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Sample records for postnatal lead exposure

  1. Prenatal and early postnatal lead exposure in mice: neuroimaging findings

    PubMed Central

    Lindquist, Diana M.; Beckwith, Travis; Sánchez-Martín, Francisco Javier; Landero-Figueroa, Julio; Puga, Alvaro

    2015-01-01

    Background Childhood lead exposure has been linked to adult gray matter loss accompanied by changes in myelination and neurochemistry noninvasively revealed by magnetic resonance imaging (MRI) methods. However, the extent, duration and timing of lead exposure required to produce such imaging changes in humans are difficult to ascertain. Methods To determine if such changes are related to early exposure to low levels of lead, we treated mouse dams with 0, 3, or 30 ppm of lead acetate in drinking water for 2 months prior to mating through gestation until weaning of the offspring at post-natal day 21. Two male and two female pups from each litter were imaged at post-natal day 60. Volumetric, diffusion tensor imaging and magnetic resonance spectroscopy (MRS) measurements were obtained using a seven Tesla Bruker animal MRI scanner. Results Postnatal blood lead levels were identical between groups at the time of imaging. No effects of lead exposure were detected in the volumetric or MRS data. Mean diffusivity in the hippocampus showed significant effects of lead exposure and gender. Conclusions These data suggest that low-level, gestational lead exposure in a mouse model produces minimal changes observed by MRI. PMID:26435914

  2. Pre- and postnatal lead exposure and behavior problems in school-aged children

    SciTech Connect

    Bellinger, D.; Leviton, A.; Allred, E.; Rabinowitz, M. )

    1994-07-01

    The association between early lead exposure and later problem behaviors was evaluated prospectively in a cohort of 8-year-old children born during a 12-month period at one hospital. Lead levels in umbilical cord blood ([bar X] = 6.8 [mu]g/dl, SD = 3.1) and the dentin of a shed deciduous tooth ([bar X] = 3.4 [mu]g/g, SD = 2.4) provided measures of prenatal and postnatal exposure, respectively. Ratings on the Teacher Report Form of the Child Behavior Profile provided information about children's problem behaviors. Cord blood lead level was not associated with the overall prevalence or nature of problem behaviors. In both crude and adjusted analyses, tooth lead level was significantly associated with total problem behavior scores (approximately 2 points in T score per log unit increase in tooth lead). Significant tooth lead-associated increases in both internalizing and externalizing scores were also observed (approximately 1.5 points in T score per log unit increase). Weaker associations were noted between tooth lead level and the prevalence of [open quotes]extreme[close quotes] problem behavior scores. The extent to which these associations reflect residual confounding is uncertain. These data suggest, however, that social and emotional dysfunctions are correlates and may be expressions of increased lead exposure. 64 refs., 2 figs., 9 tabs.

  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. Effects of maternal lead exposure on central nervous system maturation in postnatal rats

    SciTech Connect

    Coleman, J.C.

    1984-01-01

    Pups from female rats exposed to 40-to-80 mg of lead per liter in their drinking water (low-lead group) and 160-to-320 mg of lead per liter water (high-lead group) were examined at 1 to 18 days of age. Maximal electroshock seizure (MES) patterns were determined and, upon recovery, whole blood, plasma, cerebrospinal fluid (CSF) and cerebral cortex samples were collected. Approximately one-half of the pups was used to determine the cerebral cortical extracellular water space (ECS). The other half was used to determine whole blood lead concentrations, plasma electrolytes (Na/sup +/, K/sup +/ and Cl/sup -/), CSF electrolytes, and cerebral cortical lead content, electrolytes, total water spaces, protein content, DNA content, carbonic anhydrase (CA) activity, and sodium- potassium-activated adenosinetriphosphatase (Na/sup +//K/sup +/-ATPase) activity. Neither the low- nor the high-lead groups had significant changes in body weight, body length, hematocrit or cerebral wet weight at any age studied. Whole blood and cerebral cortical lead contents were increased, dose-dependently, at each day of age. Hyperexcitability as measured by MES was observed in lead-exposed pups at 6, 9 and 12 days of age. These observations demonstrate that prenatal and postnatal exposure to lead causes increased susceptibility to MES and alterations in normal developmental patterns of the cerebral cortex. Such alterations appear to result from the greater vulnerability of the glial population to the adverse effects of lead than are neutrons. Thus, effects on the glia can account for the electrolyte imbalances, cellular edema and hyperexcitability resulting from exposure to lead.

  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. PMID:25147304

  6. Sex-Based Differences in Gene Expression in Hippocampus Following Postnatal Lead Exposure

    PubMed Central

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

    2011-01-01

    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 a variety of genes in the hippocampus and that the response of the brain to a given lead exposure may vary depending on sex. PMID:21864555

  7. 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.

  8. Infantile Postnatal Exposure to Lead (Pb) Enhances Tau Expression in the Cerebral Cortex of Aged Mice: Relevance to AD

    PubMed Central

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

    2014-01-01

    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. PMID:24954411

  9. 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

  10. 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

  11. 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.

  12. Postnatal glucocorticoid exposure alters the adult phenotype.

    PubMed

    He, Jing; Varma, Amit; Weissfeld, Lisa A; Devaskar, Sherin U

    2004-07-01

    We examined the effect of six doses of dexamethasone (Dex) administered daily (2-7 days of age) to postnatal rats on body weight gain, food and water intake, peripheral hormonal/metabolic milieu, and hypothalamic neuropeptides that regulate food intake. We observed a Dex-induced acute (3 days of age) suppression of endogenous corticosterone and an increase in circulating leptin concentrations that were associated with a decrease in body weight in males and females. Followup during the suckling, postsuckling, and adult stages (7-120 days of age) revealed hypoleptinemia in males and females, and hypoinsulinemia, a relative increase in the glucose-to-insulin ratio, and a larger increase in skeletal muscle glucose transporter (GLUT 4) concentrations predominantly in the males, reflective of a catabolic state associated with a persistent decrease in body weight gain. The increase in the glucose-to-insulin ratio and hyperglycemia was associated with an increase in water intake. In addition, the changes in the hormonal/metabolic milieu were associated with an increase in hypothalamic neuropeptide Y content in males and females during the suckling phase, which persisted only in the 120-day-old female with a transient postnatal decline in alpha-melanocyte-stimulating hormone and corticotropin-releasing factor. This increase in neuropeptide Y (NPY) during the suckling phase in males and females was associated with a subsequent increase in adult food intake that outweighed the demands of body weight gain. In contrast to the adult hypothalamic findings, cerebral ventricular dilatation was more prominent in adult males. We conclude that postnatal Dex treatment causes permanent sex-specific changes in the adult phenotype, setting the stage for future development of diabetes (increased glucose:insulin ratio), obesity (increased NPY and food intake), and neurological impairment (loss of cerebral volume). PMID:15001431

  13. Overexpression of Dlx2 leads to postnatal condyle degradation

    PubMed Central

    Dai, Jiewen; Si, Jiawen; Zhu, Xiaofang; Zhang, Lei; Wu, Dandan; Lu, Jingting; Ouyang, Ningjuan; Wang, Xudong; Shen, Guofang

    2016-01-01

    Distal-less homeobox 2 (Dlx2), a member of the Dlx family of transcription factors, is important for the development of craniofacial tissues. Previous studies based on knock-out mutant mice revealed that Dlx2 primarily disturbed the development of tissues from maxillary arch. The present study used a transgenic mouse model to specifically overexpress Dlx2 in neural crest cells in order to investigate the role of Dlx2 overexpression in post-natal condyle in mice. The model was constructed and the phenotype observed using gross observation, micro-CT scan and histological examination. The model determined that overexpression of Dlx2 may lead to postnatal condyle malformation, subchondral bone degradation and irregular histological structure of the condylar cartilage. In addition, the expression of osteocalcin in the condyle region was markedly downregulated, whereas expression of msh homeobox 2 was upregulated. The results of the present study suggest that Dlx2 overexpression in cranial neural crest cells would disrupt the development of post-natal condyle, which demonstrates that the expression level and the spatiotemporal expression patterns of Dlx2 may be important in regulating the development of post-natal condyle in mice, and also offered a possible temporal-mandibular joint osteoarthritis model animal for future studies. PMID:27315306

  14. NEUROBEHAVIORAL CONSEQUENCES OF POSTNATAL EXPOSURE TO TOXICANTS

    EPA Science Inventory

    Behavioral teratology is the study of the functional consequences of exposure to toxicants during the period of nervous system development. These agents include therapeutic drugs, food additives, hormones, alcohol, drugs of abuse, heavy metals, pesticides, solvents, and x-irradia...

  15. 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

  16. Effects of prenatal propofol exposure on postnatal development in rats.

    PubMed

    Li, Jing; Xiong, Ming; Alhashem, Hussain M; Zhang, Yong; Tilak, Vasanti; Patel, Anuradha; Siegel, Allan; Ye, Jiang Hong; Bekker, Alex

    2014-01-01

    Preclinical studies suggest that propofol may cause damage to immature neurons. However, the effect of maternal propofol exposure on the neuronal development of the offspring is largely unknown. In this study, pregnant rats were assigned to receive continuous infusion of saline (control) or propofol for 1 h (1HP) or 2 h (2HP) on gestational day 18. An additional group (lipid) was assigned to receive continuous infusion of intralipid fat emulsion (vehicle of propofol) for 2 h. Pups were then tested on the appearance and progression of sensory and physical motor abilities between postnatal day 1 (P1) and P28. The brain and body weights of pups from 2HP group on P10 were significantly lower than those from the saline control group, although they were the same in all four groups at birth (P0). Pups from 1HP and 2HP groups, but not lipid group, showed slower maturation of eyes (delayed opening) and several neurological reflexes (hindlimb reflex, righting reflex); they also showed delayed improvement in execution on gait reflex and inclined board tests. The forelimb reflex and negative geotaxis were also delayed in 2HP group. All parameters examined except body weight of 2HP pups recovered to normal levels by P28. We conclude that administration of propofol to pregnant rats leads to retardation in physical and neurological reflex development in their offspring. PMID:24726880

  17. 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. PMID:26646100

  18. 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.

  19. 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

  20. In utero dimethadione exposure causes postnatal disruption in cardiac structure and function in the rat.

    PubMed

    Aasa, Kristiina L; Purssell, Elizabeth; Adams, Michael A; Ozolinš, Terence R S

    2014-12-01

    In utero exposure of rat embryos to dimethadione (DMO), the N-demethylated teratogenic metabolite of the anticonvulsant trimethadione, induces a high incidence of cardiac heart defects including ventricular septal defects (VSDs). The same exposure regimen also leads to in utero cardiac functional deficits, including bradycardia, dysrhythmia, and a reduction in cardiac output (CO) and ejection fraction that persist until parturition (10 days after the final dose). Despite a high rate of spontaneous postnatal VSD closure, we hypothesize that functional sequelae will persist into adulthood. Pregnant Sprague Dawley rats were administered six 300 mg/kg doses of DMO, one every 12 h in mid-pregnancy beginning on the evening of gestation day 8. Postnatal cardiac function was assessed in control (CTL) and DMO-exposed offspring using radiotelemetry and ultrasound at 3 and 11 months of age, respectively. Adult rats exposed to DMO in utero had an increased incidence of arrhythmia, elevated blood pressure and CO, greater left ventricular volume and elevated locomotor activity versus CTL. The mean arterial pressure of DMO-exposed rats was more sensitive to changes in dietary salt load compared with CTL. Importantly, most treated rats had functional deficits in the absence of a persistent structural defect. It was concluded that in utero DMO exposure causes cardiovascular deficits that persist into postnatal life in the rat, despite absence of visible structural anomalies. We speculate this is not unique to DMO, suggesting possible health implications for infants with unrecognized gestational chemical exposures. PMID:25239635

  1. 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.

  2. 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...

  3. Postnatal Sulfur Dioxide Exposure Reversibly Alters Parasympathetic Regulation of Heart Rate

    PubMed Central

    Woerman, Amanda L.; Mendelowitz, David

    2014-01-01

    Perinatal sulfur dioxide exposure disrupts parasympathetic regulation of cardiovascular activity. Here, we examine the relative risks of prenatal versus postnatal exposure to the air pollutant, and the reversibility of the cardiovascular effects. Two groups of animals were used for this study. For prenatal exposure, pregnant Sprague-Dawley dams were exposed to 5 parts per million sulfur dioxide for 1 hour daily throughout gestation, and with their pups upon birth to medical-grade air through 6 days postnatal. For postnatal exposure, dams were exposed to air, and upon delivery along with their pups to 5 parts per million sulfur dioxide through postnatal day 6. Electrocardiograms were recorded from pups on postnatal day 5 to examine changes in heart rate. Whole-cell patch-clamp electrophysiology was used to examine changes in neurotransmission to cardiac vagal neurons upon sulfur dioxide exposure. Postnatal sulfur dioxide exposure diminished glutamatergic neurotransmission to cardiac vagal neurons by 40.9% and increased heart rate, whereas prenatal exposure altered neither of these properties. When postnatal exposure concluded on postnatal day 5, excitatory neurotransmission remained decreased through day 6, and returned to basal levels by day 7. Electrocardiograms showed that heart rate remained elevated through day 6 and recovered by day 7. Upon activation of the parasympathetic diving reflex, the response was significantly blunted by postnatal sulfur dioxide exposure through day 7 but recovered by day 8. Postnatal, but not prenatal, exposure to sulfur dioxide can disrupt parasympathetic regulation of cardiovascular activity. Neonates can recover from these effects within 2–3 days of discontinued exposure. PMID:23774227

  4. Postnatal sulfur dioxide exposure reversibly alters parasympathetic regulation of heart rate.

    PubMed

    Woerman, Amanda L; Mendelowitz, David

    2013-08-01

    Perinatal sulfur dioxide exposure disrupts parasympathetic regulation of cardiovascular activity. Here, we examine the relative risks of prenatal versus postnatal exposure to the air pollutant and the reversibility of the cardiovascular effects. Two groups of animals were used for this study. For prenatal exposure, pregnant Sprague-Dawley dams were exposed to 5 parts per million sulfur dioxide for 1 hour daily throughout gestation and with their pups after birth to medical-grade air through 6 days postnatal. For postnatal exposure, dams were exposed to air, and after delivery along with their pups to 5 parts per million sulfur dioxide through postnatal day 6. ECGs were recorded from pups on postnatal day 5 to examine changes in heart rate. Whole-cell patch-clamp electrophysiology was used to examine changes in neurotransmission to cardiac vagal neurons in the nucleus ambiguus on sulfur dioxide exposure. Postnatal sulfur dioxide exposure diminished glutamatergic neurotransmission to cardiac vagal neurons by 40.9% and increased heart rate, whereas prenatal exposure altered neither of these properties. When postnatal exposure concluded on postnatal day 5, excitatory neurotransmission remained decreased through day 6 and returned to basal levels by day 7. ECGs showed that heart rate remained elevated through day 6 and recovered by day 7. On activation of the parasympathetic diving reflex, the response was significantly blunted by postnatal sulfur dioxide exposure through day 7 but recovered by day 8. Postnatal, but not prenatal, exposure to sulfur dioxide can disrupt parasympathetic regulation of cardiovascular activity. Neonates can recover from these effects within 2 to 3 days of discontinued exposure. PMID:23774227

  5. Prenatal Exposure to Lamotrigine: Effects on Postnatal Development and Behaviour in Rat Offspring

    PubMed Central

    Sathiya, Sekar; Ganesh, Murugan; Kalaivani, Periyathambi; Ranju, Vijayan; Janani, Srinivasan; Pramila, Bakthavachalam; Saravana Babu, Chidambaram

    2014-01-01

    Use of antiepileptic drugs (AEDs) in pregnancy warrants various side effects and also deleterious effects on fetal development. The present study was carried out to assess the effects of prenatal exposure to lamotrigine (LTG) on postnatal development and behavioural alterations of offspring. Adult male and female Sprague Dawley rats weighing 150–180 g b. wt. were allowed to copulate and pregnancy was confirmed by vaginal cytology. Pregnant rats were treated with LTG (11.5, 23, and 46 mg/kg, p.o) from gestational day 3 (GND 3) and this treatment continued till postnatal day 11 (PND 11). Offspring were separated from their dam on day 21 following parturition. LTG, at 46 mg/kg, p.o, produced severe clinical signs of toxicity leading to death of dam between GND 15 and 17. LTG, at 11.5 and 23 mg/kg, p.o, showed significant alterations in offspring's incisors eruption and vaginal opening when compared to age matched controls. LTG (23 mg/kg, p.o) exposed female offspring expressed hyperactive behaviour and decreased GABA-A receptor expression when compared to control rats. These results reveal that prenatal exposure to LTG may impart differential postnatal behavioural alterations between male and female rats which paves way for further investigations. PMID:24967313

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

    PubMed

    Wu, Z-X; 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

  7. Prenatal lead exposure and bone growth. Doctoral thesis

    SciTech Connect

    Hamilton, J.D.; O'Flaherty, E.J.

    1990-07-24

    An experimental system of lead (7439921) related prenatal and postnatal growth retardation in rats was developed. Sprague-Dawley-rats and Long-Evans-rats were used in these studies. Rats were exposed to lead in their drinking water at up to 1000 parts per million. A significant effect on fetal bone mineralization could not be excluded and there was a definite effect on fetal body weight following maternal lead exposure. Reduced food intake during the first week of lead exposure was the primary determinant of reduced body and skeletal growth in the lead exposed weanling female rats. When maternal lead exposure was continued during lactation a greater degree of lead related growth retardation in rat offspring occurred than when maternal lead exposure was terminated at parturition. Combined prenatal and postnatal lead exposure impaired bone resorption and increased growth plate widths. In studies using matrix induced endochondral bone plaques, locally applied lead enhanced plaque mineralization through comineralization of lead with calcium. When lead was administered in drinking water, plaque mineralization was also enhanced through the comineralization of lead with calcium.

  8. 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

  9. 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. PMID:25682472

  10. 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

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

    PubMed Central

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

    2015-01-01

    Objective The purpose of this study was to examine the association between pre and post environmental tobacco smoke (ETS) exposure and behavioral problems in schoolchildren. Methods 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. Results 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. Conclusion Postnatal ETS exposure, alone or in association with prenatal exposure, increases the risk of behavioral problems in school-age children. PMID:26244898

  12. Altered Hippocampal Lipid Profile Following Acute Postnatal Exposure to Di(2-Ethylhexyl) Phthalate in Rats.

    PubMed

    Smith, Catherine A; Farmer, Kyle; Lee, Hyunmin; Holahan, Matthew R; Smith, Jeffrey C

    2015-10-01

    Slight changes in the abundance of certain lipid species in the brain may drastically alter normal neurodevelopment via membrane stability, cell signalling, and cell survival. Previous findings have demonstrated that postnatal exposure to di (2-ethylhexyl) phthalate (DEHP) disrupts normal axonal and neural development in the hippocampus. The goal of the current study was to determine whether postnatal exposure to DEHP alters the lipid profile in the hippocampus during postnatal development. Systemic treatment with 10 mg/kg DEHP during postnatal development led to elevated levels of phosphatidylcholine and sphingomyelin in the hippocampus of female rats. There was no effect of DEHP exposure on the overall abundance of phosphatidylcholine or sphingomyelin in male rats or of lysophosphatidylcholine in male or female rats. Individual analyses of each identified lipid species revealed 10 phosphatidylcholine and six sphingomyelin lipids in DEHP-treated females and a single lysophosphatidylcholine in DEHP-treated males with a two-fold or higher increase in relative abundance. Our results are congruent with previous work that found that postnatal exposure to DEHP had a near-selective detrimental effect on hippocampal development in males but not females. Together, results suggest a neuroprotective effect of these elevated lipid species in females. PMID:26516880

  13. Altered Hippocampal Lipid Profile Following Acute Postnatal Exposure to Di(2-Ethylhexyl) Phthalate in Rats

    PubMed Central

    Smith, Catherine A.; Farmer, Kyle; Lee, Hyunmin; Holahan, Matthew R.; Smith, Jeffrey C.

    2015-01-01

    Slight changes in the abundance of certain lipid species in the brain may drastically alter normal neurodevelopment via membrane stability, cell signalling, and cell survival. Previous findings have demonstrated that postnatal exposure to di (2-ethylhexyl) phthalate (DEHP) disrupts normal axonal and neural development in the hippocampus. The goal of the current study was to determine whether postnatal exposure to DEHP alters the lipid profile in the hippocampus during postnatal development. Systemic treatment with 10 mg/kg DEHP during postnatal development led to elevated levels of phosphatidylcholine and sphingomyelin in the hippocampus of female rats. There was no effect of DEHP exposure on the overall abundance of phosphatidylcholine or sphingomyelin in male rats or of lysophosphatidylcholine in male or female rats. Individual analyses of each identified lipid species revealed 10 phosphatidylcholine and six sphingomyelin lipids in DEHP-treated females and a single lysophosphatidylcholine in DEHP-treated males with a two-fold or higher increase in relative abundance. Our results are congruent with previous work that found that postnatal exposure to DEHP had a near-selective detrimental effect on hippocampal development in males but not females. Together, results suggest a neuroprotective effect of these elevated lipid species in females. PMID:26516880

  14. 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 ...

  15. 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…

  16. 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...

  17. 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

  18. Effects of Developmental Lead Exposure on the Hippocampal Transcriptome: Influences of Sex, Developmental Period, and Lead Exposure Level

    PubMed Central

    Schneider, Jay S

    2012-01-01

    Developmental lead (Pb) exposure has profound effects on cognition and behavior. Much is known about effects of Pb on hippocampal-mediated behaviors, but little is known about the molecular consequences of Pb exposure and the influences of developmental timing of exposure, level of exposure, and sex as effect modifiers of Pb exposure on the brain. The aim of this study was to examine the effects of different levels of Pb exposure (250 and 750 ppm Pb acetate) during perinatal (gestation/lactation) and postnatal (through postnatal day 45) periods on the hippocampal transcriptome in male and female Long Evans rats. Total RNA was extracted from hippocampus from four animals per experimental condition. RNA was hybridized to Affymetrix Rat Gene RNA Arrays using standard methods. Pb exposure per se influenced the expression of 717 transcripts (328 unique annotated genes), with many influenced in a sex-independent manner. Significant differences in gene expression patterns were also influenced by timing and level of exposure, with generally larger effects at the lower level of exposure across all groups. Statistically enriched biological functions included ion binding, regulation of RNA metabolic processes, and positive regulation of macromolecule biosynthetic processes. Processes of regulation of transcription and regulation of gene expression were preferentially enriched in males, regardless of timing or amount of Pb exposure. The effect on transcription factors and the diverse pathways or networks affected by Pb suggest a substantial effect of developmental Pb exposure on plasticity and adaptability, with these effects significantly modified by sex, developmental window of exposure, and level of Pb exposure. PMID:22641619

  19. 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. PMID:3832431

  20. Prenatal puncture of a unilateral hydronephrosis leading to fetal urinoma and postnatal nephrectomy.

    PubMed

    Lunacek, Andreas; Oswald, Josef; Schwentner, Christian; Gassner, Ingmar; Bartsch, Georg; Radmayr, Christian

    2004-05-01

    Fetal pelvicaliceal dilatation due to ureteropelvic junction obstruction is the most common cause of antenatal hydronephrosis; it rarely leads to a spontaneous rupture resulting in urinoma formation. Antenatal intervention has been recommended only in those cases of large urinomas that seem to interfere with the function of other organ systems (eg, pulmonary hypoplasia secondary to diaphragmatic elevation). We report the case of a fetal intervention (transuterine puncture) in a unilateral massive hydronephrosis leading to a perirenal urinoma and the preterm birth of a female infant. Postnatally, mechanical ventilation and oxygen were required, as was forced percutaneous urinoma drainage. Evaluation revealed a fistula formation between the perirenal space and the kidney's collecting system, possibly due to the fetal intervention. Unfortunately the kidney function was very poor, and surgery to remove the impaired kidney and the urinoma was performed. We discuss the possible effects of fetal intervention in cases of obstructive uropathy and the postnatal risks associated with it. PMID:15135002

  1. 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

  2. POSTNATAL ALTERATIONS IN DEVELOPMENT RESULTING FROM PRENATAL EXPOSURE TO PESTICIDES

    EPA Science Inventory

    Alterations in the developmental processes of embryos resulting from exposure to chemicals are not limited to morphological abnormalities that can be observed in the near term fetus. In the research on the developmental toxicology of pesticides the authors have noted morphologica...

  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. Prenatal cadmium exposure alters postnatal immune cell development and function

    PubMed Central

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

    2012-01-01

    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 CdCl2 (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+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 7 weeks of age. These findings suggest that even very low levels of Cd exposure during gestation can result in long term detrimental

  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. Lead exposure at uncovered outdoor firing ranges

    SciTech Connect

    Goldberg, R.L.; Hicks, A.M.; O'Leary, L.M.; London, S. )

    1991-06-01

    Excessive lead exposure in shooting instructors at indoor firing ranges and covered outdoor firing ranges has been documented. The City of Los Angeles assessed exposure of its full-time shooting instructors at uncovered outdoor ranges via air monitoring and blood lead-level measurements. Results of these tests revealed that significant lead exposure and absorption can occur at outdoor firing ranges. The use of copper-jacketed ammunition may decrease air lead levels and decrease lead absorption by range instructors.

  7. 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

    2016-05-01

    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. Aggr. Behav. 42:209-221, 2016. © 2015 Wiley Periodicals, Inc. PMID:26660077

  8. Temporary prenatal hyperglycemia leads to postnatal neuronal 'glucose-resistance' in the chicken hypothalamus.

    PubMed

    Tzschentke, Barbara; Bogatyrev, Semjon; Schellong, Karen; Rancourt, Rebecca C; Plagemann, Andreas

    2015-08-27

    Prenatal exposures may have a distinct impact for long-term health. Exposure to maternal 'diabesity' during pregnancy increases offspring 'diabesity' risk, e.g. by malprogramming the central nervous regulation of body weight, food intake and metabolism. Critical mechanisms and concrete disrupting factors still remain unclear. Due to the independent development, from the mother, the chicken embryo could provide a valuable model to distinctively establish causal factors. Aim of this study was to determine effects of temporary prenatal hyperglycemia on postnatal hypothalamic neuronal glucose sensitivity in the chicken. To induce hyperglycemia in chicken embryos, 0.5 ml glucose solution (concentration 30 mmol/l) were daily administered via catheter into a vessel of the chorioallantoic egg membrane from days 14 to 17 of incubation. On day 21 of postnatal age, body weight, body fat content, blood glucose, neuroelectrophysiological glucose sensitivity as well as glucose transporter expression were determined in hypothalamic brain slices. No significant changes in morphometric and metabolic parameters were observed. However, strongly decreased neuronal glucose sensitivity and glucose transporter expression occurred, indicating prenatally acquired hypothalamic 'glucose-resistance'. In conclusion, temporary late prenatal hyperglycemia induces lasting changes in central glucose sensing. The prenatally glucose-treated chicken provides a valuable new model for investigating early central nervous origins of 'diabesity' and related disorders. PMID:26054304

  9. Sex differences in anxiety-like behavior and locomotor activity following prenatal and postnatal methamphetamine exposure in adult rats.

    PubMed

    Hrubá, L; Schutová, B; Šlamberová, R

    2012-01-18

    The aim of the present study was to investigate the impact of prenatal and postnatal methamphetamine (MA) exposure on behavior and anxiety in adult male and female rats. Mothers were daily exposed to injection of MA (5 mg/kg) or saline (S): prior to impregnation and throughout gestation and lactation periods. On postnatal day 1, pups were cross-fostered so that each mother raised 6 saline-exposed pups and 6 MA-exposed pups. Based on the prenatal and postnatal exposure 4 experimental groups (S/S, S/MA, MA/S, MA/MA) were tested in the Open field (OF) and in the Elevated plus maze (EPM) in adulthood. Locomotion, exploration, immobility and comforting behavior were evaluated in the OF, while anxiety was assessed in the EPM. While prenatal MA exposure did not affect behavior and anxiety in adulthood, postnatal MA exposure (i.e. MA administration to lactating mothers) induced long-term changes. Specifically, adult female rats in diestrus and adult males postnatally exposed to MA via breast milk (S/MA and MA/MA) had decreased locomotion and exploratory behavior in the OF and showed increased anxiety-like behavior in the EPM when compared to female rats in diestrus or males postnatally exposed to saline (S/S and MA/S). In adult females in proestrus, postnatal exposure to MA affected only exploratory behavior in the OF when compared to rats in proestrus postnatally exposed to saline. Thus, the present study shows that postnatal exposure to MA via breast milk impairs behavior in unfamiliar environment and anxiety-like behavior of adult male and female rats more than prenatal MA exposure. PMID:21884713

  10. 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. PMID:26506049

  11. 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.

  12. Postnatal consequences of prenatal cocaine exposure and myocardial apoptosis: does cocaine in utero imperil the adult heart?

    PubMed Central

    Feng, Qingping

    2005-01-01

    Cocaine use is common among pregnant women with a history of substance abuse, and has been shown to cause abnormalities in the heart during fetal and postnatal development. However, mechanisms underlying the detrimental effects of cocaine on the developing heart are not fully understood. In this issue, Bae and Zhang show that prenatal cocaine exposure increases the susceptibility of the postnatal heart to ischemia and reperfusion injury. Their results suggest that myocardial apoptosis induced by cocaine during fetal development may represent one of the mechanisms by which prenatal cocaine exposure exerts its long-term, deleterious consequences on postnatal cardiac function. PMID:15685202

  13. Effects of prenatal and postnatal exposure to GSM-like radiofrequency on blood chemistry and oxidative stress in infant rabbits, an experimental study.

    PubMed

    Ozgur, Elcin; Kismali, Gorkem; Guler, Goknur; Akcay, Aytac; Ozkurt, Guzin; Sel, Tevhide; Seyhan, Nesrin

    2013-11-01

    We aimed to investigate the potential hazardous effects of prenatal and/or postnatal exposure to 1800 MHz GSM-like radiofrequency radiation (RFR) on the blood chemistry and lipid peroxidation levels of infant rabbits. A total of 72 New Zealand female and male white rabbits aged 1-month were used. Thirty-six female and 36 male were divided into four groups which were composed of nine infants: (i) Group 1 were the sham exposure (control), (ii) Group 2 were exposed to RFR, 15 min daily for 7 days in the prenatal period (between 15th and 22nd days of the gestational period) (prenatal exposure group). (iii) Group 3 were exposed to RFR 15 min/day (14 days for male, whereas 7 days for female) after they reached 1-month of age (postnatal exposure group). (iv) Group 4 were exposed to RFR for 15 min daily during 7 days in the prenatal period (between 15th and 22nd days of the gestational period) and 15 min/day (14 days for male, whereas 7 days for female) after they reached 1-month of age (prenatal and postnatal exposure group). Results showed that serum lipid peroxidation level in both female and male rabbits changed due to the RFR exposure. However, different parameters of the blood biochemistry were affected by exposure in male and female infants. Consequently, the whole-body 1800 MHz GSM-like RFR exposure may lead to oxidative stress and changes on some blood chemistry parameters. Studies on RFR exposure during prenatal and postnatal periods will help to establish international standards for the protection of pregnants and newborns from environmental RFR. PMID:23526187

  14. 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.

  15. STUDIES IN SUBCLINICAL LEAD EXPOSURE

    EPA Science Inventory

    The study was initiated to examine the utility of neuropsychologic testing in identifying deficits in children with asymptomatic elevations in blood lead levels. From the files of the Boston Lead Screening Project the authors selected black male children between the ages of six a...

  16. Evaluation and management of lead exposure.

    PubMed

    Kim, Hwan-Cheol; Jang, Tae-Won; Chae, Hong-Jae; Choi, Won-Jun; Ha, Mi-Na; Ye, Byeong-Jin; Kim, Byoung-Gwon; Jeon, Man-Joong; Kim, Se-Yeong; Hong, Young-Seoub

    2015-01-01

    Lead, which is widely used in industry, is a common element found in low concentrations in the Earth's crust. Implementations to reduce environmental lead concentrations have resulted in a considerable reduction of lead levels in the environment (air) and a sustained reduction in the blood lead levels of the average citizen. However, people are still being exposed to lead through a variety of routes in everyday commodities. Lead causes health problems such as toxicity of the liver, kidneys, hematopoietic system, and nervous system. Having a carcinogenic risk as well, the IARC classifies inorganic lead compounds as probably carcinogenic to humans (Group 2A). Occupational lead poisonings have decreased due to the efforts to reduce the lead concentrations in the working environment. In contrast, health hazards associated with long-term environmental exposure to low concentrations of lead have been reported steadily. In particular, chronic exposure to low concentrations of lead has been reported to induce cognitive behavioral disturbances in children. It is almost impossible to remove lead completely from the human body, and it is not easy to treat health hazards due to lead exposure. Therefore, reduction and prevention of lead exposure are very important. We reviewed the toxicity and health hazards, monitoring and evaluation, and management of lead exposure. PMID:26677413

  17. Human lead metabolism: Chronic exposure, bone lead and physiological models

    NASA Astrophysics Data System (ADS)

    Fleming, David Eric Berkeley

    Exposure to lead is associated with a variety of detrimental health effects. After ingestion or inhalation, lead may be taken up from the bloodstream and retained by bone tissue. X-ray fluorescence was used to make in vivo measurements of bone lead concentration at the tibia and calcaneus for 367 active and 14 retired lead smelter workers. Blood lead levels following a labour disruption were used in conjunction with bone lead readings to examine the endogenous release of lead from bone. Relations between bone lead and a cumulative blood lead index differed depending on time of hiring. This suggests that the transfer of lead from blood to bone has changed over time, possibly as a result of varying exposure conditions. A common polymorphism in the δ-aminolevulinate dehydratase (ALAD) enzyme may influence the distribution of lead in humans. Blood lead levels were higher for smelter workers expressing the more rare ALAD2 allele. Bone lead concentrations, however, were not significantly different. This implies that a smaller proportion of lead in blood is distributed to tissue for individuals expressing the ALAD2 allele. The O'Flaherty physiological model of lead metabolism was modified slightly and tested with input from the personal exposure histories of smelter workers. The model results were consistent with observation in tern of endogenous exposure to lead and accumulation of lead in cortical bone. Modelling the calcaneus as a trabecular bone site did not reproduce observed trends. variations in lead metabolism between different trabecular sites may therefore be significant. The model does not incorporate a genetic component, and its output did not reflect observed differences in this respect. This result provides further support for the influence of the ALAD polymorphism on lead metabolism. Experimental trials with a digital spectrometer revealed superior energy resolution and count throughput relative to the conventional X-ray fluorescence system. The associated

  18. International perspectives of lead exposure and lead toxicity.

    PubMed

    Grandjean, P

    1993-01-01

    Three approaches have been used to examine how human body burdens of lead depend on different environments: (1) In paleopathologic studies, lead concentrations have been determined in well-preserved human bones or teeth, and pre-pollution samples generally show lead concentrations of about 1% of current levels in industrialized countries. (2) Geographic comparisons of blood-lead concentrations show low levels in, Nepal, Faroe Islands, and Sweden, while high levels occur in Mexico and Malta; average blood-lead levels may vary by a factor of 10 or more. (3) In analytical epidemiology, major exposure sources have been related to lead levels in blood, by either prospective or cross-sectional design. Increased blood-lead concentrations are related to smoking, drinking alcoholic beverages, eating vegetables for dinner, urban residence, and exposure from lead-using industries; average blood-lead values of subgroups within well-defined populations may vary by a factor of 3 or more. The dose-relationships for lead-induced neurotoxicity will depend on the sensitivity of the parameters chosen as indicators of lead exposure and of neurotoxicity. The temporal relationship between lead exposures and the development of deficits must be ascertained. Individual susceptibility and interacting factors must also be taken into account. Differences in addressing these issues impede the comparison between studies. Recently neonatal jaundice has been found to be a risk factor for subsequent neurobehavioral dysfunction in children with a birth weight above 2500 g, but only in children with increased lead exposure. Lead exposure may act in combination with several other factors and result in additive, or synergistic effects.(ABSTRACT TRUNCATED AT 250 WORDS) PMID:8247415

  19. 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

  20. Spexin is expressed in the carotid body and is upregulated by postnatal hyperoxia exposure.

    PubMed

    Porzionato, Andrea; Rucinski, Marcin; Macchi, Veronica; Stecco, Carla; Sarasin, Gloria; Sfriso, Maria M; Di Giulio, Camillo; Malendowicz, Ludwik K; De Caro, Raffaele

    2012-01-01

    Spexin is a recently identified peptide which is expressed in many different endocrine and nervous tissues. Due to the absence of data regarding spexin expression in the carotid body, the first aim of the present study was to investigate, through immunohistochemistry and Real-Time PCR, the expression and distribution of spexin in the rat and human carotid body. Moreover, the carotid body is known to undergo various structural and functional modifications in response to hyperoxic stimuli during the first postnatal period. Thus, we also evaluated if hyperoxia during the first postnatal weeks may produce changes in the spexin expression. Materials consisted of carotid bodies obtained at autopsy from five human adult subjects and sampled from 10 six-weeks old Sprague-Dawley rats. Five rats were maintained in normoxia for the first six postnatal weeks; five rats were exposed to 60% hyperoxia for 2 weeks and then maintained in normoxia for other 4 weeks. Diffuse anti-spexin immunoreactivity was found in type I cells of both humans and rats. No spexin immunoreactivity was visible in the type II cells. Hyperoxia exposure during the first 2 weeks of postnatal life caused a reduction of volume in the carotid body still apparent after 4 weeks of normoxia. Using real-time PCR, spexin expression was 6-7 times higher in hyperoxia-exposed rats than in normoxia-exposed ones. The expression of spexin in type I cells suggests a possible modulator role in peripheral chemoreception. Moreover, the ascertained role of spexin in the regulation of cell proliferation in other tissues (e.g., adrenal gland cortex) suggests a possible role of spexin also in the hyperoxia-induced plasticity of the carotid body. PMID:23080164

  1. 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. PMID:26957054

  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. Methamphetamine exposure during early postnatal development in rats: I. Acoustic startle augmentation and spatial learning deficits.

    PubMed

    Vorhees, C V; Ahrens, K G; Acuff-Smith, K D; Schilling, M A; Fisher, J E

    1994-04-01

    Methamphetamine (MA) induces neurotransmitter reductions and neurotoxicity at high doses in adult animals, but its effects on early brain development and behavior have received less attention. In this experiment the effects of MA exposure during a period equivalent to the human third trimester were examined. Rats (Sprague-Dawley CD) were injected subcutaneously with d-MA (30 mg/kg b.i.d.) early in postnatal development (days 1-10), later (postnatal days 11-20), or with water during both of these periods. Both early and later MA-exposed offspring exhibited augmented acoustic startle and impaired performance in a complex multiple-T water maze. Only the early MA exposure group showed a persistent deficit in weight while only the later MA exposure group showed impaired learning in the Morris hidden platform maze. Effects on locomoter activity are reported in the accompanying article. It was concluded that the effects of MA are both long lasting and stage dependent and involve cognitive as well as arousal functions. PMID:7855197

  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. PMID:22962062

  5. 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.

  6. 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. PMID:25106748

  7. 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 ...

  8. Oral methylphenidate alleviates the fine motor dysfunction caused by chronic postnatal manganese exposure in adult rats.

    PubMed

    Beaudin, Stéphane A; Strupp, Barbara J; Lasley, Stephen M; Fornal, Casimir A; Mandal, Shyamali; Smith, Donald R

    2015-04-01

    Developmental manganese (Mn) exposure is associated with motor dysfunction in children and animal models, but little is known about the underlying neurochemical mechanisms or the potential for amelioration by pharmacotherapy. We investigated whether methylphenidate (MPH) alleviates fine motor dysfunction due to chronic postnatal Mn exposure, and whether Mn exposure impairs brain extracellular dopamine (DA) and norepinephrine (NE) in the prefrontal cortex (PFC) and striatum in adult animals. Rats were orally exposed to 0 or 50 mg Mn/kg/day from postnatal day 1 until the end of the study (PND 145). The staircase test was used to assess skilled forelimb function. Oral MPH (2.5 mg/kg/day) was administered daily 1 h before staircase testing for 16 days. DA and NE levels were measured by dual probe microdialysis. Results show that Mn exposure impaired reaching and grasping skills and the evoked release of DA and NE in the PFC and striatum of adult rats. Importantly, oral MPH treatment fully alleviated the fine motor deficits in the Mn-exposed animals, but did not affect forelimb skills of control rats not exposed to Mn. These results suggest that catecholaminergic hypofunctioning in the PFC and striatum may underlie the Mn-induced fine motor dysfunction, and that oral MPH pharmacotherapy is an effective treatment approach for alleviating this dysfunction in adult animals. The therapeutic potential of MPH for the treatment of motor dysfunction in Mn-exposed children and adults appears promising pending further characterization of MPH efficacy in other functional areas (eg, attention) believed to be affected by developmental Mn exposure. PMID:25601986

  9. Hypothermia after chronic mild stress exposure in rats with a history of postnatal maternal separations.

    PubMed

    Mrdalj, Jelena; Lundegaard Mattson, Ase; Murison, Robert; Konow Jellestad, Finn; Milde, Anne Marita; Pallesen, Ståle; Ursin, Reidun; Bjorvatn, Bjørn; Grønli, Janne

    2014-03-01

    The circadian system develops and changes in a gradual and programmed process over the lifespan. Early in life, maternal care represents an important zeitgeber and thus contributes to the development of circadian rhythmicity. Exposure to early life stress may affect circadian processes and induce a latent circadian disturbance evident after exposure to later life stress. Disturbance of the normal regulation of circadian rhythmicity is surmised to be an etiological factor in depression. We used postnatal maternal separation in rats to investigate how the early life environment might modify the circadian response to later life unpredictable and chronic stress. During postnatal days 2-14, male Wistar rats (n = 8 per group) were daily separated from their mothers for a period of either 180 min (long maternal separation; LMS) or 10 min (brief maternal separation; BMS). In adulthood, rats were exposed to chronic mild stress (CMS) for 4 weeks. Body temperature, locomotor activity and heart rate were measured and compared before and after CMS exposure. LMS offspring showed a delayed body temperature acrophase compared to BMS offspring. Otherwise, adult LMS and BMS offspring demonstrated similar diurnal rhythms of body temperature, locomotor activity and heart rate. Exposure to CMS provoked a stronger and longer lasting hypothermia in LMS rats than in BMS rats. The thermoregulatory response appears to be moderated by maternal care following reunion, an observation made in the LMS group only. The results show that early life stress (LMS) in an early developmental stage induced a thermoregulatory disturbance evident upon exposure to unpredictable adult life stressors. PMID:24156523

  10. Oral Methylphenidate Alleviates the Fine Motor Dysfunction Caused by Chronic Postnatal Manganese Exposure in Adult Rats

    PubMed Central

    Strupp, Barbara J.; Lasley, Stephen M.; Fornal, Casimir A.; Mandal, Shyamali; Smith, Donald R.

    2015-01-01

    Developmental manganese (Mn) exposure is associated with motor dysfunction in children and animal models, but little is known about the underlying neurochemical mechanisms or the potential for amelioration by pharmacotherapy. We investigated whether methylphenidate (MPH) alleviates fine motor dysfunction due to chronic postnatal Mn exposure, and whether Mn exposure impairs brain extracellular dopamine (DA) and norepinephrine (NE) in the prefrontal cortex (PFC) and striatum in adult animals. Rats were orally exposed to 0 or 50 mg Mn/kg/day from postnatal day 1 until the end of the study (PND 145). The staircase test was used to assess skilled forelimb function. Oral MPH (2.5 mg/kg/day) was administered daily 1 h before staircase testing for 16 days. DA and NE levels were measured by dual probe microdialysis. Results show that Mn exposure impaired reaching and grasping skills and the evoked release of DA and NE in the PFC and striatum of adult rats. Importantly, oral MPH treatment fully alleviated the fine motor deficits in the Mn-exposed animals, but did not affect forelimb skills of control rats not exposed to Mn. These results suggest that catecholaminergic hypofunctioning in the PFC and striatum may underlie the Mn-induced fine motor dysfunction, and that oral MPH pharmacotherapy is an effective treatment approach for alleviating this dysfunction in adult animals. The therapeutic potential of MPH for the treatment of motor dysfunction in Mn-exposed children and adults appears promising pending further characterization of MPH efficacy in other functional areas (eg, attention) believed to be affected by developmental Mn exposure. PMID:25601986

  11. Occupational lead exposure aboard a tall ship

    SciTech Connect

    Landrigan, P.J.; Straub, W.E.

    1985-01-01

    To evaluate occupational exposures to lead in shipfitters cutting and riveting lead-painted iron plates aboard an iron-hulled sailing vessel, the authors conducted an environmental and medical survey. Lead exposures in seven personal (breathing zone) air samples ranged from 108 to 500 micrograms/mT (mean 257 micrograms/mT); all were above the Occupational Safety and Health Administration (OSHA) standard of 50 micrograms/mT. In two short-term air samples obtained while exhaust ventilation was temporarily disconnected, mean lead exposure rose to 547 micrograms/mT. Blood lead levels in ten shipfitters ranged from 25 to 53 micrograms/dl. Blood lead levels in shipfitters were significantly higher than in other shipyard workers. Smoking shipfitters had significantly higher lead levels than nonsmokers. Lead levels in shipfitters who wore respirators were not lower than in those who wore no protective gear. Four shipfitters had erythrocyte protoporphyrin (EP) concentrations above the adult upper normal limit of 50 micrograms/dl. A close correlation was found between blood lead and EP levels. Prevalence of lead-related symptoms was no higher in shipfitters than in other workers. These data indicate that serious occupational exposure to lead can occur in a relatively small boatyard.

  12. 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

  13. Docosahexaenoic Acid Rescues Synaptogenesis Impairment and Long-Term Memory Deficits Caused by Postnatal Multiple Sevoflurane Exposures

    PubMed Central

    Tao, Guorong; Luo, Yan; Xue, Qingsheng; Li, Guohui; Tan, Yongchang

    2016-01-01

    Sevoflurane exposures were demonstrated to induce neurotoxicity in the developing brain in both human and animal studies. However, there is no effective approach to reverse it. The present study aimed to evaluate the feasibility of utilizing docosahexaenoic acid (DHA) to prevent sevoflurane-induced neurotoxicity. P6 (postnatal 6 days) mice were administrated DHA after exposure to 3% sevoflurane for two hours daily in three consecutive days. Molecular expressions of synaptic makers (PSD95, synaptophysin) and synaptic morphological changes were investigated by Western blot analysis and transmission electron microscopy, respectively. Meanwhile, Morris water maze test was used to assess spatial memory of mice at P31 (postnatal 31 days). DHA restored sevoflurane-induced decreased level of PSD95 and synaptophysin expressions and increased PSD areas and also improved long-term spatial memory. These results suggest that DHA could rescue synaptogenesis impairment and long-term memory deficits in postnatal caused by multiple sevoflurane exposures. PMID:27597963

  14. Docosahexaenoic Acid Rescues Synaptogenesis Impairment and Long-Term Memory Deficits Caused by Postnatal Multiple Sevoflurane Exposures.

    PubMed

    Tao, Guorong; Luo, Yan; Xue, Qingsheng; Li, Guohui; Tan, Yongchang; Xiao, Jinglei; Yu, Buwei

    2016-01-01

    Sevoflurane exposures were demonstrated to induce neurotoxicity in the developing brain in both human and animal studies. However, there is no effective approach to reverse it. The present study aimed to evaluate the feasibility of utilizing docosahexaenoic acid (DHA) to prevent sevoflurane-induced neurotoxicity. P6 (postnatal 6 days) mice were administrated DHA after exposure to 3% sevoflurane for two hours daily in three consecutive days. Molecular expressions of synaptic makers (PSD95, synaptophysin) and synaptic morphological changes were investigated by Western blot analysis and transmission electron microscopy, respectively. Meanwhile, Morris water maze test was used to assess spatial memory of mice at P31 (postnatal 31 days). DHA restored sevoflurane-induced decreased level of PSD95 and synaptophysin expressions and increased PSD areas and also improved long-term spatial memory. These results suggest that DHA could rescue synaptogenesis impairment and long-term memory deficits in postnatal caused by multiple sevoflurane exposures. PMID:27597963

  15. 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. PMID:23935717

  16. Lead exposures from varnished floor refinishing.

    PubMed

    Schirmer, Joseph; Havlena, Jeff; Jacobs, David E; Dixon, Sherry; Ikens, Robert

    2012-01-01

    We evaluated the presence of lead in varnish and factors predicting lead exposure from floor refinishing and inexpensive dust suppression control methods. Lead in varnish, settled dust, and air were measured using XRF, laboratory analysis of scrape and wipe samples, and National Institute for Occupational Safety and Health (NIOSH) Method 7300, respectively, during refinishing (n = 35 homes). Data were analyzed using step-wise logistic regression. Compared with federal standards, no lead in varnish samples exceeded 1.0 mg/cm(2), but 52% exceeded 5000 ppm and 70% of settled dust samples after refinishing exceeded 40 μg/ft(2). Refinishing pre-1930 dwellings or stairs predicted high lead dust on floors. Laboratory analysis of lead in varnish was significantly correlated with airborne lead (r = 0.23, p = 0.014). Adding dust collection bags into drum sanders and HEPA vacuums to edgers and buffers reduced mean floor lead dust by 8293 μg Pb/ft(2) (p<0.05) on floors and reduced most airborne lead exposures to less than 50 μg/m(3). Refinishing varnished surfaces in older housing produces high but controllable lead exposures. PMID:22494405

  17. Prenatal nicotine exposure alters postnatal cardiorespiratory integration in young male but not female rats

    PubMed Central

    Boychuk, Carie R.; Hayward, Linda F.

    2011-01-01

    The present study tested the hypothesis that prenatal nicotine exposure (PNE) induces sex specific alternations in indices of cardiorespiratory coupling during early development. Rat pups exposed to either nicotine (6mg/kg/day) or saline (control) in utero were chronically instrumented with ECG electrodes for measurement of heart rate (HR) and respiratory frequency (RF) was monitored by whole body plethysmography on postnatal days (P)13, P16 and P26. PNE had no identifiable effect on resting respiratory frequency (RF) in either sex. There was however a strong trend (p=0.057) for resting HR to be elevated by PNE in male offspring only. Alternatively, the HR response to hypoxia (10% O2), was significantly blunted at P13 but significantly elevated at P26 s in the absence of any significant change in RF in PNE males only. Indicators of respiratory sinus arrhythmia (RSA) were also significantly reduced in P26 PNE males. No significant effects of PNE on HR, RF or RSA were identified in female offspring at any age. Our results demonstrate that PNE induces very specific changes in cardiorespiratory integration at select postnatal ages and these changes are more prominent in males. Additionally, alternations in cardiorespiratory integration appear to persist into later development in males only, potentially increasing the risk for cardiovascular diseases such as hypertension later in life. PMID:21945005

  18. 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. PMID:26960969

  19. 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.

  20. 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

  1. Early Postnatal Parathion Exposure in Rats Causes Sex-Selective Cognitive Impairment and Neurotransmitter Defects Which Emerge in Aging

    PubMed Central

    Levin, Edward D.; Timofeeva, Olga A.; Yang, Liwei; Petro, Ann; Ryde, Ian T.; Wrench, Nicola; Seidler, Frederic J.; Slotkin, Theodore A.

    2010-01-01

    Developmental exposure of rats to the organophosphate (OP) pesticides leads to altered neurobehavioral function in juvenile and young adult stages. The current study was conducted to determine whether effects of neonatal parathion exposure on cognitive performance persist in older adult and aged rats, and the relationship of behavioral changes to underlying cholinergic and serotonergic mechanisms. We administered parathion to rat pups on postnatal days 1–4, at doses spanning the threshold for the initial signs of systemic toxicity and for barely-detectable cholinesterase inhibition (0.1 or 0.2 mg/kg/day). Beginning at 14 months of age and continuing until 19 months, the rats were trained in the 16-arm radial maze. Controls showed the normal sex difference in this spatial learning and memory task, with the males committing significantly fewer working memory errors than females. Neonatal parathion exposure eliminated the sex difference primarily by causing impairment in males. In association with the effects on cognitive performance, neonatal parathion exposure elicited widespread abnormalities in indices of serotonergic and cholinergic synaptic function, characterized by upregulation of 5HT2 receptors and the 5HT transporter, deficits in choline acetyltransferase activity and nicotinic cholinergic receptors, and increases in hemicholinium-3 binding to the presynaptic choline transporter. Within-animal correlations between behavior and neurochemistry indicated a specific correlation between working memory performance and hippocampal hemicholinium-3 binding; parathion exposure destroyed this relationship. Like the behavioral effects, males showed greater effects of parathion on neurochemical parameters. This study demonstrates the sex-selective, long-term behavioral alterations caused by otherwise nontoxic neonatal exposure to parathion, with effects persisting into the beginning of senescence. PMID:20015457

  2. Adolescent Initiation of Licit and Illicit Substance Use: Impact of Intrauterine Exposures and Post-natal Exposure to Violence

    PubMed Central

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

    2010-01-01

    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 postnatal 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. PMID:20600847

  3. 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. PMID:25112558

  4. 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

  5. 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. PMID:2773946

  6. Early postnatal oestradiol exposure causes insulin resistance and signs of inflammation in circulation and skeletal muscle.

    PubMed

    Alexanderson, Camilla; Eriksson, Elias; Stener-Victorin, Elisabet; Lönn, Malin; Holmäng, Agneta

    2009-04-01

    Early postnatal events can predispose to metabolic and endocrine disease in adulthood. In this study, we evaluated the programming effects of a single early postnatal oestradiol injection on insulin sensitivity in adult female rats. We also assessed the expression of genes involved in inflammation and glucose metabolism in skeletal muscle and adipose tissue and analysed circulating inflammation markers as possible mediators of insulin resistance. Neonatal oestradiol exposure reduced insulin sensitivity and increased plasma levels of monocyte chemoattractant protein-1 (MCP-1) and soluble intercellular adhesion molecule-1. In skeletal muscle, oestradiol increased the expression of genes encoding complement component 3 (C3), Mcp-1, retinol binding protein-4 (Rbp4) and transforming growth factor beta1 (Tgfbeta1). C3 and MCP-1 are both related to insulin resistance, and C3, MCP-1 and TGFbeta1 are also involved in inflammation. Expression of genes encoding glucose transporter-4 (Glut 4), carnitine-palmitoyl transferase 1b (Cpt1b), peroxisome proliferator-activated receptor delta (Ppard) and uncoupling protein 3 (Ucp3), which are connected to glucose uptake, lipid oxidation, and energy uncoupling, was down regulated. Expression of several inflammatory genes in skeletal muscle correlated negatively with whole-body insulin sensitivity. In s.c. inguinal adipose tissue, expression of Tgfbeta1, Ppard and C3 was decreased, while expression of Rbp4 and Cpt1b was increased. Inguinal adipose tissue weight was increased but adipocyte size was unaltered, suggesting an increased number of adipocytes. We suggest that early neonatal oestrogen exposure may reduce insulin sensitivity by inducing chronic, low-grade systemic and skeletal muscle inflammation and disturbances of glucose and lipid metabolism in skeletal muscle in adulthood. PMID:19193715

  7. Developmental alterations in olivary climbing fiber distribution following postnatal ethanol exposure in the rat.

    PubMed

    Pierce, D R; Hayar, A; Williams, D K; Light, K E

    2010-09-01

    Ethanol exposure during postnatal days (PN) 4-6 in rats alters cerebellar development resulting in significant loss of Purkinje cells. There is little knowledge, however, on what happens to the neurons that survive. In this study, rat pups were treated with a daily dose of ethanol (either 3.6 or 4.5 g/kg body weight) delivered by intragastric intubation on PN4, PN4-6, or PN7-9. Then the interactions between climbing fibers and Purkinje cells were examined on PN14 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 in the PN4 and PN4-6 ethanol groups for the 4.5 g/kg dose level, compared to controls, indicating that the cerebellar circuitry was significantly altered following developmental ethanol exposure. Not only were there fewer Purkinje cells following ethanol exposure, but the surviving neurons had significantly fewer VGluT2-labeled synapses. These alterations in the synaptic integrity were both dose dependent and temporally dependent. PMID:20542091

  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. PMID:25242292

  9. 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…

  10. 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…

  11. POSTNATAL METHYL MERCURY EXPOSURE: EFFECTS ON ONTOGENY OF RENAL AND HEPATIC ORNITHINE DECARBOXYLASE RESPONSES TO TROPHIC STIMULI

    EPA Science Inventory

    The effects of postnatal methylmercury exposure on the ongoteny of kidney and liver responsiveness to trophic stimuli were examined. Increased ornithine decarboxylase (ODC) activity was used as an index of tissue stimulation. In the rat, kidney ODC responsiveness to growth hormon...

  12. 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

  13. AUDITORY AND VISUAL DYSFUNCTION FOLLOWING LEAD EXPOSURE

    EPA Science Inventory

    The effects of lead exposure on cognitive function have been intensively studied during the past decade, but relatively little effort has been made to understand the impact on sensory function. Subtle impairments of visual and/or auditory processing, however, could have profound ...

  14. 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. PMID:25087065

  15. Exposure to lead affects male biothiols metabolism.

    PubMed

    Kasperczyk, Sławomir; Błaszczyk, Iwona; Dobrakowski, Michał; Romuk, Ewa; Kapka-Skrzypczak, Lucyna; Adamek, Mariusz; Birkner, Ewa

    2013-01-01

    The most important biothiols include glutathione, homocysteine (HCY), cysteine and proteins. The aim of the presented study was to evaluate the influence of lead on the biothiol turnover--the concentration of HCY and protein sulfhydryl groups (P-SH) in the serum and reduced glutathione (G-SH) in erythrocytes--in individuals (employees of metal works) exposed to lead and to evaluate its probable oxidative disorders, measured as the carbonyl protein (CP) concentration in serum. The exposed workers were divided into 2 subgroups: 1) low lead exposure (LPb), with a lead concentration in the blood (PbB) of 20-45 µg dl(-1) (n= 102), and 2) high lead exposure (HPb), with PbB = 45-60 µg dl(-1) (n= 81). The control group consisted of 72 office workers or other healthy subjects with no history of occupational exposure to lead. All the controls had normal PbB (<10 μg dl(-1)) and ZPP (<2.5 μg dl(-1)) levels. The concentration of HCY was higher in the LPb group by 11% and in the HPb group by 26%, compared with the control group (n=72). The CP concentration in these 2 groups was more than twice as high as that of the control group, with 108% and 125% increases for the LPb and HPb groups, respectively; G-SH was lower by 6.6% and 7.4% for the LPb and HPb groups, respectively; P-SH was lower by 8.2% and 13% for the LPb and HPb groups, respectively. Lead decreases levels of glutathione and protein thiol groups. Lead-induced oxidative stress contributes to the observed elevation of protein carbonyl groups. Besides, lead poisoning seems to be associated with hyperhomocysteinaemia, which may promote the development of atherosclerosis. PMID:24364442

  16. Postnatal manganese exposure alters dopamine transporter function in adult rats: Potential impact on nonassociative and associative processes.

    PubMed

    McDougall, S A; Reichel, C M; Farley, C M; Flesher, M M; Der-Ghazarian, T; Cortez, A M; Wacan, J J; Martinez, C E; Varela, F A; Butt, A E; Crawford, C A

    2008-06-23

    In the present study, we examined whether exposing rats to a high-dose regimen of manganese chloride (Mn) during the postnatal period would depress presynaptic dopamine functioning and alter nonassociative and associative behaviors. To this end, rats were given oral supplements of Mn (750 microg/day) on postnatal days (PD) 1-21. On PD 90, dopamine transporter (DAT) immunoreactivity and [3H]dopamine uptake were assayed in the striatum and nucleus accumbens, while in vivo microdialysis was used to measure dopamine efflux in the same brain regions. The effects of postnatal Mn exposure on nigrostriatal functioning were evaluated by assessing rotorod performance and amphetamine-induced stereotypy in adulthood. In terms of associative processes, both cocaine-induced conditioned place preference (CPP) and sucrose-reinforced operant responding were examined. Results showed that postnatal Mn exposure caused persistent declines in DAT protein expression and [3H]dopamine uptake in the striatum and nucleus accumbens, as well as long-term reductions in striatal dopamine efflux. Rotorod performance did not differ according to exposure condition, however Mn-exposed rats did exhibit substantially more amphetamine-induced stereotypy than vehicle controls. Mn exposure did not alter performance on any aspect of the CPP task (preference, extinction, or reinstatement testing), nor did Mn affect progressive ratio responding (a measure of motivation). Interestingly, acquisition of a fixed ratio task was impaired in Mn-exposed rats, suggesting a deficit in procedural learning. In sum, these results indicate that postnatal Mn exposure causes persistent declines in various indices of presynaptic dopaminergic functioning. Mn-induced alterations in striatal functioning may have long-term impact on associative and nonassociative behavior. PMID:18485605

  17. 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.

  18. Effects of Low Level Lead Exposure on Associative Learning and Memory in the Rat: Influences of Sex and Developmental Timing Of Exposure

    PubMed Central

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

    2016-01-01

    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. PMID:26812500

  19. 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. PMID:26812500

  20. 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.

  1. 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. PMID:26391019

  2. Prenatal exposure to maternal voluntary exercise during pregnancy provides protection against mild chronic postnatal hypoxia in rat offspring.

    PubMed

    Akhavan, Maziar Mohammad; Foroutan, Tahereh; Safari, Manouchehr; Sadighi-Moghaddam, Bizhan; Emami-Abarghoie, Mitra; Rashidy-Pour, Ali

    2012-01-01

    Postnatal hypoxia is a main cause of neuronal damage in newborn. However, our understanding of the possible preventive or therapeutic methods to reduce the harmful effects of hypoxia is still primary. Pregnant rats were provided with running wheels during their pregnancy. On PND4 (postnatal day 4)to PND8, the rat pups were exposed to postnatal chronic hypoxia (11% O(2), 89% N(2)) in an air-tight plastic chamber for a period of six hours per day. The number of neurons and also angiogenesis in hippocampus were studied. Postnatal exposure to mild hypoxia decreased the number of the neurons in all studied regions of the hippocampus CA1, CA3 (cornu ammonis), DG(dentate gyrus) and SUB(cubiculum) in rat pups. In other words the number of the neurons in rat pups born from voluntary exercise group was not significantly less than control group in CA1, CA3 and DG regions. So maternal Voluntary exercise during pregnancy increases the blood vessel density in the DG region of the hippocampus of the rat pups. In this study for the first time we provide evidences that show the protective effect of maternal voluntary exercise during pregnancy on rat offspring against postnatal hypoxia. We revealed that maternal exercise during pregnancy increases the hippocampal neuron number and angiogenesis in offspring. PMID:22186335

  3. 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.

  4. Olivary climbing fiber alterations in PN40 rat cerebellum following postnatal ethanol exposure.

    PubMed

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

    2011-03-10

    Developmental ethanol exposure in rats during postnatal days (PN) 4-6 is known to cause significant loss of the 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 (4.5g/kg body weight) delivered by intragastric intubation on PN4, PN4-6, or PN7-9. The interactions between the climbing fibers and the 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

  5. Postnatal manganese exposure does not alter dopamine autoreceptor sensitivity in adult and adolescent male rats.

    PubMed

    McDougall, Sanders A; Mohd-Yusof, Alena; Kaplan, Graham J; Abdulla, Zuhair I; Lee, Ryan J; Crawford, Cynthia A

    2013-04-15

    Administering manganese chloride (Mn) to rats on postnatal day (PD) 1-21 causes long-term reductions in dopamine transporter levels in the dorsal striatum, as well as a persistent increase in D1 and D2 receptor concentrations. Whether dopamine autoreceptors change in number or sensitivity is uncertain, although D2S receptors, which may be presynaptic in origin, are elevated in Mn-exposed rats. The purpose of this study was to determine if early Mn exposure causes long-term changes in dopamine autoreceptor sensitivity that persist into adolescence and adulthood. To this end, male rats were exposed to Mn on PD 1-21 and autoreceptor functioning was tested 7 or 70 days later by measuring (a) dopamine synthesis (i.e., DOPA accumulation) in the dorsal striatum after quinpirole or haloperidol treatment and (b) behavioral responsiveness after low-dose apomorphine treatment. Results showed that low doses (i.e., "autoreceptor" doses) of apomorphine (0.06 and 0.12 mg/kg) decreased the locomotor activity of adolescent and adult rats, while higher doses increased locomotion. The dopamine synthesis experiment also produced classic autoreceptor effects, because quinpirole decreased dorsal striatal DOPA accumulation; whereas, haloperidol increased DOPA levels in control rats, but not in rats given the nerve impulse inhibitor γ-butyrolactone. Importantly, early Mn exposure did not alter autoreceptor sensitivity when assessed in early adolescence or adulthood. The lack of Mn-induced effects was evident in both the dopamine synthesis and behavioral experiments. When considered together with past studies, it is clear that early Mn exposure alters the functioning of various dopaminergic presynaptic mechanisms, while dopamine autoreceptors remain unimpaired. PMID:23458069

  6. Postnatal manganese exposure does not alter dopamine autoreceptor sensitivity in adult and adolescent male rats

    PubMed Central

    McDougall, Sanders A.; Mohd-Yusof, Alena; Kaplan, Graham J.; Abdulla, Zuhair I.; Lee, Ryan J.; Crawford, Cynthia A.

    2013-01-01

    Administering manganese chloride (Mn) to rats on postnatal day (PD) 1–21 causes long-term reductions in dopamine transporter levels in the dorsal striatum, as well as persistent increases in D1 and D2 receptor concentrations. Whether dopamine autoreceptors change in number or sensitivity is uncertain, although D2S receptors, which may be presynaptic in origin, are elevated in Mn-exposed rats. The purpose of this study was to determine if early Mn exposure causes long-term changes in dopamine autoreceptor sensitivity that persist into adolescence and adulthood. To this end, male rats were exposed to Mn on PD 1–21 and autoreceptor functioning was tested 7 or 70 days later by measuring (a) dopamine synthesis (i.e., DOPA accumulation) in the dorsal striatum after quinpirole or haloperidol treatment and (b) behavioral responsiveness after low-dose apomorphine treatment. Results showed that low doses (i.e., “autoreceptor” doses) of apomorphine (0.06 and 0.12 mg/kg) decreased the locomotor activity of adolescent and adult rats, while higher doses increased locomotion. The dopamine synthesis experiment also produced classic autoreceptor effects, because quinpirole decreased dorsal striatal DOPA accumulation; whereas, haloperidol increased DOPA levels in control rats, but not in rats given the nerve impulse inhibitor γ-butyrolactone. Importantly, early Mn exposure did not alter autoreceptor sensitivity when assessed in early adolescence or adulthood. The lack of Mn-induced effects was evident in both the dopamine synthesis and behavioral experiments. When considered together with past studies, it is clear that early Mn exposure alters the functioning of various dopaminergic presynaptic mechanisms, while dopamine autoreceptors remain unimpaired. PMID:23458069

  7. 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

  8. Stress exposure in early post-natal life reduces telomere length: an experimental demonstration in a long-lived seabird

    PubMed Central

    Herborn, Katherine A.; Heidinger, Britt J.; Boner, Winnie; Noguera, Jose C.; Adam, Aileen; Daunt, Francis; Monaghan, Pat

    2014-01-01

    Exposure to stressors early in life is associated with faster ageing and reduced longevity. One important mechanism that could underlie these late life effects is increased telomere loss. Telomere length in early post-natal life is an important predictor of subsequent lifespan, but the factors underpinning its variability are poorly understood. Recent human studies have linked stress exposure to increased telomere loss. These studies have of necessity been non-experimental and are consequently subjected to several confounding factors; also, being based on leucocyte populations, where cell composition is variable and some telomere restoration can occur, the extent to which these effects extend beyond the immune system has been questioned. In this study, we experimentally manipulated stress exposure early in post-natal life in nestling European shags (Phalacrocorax aristotelis) in the wild and examined the effect on telomere length in erythrocytes. Our results show that greater stress exposure during early post-natal life increases telomere loss at this life-history stage, and that such an effect is not confined to immune cells. The delayed effects of increased telomere attrition in early life could therefore give rise to a ‘time bomb’ that reduces longevity in the absence of any obvious phenotypic consequences early in life. PMID:24648221

  9. Transient postnatal fluoxetine leads to decreased brain arachidonic acid metabolism and cytochrome P450 4A in adult mice

    PubMed Central

    Ramadan, Epolia; Blanchard, Helene; Cheon, Yewon; Fox, Meredith A.; Chang, Lisa; Chen, Mei; Ma, Kaizong; Rapoport, Stanley I.; Basselin, Mireille

    2014-01-01

    Fetal and perinatal exposure to selective serotonin (5-HT) reuptake inhibitors (SSRIs) has been reported to alter childhood behavior, while transient early exposure in rodents is reported to alter their behavior and decrease brain extracellular 5-HT in adulthood. Since 5-HT2A/2C receptor-mediated neurotransmission can involve G-protein coupled activation of cytosolic phospholipase A2 (cPLA2), releasing arachidonic acid (ARA) from synaptic membrane phospholipid, we hypothesized that transient postnatal exposure to fluoxetine would decrease brain ARA metabolism in adult mice. Brain ARA incorporation coefficients k* and rates Jin were quantitatively imaged following intravenous [1-14C]ARA infusion of unanesthetized adult mice that had been injected daily with fluoxetine (10 mg/kg i.p.) or saline during postnatal days P4–P21. Expression of brain ARA metabolic enzymes and other relevant markers also was measured. On neuroimaging, k* and Jin was decreased widely in early fluoxetine- compared to saline-treated adult mice. Of the enzymes measured, cPLA2 activity was unchanged, while Ca2+-independent iPLA2 activity was increased. There was a significant 74% reduced protein level of cytochrome P450 (CYP) 4A, which can convert ARA to 20-HETE. Reduced brain ARA metabolism in adult mice transiently exposed to postnatal fluoxetine, and a 74% reduction in CYP4A protein, suggest long-term effects independent of drug presence in brain ARA metabolism, and in CYP4A metabolites. Comparable changes in humans might contribute to reported altered behavior following early SSRI. PMID:24529827

  10. 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

  11. 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

  12. Postnatal Isoflurane Exposure Induces Cognitive Impairment and Abnormal Histone Acetylation of Glutamatergic Systems in the Hippocampus of Adolescent Rats.

    PubMed

    Liang, Bing; Fang, Jie

    2016-09-01

    Isoflurane can elicit cognitive impairment. However, the pathogenesis in the brain remains inconclusive. The present study investigated the mechanism of glutamate neurotoxicity in adolescent male rats that underwent postnatal isoflurane exposure and the role of sodium butyrate (NaB) in cognitive impairment induced by isoflurane exposure. Seven-day-old rats were exposed to 1.7 % isoflurane for 35 min every day for four consecutive days, and then glutamate neurotoxicity was examined in the hippocampus. Morris water maze analysis showed cognitive impairments in isoflurane-exposed rats. High-performance liquid chromatography found higher hippocampal glutamate concentrations following in vitro and in vivo isoflurane exposure. The percentage of early apoptotic hippocampal neurons was markedly increased after isoflurane exposure. Decreased acetylation and increased HDAC2 activity were observed in the hippocampus of isoflurane-exposed rats and hippocampal neurons. Furthermore, postnatal isoflurane exposure decreased histone acetylation of hippocampal neurons in the promoter regions of GLT-1 and mGLuR1/5, but not mGLuR2/3. Treatment with NaB not only restored the histone acetylation of the GLT-1 and mGLuR1/5 promoter regions and glutamate excitatory neurotoxicity in hippocampal neurons, but also improved cognitive impairment in vivo. Moreover, NaB may be a potential therapeutic drug for cognitive impairment caused by isoflurane exposure. These results suggest that postnatal isoflurane exposure contributes to cognitive impairment via decreasing histone acetylation of glutamatergic systems in the hippocampus of adolescent rats. PMID:27307148

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

    PubMed

    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

  14. 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

  15. Exterior surface dust lead, interior house dust lead and childhood lead exposure in an urban environment

    SciTech Connect

    Bornschein, R.L.; Succop, P.A.; Krafft, K.M.; Clark, C.S.; Peace, B.; Hammond, P.B.

    1986-01-01

    The impact of urban lead exposure is being examined in a prospective study of several hundred children followed from birth to five years of age. A wide range of social, behavioral, biological and environmental factors are being assessed at approximately one year intervals beginning at birth. Previous analyses on this cohort have indicated a strong relationship between hand lead and hand-to-mouth activity and suggests that this is an important mechanism of inadvertent ingestion of lead in infants and young children. The present analyses was undertaken to examine the joint influence of lead in exterior surface dust and interior lead-containing painted surfaces on lead levels in house dust. In addition the joint influence of exterior and interior surface dust lead on children's hand lead content and blood lead concentration was examined. At 18 months of age 38% of the observed variation in blood lead was accounted for by hand lead and dust lead. Interior paint lead and exterior surface dust lead accounted for 52% of the observed variation in interior surface dust lead concentration. Exterior surface dust lead, obtained from exterior surface scrapings, indirectly influenced blood lead through its impact on interior house dust lead and children's hand lead content, but had no observable direct impact on blood lead. 13 references, 4 figures, 3 tables.

  16. Long-term behavioral effects in a rat model of prolonged postnatal morphine exposure.

    PubMed

    Craig, Michael M; Bajic, Dusica

    2015-10-01

    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 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 (10 mg/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 nonstressful testing (locomotor activity recording and a novel-object recognition test) at a young age (Postnatal Days [PDs] 27-31) or later in adulthood (PDs 55-56), 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, but 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

  17. Tooth analyses of sources and intensity of lead exposure in children.

    PubMed Central

    Gulson, B L

    1996-01-01

    The sources and intensity of lead exposure in utero and in early childhood were determined using stable lead isotopic ratios and lead concentrations of incisal and cervical sections of deciduous teeth from 30 exposed and nonexposed children from the Broken Hill lead mining community in Australia. Incisal sections, consisting mostly of enamel, generally have low amounts of lead and isotopic compositions consistent with those expected in the mother during pregnancy. Cervical sections, consisting mostly of dentine with secondary dentine removed by resorption and reaming, generally have higher amounts of lead than the enamel and isotopic compositions consistent with the source of postnatal exposure. There are statistically significant differences in lead concentrations between incisal and cervical sections, representing within-tooth variation, for children with low and high lead exposure (p = 0.0007, 2 x 10(-6), respectively) and for those who have ingested leaded paint (p = 0.009). Statistically significant differences between incisal and cervical sections in these three exposure groups are also exhibited by the three sets of lead isotope ratios (e.g., p = 0.001 for 206Pb/204Pb ratio in the low exposure group). There are statistically significant differences between the low and high lead exposure groups for lead concentrations and isotopic ratios in incisal (p = 0.005 for lead concentration and 6 x 10(-6) for 206Pb/204Pb ratio) and cervical sections (p = 5 x 10(-5) for lead concentration and 6 x 10(-6) for 206Pb/204Pb ratio). The dentine results reflect an increased exposure to lead from the lead-zinc-silver mineral deposit (orebody lead) during early childhood, probably associated with hand-to-mouth activity. Leaded paint was identified as the source of elevated tooth lead in at least two cases. Increased exposure to lead from orebody and paint sources in utero was implicated in two cases, but there was no indication of previous exposure from the mothers' current

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

    PubMed

    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;Fam20B(fl/fl) mice, indicating that FAM20B-catalyzed proteoglycans regulate postnatal endochondral ossification partially through the mediation of WNT signaling. PMID:27405802

  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. Postnatal Exposure to Sodium Arsenite (NaAsO2) Induces Long Lasting Effects in Rat Testes

    PubMed Central

    Kaushal, Parul; Dhar, Pushpa; Shivaprasad, Somesh Meludurga; Mehra, Raj D.

    2012-01-01

    Objective: The present study was undertaken to investigate the effects of early postnatal exposure to sodium arsenite (NaAsO2) on rat testis. Materials and Methods: Wistar rat pups were administered aqueous solution of NaAsO2, 1.5 mg/kg body weight (bw) (experimental) and distilled water (control), respectively, by intraperitoneal route (i.p.) from postnatal day (PND) 1 to 14. Testes were collected after 1, 7 and 36 days (at PND 15, 21 and 50) after the treatment period (PND1-14) from the animals and immersion fixed in Bouin's fluid followed by paraffin embedding. Seven micrometer thick serial sections were cut and stained with hematoxylin and eosin for light microscopic observations. At PND 50, morphological features of sperms and their counting was carried out besides processing the perfusion-fixed testes for electron microscopy (EM). Results and Conclusions: The observations revealed an altered morphology of the seminiferous tubules (ST) along with degeneration and dissociation of spermatogenic cells in the experimental animals at PND 15, 21 and 50. Also, increased number of sperms with abnormal morphology and decreased sperm count was noted in the experimental animals. These features together with electron microscopic observations of abnormal mitochondria and apoptotic nuclei of spermatogonia and spermatocytes could be indicative of long-lasting adverse effects on the rat testis induced by exposure to As during early postnatal period. PMID:22778523

  1. 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

  2. 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.

  3. Postnatal overnutrition in mice leads to impaired pulmonary mechanics in response to salbutamol.

    PubMed

    Teixeira, Vanessa P; Cervilha, Daniela A B; Cabral, Layla D M; Oliveira, Luiz M; Incerpi, Erika K; Novaes, Rômulo D; Ionta, Marisa; Soncini, Roseli

    2016-05-01

    Obesity increases the risk of respiratory disease, which is associated with airway hyperresponsiveness. Although the molecular underpinnings of this phenomenon are not well established, lung remodeling is known as an important factor in this process and could potentially explain compromised lung functions. In the present study, the obesity was induced by postnatal overnutrition in Swiss mice and we investigated the pulmonary mechanics after aerosolization of saline, methacholine, and salbutamol. The lungs were prepared for morphometric analysis. Obese animals showed bronchoconstriction in response to methacholine, as evidenced by airway and tissue resistance, tissue elastance, and hysteresivity. Salbutamol was effective at recovering the response only for airway resistance but not for tissue mechanics. We suggest that this impaired response in obese mice is related to collapsed alveolar, to inflammatory cells, and to elevated deposition collagen fibers in parenchymal tissue. PMID:26497334

  4. Lead exposure in students in Mexico City.

    PubMed

    Alvear Galindo, M G; Carreón García, J; Moreno Altamirano, A; Cuéllar López, J A; Kimura, L Y

    1994-10-01

    The present study was done between 1989 and 1991 and performed on 263 children 7 to 9 years of age who lived in Mexico City. The goal was to determine the association between risk factors entering the body through the respiratory or digestive path and lead concentration in deciduous teeth. Exposure to risk factors was surveyed through a questionnaire; lead was determined by atomic absorption spectrophotometry with a graphite oven and reported in microgram Pb/g tooth. Statistical significance was found for the habit of sucking toys OR 4.98 (IC 95% 1.23-28.67), the use of glazed earthenware utensils for the preparation and serving of food and drinks OR 2.47 (IC 0.80-8.47), and the ingestion of tinned food, particularly juices OR 3.31 (IC 1.03-12.50). No positive results were found for risk factors involving the respiratory path. A possible explanation for these results is a different risk level for each of the two paths of access. PMID:7529159

  5. 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

  6. 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.

  7. 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 ...

  8. SEPARATE AND JOINT EFFECTS OF TRANPLACENTAL AND POSTNATAL INHALATORY EXPOSURE TO POLYCYCLIC AROMATIC HYDROCARBONS. PROSPECTIVE BIRTH COHORT STUDY ON WHEEZING EVENTS

    PubMed Central

    Jedrychowski, Wiesław A.; Perera, Frederica P.; Majewska, Renata; Camman, David; Spengler, John D.; Mroz, Elzbieta; Stigter, Laura; Flak, Elżbieta; Jacek, Ryszard

    2014-01-01

    The goal of this epidemiologic investigation was to analyze the associations between prenatal and postnatal exposure to airborne polycyclic aromatic hydrocarbons (PAH) and severity of wheeze and recurrent wheeze. The 257 children included in this analysis had a complete set of prenatal and postnatal PAH measurements and attended regular health checkups over a four-year follow-up period since birth. Transplacental PAH exposure was measured by personal air monitoring of the mothers during the second trimester of pregnancy; postnatal exposure was estimated using the same instruments indoors at the children’s’ residences at age 3. Chemical analysis tests were performed to determine airborne concentrations of nine PAH compounds. The results show that both prenatal and postnatal exposure were associated positively with the severity of wheezing days and recurrent wheezing reported in the follow-up. While the IRR (incidence rate ratio) for severity of wheeze and prenatal PAH exposure was 1.53 (95%CI: 1.43 – 1.64) that for postnatal PAH exposure was 1.13 (95%CI: 1.08 – 1.19). However, recurrent wheezing was more strongly associated with airborne PAH levels measured at age 3 (OR= 2.31, 95%CI: 1.26 – 4.22) than transplacental PAH exposure (OR = 1.40, 95% CI: 0.85 – 2.09), but the difference was statistically insignificant. In conclusion, it appears that prenatal PAH exposure may precipitate and intensify early onset of wheezing symptoms in childhood, resulting from the postnatal exposure and suggest that success in reducing the incidence of respiratory diseases in children would depend on reducing both fetal and childhood exposure to air pollution. PMID:24155203

  9. 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

  10. 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.

  11. 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.

  12. 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

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

    PubMed

    Merrill, Loren; Grindstaff, Jennifer L

    2015-03-01

    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 28days post-hatch. When offspring were at least 18months 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

  14. 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

  15. Prenatal and Early Postnatal Exposure to Cigarette Smoke Decreases BDNF/TrkB Signaling and Increases Abnormal Behaviors Later in Life

    PubMed Central

    Xiao, Lan; Kish, Vincent L.; Benders, Katherine M.

    2016-01-01

    Background: Cigarette smoke exposure during prenatal and early postnatal periods increases the incidence of a variety of abnormal behaviors later in life. The purpose of this study was to identify the possible critical period of susceptibility to cigarette smoke exposure and evaluate the possibe effects of cigarette smoke during early life on brain-derived neurotrophic factor/neurotrophic tyrosine kinase receptor B signaling in the brain. Methods: Three different age of imprinting control region mice were exposed to cigarette smoke or filtered air for 10 consecutive days beginning on either gestational day 7 by maternal exposure, or postnatal days 2 or 21 by direct inhalation. A series of behavioral profiles and neurotrophins in brain were measured 24 hours after mice received acute restraint stress for 1 hour on postnatal day 59. Results: Cigarette smoke exposure in gestational day 7 and postnatal day 2 produced depression-like behaviors as evidenced by significantly increased immobility in both tail suspension and forced-swim test. Increased entry latencies, but not ambulation in the open field test, were also observed in the gestational day 7 and postnatal day 2 cigarette smoke exposure groups. Genetic analysis showed that gestational day 7 cigarette smoke exposure significantly altered mRNA level of brain-derived neurotrophic factor/tyrosine kinase receptor B in the hippocampus. However, behavioral profiles and brain-derived neurotrophic factor/tyrosine kinase receptor B signaling were not significantly changed in PND21 cigarette smoke exposure group compared with FA group. Conclusions: These results suggest that a critical period of susceptibility to cigarette smoke exposure exists in the prenatal and early postnatal period, which results a downregulation in brain-derived neurotrophic factor/tyrosine kinase receptor B signaling in the hippocampus and enhances depression-like behaviors later in life. PMID:26503133

  16. LEAD EXPOSURES IN THE HUMAN ENVIRONMENT

    EPA Science Inventory

    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,...

  17. Behavioral effects in mice of postnatal exposure to low-doses of 137-cesium and bisphenol A.

    PubMed

    Heredia, Luis; Bellés, Montserrat; LLovet, Maria Isabel; Domingo, Jose L; Linares, Victoria

    2016-01-18

    Bisphenol A (BPA) is the most important plasticizer used in many household products such as polycarbonate plastics or epoxy resins. Public and scientific concerns exist regarding the possibility that the neonatal exposure to BPA may contribute to neurobehavioral disorders. On the other hand, there is little information on the effects of low doses of ionizing radiation during critical phases of postnatal brain development, as well as the combination of radiation and environmental chemicals. In this study, C57BL/6J mice were exposed to low doses of internal radiation ((137)Cs), and/or BPA on postnatal day 10 (PND10). At the age of two months, animals were submitted to several tests to assess anxiety, activity, learning, and memory. Results showed that exposure to (137)Cs, alone or in combination with BPA, increased the anxiety-like of the animals without changing the activity levels. Animals exposed to (137)Cs showed impaired learning, and spatial memory, an impairment that was not observed in the groups co-exposed to BPA. PMID:26719215

  18. Post-Natal Inhibition of NF-κB Activation Prevents Renal Damage Caused by Prenatal LPS Exposure.

    PubMed

    Guo, Wei; Guan, Xiao; Pan, Xiaodong; Sun, Xiongshan; Wang, Fangjie; Ji, Yan; Huang, Pei; Deng, Yafei; Zhang, Qi; Han, Qi; Yi, Ping; Namaka, Michael; Liu, Ya; Deng, Youcai; Li, Xiaohui

    2016-01-01

    Prenatal exposure to an inflammatory stimulus has been shown to cause renal damage in offspring. Our present study explored the role of intra-renal NF-κB activation in the development of progressive renal fibrosis in offspring that underwent prenatal exposure to an inflammatory stimulus. Time-dated pregnant rats were treated with saline (control group) or 0.79 mg/kg lipopolysaccharide (LPS) through intra-peritoneal injection on gestational day 8, 10 and 12. At the age of 7 weeks, offspring from control or LPS group were treated with either tap water (Con+Ve or LPS+Ve group) or pyrollidine dithiocarbamate (PDTC, 120mg/L), a NF-κB inhibitor, via drinking water starting (Con+PDTC or LPS+PDTC group), respectively, till the age of 20 or 68 weeks. The gross structure of kidney was assessed by hematoxylin-eosin, periodic acid-Schiff staining and Sirius red staining. The expression levels of TNF-α, IL-6, α-smooth muscle actin (α-SMA) and renin-angiotensin system (RAS) genes were determined by real time polymerase chain reaction and/or immunohistochemical staining. Our data showed that post-natal persistent PDTC administration efficiently repressed intra-renal NF-κB activation, TNF-α and IL-6 expression. Post-natal PDTC also prevented intra-renal glycogen deposition and collagenous fiber generation as evident by the reduced expression of collagen III and interstitial α-SMA in offspring of prenatal LPS exposure. Furthermore, post-natal PDTC administration reversed the intra-renal renin-angiotensin system (RAS) over-activity in offspring of prenatal LPS exposure. In conclusion, prenatal inflammatory exposure results in offspring's intra-renal NF-κB activation along with inflammation which cross-talked with excessive RAS activation that caused exacerbation of renal fibrosis and dysfunction in the offspring. Thus, early life prevention of NF-κB activation may be a potential preventive strategy for chronic renal inflammation and progressive renal damage. PMID:27073902

  19. Post-Natal Inhibition of NF-κB Activation Prevents Renal Damage Caused by Prenatal LPS Exposure

    PubMed Central

    Sun, Xiongshan; Wang, Fangjie; Ji, Yan; Huang, Pei; Deng, Yafei; Zhang, Qi; Han, Qi; Yi, Ping; Namaka, Michael; Liu, Ya; Li, Xiaohui

    2016-01-01

    Prenatal exposure to an inflammatory stimulus has been shown to cause renal damage in offspring. Our present study explored the role of intra-renal NF-κB activation in the development of progressive renal fibrosis in offspring that underwent prenatal exposure to an inflammatory stimulus. Time-dated pregnant rats were treated with saline (control group) or 0.79 mg/kg lipopolysaccharide (LPS) through intra-peritoneal injection on gestational day 8, 10 and 12. At the age of 7 weeks, offspring from control or LPS group were treated with either tap water (Con+Ve or LPS+Ve group) or pyrollidine dithiocarbamate (PDTC, 120mg/L), a NF-κB inhibitor, via drinking water starting (Con+PDTC or LPS+PDTC group), respectively, till the age of 20 or 68 weeks. The gross structure of kidney was assessed by hematoxylin-eosin, periodic acid–Schiff staining and Sirius red staining. The expression levels of TNF-α, IL-6, α-smooth muscle actin (α-SMA) and renin-angiotensin system (RAS) genes were determined by real time polymerase chain reaction and/or immunohistochemical staining. Our data showed that post-natal persistent PDTC administration efficiently repressed intra-renal NF-κB activation, TNF-α and IL-6 expression. Post-natal PDTC also prevented intra-renal glycogen deposition and collagenous fiber generation as evident by the reduced expression of collagen III and interstitial α-SMA in offspring of prenatal LPS exposure. Furthermore, post-natal PDTC administration reversed the intra-renal renin-angiotensin system (RAS) over-activity in offspring of prenatal LPS exposure. In conclusion, prenatal inflammatory exposure results in offspring’s intra-renal NF-κB activation along with inflammation which cross-talked with excessive RAS activation that caused exacerbation of renal fibrosis and dysfunction in the offspring. Thus, early life prevention of NF-κB activation may be a potential preventive strategy for chronic renal inflammation and progressive renal damage. PMID

  20. Lead, Mercury, and Cadmium Exposure and Attention Deficit Hyperactivity Disorder in Children

    PubMed Central

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

    2013-01-01

    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. PMID:24034783

  1. 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. PMID:27286044

  2. 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.

  3. 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

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

    PubMed

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

    2016-03-01

    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 µm(2) of endometrium nor in the height of the uterine epithelium. PMID:27051347

  5. 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.

  6. Lifetime exposure to environmental lead and children's intelligence at 11-13 years: the Port Pirie cohort study.

    PubMed Central

    Tong, S.; Baghurst, P.; McMichael, A.; Sawyer, M.; Mudge, J.

    1996-01-01

    OBJECTIVE--To examine the association between environmental exposure to lead and children's intelligence at age 11-13 years, and to assess the implications of exposure in the first seven years of life for later childhood development. DESIGN--Prospective cohort study. SUBJECTS--375 children born in or around the lead smelting town of Port Pirie, Australia, between 1979 and 1982. MAIN OUTCOME MEASURE--Children's intelligence quotient (IQ) measured at 11-13 years of age. RESULTS--IQ was inversely associated with both antenatal and postnatal blood lead concentrations. Verbal, performance, and full scale IQ were inversely related to blood lead concentration with no apparent threshold. Multivariate analyses indicated that after adjustment for a wide range of confounders, the postnatal blood lead concentrations (particularly within the age range 15 months to 7 years) exhibited inverse associations with IQ. Strong associations with IQ were observed for lifetime average blood lead concentrations at various ages. The expected mean full scale IQ declined by 3.0 points (95% confidence interval 0.07 to 5.93) for an increase in lifetime average blood lead concentration from 0.48 to 0.96 mumol/l (10 to 20 micrograms/dl). CONCLUSION--Exposure to environmental lead during the first seven years of life is associated with cognitive deficits that seem to persist into later childhood. PMID:8664666

  7. Effects of postnatal exposure to a PCB mixture in monkeys on nonspatial discrimination reversal and delayed alternation performance.

    PubMed

    Rice, D C; Hayward, S

    1997-01-01

    Behavioral impairment as a consequence of PCB exposure beginning in utero has been reported in both humans and animals. The present study assessed the behavioral consequences of postnatal exposure to PCBs. Male monkeys (Macaca fascicularis) were dosed from birth to 20 weeks of age with 7.5 micrograms/kg/day of a PCB mixture representative of the PCBs typically found in human breast milk (8 monkeys) or vehicle (5 monkeys). At 20 weeks of age, PCB levels in fat and blood of treated monkeys were 1.7-3.6 ppm and 2-3 ppb respectively. Beginning at three years of age, monkeys were tested on a series of nonspatial discrimination reversal problems followed by a spatial delayed alternation task. Treated monkeys exhibited decreased median response latencies and variable increases in mean response latencies across the three tasks of the nonspatial discrimination reversal. There were no group differences on accuracy of performance, although some treated individuals made more mistakes at the beginning of the experiment than did control monkeys. On the delayed alteration task, the PCB-exposed group displayed retarded acquisition of the task and increased errors at short delay values, which were tested at the beginning of the experiment. There was no increase in the total number of errors in treated monkeys at long delay values. Treated monkeys engaged in more perseverative responding than controls over the entire course of the experiment, in some instances even in the absence of an increase in overall error rate. These findings are interpreted as a learning/performance decrement rather than an effect on spatial memory per se. The results of this study suggest that PCB exposure which is limited to the early postnatal period and results in environmentally-relevant body burdens produces long-term behavioral impairment. PMID:9291496

  8. Results of lead research: prenatal exposure and neurological consequences.

    PubMed Central

    Goyer, R A

    1996-01-01

    The history of advances in the understanding of the toxic effects of lead over the past 20 years is an outstanding example of how knowledge learned from research can impact public health. Measures that have had the greatest impact on reducing exposure to lead are reduction of lead from gasoline, elimination of lead solder from canned food, removal of lead from paint, and abatement of housing containing lead-based paint. Nevertheless, continuing factors that enhance risk to lead exposure, particularly during fetal life, are low socioeconomic status, old housing with lead-containing paint, and less than ideal nutrition, particularly low dietary intake of calcium, iron, and zinc. Prenatal exposure may result from endogenous sources such as lead in the maternal skeletal system or maternal exposures from diet and the environment. Experimental studies have shown that the developing nervous system is particularly sensitive to the toxic effects of lead and that a large number of the effects in the nervous system are due to interference of lead with biochemical functions dependent on calcium ions and impairment of neuronal connections dependent on dendritic pruning. There is need for more study to determine whether these effects are a continuum of prenatal lead exposure or whether prenatal exposure to lead produces unique effects. Images p1050-a Figure 1. A Figure 1. B Figure 2. Figure 3. PMID:8930545

  9. Early postnatal exposure to methylphenidate alters stress reactivity and increases hippocampal ectopic granule cells in adult rats.

    PubMed

    Torres-Reveron, Annelyn; Gray, Jason D; Melton, Jay T; Punsoni, Michael; Tabori, Nora E; Ward, Mary J; Frys, Kelly; Iadecola, Costantino; Milner, Teresa A

    2009-03-16

    To mimic clinical treatment with methylphenidate (MPH; Ritalin) for attention deficit/hyperactivity disorder (ADHD), rat pups were injected with MPH (5 mg/kg, i.p.) or placebo twice daily during their nocturnal active phase from postnatal day (PND) 7-35. Thirty-nine days after the last MPH administration (PND 76), four litters of rats experienced stressful conditions during the 2003 New York City blackout. MPH-treated rats that endured the blackout lost more weight and regained it at a slower pace than controls (p<0.05; N=7-11 per group). Furthermore, MPH-treated rats had elevated systolic arterial blood pressure (from 115.6+/-1.2 to 126+/-1.8 mmHg; p<0.05), assessed on PND 130 by tail cuff plethysmography. Immunocytochemical studies of transmitter systems in the brain demonstrated rearrangements of catecholamine and neuropeptide Y fibers in select brain regions at PND 135, which did not differ between blackout and control groups. However, MPH-treated rats that endured the blackout had more ectopic granule cells in the hilus of the dorsal hippocampal dentate gyrus compared to controls at PND 135 (p<0.05; N=6 per group). These findings indicate that early postnatal exposure to high therapeutic doses of MPH can have long lasting effects on the plasticity of select brain regions and can induce changes in the reactivity to stress that persist into adulthood. PMID:19100815

  10. 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

  11. 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

  12. 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

  13. Effectiveness of employee training and motivation programs in reducing exposure to inorganic lead and lead alkyls.

    PubMed

    Maples, T W; Jacoby, J A; Johnson, D E; Ter Haar, G L; Buckingham, F M

    1982-09-01

    The Occupational Safety and Health Administration has advanced engineering controls over administrative controls and protective equipment to reduce exposures to chemicals in the workplace. The application of employee training and motivation programs (such as job safety analysis) to reduce exposures to chemicals has not been emphasized. To determine the effectiveness of such programs, a pilot project in an alkyl lead production facility was conducted with 35 employees in an effort to reduce exposures to organic and inorganic lead. Results after 12 months show a 40% reduction in lead-in-urine and a 24% reduction in lead-in-blood, both indicators of total exposure to organic inorganic lead. PMID:7148690

  14. Sex and Rearing Condition Modify the Effects of Perinatal Lead Exposure on Learning and Memory

    PubMed Central

    Anderson, D. W.; Pothakos, K.; Schneider, J.S.

    2012-01-01

    Developmental lead (Pb) exposure is associated with cognitive impairments in humans and rodents alike. In particular, impaired spatial learning and memory, as assessed using the Morris water maze (MWM), has been noted in developmentally Pb –exposed rats. Although sex and rearing environment can influence MWM performance in normal animals, the interactions of sex and rearing environment on the impact of developmental Pb exposure on hippocampal-dependent processes has not been well characterized. The present study examined the effects of perinatal exposure (i.e., gestation through weaning) to different levels of Pb (250, 750 and 1,500 ppm Pb acetate in food) in males and females raised in a non-enriched environment (standard cage with 3 animals and no toys) or an enriched environment (large cage containing a variety of toys that were changed twice weekly). Testing in the MWM began at postnatal day 55. Behavioral outcomes were influenced by sex and rearing environment, with complex interactions with Pb exposure. In non-Pb exposed control animals, beneficial effects of environmental enrichment on spatial learning and memory were observed in males and females, with greater effects in females. Pb exposure in females mitigated at least some of the benefits of enrichment on learning, particularly at the lowest and highest exposure levels. In males, enrichment conferred a modest learning advantage and for the most part, Pb exposure did not affect this. However, in males with the highest Pb exposure, enrichment did help to overcome detrimental effects of Pb on learning. In females, any potential benefit to reference memory contributed by enrichment was muted by exposure to Pb and for the most part, this was not reproduced in males. Thus, there are complex interactions between sex, environment, and Pb exposure on spatial learning and memory. Environmental manipulation is a potential risk modifier of developmental Pb exposure and interacts with other factors including sex

  15. 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.

  16. Chronic neonatal nicotine exposure increases mRNA expression of neurotrophic factors in the postnatal rat hippocampus.

    PubMed

    Son, Jong-Hyun; Winzer-Serhan, Ursula H

    2009-06-30

    Nicotine, the psychoactive ingredient in tobacco, can be neuroprotective but the mechanism is unknown. In the adult hippocampus, chronic nicotine can increase expression of growth factors which could contribute to nicotine's neuroprotective effects. During development, nicotine could also increase expression of neurotrophic factors. Therefore, we determined whether chronic neonatal nicotine (CNN) exposure increased mRNA expression levels of brain-derived neurotrophic factor (BDNF), nerve-growth factor (NGF), neurotrophin-3 (NT-3), fibroblast growth factor-2 (FGF-2), and insulin-like growth factor-1 (IGF-1). Nicotine (6 mg/kg/day in milk formula) or milk formula (controls) were delivered in three daily doses via oral gastric intubation to rat pups from postnatal day (P)1 to P8, and then sacrificed. Brains were processed for in situ hybridization using specific (35)S-labeled cRNA probes. At P8, CNN had a significant stimulant treatment effect on the expression of BDNF, FGF-2, NT-3 and IGF-1 [p<0.01], but not NGF. Specifically, BDNF mRNA expression, detected in CA1, CA3 stratum (s.) pyramidal and granule cell layer of the dentate gyrus (DG), was increased by 27.4%, 23.26% and 27.3%, respectively. FGF-2 mRNA expression, detected in neurons and astrocytes in CA1 s. radiatum, CA2 and CA3 s. pyramidale, and molecular layer of the DG, was increased by 34.0%, 8.9%, 31.0% and 23.1%, respectively. NT-3 mRNA expression in CA2 s. pyramidale was increased by 80.0%, and CNN increased the number of IGF-1-expressing cells in CA1 (18.0%), CA3 (20.9%) and DG (17.7%). Thus, nicotine exposure during early postnatal development differentially up-regulated expression of neurotrophic factor mRNAs in the hippocampus, which could increase neurotrophic tone and alter developmental processes. PMID:19410565

  17. Renal effects of environmental and occupational lead exposure.

    PubMed Central

    Loghman-Adham, M

    1997-01-01

    Environmental and industrial lead exposures continue to pose major public health problems in children and in adults. Acute exposure to high concentrations of lead can result in proximal tubular damage with characteristic histologic features and manifested by glycosuria and aminoaciduria. Chronic occupational exposure to lead, or consumption of illicit alcohol adulterated with lead, has also been linked to a high incidence of renal dysfunction, which is characterized by glomerular and tubulointerstitial changes resulting in chronic renal failure, hypertension, hyperuricemia, and gout. A high incidence of nephropathy was reported during the early part of this century from Queensland, Australia, in persons with a history of childhood lead poisoning. No such sequela has been found in studies of three cohorts of lead-poisoned children from the United States. Studies in individuals with low-level lead exposure have shown a correlation between blood lead levels and serum creatinine or creatinine clearance. Chronic low-level exposure to lead is also associated with increased urinary excretion of low molecular weight proteins and lysosomal enzymes. The relationship between renal dysfunction detected by these sensitive tests and the future development of chronic renal disease remains uncertain. Epidemiologic studies have shown an association between blood lead levels and blood pressure, and hypertension is a cardinal feature of lead nephropathy. Evidence for increased body lead burden is a prerequisite for the diagnosis of lead nephropathy. Blood lead levels are a poor indicator of body lead burden and reflect recent exposure. The EDTA lead mobilization test has been used extensively in the past to assess body lead burden. It is now replaced by the less invasive in vivo X-ray fluorescence for determination of bone lead content. Images p928-a Figure 1. Figure 2. Figure 2. Figure 3. PMID:9300927

  18. Early Postnatal Exposure to Ultrafine Particulate Matter Air Pollution: Persistent Ventriculomegaly, Neurochemical Disruption, and Glial Activation Preferentially in Male Mice

    PubMed Central

    Allen, Joshua L.; Liu, Xiufang; Pelkowski, Sean; Palmer, Brian; Conrad, Katherine; Oberdörster, Günter; Weston, Douglas; Mayer-Pröschel, Margot

    2014-01-01

    Background: Air pollution has been associated with adverse neurological and behavioral health effects in children and adults. Recent studies link air pollutant exposure to adverse neurodevelopmental outcomes, including increased risk for autism, cognitive decline, ischemic stroke, schizophrenia, and depression. Objectives: We sought to investigate the mechanism(s) by which exposure to ultrafine concentrated ambient particles (CAPs) adversely influences central nervous system (CNS) development. Methods: We exposed C57BL6/J mice to ultrafine (< 100 nm) CAPs using the Harvard University Concentrated Ambient Particle System or to filtered air on postnatal days (PNDs) 4–7 and 10–13, and the animals were euthanized either 24 hr or 40 days after cessation of exposure. Another group of males was exposed at PND270, and lateral ventricle area, glial activation, CNS cytokines, and monoamine and amino acid neurotransmitters were quantified. Results: We observed ventriculomegaly (i.e., lateral ventricle dilation) preferentially in male mice exposed to CAPs, and it persisted through young adulthood. In addition, CAPs-exposed males generally showed decreases in developmentally important CNS cytokines, whereas in CAPs-exposed females, we observed a neuroinflammatory response as indicated by increases in CNS cytokines. We also saw changes in CNS neurotransmitters and glial activation across multiple brain regions in a sex-dependent manner and increased hippocampal glutamate in CAPs-exposed males. Conclusions: We observed brain region– and sex-dependent alterations in cytokines and neurotransmitters in both male and female CAPs-exposed mice. Lateral ventricle dilation (i.e., ventriculomegaly) was observed only in CAPs-exposed male mice. Ventriculomegaly is a neuropathology that has been associated with poor neurodevelopmental outcome, autism, and schizophrenia. Our findings suggest alteration of developmentally important neurochemicals and lateral ventricle dilation may be

  19. 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. PMID:26812760

  20. Effects of in utero and lactational exposure to triphenyltin chloride on pregnancy outcome and postnatal development in rat offspring.

    PubMed

    Grote, Konstanze; Hobler, Carolin; Andrade, Anderson J M; Grande, Simone Wichert; Gericke, Christine; Talsness, Chris E; Appel, Klaus E; Chahoud, Ibrahim

    2007-09-01

    The organotin compound (OTC) triphenyltin (TPT) is used extensively as a herbicide, pesticide and fungicide in agriculture as well as, together with tributyltin (TBT), in marine antifouling paints. We studied the effects of in utero exposure to 2 or 6 mg triphenyltinchloride (TPTCl)/kgb.w. on pregnancy outcome and postnatal development in rat offspring. Gravid Wistar rats were treated per gavage from gestational day 6 until the end of lactation. In the 6 mg TPTCl dose group gestational mortality in dams as well as an increased incidence of anticipated and delayed parturition was observed. Furthermore, treatment resulted in a significant increase in perinatal mortality, a decrease in lactational body weight gain as well as in delayed physical maturation of offspring. Similarily, exposure to 2mg TPTCl/kgb.w. resulted in a significant increase in perinatal mortality and in delayed eye opening. Lactational body weight gain and other landmarks of physical maturation were unaffected in the low dose group. We conclude, that in utero exposure to TPTCl at the described dose levels severely affected pregnancy outcome and perinatal survival of offspring. These results were unexpected, as in two earlier studies with pubertal rats TPTCl at the same dose levels no signs of general toxicity were observed. PMID:17644232

  1. Low-Dose, Gestational Exposure to Atrazine Does Not Alter Postnatal Reproductive Development of Male Offspring

    EPA Science Inventory

    There is growing evidence that xenobiotic exposure during the perinatal period may result in a variety of adverse outcomes when the developing organism attains adulthood. Maternal stress and subsequent exposure of the fetus to excess glucocorticoids may underlie these effects. Pr...

  2. 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. PMID:27295315

  3. 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...

  4. 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...

  5. 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.

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

    PubMed

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

    1997-04-01

    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. PMID:9189705

  7. 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

  8. Moderate postnatal hyperoxia accelerates lung growth and attenuates pulmonary hypertension in infant rats after exposure to intra-amniotic endotoxin.

    PubMed

    Tang, Jen-Ruey; Seedorf, Gregory J; Muehlethaler, Vincent; Walker, Deandra L; Markham, Neil E; Balasubramaniam, Vivek; Abman, Steven H

    2010-12-01

    To determine the separate and interactive effects of fetal inflammation and neonatal hyperoxia on the developing lung, we hypothesized that: 1) antenatal endotoxin (ETX) causes sustained abnormalities of infant lung structure; and 2) postnatal hyperoxia augments the adverse effects of antenatal ETX on infant lung growth. Escherichia coli ETX or saline (SA) was injected into amniotic sacs in pregnant Sprague-Dawley rats at 20 days of gestation. Pups were delivered 2 days later and raised in room air (RA) or moderate hyperoxia (O₂, 80% O₂ at Denver's altitude, ∼65% O₂ at sea level) from birth through 14 days of age. Heart and lung tissues were harvested for measurements. Intra-amniotic ETX caused right ventricular hypertrophy (RVH) and decreased lung vascular endothelial growth factor (VEGF) and VEGF receptor-2 (VEGFR-2) protein contents at birth. In ETX-exposed rats (ETX-RA), alveolarization and vessel density were decreased, pulmonary vascular wall thickness percentage was increased, and RVH was persistent throughout the study period compared with controls (SA-RA). After antenatal ETX, moderate hyperoxia increased lung VEGF and VEGFR-2 protein contents in ETX-O₂ rats and improved their alveolar and vascular structure and RVH compared with ETX-RA rats. In contrast, severe hyperoxia (≥95% O₂ at Denver's altitude) further reduced lung vessel density after intra-amniotic ETX exposure. We conclude that intra-amniotic ETX induces fetal pulmonary hypertension and causes persistent abnormalities of lung structure with sustained pulmonary hypertension in infant rats. Moreover, moderate postnatal hyperoxia after antenatal ETX restores lung growth and prevents pulmonary hypertension during infancy. PMID:20709730

  9. 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.

  10. Prenatal and Postnatal Bisphenol A Exposure and Body Mass Index in Childhood in the CHAMACOS Cohort

    PubMed Central

    Schall, Raul Aguilar; Chevrier, Jonathan; Tyler, Kristin; Aguirre, Helen; Bradman, Asa; Holland, Nina T.; Lustig, Robert H.; Calafat, Antonia M.; Eskenazi, Brenda

    2013-01-01

    Background: Bisphenol A (BPA), a widely used endocrine-disrupting chemical, has been associated with increased body weight and fat deposition in rodents. Objectives: We examined whether prenatal and postnatal urinary BPA concentrations were associated with body mass index (BMI), waist circumference, percent body fat, and obesity in 9-year-old children (n = 311) in the CHAMACOS longitudinal cohort study. Methods: BPA was measured in spot urine samples collected from mothers twice during pregnancy and from children at 5 and 9 years of age. Results: Prenatal urinary BPA concentrations were associated with decreased BMI at 9 years of age in girls but not boys. Among girls, being in the highest tertile of prenatal BPA concentrations was associated with decreased BMI z-score (β = –0.47, 95% CI: –0.87, –0.07) and percent body fat (β = –4.36, 95% CI: –8.37, –0.34) and decreased odds of overweight/obesity [odds ratio (OR) = 0.37, 95% CI: 0.16, 0.91] compared with girls in the lowest tertile. These findings were strongest in prepubertal girls. Urinary BPA concentrations at 5 years of age were not associated with any anthropometric parameters at 5 or 9 years, but BPA concentrations at 9 years were positively associated with BMI, waist circumference, fat mass, and overweight/obesity at 9 years in boys and girls. Conclusions: Consistent with other cross-sectional studies, higher urinary BPA concentrations at 9 years of age were associated with increased adiposity at 9 years. However, increasing BPA concentrations in mothers during pregnancy were associated with decreased BMI, body fat, and overweight/obesity among their daughters at 9 years of age. PMID:23416456

  11. Postnatal exposure to MK801 induces selective changes in GAD67 or parvalbumin.

    PubMed

    Turner, Christopher Paul; DeBenedetto, Danielle; Ware, Emily; Stowe, Robert; Lee, Andrew; Swanson, John; Walburg, Caroline; Lambert, Alexandra; Lyle, Melissa; Desai, Priyanka; Liu, Chun

    2010-03-01

    Brain injury during the last trimester to the first 1-4 years in humans is now thought to trigger an array of intellectual and emotional problems later in life, including disorders such as schizophrenia. In adult schizophrenic brains, there is a specific loss of neurons that co-express glutamic acid decarboxylase-parvalbumin (GAD67-PV). Loss of this phenotype is thought to occur in mature animals previously exposed to N-methyl-D: -aspartate receptor (NMDAR) antagonists during late gestation or at postnatal day 7 (P7). However, in similarly treated animals, we have previously shown that GAD67 and PV are unaltered in the first 24 h. To more precisely define when changes in these markers first occur, we exposed rat pups (P7 or P6-P10) to the NMDAR antagonist MK801 and at P11 co-stained brain sections for GAD67 or PV. In the cingulate cortex, we found evidence for a reduction in PV (GAD67 levels were very low to undetectable). In contrast, in the somatosensory cortex, we found that expression of GAD67 was reduced, but PV remained stable. Further, repeated but not single doses of MK801 were necessary to see such changes. Thus, depending on the region, NMDAR antagonism appears to influence expression of PV or GAD67, but not both. These observations could not have been predicted by previous studies and raise important questions as to how the GAD67-PV phenotype is lost once animals reach maturity. More importantly, such differential effects may be of great clinical importance, given that cognitive deficits are seen in children exposed to anesthetics that act by blocking the NMDAR. PMID:19885653

  12. Lead exposure causes thyroid abnormalities in diabetic rats

    PubMed Central

    Zadjali, Salah Al; Nemmar, Abderrahim; Fahim, Mohamed Abdelmonem AY; Azimullah, Sheikh; Subramanian, Dhanasekaran; Yasin, Javed; Amir, Naheed; Hasan, Mohammed Yousif; Adem, Abdu

    2015-01-01

    Lead is a widely-spread environmental pollutant and a commonly-used industrial chemical that can cause multisystemic adverse health effects. However, the effects of lead exposure on diabetic animals have not been reported so far. The aim of this study is to evaluate the effects of lead exposure on thyroid, renal and oxidative stress markers in diabetic Wistar rats. Diabetes was induced with an intraperitoneal (i.p.) injection of streptozocin (STZ). Six weeks later, rats were exposed i.p. to either distilled water (control group) or 25, 50 and 100 mg/kg of lead acetate (treatment groups). We found a positive relationship between the administered doses of lead acetate and its measured levels in blood samples (P < 0.01). Treatment of diabetic animals with lead acetate resulted in significant weight loss (P < 0.001). It also caused an increase in thyroid stimulating hormone levels (P < 0.05) and reductions in thyroxine (P < 0.05) and triiodothyronine levels (P < 0.01), a clinical picture consistent with hypothyroidism. Lead acetate exposure increased urea levels (P < 0.05) and caused a significant decrease in creatinine (P < 0.05). Besides, while the concentrations of malondialdehyde were not affected, glutathione stores were depleted (P < 0.01); in response to lead exposure. In conclusion, exposure of diabetic rats to lead acetate resulted in weight loss, clinical hypothyroidism, renal damage and oxidative stress. PMID:26221254

  13. Childhood Lead Exposure from Battery Recycling in Vietnam

    PubMed Central

    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

    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

  14. Lead exposure causes thyroid abnormalities in diabetic rats.

    PubMed

    Zadjali, Salah Al; Nemmar, Abderrahim; Fahim, Mohamed Abdelmonem Ay; Azimullah, Sheikh; Subramanian, Dhanasekaran; Yasin, Javed; Amir, Naheed; Hasan, Mohammed Yousif; Adem, Abdu

    2015-01-01

    Lead is a widely-spread environmental pollutant and a commonly-used industrial chemical that can cause multisystemic adverse health effects. However, the effects of lead exposure on diabetic animals have not been reported so far. The aim of this study is to evaluate the effects of lead exposure on thyroid, renal and oxidative stress markers in diabetic Wistar rats. Diabetes was induced with an intraperitoneal (i.p.) injection of streptozocin (STZ). Six weeks later, rats were exposed i.p. to either distilled water (control group) or 25, 50 and 100 mg/kg of lead acetate (treatment groups). We found a positive relationship between the administered doses of lead acetate and its measured levels in blood samples (P < 0.01). Treatment of diabetic animals with lead acetate resulted in significant weight loss (P < 0.001). It also caused an increase in thyroid stimulating hormone levels (P < 0.05) and reductions in thyroxine (P < 0.05) and triiodothyronine levels (P < 0.01), a clinical picture consistent with hypothyroidism. Lead acetate exposure increased urea levels (P < 0.05) and caused a significant decrease in creatinine (P < 0.05). Besides, while the concentrations of malondialdehyde were not affected, glutathione stores were depleted (P < 0.01); in response to lead exposure. In conclusion, exposure of diabetic rats to lead acetate resulted in weight loss, clinical hypothyroidism, renal damage and oxidative stress. PMID:26221254

  15. 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. PMID:24411572

  16. Assessment of lead exposure in waterfowl species, Korea.

    PubMed

    Kim, Jungsoo; Oh, Jong-Min

    2014-11-01

    Lead concentrations were analyzed in white-fronted geese (Anser albifrons, n = 15), mallards (Anas platyrhynchos, n = 4), and spot-billed ducks (A. poecilorhyncha, n = 13) found dead near Gimpo, Korea, to determine tissue- and species-specific lead concentration differences and to assess the effect of embedded lead shot. In livers, kidneys, and bones (tarsus), mallards and spot-billed ducks with embedded shot had greater lead concentrations than white-fronted geese and spot-billed ducks without lead shot. Lead concentrations in spot-billed ducks were greater in bones than in livers and kidneys suggesting chronic exposure to lead. Lead concentrations in 8 of 32 livers, 5 of 32 kidneys, and 9 of 32 bones exceeded the threshold level of abnormal exposure for wild birds (>5 µg/g dw in lives, >6 µg/g dw in kidney, and >6.75 µg/g dw in bone). Increased lead concentrations in soft tissues and bones might be attributed to increased lead shot ingestion and embedded shot. Lead concentrations were correlated between livers and kidneys, between livers and bones, and between kidneys and bones. These results suggest that a relationship between acute exposure in livers and kidneys and chronic exposure in bones. PMID:24854704

  17. Persistent Cognitive Alterations in Rats after Early Postnatal Exposure to Low Doses of the Organophosphate Pesticide, Diazinon

    PubMed Central

    Timofeeva, Olga A.; Roegge, Cindy S.; Seidler, Frederic J.; Slotkin, Theodore A.; Levin, Edward D.

    2008-01-01

    Background Developmental neurotoxicity of organophosphorous insecticides (OPs) involves multiple mechanisms in addition to cholinesterase inhibition. We have found persisting effects of developmental chlorpyrifos (CPF) and diazinon (DZN) on cholinergic and serotonergic neurotransmitter systems and gene expression as well as behavioral function. Both molecular/neurochemical and behavioral effects of developmental OP exposure have been seen at doses below those which cause appreciable cholinesterase inhibition. Objectives We sought to determine if developmental DZN exposure at doses which do not produce significant acetylcholinesterase inhibition cause cognitive deficits. Methods Rats were exposed to DZN on postnatal days 1-4 at doses (0.5 and 2 mg/kg/d) that span the threshold for cholinesterase inhibition. They were later examined with a cognitive battery tests similar to that used with CPF. Results In the T-maze DZN caused significant hyperactivity in the initial trials of the session, but not later. In a longer assessment of locomotor activity no DZN-induced changes were seen over a 1-hour session. Prepulse inhibition was reduced by DZN exposure selectively in males vs. females; DZN eliminated the sex difference present in controls. In the radial maze, the lower but not higher DZN dose significantly impaired spatial learning. This has previously been seen with CPF as well. The lower dose DZN group also showed significantly greater sensitivity to the memory-impairing effects of the anticholinergic drug scopolamine. Conclusions Neonatal DZN exposure below the threshold for appreciable cholinesterase inhibition caused neurocognitive deficits in adulthood. The addition of some inhibition of AChE with a higher dose reversed the cognitive impairment. This non-monotonic dose-effect function has also been seen with neurochemical effects. Some of the DZN effects on cognition resemble those seen earlier for CPF, some differ. Our data suggest that DZN and CPF affect

  18. 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

  19. Alcohol exposure during late gestation adversely affects myocardial development with implications for postnatal cardiac function.

    PubMed

    Goh, Joanna M; Bensley, Jonathan G; Kenna, Kelly; Sozo, Foula; Bocking, Alan D; Brien, James; Walker, David; Harding, Richard; Black, M Jane

    2011-02-01

    Prenatal exposure to high levels of ethanol is associated with cardiac malformations, but the effects of lower levels of exposure on the heart are unclear. Our aim was to investigate the effects of daily exposure to ethanol during late gestation, when cardiomyocytes are undergoing maturation, on the developing myocardium. Pregnant ewes were infused with either ethanol (0.75 g/kg) or saline for 1 h each day from gestational days 95 to 133 (term ∼145 days); tissues were collected at 134 days. In sheep, cardiomyocytes mature during late gestation as in humans. Within the left ventricle (LV), cardiomyocyte number was determined using unbiased stereology and cardiomyocyte size and nuclearity determined using confocal microscopy. Collagen deposition was quantified using image analysis. Genes relating to cardiomyocyte proliferation and apoptosis were examined using quantitative real-time PCR. Fetal plasma ethanol concentration reached 0.11 g/dL after EtOH infusions. Ethanol exposure induced significant increases in relative heart weight, relative LV wall volume, and cardiomyocyte cross-sectional area. Ethanol exposure advanced LV maturation in that the proportion of binucleated cardiomyocytes increased by 12%, and the number of mononucleated cardiomyocytes was decreased by a similar amount. Apoptotic gene expression increased in the ethanol-exposed hearts, although there were no significant differences between groups in total cardiomyocyte number or interstitial collagen. Daily exposure to a moderate dose of ethanol in late gestation accelerates the maturation of cardiomyocytes and increases cardiomyocyte and LV tissue volume in the fetal heart. These effects on cardiomyocyte growth may program for long-term cardiac vulnerability. PMID:21076018

  20. 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 Central

    Nakauchi, Sakura; Malvaez, Melissa; Su, Hailing; Kleeman, Elise; Dang, Richard; Wood, Marcelo A.; Sumikawa, Katumi

    2014-01-01

    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. PMID:25545599

  1. Home lead-work as a potential source of lead exposure for children.

    PubMed

    Kawai, M; Toriumi, H; Katagiri, Y; Maruyama, Y

    1983-01-01

    Health examinations for lead poisoning were made on 62 family members from 15 families of homes carrying on lead work, such as quench-hardening in a molten lead bath and type-printing, as work at home. The most interesting findings concern the occurrence of cases with an unduly high lead absorption among children, but not among adult family members other than home lead-workers. The home environments of the children with an unduly high lead absorption represented contamination with housedust high in lead contents. The ingestion of the contaminated housedust by hand-to-mouth is probably responsible for the excessive lead exposure of the affected children. The results of the present study suggest that contamination of housedust with lead due to home lead-work constitutes a possible hazardous source of lead exposure for children. PMID:6654500

  2. PERSPECTIVES ON THE CONCERN FOR AND MANAGEMENT OF PRENATAL CHEMICAL EXPOSURE AND POSTNATAL EFFECTS

    EPA Science Inventory

    This paper was presented as the introduction to a session on the history and epidemiology of prenatal chemical exposure. lthough teratology and developmental toxicology had its experimental beginnings in the early part of this century, the potential for human developmental toxici...

  3. 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...

  4. 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. PMID:26394891

  5. 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.

  6. 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

  7. 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. PMID:6517025

  8. Genistein Exposure During the Early Postnatal Period Favors the Development of Obesity in Female, But Not Male Rats

    PubMed Central

    Helferich, William G.

    2014-01-01

    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. PMID:24361872

  9. 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. PMID:27038133

  10. 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

  11. Maternal lead exposure during lactation persistently impairs testicular development and steroidogenesis in male offspring.

    PubMed

    Wang, Hua; Ji, Yan-Li; Wang, Qun; Zhao, Xian-Feng; Ning, Huan; Liu, Ping; Zhang, Cheng; Yu, Tao; Zhang, Ying; Meng, Xiu-Hong; Xu, De-Xiang

    2013-12-01

    Lead (Pb) is a testicular toxicant. In the present study, we investigated the effects of maternal Pb exposure during lactation on testicular development and steroidogenesis in male offspring. Maternal mice were exposed to different concentration of lead acetate (200 or 2000 ppm) through drinking water from postnatal day (PND) 0 to PND21. As expected, a high concentration of Pb was measured in the kidneys and liver of pups whose mothers were exposed to Pb during lactation. In addition, maternal Pb exposure during lactation elevated, to a less extent, Pb content in testes of weaning pups. Testis weight in weaning pups was significantly decreased when maternal mice were exposed to Pb during lactation. The level of serum and testicular T was reduced in Pb-exposed pups. The expression of P450scc, P450(17α) and 17β-HSD, key enzymes for T synthesis, was down-regulated in testes of weaning pups whose mothers were exposed to Pb during lactation. Interestingly, the level of serum and testicular T remained decreased in adult offspring whose mothers were exposed to Pb during lactation. Importantly, the number of spermatozoa was significantly reduced in Pb-exposed male offspring. Taken together, these results suggest that Pb could be transported from dams to pups through milk. Maternal Pb exposure during lactation persistently disrupts testicular development and steroidogenesis in male offspring. PMID:22806249

  12. 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.

  13. Effects of pre- and postnatal polychlorinated biphenyl exposure on emotional reactivity observed in lambs before weaning.

    PubMed

    Gutleb, Arno C; Lilienthal, Hellmuth; Erhard, Hans W; Zimmer, Karin E; Skaare, Janneche Utne; Ropstad, Erik

    2011-07-01

    Humans and animals are exposed to PCBs and influences on developmental and endocrine processes are among the most pronounced effects. In the present study it was hypothesised that exposure to PCBs may interfere with sexually dimorphic behaviour. To test this hypothesis, behavioural studies in developmentally exposed sheep were conducted. Ewes were orally administered PCB 153 (98 μg/kg bw day), PCB 118 (49 μg/kg bw day) or corn oil from conception until delivery. However, because of accidental cross-contamination occurring twice causing a mixed exposure scenario in all three groups, the focus of this paper is to compare three distinct groups of lambs with different PCB levels (PCB 153 high-PCB 153 h, PCB 118 high-PCB 118 h, and low combined group-LC) rather than comparing animals exposed to single PCB congeners to those of a control group. Lambs were tested between 2 and 6 weeks of age. When LC males started the light/dark choice test in a dark box, they spent significantly more time in the dark part of the pen than LC females. This gender-related difference was not found in groups exposed to PCBs. A significant inhibitory effect on the activity level of males exposed to stress of confinement was found in the PCB 118 h group. In a high stress situation females from PCB 118 h and males from PCB 153 h were less active than their gender counterparts. The results support the hypothesis that intrauterine exposure to PCBs can alter sexually dimorphic behaviour of offspring. PMID:21450342

  14. Lead exposure in Nunavik: from research to action

    PubMed Central

    Couture, Ariane; Levesque, Benoît; Dewailly, Éric; Muckle, Gina; Déry, Serge; Proulx, Jean-François

    2012-01-01

    Background In 1999, the Government of Canada regulated the use of lead shot for hunting. Concurrently, the Nunavik Regional Board of Health and Social Services (NRBHSS) was informed of the results of an isotope study that pointed to lead ammunition as a likely source of lead exposure in Nunavik. Rapidly thereafter, a coalition for the banning of lead shot was implemented by the NRBHSS as well as by regional/local partners and by Inuit hunters in order to disseminate this information to the public. Objectives The purpose of this article is to describe the intervention conducted in the winter of 1999 by the NRBHSS and to assess the combined impact of national legislation and an awareness campaign on blood lead levels in Nunavik. Study design Impact assessment of the intervention for the banning of lead shot conducted in 1999 in Nunavik using blood lead levels data before and after the intervention. Methods Data on blood lead levels in Nunavik describing foetal exposure as well as during childhood and in adults published between 1992 and 2009 were compiled. Blood lead levels in Nunavik prior to and after the interventions were compared. To assess the current situation, the most recent blood lead levels were compared with those from surveys conducted during the same period in North America. Results Analysis of blood samples collected from umbilical cord and from adults show that blood lead levels in Nunavik significantly declined between 1992 and 2004. Nevertheless, lead exposure in Nunavik still remains higher in comparison to that observed in other North American surveys. Conclusions The current situation regarding lead exposure in Nunavik has significantly improved as a result of the implemented intervention. However, according to recent data, a gap still subsists relative to other North American populations. PMID:22818717

  15. 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

  16. 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.

  17. 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.

  18. Environmental lead exposure and children’s cognitive function

    PubMed Central

    CANFIELD, R. L.; JUSKO, T. A.; KORDAS, K.

    2015-01-01

    Summary Recent research has substantially increased knowledge about the effects of low-level lead exposure on children’s neurobehavioral development. This update article focuses on two specific areas of recent research: low-level effects on cognitive function, and results from experimental and observational studies designed to prevent or reverse the damaging effects of lead on intellectual development, either through chelation therapy or micronutrient supplementation. Taken as a whole, these studies suggest that there is no safe level of lead exposure for young children and, although small, these effects are enduring and possibly permanent. PMID:26660292

  19. Sex-dependent effects of lead and prenatal stress on post-translational histone modifications in frontal cortex and hippocampus in the early postnatal brain.

    PubMed

    Schneider, Jay S; Anderson, David W; Kidd, Sarah K; Sobolewski, Marissa; Cory-Slechta, Deborah A

    2016-05-01

    Environmental lead (Pb) exposure and prenatal stress (PS) are co-occurring risk factors for impaired cognition and other disorders/diseases in adulthood and target common biological substrates in the brain. Sex-dependent differences characterize the neurochemical and behavioral responses of the brain to Pb and PS and sexually dimorphic histone modifications have been reported to occur in at-risk brain regions (cortex and hippocampus) during development. The present study sought to examine levels and developmental timing of sexually dimorphic histone modifications (i.e., H3K9/14Ac and H3K9Me3) and the extent to which they may be altered by Pb±PS. Female C57/Bl6 mice were randomly assigned to receive distilled deionized drinking water containing 0 or 100ppm Pb acetate for 2 months prior to breeding and throughout lactation. Half of the dams in each group were exposed to restraint stress (PS, three restraint sessions in plastic cylindrical devices 3×/day at for 30min/day (1000, 1300, and 1600h)) from gestational day 11-19 or no stress (NS). At delivery (PND0) and postnatal day 6 (PND6), pups were euthanized and frontal cortex and hippocampus were removed, homogenized, and assayed for levels of H3K9/14Ac and H3K9Me3. Sex-dependent differences in both levels of histone modifications as well as the developmental trajectory of changes in these levels were observed in both structures and these parameters were differentially affected by Pb±PS in a sex and brain-region-dependent manner. Disruptions of these epigenetic processes by developmental Pb±PS may underlie some of the sex-dependent neurobehavioral differences previously observed in these animals. PMID:27018513

  20. 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.

  1. The association between caries and childhood lead exposure.

    PubMed Central

    Campbell, J R; Moss, M E; Raubertas, R F

    2000-01-01

    Epidemiologic studies suggest an association between lead exposure and caries. Our objective was to establish whether children with a higher lead exposure as toddlers had more caries at school age than children with a lower lead exposure. We used a retrospective cohort design. A sample of children who attended second and fifth grades in the Rochester, New York, public schools during the 1995-1996 and 1996-1997 school years were examined for caries through a dental screening program. For each child we assessed the number of decayed, missing, or filled surfaces on permanent teeth (DMFS), and the number of decayed or filled surfaces on deciduous teeth (dfs); the number of surfaces at risk (SAR) was also recorded. Lead exposure was defined as the mean of all blood lead levels collected between 18 and 37 months of age by fingerstick [provided the blood lead level was [less than/equal to] 10 microg/dL)] or venipuncture. A total of 248 children (197 second graders and 51 fifth graders) were examined for caries and had a record of blood lead levels to define lead exposure. The mean dfs was 3.4 (range 0-29); the mean DMFS was 0.5 (range 0-8). Logistic regression was used to examine the association between the proportion of children with DMFS [Greater/equal to] 1, and the proportion with dfs [Greater/equal to] 1, and lead exposure [< 0.48 micromol/L vs. [Greater/equal to] 0.48 micromol/L (< 10 microg/dL vs. [Greater/equal to] 10 microg/dL)] while controlling for SAR, age at examination, and grade in school. For DMFS, the adjusted odds ratio was 0.95 [95% confidence interval (CI), 0.43-2.09; p = 0.89); for dfs, the odds ratio was 1.77 (95% CI, 0.97-3.24; p = 0.07). This study did not demonstrate that lead exposure > 10 microg/dL as a toddler was a strong predictor of caries among school-age children. However, the results should be interpreted cautiously because of limitations in the assessment of lead exposure and limited statistical power. PMID:11102303

  2. Associations between Prenatal and Recent Postnatal Methylmercury Exposure and Auditory Function at age 19 years in the Seychelles Child Development Study

    PubMed Central

    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

    Objectives 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. Design The peripheral and central auditory function of 534 subjects in the Seychelles Child Development Study (SCDS) Main Cohort was examined at age 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. Results 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/sec 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

  3. 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. PMID:11234531

  4. Late-Postnatal Cannabinoid Exposure Persistently Increases FoxP2 Expression within Zebra Finch Striatum

    PubMed Central

    Soderstrom, Ken; Luo, Bin

    2010-01-01

    Prior work has shown that cannabinoid exposure of zebra finches during sensorimotor stages of vocal development alters song patterns produced in adulthood. We are currently working to identify physiological substrates for this altered song learning. FoxP2 is a transcription factor associated with altered vocal development in both zebra finches and humans. This protein shows a distinct pattern of expression within Area X of striatum that coincides with peak expression of CB1 cannabinoid receptors during sensorimotor learning. Coincident expression in a brain region essential for song learning led us to test for a potential signaling interaction. We have found that cannabinoid agonists acutely increase expression of FoxP2 throughout striatum. When administered during sensorimotor song learning, cannabinoids increase basal levels of striatal FoxP2 expression in adulthood. Thus, song-altering cannabinoid treatments are associated with persistent increases in basal expression of FoxP2 in zebra finch striatum. PMID:20017118

  5. Maternal nicotinic exposure produces a depressed hypoxic ventilatory response and subsequent death in postnatal rats

    PubMed Central

    Zhuang, Jianguo; Zhao, Lei; Xu, Fadi

    2014-01-01

    Abstract In this study, we asked whether a “full term” prenatal nicotinic exposure (fPNE, 6 mg·kg−1·day−1 nicotinic delivery) over the full gestation, compared to a traditional PNE (tPNE) over the last two‐thirds of the gestation, caused a higher mortality following a remarkable depressed hypoxic ventilatory response (dHVR) independent of brain and pulmonary edema and change in serum corticosterone. P12‐14 pups pretreated with tPNE, fPNE or their vehicle (tCtrl and fCtrl) were exposed to 5% O2 for up to 60 min followed by harvesting the brain and lungs or anesthetized to collect blood for detecting arterial blood pH/gases and serum cotinine and corticosterone levels. We found that fPNE had little effect on baseline VE and heart rate, but consistently induced a dHVR and prolonged apnea that were rarely observed after tPNE. The severity of the dHVR in PNE pups were closely correlated to an earlier appearance of lethal ventilatory arrest (the hypoxia‐induced mortality). PNE did not induce brain and pulmonary edema, but significantly increased serum corticosterone levels similarly in tPNE and fPNE pups. Moreover, the accumulated nicotinic dose given to the individual was significantly higher in fPNE than tPNE pups, though there was no difference in serum cotinine levels and arterial blood pH/gases between the two groups. Our results suggest that nicotinic exposure at the early stage of gestation achieved by fPNE, rather than tPNE, is critical in generating the dHVR and subsequent death occurring independently of brain/pulmonary edema and changes in arterial blood pH/gases and serum corticosterone. PMID:24872357

  6. Maternal nicotinic exposure produces a depressed hypoxic ventilatory response and subsequent death in postnatal rats.

    PubMed

    Zhuang, Jianguo; Zhao, Lei; Xu, Fadi

    2014-05-01

    In this study, we asked whether a "full term" prenatal nicotinic exposure (fPNE, 6 mg·kg(-1)·day(-1) nicotinic delivery) over the full gestation, compared to a traditional PNE (tPNE) over the last two-thirds of the gestation, caused a higher mortality following a remarkable depressed hypoxic ventilatory response (dHVR) independent of brain and pulmonary edema and change in serum corticosterone. P12-14 pups pretreated with tPNE, fPNE or their vehicle (tCtrl and fCtrl) were exposed to 5% O2 for up to 60 min followed by harvesting the brain and lungs or anesthetized to collect blood for detecting arterial blood pH/gases and serum cotinine and corticosterone levels. We found that fPNE had little effect on baseline VE and heart rate, but consistently induced a dHVR and prolonged apnea that were rarely observed after tPNE. The severity of the dHVR in PNE pups were closely correlated to an earlier appearance of lethal ventilatory arrest (the hypoxia-induced mortality). PNE did not induce brain and pulmonary edema, but significantly increased serum corticosterone levels similarly in tPNE and fPNE pups. Moreover, the accumulated nicotinic dose given to the individual was significantly higher in fPNE than tPNE pups, though there was no difference in serum cotinine levels and arterial blood pH/gases between the two groups. Our results suggest that nicotinic exposure at the early stage of gestation achieved by fPNE, rather than tPNE, is critical in generating the dHVR and subsequent death occurring independently of brain/pulmonary edema and changes in arterial blood pH/gases and serum corticosterone. PMID:24872357

  7. 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

  8. 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

  9. 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.

  10. Lead level in seminal plasma may affect semen quality for men without occupational exposure to lead

    PubMed Central

    2012-01-01

    Background Infertility affects approximately 10–15% of reproductive-age couples. Poor semen quality contributes to about 25% of infertile cases. Resulting from the direct effect on testicular function or hormonal alterations, heavy metals exposure has been related to impaired semen quality. The objective of this study was to assess the level of lead in the seminal plasma in men without occupational exposure to lead, and to determine the relationship between semen quality and lead concentration in the semen. Methods This is a prospective and nonrandomized clinical study conducted in University infertility clinic and academic research laboratory. Three hundred and forty-one male partners of infertile couples undergoing infertility evaluation and management were recruited to the study. Semen samples collected for the analyses of semen quality were also used for the measurement of lead concentrations. Semen samples were evaluated according to the WHO standards. Results All subjects were married and from infertile couples without occupational exposure to lead. There is a significant inverse correlation between the lead concentration in seminal plasma and sperm count. A higher semen lead concentration was correlated with lower sperm count, but not with semen volume, sperm motility or sperm morphology as assessed by simple linear regression. Conclusions We found that semen lead concentration was significantly higher among the patients with lower sperm count. To our knowledge, this is the first study to demonstrate that a high level of lead accumulation in semen may reduce the sperm count contributing to infertility of men without occupational exposure to lead. PMID:23137356

  11. 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. PMID:21888039

  12. 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. PMID:24943230

  13. Elevated blood lead levels from exposure via a radiator workshop

    SciTech Connect

    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 {micro}mol/L, respectively. The father`s blood lead level was just below the Canadian occupational health and safety intervention level. The two children had blood lead levels of 1.0 and 0.8 {micro}mol/L, both of which are in excess of the recommended guideline for intervention in the case of children. 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.

  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

    2016-05-01

    Purpose 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. Methods 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. Results 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). Conclusion 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. PMID:26905323

  15. 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.

  16. Lead exposure in the lead-acid storage battery manufacturing and PVC compounding industries.

    PubMed

    Ho, S F; Sam, C T; Embi, G B

    1998-09-01

    This study was conducted as part of the Human Exposure Assessment Location (HEAL) Project which comes under the United Nations Environment Programme/World Health Organisation (UNEP/WHO) Global environmental Monitoring System (GEMS). The objective of the study was to evaluate workers' exposure to lead in industries with the highest exposure. All subjects were interviewed about their occupational and smoking histories, the use of personal protective equipment and personal hygiene. The contribution of a dietary source of lead intake from specified foods known to contain lead locally and personal air sampling for lead were assessed. A total of 61 workers from two PVC compounding and 50 workers from two lead acid battery manufacturing plants were studied together with 111 matched controls. In the PVC compounding plants the mean lead-in-air level was 0.0357 mg/m3, with the highest levels occurring during the pouring and mixing operations. This was lower than the mean lead-in-air level of 0.0886 mg/m3 in the lead battery manufacturing plants where the highest exposure was in the loading of lead ingots into milling machines. Workers in lead battery manufacturing had significantly higher mean blood lead than the PVC workers (means, 32.51 and 23.91 mcg/100 ml respectively), but there was poor correlation with lead-in-air levels. Among the lead workers, the Malays had significantly higher blood lead levels than the Chinese (mean blood levels were 33.03 and 25.35 mcg/100 ml respectively) although there was no significant difference between the two ethnic groups in the control group. There were no significant differences between the exposed and control group in terms of dietary intake of specified local foods known to contain lead. However, Malays consumed significantly more fish than the Chinese did. There were no ethnic differences in the hours of overtime work, number of years of exposure, usage of gloves and respirators and smoking habits. Among the Malays, 94.3% eat with

  17. 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).

  18. 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.

  19. 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

  20. Effects of chronic prenatal ethanol exposure on locomotor activity, and hippocampal weight, neurons, and nitric oxide synthase activity of the young postnatal guinea pig.

    PubMed

    Gibson, M A; Butters, N S; Reynolds, J N; Brien, J F

    2000-01-01

    Decreased nitric oxide synthase (NOS)-catalyzed formation of NO from L-arginine may be involved in ethanol teratogenesis involving the hippocampus. This hypothesis was tested by determining the effects of chronic prenatal ethanol exposure on locomotor activity and on hippocampal weight, number of CA1 and CA3 pyramidal cells and dentate gyrus granule cells, and NOS activity of the postnatal guinea pig. Timed, pregnant guinea pigs received one of the following chronic oral regimens throughout gestation: 4 g ethanol/kg maternal body weight/day, isocaloric-sucrose/pair-feeding, or water. At postnatal day (PD) 10, spontaneous locomotor activity was measured. At PD 12, histological analysis was performed on the hippocampal formation, in which hippocampal CA1 and CA3 pyramidal cells and dentate gyrus granule cells were counted; body, brain, and hippocampal weights were measured; and hippocampal NOS enzymatic activity was determined using a radiometric assay. Chronic prenatal ethanol exposure produced hyperactivity, decreased the brain and hippocampal weights with no change in body weight, decreased the number of hippocampal CA1 pyramidal cells by 25-30%, and had no effect on hippocampal NOS activity compared with the two control groups. These data, together with our previous findings in the fetal guinea pig, demonstrate that chronic prenatal ethanol exposure decreases hippocampal NOS activity in near-term fetal life that temporally precedes the selective loss of hippocampal CA1 pyramidal cells in postnatal life. PMID:10758347

  1. Lead exposure assessment from study near a lead-acid battery factory in China.

    PubMed

    Chen, Laiguo; Xu, Zhencheng; Liu, Ming; Huang, Yumei; Fan, Ruifang; Su, Yanhua; Hu, Guocheng; Peng, Xiaowu; Peng, Xiaochun

    2012-07-01

    The production of lead-acid battery in China covered about one-third of the world total output and there are more than 2000 lead-acid battery factories. They may cause the major environment lead pollution. Blood lead levels of several hundreds of residents were over 100 μg/L due to the waste discharges from a lead-acid battery factory in Heyuan, Guangdong province. This study aimed to find out the environmental lead sources, the human lead exposure pathways, and the amplitudes from a lead-acid battery factory. The study results showed that lead levels in soil, dust, tree leaves and human blood declined with the distances increased from the production site. Twenty nine of 32 participants had blood lead levels of over 100 μg/L with an exceptional high value of 639 μg/L for one child. This result suggested that the lead-acid battery production from this factory has caused the elevated lead levels in its neighboring environment and residents. Dust intake was the dominant exposure pathway for humans (over 90%). The lead levels found in adult and toddler (6.19 and 50.1 μg/kg/d, respectively) in the polluted area were far higher than the provisional tolerable weekly intake (PTWI) of 25 μg/kg body weight (translated into 3.5 μg/kg/d), which was established by the joint FAO/WHO Expert Committee. Blood lead levels within the family members were strongly correlated with the house dust lead levels. Our results in this study suggested that further studies in this area should be performed to assess human exposure and relevant human health risks from living close to lead-acid battery factories. PMID:22578522

  2. 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

  3. The effect of lead exposure on expression of SIRT1 in the rat hippocampus.

    PubMed

    Feng, Chang; Gu, Junwang; Zhou, Fankun; Li, Jiaoyang; Zhu, Gaochun; Guan, Linfu; Liu, Haizhen; Du, Guihua; Feng, Jiangao; Liu, Dong; Zhang, Shuyun; Fan, Guangqin

    2016-06-01

    Based on how the silent information regulator 2 homolog 1 (SIRT1) regulates the cyclic AMP response element binding protein (CREB), which is the molecular switch of long-term memory that maintains cognitive function, it is postulated that the impact of lead (Pb) on SIRT1 is one of the mechanisms leading to Pb-induced cognitive and learning deficits. Hence, the purpose of this study was to investigate the effect of Pb exposure on the expression of SIRT1, and the reversion effect of resveratrol, which is an activator of SIRT1. We examined the effects of maternal rat ingestion of Pb in drinking water during gestation and lactation on the expression of SIRT1 and CREB in the hippocampus of their offspring at postnatal week 3 (PNW3) and 52 (PNW52), and then reexamined these effects in offspring after intragastric administration of resveratrol for 4 weeks. Pb exposure decreased SIRT1 and CREB phosphorylation in a dose-dependent manner in the rat hippocampus at both PNW3 and 52, and resveratrol reversed those losses. These results indicated that SIRT1 might be a novel target to prevent Pb neurotoxicity. PMID:27131751

  4. Fetal chlorpyrifos exposure: adverse effects on brain cell development and cholinergic biomarkers emerge postnatally and continue into adolescence and adulthood.

    PubMed Central

    Qiao, Dan; Seidler, Frederic J; Tate, Charlotte A; Cousins, Mandy M; Slotkin, Theodore A

    2003-01-01

    Fetal and childhood exposures to widely used organophosphate pesticides, especially chlorpyrifos (CPF), have raised concerns about developmental neurotoxicity. Previously, biomarkers for brain cell number, cell packing density, and cell size indicated that neonatal rats were more sensitive to CPF than were fetal rats, yet animals exposed prenatally still developed behavioral deficits in adolescence and adulthood. In the present study, we administered CPF to pregnant rats on gestational days 17-20, using regimens devoid of overt fetal toxicity. We then examined subsequent development of acetylcholine systems in forebrain regions involved in cognitive function and compared the effects with those on general biomarkers of cell development. Choline acetyltransferase, a constitutive marker for cholinergic nerve terminals, showed only minor CPF-induced changes during the period of rapid synaptogenesis. In contrast, hemicholinium-3 binding to the presynaptic choline transporter, which is responsive to nerve impulse activity, displayed marked suppression in the animals exposed to CPF; despite a return to nearly normal values by weaning, deficits were again apparent in adolescence and adulthood. There was no compensatory up-regulation of cholinergic receptors, as m2-muscarinic cholinergic receptor binding was unchanged. CPF also elicited delayed-onset alterations in biomarkers for general aspects of cell integrity, with reductions in cell packing density, increases in relative cell size, and contraction of neuritic extensions; however, neither the magnitude nor timing of these changes was predictive of the cholinergic defects. The present findings indicate a wide window of vulnerability of cholinergic systems to CPF, extending from prenatal through postnatal periods, occurring independently of adverse effects on general cellular neurotoxicity. PMID:12676612

  5. 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.

  6. 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.
    ...

  7. Lead exposure among five distinct occupational groups: a comparative study.

    PubMed

    Gharaibeh, Mohammad Younis; Alzoubi, Karem Hasan; Khabour, Omar Falah; Khader, Yousef Saleh; Gharaibeh, Mamoun Abdallah; Matarneh, Sulaiman Khalid

    2014-01-01

    This study was conducted to evaluate blood lead concentration among five selected occupational groups. The five groups were: hospital health workers, shop workers, taxi drivers, automobiles mechanics, and wood workers. The groups did not significantly differ among each other in the average of age and work years. ANOVA test revealed significantly higher mean lead blood concentration in taxi drivers, automechanics, and wood workers compared to other groups. Additionally, workers with lead concentration >0.483 umol/L (10μg/dL) were more likely to have frequent muscle pain compared to those with lower concentrations. No association between other symptoms of lead exposure/toxicity and blood lead concentration was detected. In conclusion, special attention must be directed toward lead blood levels and lead poisoning symptoms when examining patients from certain occupational groups such as taxi drivers, automechanics, and wood workers. Special safety precautions and educational programs are also needed to limit the lead exposure in these occupational groups. PMID:24374433

  8. 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.

  9. 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

  10. 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.

  11. 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

  12. Census tract analysis of lead exposure in Rhode Island children.

    PubMed

    Sargent, J D; Bailey, A; Simon, P; Blake, M; Dalton, M A

    1997-01-01

    There has been increasing interest in a targeted approach to the screening and prevention of lead exposure in children. Targeted screening requires an understanding of variation in lead exposure in individual children or by region. In order to better understand variation by region, we studied Rhode Island lead poisoning screening data, examining average lead exposure to children living in 136 Providence County census tracts (CTs). The study population included 17,956 children aged 59 months and under, who were screened between May 1, 1992, and April 30, 1993. We evaluated the relationship between the percentage of children with blood lead > or = 10 micrograms/dL (pe10) and sociodemographic and housing characteristics, derived from United States 1990 Census data, of these CTs. CT descriptors included population density, percentage of households receiving public assistance income, median per capita income, percentage of households female headed, percentage of houses owner occupied, percentage of houses built before 1950, percentage of houses vacant, percentage of population Black, percentage of recent immigrants, and intraurban mobility. On average, 109 children were screened in each census tract; mean screening rate was 44%. There was wide variation in average lead exposure among census tracts, with pe10 ranging from 3 to 60% of screened children (mean 27%). Individual census variables explained between 24 and 67% of the variance in pe10 among CTs. A multiple regression model including percentage screened, percentage of households receiving public assistance, percentage of houses built before 1950, In (percentage of houses vacant), and percentage of recent immigrants explained 83% of variance in pe10. The percentage of houses built before 1950, a variable which models the presence of lead paint in old houses, displayed the largest adjusted effect on pe10 over the range observed for that variable in RI CTs. The percentage of houses vacant was also a highly

  13. Chronic Lead Poisoning From Industrial Exposure: A Review

    PubMed Central

    Yassi, Annalee

    1980-01-01

    Lead poisoning from chronic industrial exposure is not uncommon. Early diagnosis is important in avoiding irreversible effects. A good occupational history is key to alerting the unsuspecting physician to the correct diagnosis. Blood lead levels are useful but ridden with shortcomings. Specific tests to assess functional impairment, such as urinary aminolevulinic acid (ALA) and coproporphyrins should be included in the diagnostic work-up. Lead poisoning is a preventable disease well worth the consideration of the family practitioner. (Can Fam Physician 1980; 26:1056-1062). PMID:21293668

  14. 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. PMID:25824762

  15. 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.

  16. Comparison of three models for predicting blood lead levels in children: episodic exposures to lead.

    PubMed

    Lakind, J S

    1998-01-01

    A threshold blood lead level in children below which no adverse effects occur has not been identified (CDC, 1991), Therefore, the traditional risk assessment method of relating dose to a reference dose (RfD) for noncancer effects is not applicable to lead. To assess whether environmental lead concentrations may result in adverse health effects, predicted blood lead levels are compared to a blood lead level of 10 micrograms/dL, the current Centers for Disease Control and Prevention level of concern. Children's blood lead levels may be predicted with one of at least three models: USEPA'S Integrated Exposure Uptake Biokinetic Model (IEUBK), and models by O'Flaherty (1993) and Carlisle and Wade (1992). This paper explores the utility of these models for predicting blood lead levels in children, and discusses areas of uncertainty associated with the use of these models in evaluating episodic exposures. It is hoped that this discussion will stimulate interest further researching exposure and health effects from episodic contact with lead contaminated media. PMID:9679219

  17. 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

  18. Proton Magnetic Resonance Spectroscopy in Adults with Childhood Lead Exposure

    PubMed Central

    Cecil, Kim M.; Dietrich, Kim N.; Altaye, Mekibib; Egelhoff, John C.; Lindquist, Diana M.; Brubaker, Christopher J.; Lanphear, Bruce P.

    2011-01-01

    Background Childhood lead exposure adversely affects neurodevelopment. However, few studies have examined changes in human brain metabolism that may underlie known adverse cognitive and behavioral outcomes. Objective We examined the association between mean childhood blood lead levels and in vivo brain metabolite concentrations as adults, determined by proton magnetic resonance spectroscopy (MRS) in a birth cohort with documented low-to-moderate lead exposure. Methods Adult participants from the Cincinnati Lead Study [n = 159; mean age (± SD), 20.8 ± 0.9 years] completed a quantitative, short-echo proton MRS protocol evaluating seven regions to determine brain concentrations of N-acetyl aspartate (NAA), creatine and phosphocreatine (Cr), cholines (Cho), myo-inositol, and a composite of glutamate and glutamine (GLX). Correlation and multiple linear regression analyses were conducted. Results Mean childhood blood lead levels were associated with regionally specific brain metabolite concentrations adjusted for age at imaging and Full-Scale intelligence quotient. Adjusted analyses estimated for a unit (micrograms per deciliter) increase in mean childhood blood lead concentrations, a decrease of NAA and Cr concentration levels in the basal ganglia, a decrease of NAA and a decrease of Cho concentration levels in the cerebellar hemisphere, a decrease of GLX concentration levels in vermis, a decrease of Cho and a decrease of GLX concentration levels in parietal white matter, and a decrease of Cho concentration levels in frontal white matter. Conclusions Gray-matter NAA reductions associated with increasing childhood blood lead levels suggest that sustained childhood lead exposure produces an irreversible pattern of neuronal dysfunction, whereas associated white-matter choline declines indicate a permanent alteration to myelin architecture. PMID:20947467

  19. Lead exposure and hair lead level of workers in a lead refinery industry in Iran

    PubMed Central

    Pirsaraei, Seyed Reza Azimi

    2007-01-01

    This study was carried out on the workers of a lead refinery industry and two control groups in Zanjan city in Iran. The scalp hair samples were collected from 25 workers who were occupationally exposed to lead contamination as a case group and from 25 subjects among the staff of the same industry and 25 subjects among Zanjan citizens as the first and second control groups respectively. A flame atomic absorption spectrophotometer used to determine lead level in all of the samples. The age of all subjects in the three groups was matched. The mean concentrations of hair lead in the workers (case group), the staff (control groupA) and the citizens (control group B) were 131.7±93.4 µgr/gr, 21.1±13.2 µgr/gr and 27.9±14.1 µgr/gr respectively. The mean concentration of hair lead in the case group was more than hair lead of normal range found in humans (0-30 µgr/gr). The mean of hair lead level in the citizens who had used gas vehicles was statistically higher than who had not used it (36.9±12.2 µgr/gr vs. 16.6±4.9 µgr/gr, P<0.001). PMID:21957365

  20. Child lead-exposure study, Leeds, Alabama. Final report

    SciTech Connect

    Woernle, C.; Rao, R.; White, J.; Amler, R.

    1991-09-01

    In August 1989, a human exposure study was undertaken near a secondary battery lead reclamation factory in Leeds, Alabama. A door-to-door census survey was conducted in two targeted residential areas near the factory. Venous blood samples were analyzed for lead, erthrocyte protoporphyrin, hemoglobin, and hematocrit. Among 81 children (9-71 months) studied the mean blood lead value was 6.96 micrograms per deciliter (mcg/dl), with a range of 3 to 16 mcg/dl; 85% of the values were below 10 mcg/dl. A multivariate linear regression model and a logistic regression model identified several following factors as being associated with an increased blood lead value or, having a blood lead concentration in the upper 15th percentile (>10 mcg/dl).

  1. Pre- and postnatal exposure to ambient levels of urban particulate matter (PM(2.5)) affects mice spermatogenesis.

    PubMed

    Pires, Adriana; de Melo, Elizabeth Neves; Mauad, Thais; Nascimento Saldiva, Paulo Hilário; de Siqueira Bueno, Heloisa Maria

    2011-03-01

    This work characterizes the effects of ambient levels of urban particulate matter (PM(2.5)) from the city of Sao Paulo on spermatogenesis using mice exposed during the embryo-fetal and/or postnatal phases of development. Parental generations (BALB/c mice) were exposed to air pollution in chambers with or without filtering PM(2.5) for 4 months. Animals were mated, and half of the 1-day-old offspring were moved between chambers, which yielded prenatal and postnatal groups. Remaining offspring comprised the non-exposed and pre+postnatal exposed groups. After 90 days, the animals were sacrificed for testis collection and weighing. Optical microscopy was used for the morphometric analyses of the cell counts, spermatogenic cycle, proliferation, and apoptosis. Prenatally exposed animals presented reduced body and testicular weight with an increased gonadosomatic index (GSI). Testicular volume also decreased, as well as the tubular diameter in testes of the same animals. Proliferation, apoptosis, and spermatogenic cycle analyses showed no significant differences among groups. However, the tubules at stage VII of pre- and postnatal animals presented a reduced number of elongated spermatids. Pre+postnatal group presented higher spermatid head retention at stages VIII-XII. These results show that ambient levels of PM(2.5) from Sao Paulo city affect spermatogenesis by damaging sperm production. PMID:21456956

  2. Exposure to lead of boatyard workers in southern Thailand.

    PubMed

    Thanapop, Chamnong; Geater, Alan F; Robson, Mark G; Phakthongsuk, Pitchaya; Viroonudomphol, Duangkamol

    2007-09-01

    Lead oxide is used extensively in the construction and repair of wooden boats in Thailand, but the behaviors of boatyard workers that could place them at risk of contamination have not previously been documented. Baseline data on practices and behaviors of boatyard workers and on the level of worker and workplace contamination with lead were therefore collected. Fifty workers in two boatyards participated in this study. Lead exposure of workers was assessed by determining airborne and blood lead levels. A questionnaire was administered to collect information on work history, suspected exogenous lead sources, personal behavior and knowledge about lead. Evidence obtained by the study indicated that safety behavior and personal hygiene were poor--workers used no mask, gloves or hood, wore open sandals, smoked, drank, chewed and ate during work and did not wash their hands before drinking or eating. Some workers had lunch in the working area. The mean personal airborne lead of caulkers (36.4 microg/m3) was higher than that of carpenters (8.3 microg/m3). Forty-eight percent of all workers and 67% of caulkers had a blood lead level (BLL) exceeding 40 microg/dl. Multiple linear regression indicated that blood lead levels of workers were significantly related to job and education level, with significant differences between boatyards. In addition, the potential for "take-home" contamination was high; none of the workers took a shower or changed their clothes prior to going home. These results indicate a problem of lead exposure of sufficient magnitude to be a public health concern. PMID:17951965

  3. Prenatal lead exposure, delta-aminolevulinic acid, and schizophrenia.

    PubMed Central

    Opler, Mark G A; Brown, Alan S; Graziano, Joseph; Desai, Manisha; Zheng, Wei; Schaefer, Catherine; Factor-Litvak, Pamela; Susser, Ezra S

    2004-01-01

    Schizophrenia is a severe mental disorder of unknown etiology. Recent reports suggest that a number of environmental factors during prenatal development may be associated with schizophrenia. We tested the hypothesis that environmental lead exposure may be associated with schizophrenia using archived serum samples from a cohort of live births enrolled between 1959 and 1966 in Oakland, California. Cases of schizophrenia spectrum disorder were identified and matched to controls. A biologic marker of lead exposure, delta-aminolevulinic acid (delta-ALA), was determined in second-trimester serum samples of 44 cases and 75 controls. delta-ALA was stratified into high and low categories, yielding 66 subjects in the high category, corresponding to a blood lead level (BPb) greater than or equal to 15 micro g/dL, and 53 in the low category, corresponding to BPb less than 15 micro g/dL. Using logistic regression, the odds ratio (OR) for schizophrenia associated with higher delta-ALA was 1.83 [95% confidence interval (CI), 0.87-3.87; p = 0.1]. Adjusting for covariates gave an OR of 2.43 (95% CI, 0.99-5.96; p = 0.051). This finding suggests that the effects of prenatal exposure to lead and/or elevated delta-ALA may extend into later life and must be further investigated as risk factors for adult psychiatric diseases. PMID:15064159

  4. 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

    Cezard, C; Demarquilly, C; Boniface, M; Haguenoer, J M

    1992-09-01

    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

  5. Prenatal and postnatal exposure to phthalate esters and asthma: a 9-year follow-up study of a taiwanese birth cohort.

    PubMed

    Ku, Hsiu Ying; Su, Pen Hua; Wen, Hui Ju; Sun, Hai Lun; Wang, Chien Jen; Chen, Hsiao Yen; Jaakkola, Jouni J K; Wang, Shu-Li

    2015-01-01

    Previous studies have shown that phthalate exposure in childhood is associated with the development of respiratory problems. However, few studies have assessed the relative impact of prenatal and postnatal exposure to phthalates on the development of asthma later in childhood. Therefore, we assessed the impact of prenatal and postnatal phthalate exposure on the development of asthma and wheezing using a Taiwanese birth cohort. A total of 430 pregnant women were recruited, and 171 (39.8%) of them had their children followed when they were aged 2, 5, and 8 years. The International Study of Asthma and Allergies in Childhood questionnaire was used to assess asthma and wheezing symptoms and serum total immunoglobulin E levels were measured at 8 years of age. Urine samples were obtained from 136 women during their third trimester of pregnancy, 99 children at 2 years of age, and 110 children at 5 years. Four common phthalate monoester metabolites in maternal and children's urine were measured using liquid chromatography-electrospray ionization-tandem mass spectrometry. Maternal urinary mono-benzyl phthalate [MBzP] concentrations were associated with an increased occurrence of wheezing in boys at 8 years of age (odds ratio [OR] = 4.95 (95% CI 1.08-22.63)), for upper quintile compared to the others) after controlling for parental allergies and family members' smoking status. Urinary mono-2-ethylhexyl phthalate [MEHP] levels over the quintile at 2-year-old were associated with increased asthma occurrence (adjusted OR = 6.14 (1.17-32.13)) in boys. Similarly, the sum of di-2-ethyl-hexyl phthalate [DEHP] metabolites at 5 years was associated with asthma in boys (adjusted OR = 4.36 (1.01-18.86)). Urinary MEHP in maternal and 5-year-old children urine were significantly associated with increased IgE in allergic children at 8 years. Prenatal and postnatal exposure to phthalate was associated with the occurrence of asthma in children, particularly for boys. PMID:25875379

  6. Di(2-Ethylhexyl) Phthalate Exposure In Utero Damages Sertoli Cell Differentiation Via Disturbance of Sex Determination Pathway in Fetal and Postnatal Mice.

    PubMed

    Wang, Yongan; Yang, Qing; Liu, Wei; Yu, Mingxi; Zhang, Zhou; Cui, Xiaoyu

    2016-07-01

    Mice may share similar mechanism with human underlying reproductive toxicity induced by di(2-ethylhexyl) phthalate (DEHP), which is not supposed to be associated with decreased testicular testosterone. Pregnant mice were exposed to DEHP by gavage, with the dosage regime beginning at human relevant exposure level. After in utero DEHP exposure, loss of Sertoli cells and germ cells were observed in the male pups at postnatal days 21. And SRY-related HMG box 9 (SOX9), Fibroblast growth factor-9 (FGF9), and Double-sex and Mab-3 related transcripttion factor 1 (DMRT1) proteins were significantly downregulated by DEHP at 2 mg/kg/d and above, suggesting the depression of Sertoli cell differentiation. The repression of Sox9 genes expression was supported by whole-mount in situ hybridization and real-time real-time-quantitative PCR. The expressions of Cyp11α1 and Star were not significantly affected by in utero DEHP exposure, indicating the absence of effects on testosterone biosynthesis. Furthermore, the testosterone-independent pathway regulating Sertoli cells differentiation was disturbed in fetus by DEHP at 2 mg/kg/d and above during the critical time window of sex determination, involving Gadd45g → Gata4/Fog2 → Sry → Sox9 → Fgf9 The results suggest that in utero DEHP exposure damaged Sertoli cells in the postnatal life of mice offspring via disturbance of the differentiation regulating pathway, potentially inducing declines in spermatogenesis. PMID:27060630

  7. 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.

  8. Smad2 protein disruption in the central nervous system leads to aberrant cerebellar development and early postnatal ataxia in mice.

    PubMed

    Wang, Lixiang; Nomura, Masatoshi; Goto, Yutaka; Tanaka, Kimitaka; Sakamoto, Ryuichi; Abe, Ichiro; Sakamoto, Shohei; Shibata, Atsushi; Enciso, Patricio L M; Adachi, Masahiro; Ohnaka, Keizo; Kawate, Hisaya; Takayanagi, Ryoichi

    2011-05-27

    Smad2 is a critical mediator of TGF-β signals that are known to play an important role in a wide range of biological processes in various cell types. Its role in the development of the CNS, however, is largely unknown. Mice lacking Smad2 in the CNS (Smad2-CNS-KO) were generated by a Cre-loxP approach. These mice exhibited behavioral abnormalities in motor coordination from an early postnatal stage and mortality at approximately 3 weeks of age, suggestive of severe cerebellar dysfunction. Gross observation of Smad2-CNS-KO cerebella demonstrated aberrant foliations in lobule IX and X. Further analyses revealed increased apoptotic cell death, delayed migration and maturation of granule cells, and retardation of dendritic arborization of Purkinje cells. These findings indicate that Smad2 plays a key role in cerebellar development and motor function control. PMID:21464123

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

    PubMed Central

    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

    2015-01-01

    Background: 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. Objectives: 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. Methods: 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. Results: 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

  10. Postnatal testosterone exposure results in insulin resistance, enlarged mesenteric adipocytes, and an atherogenic lipid profile in adult female rats: comparisons with estradiol and dihydrotestosterone.

    PubMed

    Alexanderson, Camilla; Eriksson, Elias; Stener-Victorin, Elisabet; Lystig, Theodore; Gabrielsson, Britt; Lönn, Malin; Holmäng, Agneta

    2007-11-01

    Postnatal events contribute to features of the metabolic syndrome in adulthood. In this study, postnatally administered testosterone reduced insulin sensitivity and increased the mesenteric fat depot, the size of mesenteric adipocytes, serum levels of total cholesterol, low-density lipoprotein cholesterol, and triglycerides, and the atherogenic index in adult female rats. To assess the involvement of estrogen and androgen receptors in these programming effects, we compared testosterone-exposed rats to rats exposed to estradiol or dihydrotestosterone (DHT). Estradiol-treated rats had lower insulin sensitivity than testosterone-treated rats and, like those rats, had enlarged mesenteric adipocytes and increased triglyceride levels. DHT also reduced insulin sensitivity but did not mimic the other metabolic effects of testosterone. All treated rats were probably anovulatory, but only those treated with testosterone had reduced testosterone levels. This study confirms our previous finding that postnatal administration of testosterone reduces insulin sensitivity in adult female rats and shows that this effect is accompanied by unfavorable changes in mesenteric fat tissue and in serum lipid levels. The findings in the estradiol and DHT groups suggest that estrogen receptors exert stronger metabolic programming effects than androgen receptors. Thus, insults such as sex hormone exposure in early life may have long-lasting effects, thereby creating a predisposition to disturbances in insulin sensitivity, adipose tissue, and lipid profile in adulthood. PMID:17656458