets from implantation through weaning that were either untreated or that contained Cr(pic)3 (200 mg kg(-1) day(-1)) or picolinic acid (174 mg kg(-1) day(-1)). A comprehensive battery of postnatal tests was administered, including a modified Fox battery, straight-channel swim, open-field activity, and odor-discrimination tests. Pups exposed to picolinic acid tended to weigh less than either control or Cr(pic)3-exposed pups, although the differences were not significant. Offspring of picolinic acid-treated dams also appeared to display impaired learning ability, diminished olfactory orientation ability, and decreased forelimb grip strength, although the differences among the treatment groups were not significant. The results indicate that there were no significant effects on the offspring with regard to neurological development from supplementation of the dams with either Cr(pic)3 or picolinic acid.

  16. Testicular steroidogenesis is not altered by 137 cesium Chernobyl fallout, following in utero or post-natal chronic exposure.

    PubMed

    Grignard, Elise; Guéguen, Yann; Grison, Stéphane; Dublineau, Isabelle; Gourmelon, Patrick; Souidi, Maâmar

    2010-05-01

    The testis is especially sensitive to pollutants, including radionuclides. Following the Chernobyl nuclear power plant accident, several of these radionuclides were emitted and spread in the environment. Subsequently, children presented some disruptions of the endocrine system. To determine whether these disruptions were due to 137 cesium ((137)Cs) exposure, the effects of chronic contamination with low doses of (137)Cs in utero or from birth on testicular steroidogenesis in rats were studied. Contamination was continued for 9 months. No modification was observed in circulating level of hormones (17beta-estradiol, testosterone, follicle-stimulating hormone, luteinizing hormone) following in utero or post-natal contamination. Expression of several genes involved in testicular steroidogenesis was affected (cyp19a1, fxr, sf-1), without modification of protein expression or activity. Our results suggest that growing organisms may be affected at the molecular level by (137)Cs contamination at this post-accidental dose. Copyright 2010 Académie des sciences. Published by Elsevier SAS. All rights reserved.

  17. Influence of the degree of exposure to lead on relations between alcohol consumption and the biological indices of lead exposure: epidemiological study in a lead acid battery factory.

    PubMed Central

    Cezard, C; Demarquilly, C; Boniface, M; Haguenoer, J M

    1992-01-01

    Alcohol has been shown to interact with lead to influence haem biosynthesis. The aim of this study was to define the dependence of this interaction on the degree of exposure to lead. Exposure to alcohol was estimated by measurement of alcohol concentrations in a sample of urine collected during the morning (AlcUM) (0.82 (SD 4.36) mmol/l) and in a sample collected during the afternoon (AlcUA) (1.15 (SD 3.49) mmol/l). The biological monitoring of exposure to lead included measurements of blood lead (Pb-B) (1.82 (SD 0.72) mumol/l), urinary delta-aminolaevulinic acid (ALAU) (35.33 (SD 28.00) mumol/l; d = 1.015), and erythrocyte zinc-protoporphyrin (ZPP) (112.90 (SD 83.71) nmol/mmol Hb) concentrations. The study of the influence of the degree of occupational exposure to lead on relations between alcohol consumption and effects of the exposure to lead led to the consideration of two different groups--namely, mildly and strongly exposed subjects. In the first group, individual biological susceptibility seemed to play a preponderant part. In the second, the pool of lead present in the body seemed to be sufficiently important to mask the effects of individual susceptibility. PMID:1390270

  18. Associations between prenatal and recent postnatal methylmercury exposure and auditory function at age 19 years in the Seychelles Child Development Study.

    PubMed

    Orlando, Mark S; Dziorny, Adam C; Harrington, Donald; Love, Tanzy; Shamlaye, Conrad F; Watson, Gene E; van Wijngaarden, Edwin; Davidson, Philip W; Myers, Gary J

    2014-01-01

    The aim of this study was to determine if prenatal or recent postnatal methylmercury (MeHg) exposure from consuming ocean fish and seafood is associated with auditory deficits in young adults. Some investigators have reported adverse associations while others have found no associations. Ocean fish is an important nutrient source for billions of people around the world. Consequently, determining if there is an adverse association with objective auditory measures is important in assessing whether a risk is present or not. The peripheral and central auditory function of 534 subjects in the Seychelles Child Development Study (SCDS) Main Cohort was examined at age of 19 years. The auditory test battery included standard pure-tone audiometry, tympanometry, auditory brainstem response (ABR) latencies, and both click-evoked and distortion product otoacoustic emissions (OAE). Associations with MeHg were evaluated with multiple linear regression models, adjusting for sex, recent postnatal MeHg exposure, and hearing loss. Bilateral hearing loss (defined as a mean pure-tone threshold of greater than 25 dB) was present in 1.1%of the subjects and was not associated with prenatal or recent postnatal MeHg exposure. As expected, absolute and interwave ABR latencies were shorter for women as compared to men, as the stimulus presentation rate decreased from 69.9 to 19.9 clicks/s and as the stimulus intensity increased from 60 to 80 dBnHL. Similarly, larger OAE amplitudes were elicited in women as compared to men and in the right ears as compared to the left. There was no association of prenatal MeHg exposure with hearing loss, ABR absolute and interwave latencies or OAE amplitudes. As recent postnatal MeHg increased, some associations were found with a few ABR absolute and interwave latencies and a few OAE amplitudes. However, the direction of these associations was inconsistent. As recent postnatal MeHg levels increased the wave I absolute latencies were shorter at 80 dBnHL for all

  19. Primary Prevention of Lead Exposure: The Philadelphia Lead Safe Homes Study

    PubMed Central

    Campbell, Carla; Tran, Mary; Gracely, Edward; Starkey, Naomi; Kersten, Hans; Palermo, Peter; Rothman, Nancy; Line, Laura; Hansen-Turton, Tine

    2011-01-01

    Objective Lead exposure in children can lead to neuropsychological impairment. This study tested whether primary prevention interventions in the newborn period prevent elevated blood lead levels (BLLs). Methods The Philadelphia Lead Safe Homes (LSH) Study offered parental education, home evaluation, and lead remediation to the families of urban newborns. Households were randomized to a standard lead education group or maintenance education group. We conducted home visits at baseline, six months, and 12 months. To compare BLLs, we identified a matched comparison group. Results We enrolled and randomized 314 newborns in the intervention component; 110 completed the study. There were few significant differences between the randomized groups. In the combined intervention groups, positive results on visual inspection declined from baseline to 12 months (97.0% to 90.6%, p=0.007). At baseline, 36.9% of homes were above the U.S. Environmental Protection Agency's lead dust standard, compared with 26.9% at 12 months (p=0.032), mainly due to a drop in windowsill dust levels. Both groups showed a significant increase in parental scores on a lead education test. Children in the intervention and matched control groups had similar geometric mean initial BLLs (2.6 vs. 2.7, p=0.477), but a significantly higher percentage of children in the intervention group had an initial blood lead screening compared with those in the matched group (88.9% vs. 84.4%, p=0.032). Conclusions A study of primary prevention of lead exposure showed a higher blood lead screening rate for the combined intervention groups and mean BLLs at one year of age not statistically different from the comparison group. Most homes had lead hazards. Lead education significantly increased knowledge. PMID:21563715

  20. In utero and lactational exposure to ammonium perchlorate in drinking water: effects on developing deer mice at postnatal day 21.

    PubMed

    Thuett, Kerry A; Roots, Ellen H; Mitchell, Lisa P; Gentles, B Angella; Anderson, Todd A; Smith, Ernest E

    2002-08-09

    The effects of in utero and lactational exposure to ammonium perchlorate (AP), a component of rocket fuel and a thyroid toxicant, on developing deer mice (Peromyscus maniculatus) were evaluated. Breeding pairs were dosed continuously with 0, 1 nM, 1 micro M, or 1 mM AP in drinking water, from cohabitation until pups were euthanized at postnatal day (PND) 21. Pups from the second litter were used for evaluation in this study. No significant differences were observed in any analysis performed when litter means were used in statistical analysis. All reported significant differences occurred when statistical analysis was performed on individual pup data. Body weights were significantly different between treatments at PND 5 and PND 20, with the 1- micro M body weights being lower than that of controls. Body weight and liver weight in the 1-mM group were significantly higher than the 1- micro M weights at PND 21 when analyzed by analysis of variance (ANOVA). However, there were no significant differences in liver weights when analyzed with body weight as the covariate. Heart weights were significantly different between males and females. Male heart weights in the 1- microM and 1-mM groups were significantly lower than in controls when analyzed by analysis of covariance (ANCOVA) with body weight as the covariate. Litter size and survival percentage were not significantly different among treatments. Although significant differences were observed only when the individual pup was used as the experimental unit, these data suggest that AP exposure at different concentrations may variably alter body weight and male heart weight during mammalian development.

  1. Effect of pre- and postnatal manganese exposure on brain histamine content in a rodent model of Parkinson's disease.

    PubMed

    Brus, Ryszard; Jochem, Jerzy; Nowak, Przemysław; Adwent, Marta; Boroń, Dariusz; Brus, Halina; Kostrzewa, Richard M

    2012-02-01

    Rats lesioned shortly after birth with 6-hydroxydopamine (6-OHDA; 134 μg icv) represent a near-ideal model of severe Parkinson's disease because of the near-total destruction of nigrostriatal dopaminergic fibers. There are scarce data that in Parkinson's disease, activity of the central histaminergic system is increased. The element manganese, an essential cofactor for many enzymatic reactions, itself in toxic amount, replicates some clinical features similar to those of Parkinson's disease. The aim of this study was to examine the effect of neonatal manganese exposure on 6-OHDA modeling of Parkinson's disease in rats, and to determine effects on histamine content in the brain of these rats in adulthood. Manganese (MnCl₂·4H₂O; 10,000 ppm) was included in the drinking water of pregnant Wistar rats from the time of conception until the 21st day after delivery, the age when neonatal rats were weaned. Control rats consumed tap water. Other groups of neonatal rat pups, on the 3rd day after birth, were pretreated with desipramine (20 mg/kg ip 1 h) prior to bilateral icv administration of 6-OHDA (60 or 134 μg) or its vehicle saline-ascorbic (0.1%) (control). At 2 months after birth, in rats lesioned with 60 or 134 μg 6-OHDA, endogenous striatal dopamine (DA) content was reduced, respectively, by 92 and 98% (HPLC/ED), while co-exposure of these groups to perinatal manganese did not magnify the DA depletion. However, there was prominent enhancement of histamine content in frontal cortex, hippocampus, hypothalamus, and medulla oblongata of adult rat brain after 6-OHDA (60 and 134 μg) injection on the day 3rd postnatal day. These findings indicate that histamine and the central histaminergic system are altered in the brain of rats lesioned to model Parkinson's disease, and that manganese enhances effects of 6-OHDA on histamine in brain.

  2. Genetic Diversity Influences the Response of the Brain to Developmental Lead Exposure

    PubMed Central

    Schneider, Jay S.; Talsania, Keyur; Mettil, William; Anderson, David W.

    2014-01-01

    Although extrinsic factors, such as nutritional status, and some intrinsic genetic factors may modify susceptibility to developmental lead (Pb) poisoning, no studies have specifically examined the influence of genetic background on outcomes from Pb exposure. In this study, we used gene microarray profiling to identify Pb-responsive genes in rats of different genetic backgrounds, including inbred (Fischer 344 (F344)) and outbred (Long Evans (LE), Sprague Dawley (SD)) strains, to investigate the role that genetic variation may play in influencing outcomes from developmental Pb exposure. Male and female animals received either perinatal (gestation through lactation) or postnatal (birth through weaning) exposure to Pb in food (0, 250, or 750 ppm). RNA was extracted from the hippocampus at day 55 and hybridized to Affymetrix Rat Gene 1.0 ST Arrays. There were significant strain-specific effects of Pb on the hippocampal transcriptome with 978 transcripts differentially expressed in LE rats across all experimental groups, 269 transcripts differentially expressed in F344 rats, and only 179 transcripts differentially expressed in SD rats. These results were not due to strain-related differences in brain accumulation of Pb. Further, no genes were consistently differentially regulated in all experimental conditions. There was no set of “Pb toxicity” genes that are a molecular signature for Pb neurotoxicity that transcended sex, exposure condition, and strain. These results demonstrate the influence that strain and genetic background play in modifying the brain's response to developmental Pb exposure and may have relevance for better understanding the molecular underpinnings of the lack of a neurobehavioral signature in childhood Pb poisoning. PMID:24913800

  3. Genetic diversity influences the response of the brain to developmental lead exposure.

    PubMed

    Schneider, Jay S; Talsania, Keyur; Mettil, William; Anderson, David W

    2014-09-01

    Although extrinsic factors, such as nutritional status, and some intrinsic genetic factors may modify susceptibility to developmental lead (Pb) poisoning, no studies have specifically examined the influence of genetic background on outcomes from Pb exposure. In this study, we used gene microarray profiling to identify Pb-responsive genes in rats of different genetic backgrounds, including inbred (Fischer 344 (F344)) and outbred (Long Evans (LE), Sprague Dawley (SD)) strains, to investigate the role that genetic variation may play in influencing outcomes from developmental Pb exposure. Male and female animals received either perinatal (gestation through lactation) or postnatal (birth through weaning) exposure to Pb in food (0, 250, or 750 ppm). RNA was extracted from the hippocampus at day 55 and hybridized to Affymetrix Rat Gene 1.0 ST Arrays. There were significant strain-specific effects of Pb on the hippocampal transcriptome with 978 transcripts differentially expressed in LE rats across all experimental groups, 269 transcripts differentially expressed in F344 rats, and only 179 transcripts differentially expressed in SD rats. These results were not due to strain-related differences in brain accumulation of Pb. Further, no genes were consistently differentially regulated in all experimental conditions. There was no set of "Pb toxicity" genes that are a molecular signature for Pb neurotoxicity that transcended sex, exposure condition, and strain. These results demonstrate the influence that strain and genetic background play in modifying the brain's response to developmental Pb exposure and may have relevance for better understanding the molecular underpinnings of the lack of a neurobehavioral signature in childhood Pb poisoning. © The Author 2014. Published by Oxford University Press on behalf of the Society of Toxicology. All rights reserved. For permissions, please email: journals.permissions@oup.com.

  4. LONG TERM EFFECTS OF PRENATAL AND POSTNATAL AIRBORNE PAH EXPOSURE ON VENTILATORY LUNG FUNCTION OF NON-ASTHMATIC PREADOLESCENT CHILDREN. PROSPECTIVE BIRTH COHORT STUDY IN KRAKOW

    PubMed Central

    Jedrychowski, Wieslaw A.; Perera, Frederica P.; Maugeri, Umberto; Majewska, Renata; Mroz, Elzbieta; Flak, Elzbieta; Camman, David; Sowa, Agata; Jacek, Ryszard

    2014-01-01

    The main goal of the study was to test the hypothesis that prenatal and postnatal exposure to polycyclic aromatic hydrocarbons (PAH) is associated with depressed lung function in non-asthmatic children. The study sample comprises 195 non-asthmatic children of non-smoking mothers, among whom the prenatal PAH exposure was assessed by personal air monitoring in pregnancy. At the age of 3, residential air monitoring was carried out to evaluate the residential PAH exposure indoors and outdoors. At the age of 5 to 8, children were given allergic skin tests for indoor allergens; and between 5–9 years lung function testing (FVC, FEV05, FEV1 and FEF25–75) was performed. The effects of prenatal PAH exposure on lung function tests repeated over the follow-up were adjusted in the General Estimated Equation (GEE) model for the relevant covariates. No association between FVC with prenatal PAH exposure was found; however for the FEV1 deficit associated with higher prenatal PAH exposure (above 37ng/m3) amounted to 53 mL (p = 0.050) and the deficit of FEF25–75 reached 164 mL (p=0.013). The corresponding deficits related to postnatal residential indoor PAH level (above 42 ng/m3) were 59 mL of FEV1 (p=0.028) and 140 mL of FEF25–75 (p=0.031). At the higher residential outdoor PAH level (above 90 ng/m3) slightly greater deficit of FEV1 (71mL, p = 0.009) was observed. The results of the study suggest that transplacental exposure to PAH compromises the normal developmental process of respiratory airways and that this effect is compounded by postnatal PAH exposure. PMID:25300014

  5. Long term effects of prenatal and postnatal airborne PAH exposures on ventilatory lung function of non-asthmatic preadolescent children. Prospective birth cohort study in Krakow.

    PubMed

    Jedrychowski, Wieslaw A; Perera, Frederica P; Maugeri, Umberto; Majewska, Renata; Mroz, Elzbieta; Flak, Elzbieta; Camann, David; Sowa, Agata; Jacek, Ryszard

    2015-01-01

    The main goal of the study was to test the hypothesis that prenatal and postnatal exposures to polycyclic aromatic hydrocarbons (PAH) are associated with depressed lung function in non-asthmatic children. The study sample comprises 195 non-asthmatic children of non-smoking mothers, among whom the prenatal PAH exposure was assessed by personal air monitoring in pregnancy. At the age of 3, residential air monitoring was carried out to evaluate the residential PAH exposure indoors and outdoors. At the age of 5 to 8, children were given allergic skin tests for indoor allergens; and between 5 and 9 years lung function testing (FVC, FEV05, FEV1 and FEF25-75) was performed. The effects of prenatal PAH exposure on lung function tests repeated over the follow-up were adjusted in the General Estimated Equation (GEE) model for the relevant covariates. No association between FVC with prenatal PAH exposure was found; however for the FEV1 deficit associated with higher prenatal PAH exposure (above 37 ng/m(3)) amounted to 53 mL (p=0.050) and the deficit of FEF25-75 reached 164 mL (p=0.013). The corresponding deficits related to postnatal residential indoor PAH level (above 42 ng/m(3)) were 59 mL of FEV1 (p=0.028) and 140 mL of FEF25-75 (p=0.031). At the higher residential outdoor PAH level (above 90 ng/m(3)) slightly greater deficit of FEV1 (71 mL, p=0.009) was observed. The results of the study suggest that transplacental exposure to PAH compromises the normal developmental process of respiratory airways and that this effect is compounded by postnatal PAH exposure.

  6. Protoporphyrin (FEP/ZPP) screening in industrial lead exposure

    SciTech Connect

    Saryan, L.A.

    1988-11-01

    Lead-acid battery manufacturers, as a group, are among the largest industrial users of lead in the United States, and every industry using this metal is confronted with a maze of federal regulations governing workplace conditions and employee health. In the biological testing category, particular emphasis has been placed on the periodic testing of blood for lead, to assess absorption of the metal, and protoporphyrin (abbreviated ZPP or FEP) testing as a means of monitoring the biological effects resulting from lead exposure. The protoporphyrin test, however, remains a matter of general confusion among industry managers and medical directors, and this article attempts to provide a concise and understandable explanation of this topic. 10 references, 3 figures, 1 table.

  7. Behavioral effects of pre- and postnatal exposure to individual polychlorinated biphenyl congeners in rats

    SciTech Connect

    Holene, E.; Bernhoft, A.; Engen, P.; Nafstad, I. |; Skaare, J.U. |; Sagvolden, T.

    1995-06-01

    Rats were exposed in utero and through mother`s milk either to the coplanar PCB congener 3,3{prime},4,4{prime},5-CB (IUPAC no. 126) or to the mono-ortho-substituted PCB congener 2,3{prime},4,4{prime},5-CB (IUPAC no. 118). The different groups of mothers were exposed to 1 and 5 mg/kg body weight of PCB 118, and 2 {mu}g/kg b.w. of PCB 126 every second day from day 10 to day 20 of gestation. The exposure did not affect the body weight of the dams or the size, weight, sex ratio, or physical development of the offspring. Operant behavioral testing revealed that the PCB-exposed offspring showed both poorer visual discrimination and higher activity level than did the controls. The coplanar PCB 126 congener was the most potent treatment. These results show that both PCB 118 and PCB 126 produced significant neurotoxic effects in the offspring of exposed females in absence of clinical maternotoxic and fetotoxic effects.

  8. Peripheral blood findings associated with asymptomatic lead exposure

    SciTech Connect

    Day, C.M.; Tennant, F.S. Jr.

    1982-02-01

    This study was done to determine whether erythroid alterations can be found on a peripheral blood smear from an asymptomatic person exposure to excess atmospheric lead. Thirty healthy, asymptomatic adults who lived within five miles of a major Los Angeles, California freeway for five consecutive years were studied. Erythroid cytologic alterations-including-anisocytosis, poikilocytosis, polychromasia and basophilic stippling were statistically associated with increased free erythrocyte protoporphyrin levels. These findings indicate that erythroid alterations may be found on a peripheral blood smear prior to the development of clinical symptoms of lead intoxication.

  9. Exposure to lead in South African shooting ranges.

    PubMed

    Mathee, Angela; de Jager, Pieter; Naidoo, Shan; Naicker, Nisha

    2017-02-01

    Lead exposure in shooting ranges has been under scrutiny for decades, but no information in this regard is available in respect of African settings, and in South Africa specifically. The aim of this study was to determine the blood lead levels in the users of randomly selected private shooting ranges in South Africa's Gauteng province. An analytical cross sectional study was conducted, with participants recruited from four randomly selected shooting ranges and three archery ranges as a comparator group. A total of 118 (87 shooters and 31 archers) were included in the analysis. Shooters had significantly higher blood lead levels (BLL) compared to archers with 36/85 (42.4%) of shooters versus 2/34 (5.9%) of archers found to have a BLL ≥10μg/dl (p<0.001). Shooting ranges may constitute an import site of elevated exposure to lead. Improved ventilation, low levels of awareness of lead hazards, poor housekeeping, and inadequate personal hygiene facilities and practices at South African shooting ranges need urgent attention. Copyright © 2016 The Authors. Published by Elsevier Inc. All rights reserved.

  10. Elevated blood lead levels from exposure via a radiator workshop.

    PubMed

    Treble, R G; Thompson, T S; Morton, D N

    1998-04-01

    Elevated lead levels were discovered in blood samples collected from family members where both the father and the mother worked in a radiator repair workshop. The father and mother were found to have blood lead levels of 2.0 and 0.5 mumol/L (41.7 and 10.4 micrograms/dL), respectively. The father's blood lead level was just below the Canadian occupational health and safety intervention level (2.5 mumol/L or 52.1 micrograms/dL). The two children had blood lead levels of 1.0 and 0.8 mumol/L (20.8 and 16.7 micrograms/dL), both of which are in excess of the recommended guideline for intervention in the case of children (0.5 mumol/L or 10.4 micrograms/dL). The exposure of the two children was possibly due to a combination of pathways including exposure at the workshop itself during visits and also the transportation of lead-containing dust to the home environment.

  11. LONG-TERM BEHAVIORAL EFFECTS IN A RAT MODEL OF PROLONGED POSTNATAL MORPHINE EXPOSURE

    PubMed Central

    Craig, Michael M.; Bajic, Dusica

    2015-01-01

    Prolonged morphine treatment in neonatal pediatric populations is associated with a high incidence of opioid tolerance and dependence. Despite the clinical relevance of this problem, our knowledge of the long-term consequences is sparse. The main objective of this study was to investigate whether prolonged morphine administration in a neonatal rat is associated with long-term behavioral changes in adulthood. Newborn animals received either morphine (10mg/kg) or equal volume of saline subcutaneously twice daily for the first 2 weeks of life. Morphine treated animals underwent 10 days of morphine weaning to reduce the potential for observable physical signs of withdrawal. Animals were subjected to non-stressful testing (locomotor activity recording and a Novel-Object Recognition test) at a young age (PD27-31) or later in adulthood (PD55-56), as well as stressful testing (calibrated forceps test, Hot Plate test, and Forced Swim test) only in adulthood. Analysis revealed that prolonged neonatal morphine exposure resulted in decreased thermal, but not mechanical threshold. Importantly, no differences were found for total locomotor activity (proxy of drug reward/reinforcement behavior), individual Forced Swim test behaviors (proxy of affective processing), or Novel-Object Recognition test. Performance on the Novel-Object Recognition test was compromised in the morphine treated group at the young age, however the effect disappeared in adulthood. These novel results provide insight into the long-term consequences of opioid treatment during an early developmental period and suggest long-term neuroplastic differences in sensory processing related to thermal stimuli. PMID:26214209

  12. Early (in uterus and infant) exposure to mercury and lead.

    PubMed

    Dorea, Jose G; Donangelo, Carmen M

    2006-06-01

    Mercury and lead are toxic metals widely spread in the environment with bio-accumulative features that raises public health concerns. Both metals are equally dispersed in the human food chain but exposure and risk of toxicity during early human development are modulated by the diet and nutritional status. Understanding how Hg and Pb occur and interact with nutrients is fundamental to establish guidelines for diminishing exposure and the risk of toxicity. The risk of fetal and infant exposure to Hg can be influenced by maternal amalgam filling (inorganic Hg) and fish consumption (monomethyl Hg), whereas the risk of exposure to Pb is complex: maternal absorption depends on nutrient interactions (Ca and P); and maternal body Pb accumulation responds to all factors known to interact with bone and calcium metabolism. Maternal exposure to Hg and Pb is more important during fetal development than during breastfeeding. Moreover, these metals (especially Pb) are frequently higher in infant formulas which do not carry the nutritional and psychological advantages and protection of breastfeeding. Infant's reference dose is lower for Hg than for Pb, but risk of Pb contamination for fetuses and infant (breast- or formula-fed) is higher and lasts longer than Hg. Breastfeeding is essential to complete infant development. Interruption or suppression of breast-feeding with cow's milk-based formulas is not an option to environmental pollution.

  13. Methods for integrated exposure monitoring of lead and cadmium

    SciTech Connect

    Vahter, M.; Berglund, M.; Friberg, L. ); Slorach, S. ); Saric, M. ); Zheng Xingquan ); Fujita, Masahiko )

    1991-10-01

    An international pilot monitoring study on exposure to lead (Pb) and cadmium (Cd) has been implemented in Beijing, Yokohama, Stockholm, and Zagreb as part of the UNEP/WHO human exposure assessment locations (HEAL) Program. The main objective was to develop and test methods, including methods for quality assurance, for monitoring of personal exposure to Pb and Cd. The study included analytical training for Pb and Cd in blood, air filters, dust, diets, and feces, as well as exposure monitoring activities in small groups of nonsmoking women, 23-53 years of age, during 7 consecutive days. Airborne particulates, duplicate diets, feces, and blood were collected. An extensive quality assurance program was implemented in order to assure the reliability and comparability of the monitoring data. The main problem in the sample collection was associated with the air monitoring. The pumps were noisy, and the batteries had to be recharged every 6-8 hr. Collection of duplicate diets during 1 week gave good estimates of average dietary intakes of Pb and Cd. The metal contents in feces were found useful for evaluation of total peroral intakes. The methods used made it possible to demonstrate that the diet was the main source of Cd exposure at all the HEAL sites.

  14. Effects of long-term pre- and post-natal exposure to 2.45 GHz wireless devices on developing male rat kidney.

    PubMed

    Kuybulu, Ayça Esra; Öktem, Faruk; Çiriş, İbrahim Metin; Sutcu, Recep; Örmeci, Ahmet Rıfat; Çömlekçi, Selçuk; Uz, Efkan

    2016-01-01

    The aim of the present study was to investigate oxidative stress and apoptosis in kidney tissues of male Wistar rats that pre- and postnatally exposed to wireless electromagnetic field (EMF) with an internet frequency of 2.45 GHz for a long time. The study was conducted in three groups of rats which were pre-natal, post-natal. and sham exposed groups. Oxidative stress markers and histological evaluation of kidney tissues were studied. Renal tissue malondialdehyde (MDA) and total oxidant (TOS) levels of pre-natal group were high and total antioxidant (TAS) and superoxide dismutase (SOD) levels were low. Spot urine NAG/creatinine ratio was significantly higher in pre- and post-natal groups (p < 0.001). Tubular injury was detected in most of the specimens in post-natal groups. Immunohistochemical analysis showed low-intensity staining with Bax in cortex, high-intensity staining with Bcl-2 in cortical and medullar areas of pre-natal group (p values, 0.000, 0.002, 0.000, respectively) when compared with sham group. Bcl2/Bax staining intensity ratios of medullar and cortical area was higher in pre-natal group than sham group (p = 0.018, p = 0.011). Based on this study, it is thought that chronic pre- and post-natal period exposure to wireless internet frequency of EMF may cause chronic kidney damages; staying away from EMF source in especially pregnancy and early childhood period may reduce negative effects of exposure on kidney.

  15. Short- and long-term effects of combined pre- and postnatal ethanol exposure (three trimester equivalency) on the development of myelin and axons in rat optic nerve.

    PubMed

    Phillips, D E; Krueger, S K; Rydquist, J E

    1991-01-01

    This study evaluated the effects of a combined gestational and 10 day postnatal alcohol exposure (human three trimester equivalency) on the development of myelin and axons in rat optic nerve. Rats were exposed during gestation via liquid diet, then their artificially reared pups were further exposed for 10 postnatal days via an ethanol-containing diet fed by gastrostomy. Control animals from pair-fed dams were artificially reared for 10 days on pair-fed isocaloric diets. Anesthetized animals were perfused with fixative on gestational days (G) 15 and 20 and postnatal days (P) 5, 10, 15, 20, and 90, then optic nerve tissues prepared for electron microscopy. Optic nerve cross-sectional areas were generally less from G20 through P90 in ethanol exposed animals. Counts of the number of myelinated nerve fibers per unit area and of the numbers of fibers in different stages of myelin development revealed that alcohol exposure caused a delay in myelin acquisition at 10 and 15 days that was compensated for at 20 and 90 days. Myelin thickness as a function of axon diameter was decreased in the alcohol exposed animals from 10 through 90 days, indicating a permanent reduction in the relative thickness of myelin. These results show that alcohol exposure for all of gestation and 10 postnatal days in the rat (human three trimester equivalency) causes a permanent reduction in myelin thickness along with a delay in myelin acquisition in the optic nerve. Such alterations in developing and adult myelin could help to explain some of the neurological and visual dysfunctions associated with developmental alcohol exposures.

  16. In utero and postnatal exposure to environmental tobacco smoke (ETS) alters alveolar and respiratory bronchiole (RB) growth and development in infant monkeys.

    PubMed

    Avdalovic, Mark; Putney, Lei; Tyler, Nancy; Finkbeiner, Walter; Pinkerton, Kent; Hyde, Dallas

    2009-02-01

    The direct effect of environmental tobacco smoke (ETS) exposure in utero on the development of the lung parenchyma is not known. We used design-based stereologic methods to evaluate in utero and postnatal ETS exposure on alveolar and respiratory bronchiole (RB) development in the rhesus macaque. Timed-pregnant rhesus macaques and their offspring were exposed to filtered air or various amounts of ETS during the prenatal and postnatal period. The left cranial lobe from necropsied infants was evaluated by design-based stereological methods and general pathological review. Infants in the in utero and six-month ETS groups had an 18% and 17% relative decrease, respectively, in alveolar number and a 57% and 33% increase, respectively, in alveolar size compared to filtered air (FA) monkeys. Lung volume positively correlated with alveolar number in the FA and six-month ETS group and negatively correlated in the in utero ETS group. The distribution of alveolar size was much more variable in the in utero group. Overall, RB volume was significantly increased in the six-month ETS group (p < .04). Taken together, these results indicate that in utero and postnatal ETS exposure is associated with altered parenchymal lung development.

  17. Prevalence of elevated blood leads and exposure to lead in construction trades in Iowa and Illinois.

    PubMed

    Reynolds, S J; Seem, R; Fourtes, L J; Sprince, N L; Johnson, J; Walkner, L; Clarke, W; Whitten, P

    1999-08-01

    Despite lowering of the permissible exposure level for lead in construction from 200 to 50 microg/m3 in 1993, excessive lead exposure continues to be a problem. Relatively little data are available from the Midwestern U.S. on the environmental lead concentrations generated during various construction activities and the potential for worker exposure. This study characterized the prevalence of blood lead concentrations in high-risk construction trades in Iowa/Illinois, and identified risk factors for occupational exposure to lead in these construction workers. A sample of 459 workers was selected from the total population of all union members from trade groups of painters, plumbers/pipefitters, ironworkers, laborers, and electricians. Participants completed an interviewer-administered questionnaire obtaining information on demographics, symptoms, occupational history, work practices, personal protective equipment, and training. Venous blood samples were collected from each participant and analyzed for blood lead (using atomic absorption spectroscopy) and free erythrocyte protoporphyrin levels. Blood lead levels (BLLs) of construction workers ranged from 0.1 to 50 microg/dL. Geometric mean blood lead concentrations by trade group were: laborers (7.6 microg/dL, n = 80); painters (5.9 microg/dL, n = 83); ironworkers (5.2 microg/dL, n = 87); plumbers (4.4 microg/dL, n = 82); electricians (2.4 microg/dL, n = 91). Blood lead levels for painters and laborers were significantly higher than other trade groups, and levels for electricians were significantly lower (p < 0. 01). Participants reported working primarily on commercial and industrial projects including new construction, renovation, and demolition. There were significant differences between the types of projects performed by different trade groups with laborers performing more highway/bridge renovation (p < 0.01), and plumbers reporting more residential remodeling (p = 0.05), repair of water lines containing lead (p

  18. Reproductive toxicity of low-level lead exposure in men

    SciTech Connect

    Telisman, Spomenka Colak, Bozo; Pizent, Alica; Jurasovic, Jasna; Cvitkovic, Petar

    2007-10-15

    Parameters of semen quality, seminal plasma indicators of secretory function of the prostate and seminal vesicles, sex hormones in serum, and biomarkers of lead, cadmium, copper, zinc, and selenium body burden were measured in 240 Croatian men 19-52 years of age. The subjects had no occupational exposure to metals and no known other reasons suspected of influencing male reproductive function or metal metabolism. After adjusting for age, smoking, alcohol, blood cadmium, and serum copper, zinc, and selenium by multiple regression, significant (P<0.05) associations of blood lead (BPb), {delta}-aminolevulinic acid dehydratase (ALAD), and/or erythrocyte protoporphyrin (EP) with reproductive parameters indicated a lead-related increase in immature sperm concentration, in percentages of pathologic sperm, wide sperm, round sperm, and short sperm, in serum levels of testosterone and estradiol, and a decrease in seminal plasma zinc and in serum prolactin. These reproductive effects were observed at low-level lead exposure (BPb median 49 {mu}g/L, range 11-149 {mu}g/L in the 240 subjects) common for general populations worldwide. The observed significant synergistic effect of BPb and blood cadmium on increasing serum testosterone, and additive effect of a decrease in serum selenium on increasing serum testosterone, may have implications on the initiation and development of prostate cancer because testosterone augments the progress of prostate cancer in its early stages.

  19. Environmental lead exposure as a risk for childhood aplastic anemia.

    PubMed

    Ahamed, M; Akhtar, M J; Verma, S; Kumar, A; Siddiqui, M K J

    2011-01-01

    Concern about environmental lead exposure as a significant public health threat has increased as evidence has accumulated regarding adverse health effects at successively lower levels. Aplastic anemia is a hematological disorder of unknown etiology with a high lethality rate. Lead is a known toxicant for the hematopoietic system. Oxidative stress appears to be the possible mode of lead toxicity. We evaluated the effects of blood lead level on oxidative stress parameters in children suffering from aplastic anemia disease. Seventeen children with aplastic anemia disease (15 male and 2 female, age 3-12 y) were recruited in the study group. Fifty one healthy children (45 male and 6 female, age 3-12 y) having normal blood profiles and not suffering from any chronic disease(s) were used as controls. Blood lead level and oxidative stress parameters were determined. Mean blood lead level was significantly higher while δ-aminolevulinic acid dehydratase (δ-ALAD) activity, a biomarker for lead exposure was significantly lower in the study group as compared to the control group (p < 0.05 for each). Thiobarbituric acid reactive species (TBARS), a marker of lipid peroxidation, was significantly higher while the antioxidant glutathione (GSH) level was significantly lower in the study group as compared to the control group (p < 0.05 for each). Activity of the antioxidant enzyme catalase (CAT) was significantly higher in the study group than in the control group (p < 0.05). There was a significant negative correlation of blood lead levels with δ-ALAD (r = -0.45; p < 0.05) and GSH (r = -0.32; p < 0.05), and a positive correlation with TBARS (r = 0.41; p < 0.05) and CAT (r = 0.37; p < 0.05). Although a causal pathway cannot be determined from this study, our results indicated that lead induces oxidative stress in children suffering from aplastic anemia. Lead-induced oxidative stress as an underlying mechanism for aplastic anemia warrants further research.

  20. Synaptotoxicity of chronic low-dose pre- and post-natal ethanol exposure: A new animal model

    SciTech Connect

    Walewski, J.L.

    1992-01-01

    Chronic Low-dose Pre- and Post-natal Ethanol exposure (CLPPEE) is the most frequent cause of teratogenically induced mental deficiency in the Western world. Although the Fetal Alcohol Syndrome (FAAS) is associated with high levels of alcohol consumption, the relative teratogenic risk of moderate ethanol consumption is not well defined. CLPPEE may affect some processes involved in synapse formation, affecting the proper development and maturation of the nervous system. Ethanol was admixed (3 v/v%) with high-protein liquid diet (Bio-Serve) as the only nutrient source. The controls received an isocaloric sucrose liquid diet mixture. Ethanol treatment began on day 8 of pregnancy. 3 v/v% ethanol did not significantly reduce the body weights or diet consumption of dams, nor the gross growth of ethanol-exposed pups. Standard neuromuscular twitch preparations in vivo, utilizing the sciatic nerve-gastrocnemius muscle, were done on 1, 2, 3 and 7 week old pups. The physiologic functional tests of nursing pups (1-3 weeks), indicated that the ethanol-treated pups had abnormal responses to indirect stimulation. The deficit was determined to be pre-synaptic. The ethanol-exposed at these ages demonstrated abnormal responses to presynaptic challenge. Histochemical staining revealed motor nerve terminal morphology. In 2 and 3 week ethanol-treated pups, the number of nerve terminal branches, and endplate lengths were significantly reduced. Reversibility was examined by allowing the pups to mature while receiving only standard rat chow and water. Tests were repeated at 7 weeks of age. The responses of the ethanol-exposed to pharmacologic challenge, and motor nerve terminal morphology were still significantly different in the young adult animals. CLPPEE, at doses sub-threshold for FAS, affects the normal development of the skeletal neuromuscular system, with long-lasting effects on motor nerve terminal function and morphology.

  1. The effects of postnatal alcohol exposure and galantamine on the context pre-exposure facilitation effect and acetylcholine efflux using in vivo microdialysis

    PubMed Central

    Perkins, Amy E.; Fadel, Jim R.; Kelly, Sandra J.

    2015-01-01

    Fetal alcohol spectrum disorders (FASD) affect 2–5% of children. FASD have been shown to cause damage to multiple brain regions, but damage to the hippocampus specifically may explain deficits in learning and memory that are hallmark symptoms of FASD. The acetylcholine neurotransmitter system is a major input to the hippocampus and is a possible target of developmental alcohol exposure. Alcohol (3.0 g/kg/day) was administered via intragastric intubation to developing male rat pups (postnatal day [PD] 2–10; ethanol-treated [ET]), with controls receiving a sham intubation (IC) or no treatment (NC). In Experiment 1, in vivo microdialysis was used to measure acetylcholine efflux in adolescents (PD 32–35). During microdialysis, the effects of a high K+/Ca2+ aCSF solution (PD 32–33) and an acute galantamine (acetylcholinesterase [AChE] inhibitor) injection (2.0 mg/kg; PD 34–35) on acetylcholine efflux were measured. Alcohol-exposed animals did not differ in acetylcholine efflux at baseline. However, alcohol-exposed animals had a decrease in K+/Ca2+-induced acetylcholine efflux compared to non-treated controls, and an enhanced acetylcholine response to galantamine compared to both control groups. Experiment 2 tested whether chronic administration of galantamine (2.0 mg/kg; PD 11–30) could attenuate alcohol-induced learning deficits in the context pre-exposure facilitation effect (CPFE; PD 30–32). Neither chronic galantamine nor postnatal alcohol exposure influenced performance in the CPFE task. Immunohistochemistry was used to measure expression of choline acetyltransferase (ChAT; medial septum), vesicular acetylcholine transporter (vAChT; ventral CA1), and the alpha7 nicotinic acetylcholine receptor (α7 nAChR; ventral CA1) following microdialysis (Exp. 1) or chronic galantamine and behavioral testing (Exp. 2). Neither alcohol exposure nor behavioral testing significantly altered the density of vAChT or α7 nAChRs in the ventral CA1 region of the

  2. Effects of early postnatal exposure to ethanol on retinal ganglion cell morphology and numbers of neurons in the dorsolateral geniculate in mice

    PubMed Central

    Dursun, Ilknur; Jakubowska-Doğru, Ewa; van der List, Deborah; Liets, Lauren C.; Coombs, Julie L.; Berman, Robert F.

    2012-01-01

    Background The adverse effects of fetal and early postnatal ethanol intoxication on peripheral organs and the central nervous system are well documented. Ocular defects have also been reported in about 90% of children with Fetal Alcohol Syndrome (FAS), including microphthalmia, loss of neurons in the retinal ganglion cell layer (GCL), optic nerve hypoplasia and dysmyelination. However, little is known about perinatal ethanol effects on retinal cell morphology. Examination of the potential toxic effects of alcohol on the neuron architecture is important since the changes in dendritic geometry and synapse distribution directly affect the organization and functions of neural circuits. Thus, in the present study estimations of the numbers of neurons in the GCL and dorsolateral geniculate nucleus (dLGN), and a detailed analysis of RGC morphology were carried out in transgenic mice exposed to ethanol during the early postnatal period. Methods The study was carried out in male and female transgenic mice expressing Yellow Fluorescent Protein (YFP) controlled by a Thy-1 (thymus cell antigen 1) regulator on a C57 background. Ethanol (3 g/kg/day) was administered to mouse pups by intragastric intubation throughout postnatal days (PD) 3–20. Intubation control (IC) and untreated control (C) groups were included. Blood alcohol concentration (BAC) was measured in separate groups of pups on PD3, PD10, and PD20 at 4 different time points, 1, 1.5, 2 and 3 h after the second intubation. Numbers of neurons in the GCL and in the dLGN were quantified on PD20 using unbiased stereological procedures. Retinal ganglion cell morphology was imaged by confocal microscopy and analyzed using Neurolucida software. Results Binge-like ethanol exposure in mice during the early postnatal period from PD3 through PD20 altered RGC morphology and resulted in a significant decrease in the numbers of neurons in the GCL and in the dLGN. In the alcohol exposure group, out of 13 morphological parameters

  3. Developmental alcohol exposure leads to a persistent change on astrocyte secretome.

    PubMed

    Trindade, Pablo; Hampton, Brian; Manhães, Alex C; Medina, Alexandre E

    2016-06-01

    Fetal alcohol spectrum disorder is the most common cause of mental disabilities in the western world. It has been quite established that acute alcohol exposure can dramatically affect astrocyte function. Because the effects of early alcohol exposure on cell physiology can persist into adulthood, we tested the hypothesis that ethanol exposure in ferrets during a period equivalent to the last months of human gestation leads to persistent changes in astrocyte secretome in vitro. Animals were treated with ethanol (3.5 g/kg) or saline between postnatal day (P)10-30. At P31, astrocyte cultures were made and cells were submitted to stable isotope labeling by amino acids. Twenty-four hour conditioned media of cells obtained from ethanol- or saline-treated animals (ET-CM or SAL-CM) were collected and analyzed by quantitative mass spectrometry in tandem with liquid chromatography. Here, we show that 65 out of 280 quantifiable proteins displayed significant differences comparing ET-CM to SAL-CM. Among the 59 proteins that were found to be reduced in ET-CM we observed components of the extracellular matrix such as laminin subunits α2, α4, β1, β2, and γ1 and the proteoglycans biglycan, heparan sulfate proteoglycan 2, and lumican. Proteins with trophic function such as insulin-like growth factor binding protein 4, pigment epithelium-derived factor, and clusterin as well as proteins involved on modulation of proteolysis such as metalloproteinase inhibitor 1 and plasminogen activator inhibitor-1 were also reduced. In contrast, pro-synaptogeneic proteins like thrombospondin-1, hevin as well as the modulator of extracelular matrix expression, angiotensinogen, were found increased in ET-CM. The analysis of interactome maps through ingenuity pathway analysis demonstrated that the amyloid beta A4 protein precursor, which was found reduced in ET-CM, was previously shown to interact with ten other proteins that exhibited significant changes in the ET-CM. Taken together our results

  4. Maternal self-esteem, exposure to lead, and child neurodevelopment.

    PubMed

    Surkan, Pamela J; Schnaas, Lourdes; Wright, Rosalind J; Téllez-Rojo, Martha M; Lamadrid-Figueroa, Héctor; Hu, Howard; Hernández-Avila, Mauricio; Bellinger, David C; Schwartz, Joel; Perroni, Estela; Wright, Robert O

    2008-03-01

    The notion that maternal personality characteristics influence cognitive development in their children has been grounded in stress moderation theory. Maternal personality traits, such as self-esteem, may buffer maternal stressors or lead to improved maternal-child interactions that directly impact neurodevelopment. This can be extended to suggest that maternal personality may serve to attenuate or exacerbate the effects of other neurotoxicants, although this has not been studied directly. We examined whether mothers' self-esteem had a direct or main effect on their children's cognitive outcomes. We also explored the modifying effects of maternal self-esteem on the association between exposure to lead and neurodevelopment in these children. Study participants included 379 mother-child pairs from Mexico City. Data included the Coopersmith Self-Esteem Scale in mothers, children's Bayley's Scale of Infant Development (BSID) scores, and sociodemographic information. Linear regression was used to model the relationship between maternal self-esteem and the Bayley's Mental Development Index (MDI) and Psychomotor Development Index (PDI) scores at age 24 months using models stratified by levels of maternal self-esteem. In adjusted models, each point increase in maternal self-esteem was associated with children having 0.2 higher score on the Bayley's MDI (p=0.04). Similar results were observed using the PDI outcome. Moreover, there was evidence that maternal self-esteem attenuated the negative effects of lead exposure, although the interaction fell short of conventional levels of statistical significance.

  5. Transcriptome Changes in Hirschfeldia incana in Response to Lead Exposure.

    PubMed

    Auguy, Florence; Fahr, Mouna; Moulin, Patricia; El Mzibri, Mohamed; Smouni, Abdelaziz; Filali-Maltouf, Abdelkarim; Béna, Gilles; Doumas, Patrick

    2015-01-01

    Hirschfeldia incana, a pseudometallophyte belonging to the Brassicaceae family and widespread in the Mediterranean region, was selected for its ability to grow on soils contaminated by lead (Pb). The global comparison of gene expression using microarrays between a plant susceptible to Pb (Arabidopsis thaliana) and a Pb tolerant plant (H. incana) enabled the identification of a set of specific genes expressed in response to lead exposure. Three groups of genes were particularly over-represented by the Pb exposure in the biological processes categorized as photosynthesis, cell wall, and metal handling. Each of these gene groups was shown to be directly involved in tolerance or in protection mechanisms to the phytotoxicity associated with Pb. Among these genes, we demonstrated that MT2b, a metallothionein gene, was involved in lead accumulation, confirming the important role of metallothioneins in the accumulation and the distribution of Pb in leaves. On the other hand, several genes involved in biosynthesis of ABA were shown to be up-regulated in the roots and shoots of H. incana treated with Pb, suggesting that ABA-mediated signaling is a possible mechanism in response to Pb treatment in H. incana. This latest finding is an important research direction for future studies.

  6. Transcriptome Changes in Hirschfeldia incana in Response to Lead Exposure

    PubMed Central

    Auguy, Florence; Fahr, Mouna; Moulin, Patricia; El Mzibri, Mohamed; Smouni, Abdelaziz; Filali-Maltouf, Abdelkarim; Béna, Gilles; Doumas, Patrick

    2016-01-01

    Hirschfeldia incana, a pseudometallophyte belonging to the Brassicaceae family and widespread in the Mediterranean region, was selected for its ability to grow on soils contaminated by lead (Pb). The global comparison of gene expression using microarrays between a plant susceptible to Pb (Arabidopsis thaliana) and a Pb tolerant plant (H. incana) enabled the identification of a set of specific genes expressed in response to lead exposure. Three groups of genes were particularly over-represented by the Pb exposure in the biological processes categorized as photosynthesis, cell wall, and metal handling. Each of these gene groups was shown to be directly involved in tolerance or in protection mechanisms to the phytotoxicity associated with Pb. Among these genes, we demonstrated that MT2b, a metallothionein gene, was involved in lead accumulation, confirming the important role of metallothioneins in the accumulation and the distribution of Pb in leaves. On the other hand, several genes involved in biosynthesis of ABA were shown to be up-regulated in the roots and shoots of H. incana treated with Pb, suggesting that ABA-mediated signaling is a possible mechanism in response to Pb treatment in H. incana. This latest finding is an important research direction for future studies. PMID:26793211

  7. MATERNAL SELF-ESTEEM, EXPOSURE TO LEAD, AND CHILD NEURODEVELOPMENT

    PubMed Central

    Surkan, Pamela J.; Schnaas, Lourdes; Wright, Rosalind J.; Téllez-Rojo, Martha M.; Lamadrid-Figueroa, Héctor; Hu, Howard; Hernández-Avila, E. Mauricio; Bellinger, David C.; Schwartz, Joel; Perroni, Estela; Wright, Robert O.

    2008-01-01

    The notion that maternal personality characteristics influence cognitive development in their children has been grounded in stress moderation theory. Maternal personality traits, such as self-esteem, may buffer maternal stressors or lead to improved maternal-child interactions that directly impact neurodevelopment. This can be extended to suggest that maternal personality may serve to attenuate or exacerbate the effects of other neurotoxicants, although this has not been studied directly. We examined whether mothers’ self-esteem had a direct or main effect on their children's cognitive outcomes. We also explored the modifying effects of maternal self-esteem on the association between exposure to lead and neurodevelopment in these children. Study participants included 379 mother-child pairs from Mexico City. Data included the Coopersmith self-esteem scale in mothers, children's Bayley's Scale of Infant Development (BSID) scores, and sociodemographic information. Linear regression was used to model the relationship between maternal self-esteem and the Bayley's Mental Development Index (MDI) and Psychomotor Development Index (PDI) scores at age 24 months using regression models stratified by levels of maternal self-esteem. In adjusted models, each point increase in maternal self-esteem was associated with children having 0.2 higher score on the Bayley's MDI (p=0.04). Similar results were observed using the PDI outcome. Moreover, there was evidence that maternal self-esteem attenuated the negative effects of lead exposure, although the interaction fell short of conventional levels of statistical significance. PMID:18261800

  8. Radiation exposure benefit of a lead cap in invasive cardiology.

    PubMed

    Kuon, E; Birkel, J; Schmitt, M; Dahm, J B

    2003-10-01

    Occupational head exposure to radiation in cardiologists may cause radiation induced cataracts and an increased risk of brain cancer. To determine the effectiveness of 0.5 mm lead equivalent caps, not previously used in invasive cardiology, in comparison with a 1.0 mm lead equivalent ceiling mounted lead glass screen. An anthropomorphic Alderson-Rando phantom was used to represent the patient. Scatter entrance skin air kerma to the operator position (S-ESAK-O) was measured during fluoroscopy for all standard angulations and the S-ESAK-O per dose-area product (DAP) calculated, as applied to the phantom. Measured mean (SD) left/right anterior oblique angulation ratios of S-ESAK-O without lead devices were 23.1 (10.1), and varied as a function of tube angulation, body height, and angle of incidence. S-ESAK-O/DAP decreased with incremental operator body height by 10 (3)% per 10 cm. A 1.0 mm lead glass shield reduced mean S-ESAK-O/DAP originating from coronary angiography from 1089 (764) to 54 (29) nSv/Gy x cm2. A 0.5 mm lead cap was effective in lowering measured levels to 1.8 (1.1) nSv/Gy x cm2. Both devices together enabled attenuation to 0.5 (0.1) nSv/Gy x cm2. The most advantageous line of vision for protection of the operator's eyes was > or = 60 degrees rightward. Use of 0.5 mm lead caps proved highly effective, attenuating S-ESAK-O to 2.7 (2.0) x 10(-3) of baseline, and to 1.2 (1.4) x 10(-3) of baseline where there was an additional 1.0 mm lead glass shield. These results could vary according to the x ray systems used, catheterisation protocols, and correct use of radiation protection devices.

  9. Early umbilical cord clamping contributes to elevated blood lead levels among infants with higher lead exposure.

    PubMed

    Chaparro, Camila M; Fornes, Raymond; Neufeld, Lynnette M; Tena Alavez, Gilberto; Eguía-Líz Cedillo, Raúl; Dewey, Kathryn G

    2007-11-01

    To investigate whether infant iron status, modified by umbilical cord clamping time and infant feeding mode, affected infant blood lead concentration at 6 months of age. Participants were a subset of women and their infants randomized to receive early (10 seconds) or delayed (2 minutes) umbilical cord clamping and were monitored to 6 months postpartum in Mexico City. Iron and lead status was analyzed in maternal, placental, and 6-month infant blood samples. Baseline maternal lead exposure data and infant feeding data at 2, 4, and 6 months were collected. In the total sample, maternal blood lead concentration, infant ferritin, and breast-feeding practices predicted infant blood lead concentration. Among infants with higher placental blood lead concentration and breast-fed infants not receiving any iron-fortified formula or milk at 6 months, early clamping increased infant blood lead concentration, an effect mediated in part via decreased infant iron status. Early cord clamping, by decreasing infant iron status, contributes to higher blood lead concentrations at 6 months of age among infants at high risk.

  10. [Use of urine lead level as an exposure indicator and its relationship to blood lead].

    PubMed

    Moreira, Maria de Fátima Ramos; Neves, Eduardo Borba

    2008-09-01

    The aim of this work was to verify whether there are statistically significant correlation between the concentrations of lead in blood (Pb-B) and urine (Pb-U). Electrothermal atomic absorption spectrometry was used in the determination of lead concentration in biological material. Venous blood and spot urine were collected from workers occupationally exposed (95), adults (130) and children up to 15 years old (22) environmentally exposed. After a test showing significant differences between Pb-U and the three categories previously determined, cutting points for Pb-U were established to predict Pb-B values by the ROC curve. Thus, it is expected that Pb-B is lower than 10 microg.dL-(1) with Pb-U up to 0.55 microg.dL-(1), whereas lead levels in blood below 27.6 microg.dL-(1) are expected when the amount of the metal in urine is lower than 2.05 microg.dL-(1). So, urine can be used to replace blood for the assessment of the occupational exposure to lead. However, caution is advised in the case of environmental exposure, since urinary lead should be used just as an estimation of the metal content in blood.

  11. The social costs of childhood lead exposure in the post-lead regulation era.

    PubMed

    Muennig, Peter

    2009-09-01

    To estimate the benefits that might be realized if all children in the United States had a blood lead level of less than 1 microg/dL. Data were obtained from published and electronic sources. A Markov model was used to project lifetime earnings, reduced crime costs, improvements in health, and reduced welfare costs using 2 scenarios: (1) maintaining the status quo and (2) reducing the blood lead level of all children to less than 1 microg/dL. The cohort of US children between birth and age 6 years in 2008, with economic and health outcomes projected for 65 years. Increased primary prevention efforts aimed at reducing lead exposure among children and pregnant women. Societal costs and quality-adjusted life years (QALYs) gained. Reducing blood lead levels to less than 1 microg/dL among all US children between birth and age 6 years would reduce crime and increase on-time high school graduation rates later in life. The net societal benefits arising from these improvements in high school graduation rates and reductions in crime would amount to $50 000 (SD, $14 000) per child annually at a discount rate of 3%. This would result in overall savings of approximately $1.2 trillion (SD, $341 billion) and produce an additional 4.8 million QALYs (SD, 2 million QALYs) for US society as a whole. More aggressive programs aimed at reducing childhood lead exposure may produce large social benefits.

  12. Prenatal exposure of testosterone prevents SDN-POA neurons of postnatal male rats from apoptosis through NMDA receptor.

    PubMed

    Hsu, H K; Yang, R C; Shih, H C; Hsieh, Y L; Chen, U Y; Hsu, C

    2001-11-01

    The role of N-methyl-D-aspartate (NMDA) receptor in mediating the effect of testosterone exposure prenatally on neuronal apoptosis in the sexual dimorphic nucleus of the preoptic area (SDN-POA) of rats was studied. The endogenous testosterone was diminished by prenatal stress (PNS) or simulated by testosterone exposure (TE) to understand the effect of testosterone on NR(1) (a functional subunit protein of NMDA receptor) expression and neuronal apoptosis. To further study whether the testosterone, after being converted into estradiol, modulates NR(1) expression, 4-androstein-4-ol-3,17-dione (ATD; an aromatase inhibitor) was used to block the conversion of estradiol from testosterone. The expressions of the NR(1) mRNA and NR(1) subunit protein were quantified by RT-PCR and western blotting analysis, respectively. In addition, a noncompetitive antagonist of NMDA receptor, MK-801, was used to find out whether blockage of NMDA receptor affects the naturally occurring apoptosis in SDN-POA. The results showed the following. 1) Expression of perinatal NR(1) subunit protein in the central part of the medial preoptic area of male rats was significantly higher than that of females, especially on postnatal days 1 and 3. 2) The testosterone level of male fetuses on embryonic day 18 was significantly higher than that of females, while the testosterone level of TE females or PNS males was similar to that of intact males or intact females, respectively. 3) The apoptotic incidence of intact male rats was significantly less than that of females, and the apoptosis was stimulated by PNS in male or inhibited by TE in female. 4) The expression of NR(1) subunit protein could be inhibited by PNS or ATD-treatment in male, while stimulated by TE in female. 5) NR(1) mRNA showed no significant difference among intact male, PNS male, ATD-treated male, TE female and intact female rats. 6) The low apoptotic incidence of male rats was significantly increased when NMDA receptor was blocked by MK

  13. Developmental lead exposure attenuates methamphetamine dose-effect self-administration performance and progressive ratio responding in the male rat.

    PubMed

    Rocha, Angelica; Valles, Rodrigo; Hart, Nigel; Bratton, Gerald R; Nation, Jack R

    2008-06-01

    Perinatal (gestation/lactation) lead exposure modifies the reinforcement efficacy of various psychoactive drugs (e.g., cocaine, opiates) across the phases of initial selection, use, and abuse [Nation J.R., Cardon A.L., Heard H.M., Valles R., Bratton G.R. Perinatal lead exposure and relapse to drug-seeking behavior in the rat: a cocaine reinstatement study. Psychopharmacol 2003;168: 236-243.; Nation J.R., Smith K.R., Bratton G.R. Early developmental lead exposure increases sensitivity to cocaine in a self-administration paradigm. Pharmacol Biochem Behave 2004; 77: 127-13; Rocha A., Valles R., Cardon A.L., Bratton G.R., Nation J.R. Enhanced acquisition of cocaine self-administration in rats developmentally exposed to lead. Neuropsychopharmacol 2005; 30: 2058-2064.]. However, changes in sensitivity to methamphetamine across the phases of drug abuse have not been examined in animals perinatally exposed to lead. Because the mainstream popularity of methamphetamine in the United States is increasing and lead exposure continues to be widespread, an examination of this drug and how it may be modified by perinatal exposure to lead is warranted. The studies reported here examined the effects of perinatal lead exposure on adult self-administration of intravenous (i.v.) methamphetamine across the maintenance phase of drug addiction. Experiment 1 examined dose-effect patterns in control and lead-exposed animals. Experiment 2 evaluated control and lead-exposed animals in a progressive ratio task. Female rats were administered a 16-mg lead or a control solution for 30 days prior to breeding with non-exposed males. Exposure continued through pregnancy and lactation and was discontinued at weaning (postnatal day [PND] 21). Animals born to control or lead-exposed dams received indwelling jugular catheters as adults (PND 70) and subsequently were randomly assigned to one of the two studies, using only one male rat per litter for each study. The data showed a general attenuation of

  14. Occupational Lead Exposure from Indoor Firing Ranges in Korea.

    PubMed

    Park, Won-Ju; Lee, Suk-Ho; Lee, Se-Ho; Yoon, Hye-Sik; Moon, Jai-Dong

    2016-04-01

    Military personnel often use ammunitions that contain lead. The present study aimed to identify the risks for lead exposure and lead poisoning among workers at indoor firing ranges. A special health examination, including blood lead level (BLL) testing, was performed for all 120 workers at the indoor firing ranges of the Republic of Korea's Air Force, Navy, and Armed Forces Athletic Corps. The overall mean BLL was 11.3 ± 9.4 µg/dL (range: 2.0-64.0 µg/dL). The arithmetic mean of the BLL for professional shooters belong to Armed Forces Athletic Corps was 14.0 ± 8.3 µg/dL, while those of shooting range managers and shooting range supervisors were 13.8 ± 11.1 µg/dL and 6.4 ± 3.1 µg/dL, respectively. One individual had a BLL of 64 µg/dL, and ultimately completed chelation treatment (with CaNa2-ethylenediaminetetraacetic acid) without any adverse effects. These findings indicate that indoor firing range workers are exposed to elevated levels of lead. Therefore, when constructing an indoor firing range, a specialist should be engaged to design and assess the ventilation system; and safety guidelines regarding ammunition and waste handling must be mandatory. Moreover, workplace environmental monitoring should be implemented for indoor firing ranges, and the workers should undergo regularly scheduled special health examinations.

  15. Occupational Lead Exposure from Indoor Firing Ranges in Korea

    PubMed Central

    Lee, Suk-Ho; Lee, Se-Ho; Yoon, Hye-Sik

    2016-01-01

    Military personnel often use ammunitions that contain lead. The present study aimed to identify the risks for lead exposure and lead poisoning among workers at indoor firing ranges. A special health examination, including blood lead level (BLL) testing, was performed for all 120 workers at the indoor firing ranges of the Republic of Korea’s Air Force, Navy, and Armed Forces Athletic Corps. The overall mean BLL was 11.3 ± 9.4 µg/dL (range: 2.0–64.0 µg/dL). The arithmetic mean of the BLL for professional shooters belong to Armed Forces Athletic Corps was 14.0 ± 8.3 µg/dL, while those of shooting range managers and shooting range supervisors were 13.8 ± 11.1 µg/dL and 6.4 ± 3.1 µg/dL, respectively. One individual had a BLL of 64 µg/dL, and ultimately completed chelation treatment (with CaNa2-ethylenediaminetetraacetic acid) without any adverse effects. These findings indicate that indoor firing range workers are exposed to elevated levels of lead. Therefore, when constructing an indoor firing range, a specialist should be engaged to design and assess the ventilation system; and safety guidelines regarding ammunition and waste handling must be mandatory. Moreover, workplace environmental monitoring should be implemented for indoor firing ranges, and the workers should undergo regularly scheduled special health examinations. PMID:27051231

  16. Reduced Hippocampal Dendritic Spine Density and BDNF Expression following Acute Postnatal Exposure to Di(2-Ethylhexyl) Phthalate in Male Long Evans Rats

    PubMed Central

    Smith, Catherine A.; Holahan, Matthew R.

    2014-01-01

    Early developmental exposure to di(2-ethylhexyl) phthalate (DEHP) has been linked to a variety of neurodevelopmental changes, particularly in rodents. The primary goal of this work was to establish whether acute postnatal exposure to a low dose of DEHP would alter hippocampal dendritic morphology and BDNF and caspase-3 mRNA expression in male and female Long Evans rats. Treatment with DEHP in male rats led to a reduction in spine density on basal and apical dendrites of neurons in the CA3 dorsal hippocampal region compared to vehicle-treated male controls. Dorsal hippocampal BDNF mRNA expression was also down-regulated in male rats exposed to DEHP. No differences in hippocampal spine density or BDNF mRNA expression were observed in female rats treated with DEHP compared to controls. DEHP treatment did not affect hippocampal caspase-3 mRNA expression in male or female rats. These results suggest a gender-specific vulnerability to early developmental DEHP exposure in male rats whereby postnatal DEHP exposure may interfere with normal synaptogenesis and connectivity in the hippocampus. Decreased expression of BDNF mRNA may represent a molecular mechanism underlying the reduction in dendritic spine density observed in hippocampal CA3 neurons. These findings provide initial evidence for a link between developmental exposure to DEHP, reduced levels of BDNF and hippocampal atrophy in male rats. PMID:25295592

  17. Reduced hippocampal dendritic spine density and BDNF expression following acute postnatal exposure to di(2-ethylhexyl) phthalate in male Long Evans rats.

    PubMed

    Smith, Catherine A; Holahan, Matthew R

    2014-01-01

    Early developmental exposure to di(2-ethylhexyl) phthalate (DEHP) has been linked to a variety of neurodevelopmental changes, particularly in rodents. The primary goal of this work was to establish whether acute postnatal exposure to a low dose of DEHP would alter hippocampal dendritic morphology and BDNF and caspase-3 mRNA expression in male and female Long Evans rats. Treatment with DEHP in male rats led to a reduction in spine density on basal and apical dendrites of neurons in the CA3 dorsal hippocampal region compared to vehicle-treated male controls. Dorsal hippocampal BDNF mRNA expression was also down-regulated in male rats exposed to DEHP. No differences in hippocampal spine density or BDNF mRNA expression were observed in female rats treated with DEHP compared to controls. DEHP treatment did not affect hippocampal caspase-3 mRNA expression in male or female rats. These results suggest a gender-specific vulnerability to early developmental DEHP exposure in male rats whereby postnatal DEHP exposure may interfere with normal synaptogenesis and connectivity in the hippocampus. Decreased expression of BDNF mRNA may represent a molecular mechanism underlying the reduction in dendritic spine density observed in hippocampal CA3 neurons. These findings provide initial evidence for a link between developmental exposure to DEHP, reduced levels of BDNF and hippocampal atrophy in male rats.

  18. Increased risk of childhood acute lymphoblastic leukemia (ALL) by prenatal and postnatal exposure to high voltage power lines: a case control study in Isfahan, Iran.

    PubMed

    Tabrizi, Maral Mazloomi; Bidgoli, Sepideh Arbabi

    2015-01-01

    Childhood acute lymphoblastic leukemia (ALL) is one of the most common hematologic malignancies, accounting for one fourth of all childhood cancer cases. Exposure to environmental factors around the time of conception or pregnancy can increase the risk of ALL in the offspring.This study aimed to evaluted the role of prenatal and postnatal exposure to high voltage power lines on the incidence of childhood ALL.This cross-sectional case control study was carried out on 22 cases and 100 controls who were born and lived in low socioeconomic families in Isfahan and hospitalized for therapeutic purposes in different hospitals from 2013-2014.With regard to the underlying risk factors, familial history and parental factors were noted but in this age, socioeonomic and zonal matched case control study, prenatal and childhood exposure to high voltage power lines was considered as the most important environmental risk factors of ALL (p=0.006, OR=3.651, CI 95%, 1.692-7.878). As the population was of low socioeconomic background, use of mobiles, computers and microwave was negligible. Moreover prenatal and postnatal exposure to indoor electrically charged objects was not determined to be a significant environmental factor. Thus, pre and post natal exposure to high voltage power lines and living in pollutant regions as well as familial influence could be described as risk factors of ALL for the first time in a low socioeconomic status Iranian population.

  19. Lead exposure at firing ranges-a review.

    PubMed

    Laidlaw, Mark A S; Filippelli, Gabriel; Mielke, Howard; Gulson, Brian; Ball, Andrew S

    2017-04-04

    Lead (Pb) is a toxic substance with well-known, multiple, long-term, adverse health outcomes. Shooting guns at firing ranges is an occupational necessity for security personnel, police officers, members of the military, and increasingly a recreational activity by the public. In the United States alone, an estimated 16,000-18,000 firing ranges exist. Discharge of Pb dust and gases is a consequence of shooting guns. The objectives of this study are to review the literature on blood lead levels (BLLs) and potential adverse health effects associated with the shooting population. The search terms "blood lead", "lead poisoning", "lead exposure", "marksmen", "firearms", "shooting", "guns", "rifles" and "firing ranges" were used in the search engines Google Scholar, PubMed and Science Direct to identify studies that described BLLs in association with firearm use and health effects associated with shooting activities. Thirty-six articles were reviewed that included BLLs from shooters at firing ranges. In 31 studies BLLs > 10 μg/dL were reported in some shooters, 18 studies reported BLLs > 20 μg/dL, 17 studies > 30 μg/d, and 15 studies BLLs > 40 μg/dL. The literature indicates that BLLs in shooters are associated with Pb aerosol discharge from guns and air Pb at firing ranges, number of bullets discharged, and the caliber of weapon fired. Shooting at firing ranges results in the discharge of Pb dust, elevated BLLs, and exposures that are associated with a variety of adverse health outcomes. Women and children are among recreational shooters at special risk and they do not receive the same health protections as occupational users of firing ranges. Nearly all BLL measurements compiled in the reviewed studies exceed the current reference level of 5 μg/dL recommended by the U.S. Centers for Disease Control and Prevention/National Institute of Occupational Safety and Health (CDC/NIOSH). Thus firing ranges, regardless of type and user classification

  20. The investigation of the prenatal and postnatal alcohol exposure-induced neurodegeneration in rat brain: protection by betaine and/or omega-3.

    PubMed

    Kusat Ol, Kevser; Kanbak, Güngör; Oğlakcı Ilhan, Ayşegül; Burukoglu, Dilek; Yücel, Ferruh

    2016-03-01

    We aim to study the effect of neurodegeneration on the brain of rat pups caused by prenatal and postnatal ethanol exposure with modified liquid diet to elucidate protective effects of betaine and omega-3 supplementation. When ethanol is consumed during prenatal and postnatal periods, it may result in fetal alcohol syndrome (FAS) in the offspring. Rats were divided into control, ethanol, ethanol + betaine, ethanol + omega-3, ethanol + omega-3 + betaine groups. The effect of betaine and omega-3 in response to ethanol-induced changes on the brain, by biochemical analyses cytochrome c, caspase-3, calpain, cathepsin B and L, DNA fragmentation, histological and morfometric methods were evaluated. Caspase-3, calpain, cathepsin B, and cytochrome c levels in ethanol group were significantly higher than control. Caspase-3, calpain levels were decreased in ethanol + betaine, ethanol + omega-3, and ethanol + omega-3 + betaine groups compared to ethanol group. Cathepsin B in ethanol + omega-3 + betaine group was decreased compared to ethanol, ethanol + betaine groups. Cathepsin L and DNA fragmentation were found not statistically significant. We found similar results in histological and morfometric parameters. We found that pre- and postnatal ethanol exposure is capable of triggering necrotic cell death in rat brains, omega-3, and betaine reduce neurodegeneration. Omega-3 and betaine may prove beneficial for neurodegeneration, particularly in preventing FAS.

  1. Effects of in utero and Postnatal Exposure to Secondhand Smoke on Lung Function by Gender and Asthma Status: The Seven Northeastern Cities (SNEC) Study.

    PubMed

    Hu, Li-Wen; Yang, Mo; Chen, Shu; Shah, Kuntal; Hailegiorgis, Yismaw; Burgens, Richai; Vaughn, Michael; Huang, Jin; Xaverius, Pamela; Paul, Gunther; Morawska, Lidia; Lu, Tao; Lin, Shao; Zhong, Shou-Qiang; Kong, Min-Li; Xie, Yan-Qi; Hao, Yuan-Tao; Zeng, Xiao-Wen; Qian, Zhengmin; Dong, Guang-Hui

    2017-01-01

    Little information exists on whether gender or asthma status modifies the effects of secondhand smoke (SHS) exposure on lung function. To evaluate whether gender or asthma status modifies the association of SHS exposure with lung function. A total of 6,740 children (average 11.6 years) were recruited from 24 districts of 7 cities in northeast China in 2012. SHS exposure included exposure to environmental and maternal smoking both in utero and during early childhood (postnatal). Lung function was measured using electronic spirometers. Two-step regressions were used to analyze the association between SHS and lung function. In utero and postnatal exposure to SHS was independently associated with decreased lung function in both genders; however, this association was greater among males. For example, when exposed to maternal smoking during pregnancy, the adjusted odds ratio (aOR) for decreased forced vital capacity (FVC) was 6.46 (95% confidence interval [CI]: 2.58-16.17) among males, while only 2.16 (95% CI: 0.96-4.88) among females. More positive associations between SHS exposure and decreased lung function were detected among nonasthmatic compared with asthmatic children. Nonasthmatics had significantly larger deficits from in utero exposure to maternal smoking, which concerned decreased lung FVC function (aOR = 2.58, 95% CI: 1.28-5.21) and decreased lung forced expiratory volume in 1 s (FEV1) function (aOR = 2.32, 95% CI: 1.01-5.33). A similar pattern was also observed for the associations between SHS exposure and continuous pulmonary function test measurements. SHS exposure was associated with decreased lung function. Males and nonasthmatics seem to be more susceptible than their respective counterparts. © 2017 S. Karger AG, Basel.

  2. Perinatal lead exposure and relapse to drug-seeking behavior in the rat: a cocaine reinstatement study.

    PubMed

    Nation, Jack R; Cardon, Aaron L; Heard, Heather M; Valles, Rodrigo; Bratton, Gerald R

    2003-07-01

    Intravenous self-administration of cocaine at low doses is increased by chronic low-level exposure to lead during gestation and lactation (perinatal lead exposure). Insofar as drug potency is increased by early lead exposure, it must be considered that cocaine-seeking and relapse after periods of withdrawal similarly may be enhanced by perinatal lead exposure. Employing an animal model, the present study examined the effects of lead exposure during gestation and lactation on cocaine-induced reinstatement of drug-seeking, when animals were tested as adults. Adult female rats were gavaged once daily with 0 or 16 mg lead for 30 days prior to breeding with non-exposed males. This exposure regimen continued until offspring were weaned at postnatal day (PND) 21. At PND 120, male offspring were trained to self-administer cocaine intravenously (IV) [0.50 mg/kg cocaine per infusion on a fixed-ratio schedule where two lever presses resulted in drug delivery (FR-2 schedule)]. After steady-state responding was established, cocaine reinstatement responding was assessed for each group within an extinction paradigm. During the initial 1 h of reinstatement testing, the previous baseline contingencies were in place, i.e. animals operated under an FR-2 schedule for an infusion of 0.50 mg/kg cocaine. During the 2 h, 3 h, and 4 h of testing saline infusions were substituted for cocaine infusions. After responding extinguished during hour 4, reinstatement of responding was tested by administering an intraperitoneal (IP) priming injection of 0.00, 5.00, 10.00, or 20.00 mg/kg cocaine. Following these injections, lever responding for saline infusions was monitored during hour 5. The number of saline infusions self-administered during hour 5 increased in a dose-dependent fashion for both controls (group 0-mg) and lead-exposed (group 16-mg