Joseph L Jacobson

University of Cape Town, Kaapstad, Western Cape, South Africa

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Publications (176)619.7 Total impact

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    ABSTRACT: Prenatal alcohol exposure (PAE) is known to have severe, long-term consequences for brain and behavioral development already detectable in infancy and childhood. Resulting features of fetal alcohol spectrum disorders include cognitive and behavioral effects, as well as facial anomalies and growth deficits. Diffusion tensor imaging (DTI) and tractography were used to analyze white matter (WM) development in 11 newborns (age since conception <45 weeks) whose mothers were recruited during pregnancy. Comparisons were made with nine age-matched controls born to abstainers or light drinkers from the same Cape Coloured (mixed ancestry) community near Cape Town, South Africa. DTI parameters, T1 relaxation time, proton density and volumes were used to quantify and investigate group differences in WM in the newborn brains. Probabilistic tractography was used to estimate and to delineate similar tract locations among the subjects for transcallosal pathways, cortico-spinal projection fibers, and cortico-cortical association fibers. In each of these WM networks, the axial diffusivity was the parameter that showed the strongest association with maternal drinking. The strongest relations were observed in medial and inferior WM, regions in which the myelination process typically begins. In contrast to studies of older individuals with PAE, fractional anisotropy did not exhibit a consistent and significant relation with alcohol exposure. To our knowledge, this is the first DTI-tractography study of prenatally alcohol exposed newborns. Hum Brain Mapp, 2014. © 2014 Wiley Periodicals, Inc.
    Human Brain Mapping 09/2014; · 6.88 Impact Factor
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    ABSTRACT: OBJECTIVES: Inuit in Canada experience alarming levels of food insecurity, but nutritional and physiological consequences are poorly documented, especially in school-age children. The objective of this study was to assess the relation of food insecurity to iron deficiency and stature in school-aged Inuit children from Nunavik (Northern Quebec). METHODS: Food insecurity, iron deficiency, and stature were assessed in a cohort of children. Food insecurity was determined by interviewing the children’s mothers. Multiple logistic regression was used to evaluate the association of food insecurity to iron deficiency and short stature. We defined short stature as a height in the lowest tertile for age and sex, based on Canadian growth charts. The relation of food insecurity to height (cm) was analyzed with a general linear model. Statistical models controlled for age, sex, normal/overweight/obese status, prenatal lead exposure and postnatal polychlorinated biphenyls exposure. RESULTS: Half of the children (49.7%, n=145) were food insecure, while one third were iron depleted, 12.6% had anaemia, and 8.7% had iron-deficiency anaemia. The multivariate odds ratio of anaemia was 1.82 (95% CI: 0.97, 3.42, p=0.06) for food-insecure children. Prevalence of short stature was 18.7%. Food-insecure children were an average of 2 cm shorter (95% CI: -0.48, -3.17) than food-secure children (p<0.01). CONCLUSION: In this population, food-insecure children have greater burdens of nutritional deficiencies and slower linear growth. Considering the high prevalence of food insecurity among Inuit children in Nunavik, nutritional deficiencies and adverse effects on development should be carefully monitored.
    Canadian journal of public health. Revue canadienne de santé publique 08/2014; 105(4):e233-e238. · 1.02 Impact Factor
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    ABSTRACT: Prenatal cigarette smoke exposure (PCSE) has been linked to problems in behavioral inhibition and attention deficit hyperactivity disorder in children in several epidemiological studies. We used event-related potentials (ERPs) to examine the effects of PCSE on neural correlates of inhibitory control of behavior. In a prospective longitudinal study on child development in the Canadian Arctic, we assessed 186 Inuit children (mean age=11.3years) on a visual Go/No-go response inhibition paradigm. PCSE was assessed through maternal recall. Potential confounders were documented from a maternal interview, and exposure to neurotoxic environmental contaminants was assessed from umbilical cord and child blood samples. PCSE was not related to behavioral performance on this simple response inhibition task. Nevertheless, this exposure was associated with smaller amplitudes of the N2 and P3 components elicited by No-go stimuli, suggesting an impairment in the neural processes underlying response inhibition. Amplitude of the No-go P3 component was also inversely associated with behavioral measures of externalizing problems and hyperactivity/impulsivity in the classroom. This study is the first to report neurophysiological evidence of impaired response inhibition in school-aged children exposed to tobacco smoke in utero. Effects were found on ERP components associated with conflict processing and inhibition of a prepotent response, indicating neurophysiological deficits that may play a critical role in the attention and behavior problems observed in children with PCSE.
    Neurotoxicology and Teratology 06/2014; · 3.18 Impact Factor
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    ABSTRACT: Due to their geographic location and traditional diet, rich in seafood and marine mammals, the Inuit living in Arctic Quebec are exposed to high amounts of pollutants, including organochlorine pesticides (OCPs). While the adverse developmental effects of these pesticides on child cognitive functions are well known, the effects of developmental exposure to OP on sensory processes have not been investigated. The aim of this longitudinal study was to assess the effects of prenatal and childhood exposure to 1,1,1-trichloro-2,2-bis(p-chlorophenyl)ethane (p,p'-DDT) and its major metabolite 1,1,-dichloro-2,2-bis(p-chlorophenyl)ethylene (p,p'-DDE), on visual processing in Inuit children in Nunavik (Arctic Québec). p,p'-DDT and p,p'-DDE concentrations were determined from umbilical cord and 5- and 11-year plasma samples. Visual evoked potentials (VEPs) were successfully recorded in 150 children at four contrast levels (95%, 30%, 12%, and 4%). Hierarchical multiple regressions were conducted to determine the association between p,p'-DDT, or p,p'-DDE, exposure and VEPs while controlling for the effects of various confounders, including fish nutrients and other contaminants. p,p'-DDE measured in umbilical cord plasma was significantly related to the amplitude of the N150 response at the lowest contrast (4%). In addition, 5-year p,p'-DDE plasma concentration was significantly associated with decreased N75 amplitude. These findings indicate that p,p'-DDE exposure, both pre- and postnatally, during early childhood is associated with visual processing impairment later in life.
    NeuroToxicology 05/2014; · 2.65 Impact Factor
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    ABSTRACT: Background Animal models have demonstrated fetal alcohol-related disruptions in neuroendocrine function in the hypothalamic–pituitary–gonadal axis and downstream effects on pubertal development and sexual behavior in males and females, but little is known about these effects in humans. This study examined whether prenatal alcohol exposure is associated with alterations in testosterone during adolescence and whether it affects timing of pubertal development.Methods The sample consisted of 265 African American adolescents from the Detroit Longitudinal Cohort Study for whom testosterone and/or pubertal development data were available. Subjects were offspring of women recruited at their first prenatal clinic visit to over represent moderate-to-heavy alcohol use, including a 5% random sample of low-level drinkers/abstainers. Mothers were interviewed at every prenatal visit about their alcohol consumption using a timeline follow-back approach and about their smoking and drug use and sociodemographic factors. At age 14 years, adolescents provided salivary samples, which were analyzed for testosterone (pg/ml), self-reported Tanner stages for pubertal development, and age at menarche (females).ResultsPrenatal alcohol exposure was related to elevated testosterone concentrations for males and females but not to changes in Tanner stages or age at menarche, after controlling for confounders. In regression models stratified by alcohol exposure, the expected relation between testosterone and pubic hair development was seen among males with light-to-no prenatal alcohol exposure, but not among those with moderate-to-heavy prenatal alcohol exposure. This interaction between testosterone and prenatal alcohol exposure was confirmed in multivariable models including an alcohol exposure group × testosterone interaction term and potential confounders.Conclusions This study is the first to show a relation between prenatal alcohol exposure and increased testosterone during adolescence and evidence of decreased testosterone responsiveness in tissues related to pubertal development in humans. Further studies examining androgen receptor expression and other hormonal and cellular factors affecting pubertal development may reveal important mechanisms underlying these teratogenic effects of alcohol exposure.
    Alcoholism Clinical and Experimental Research 04/2014; · 3.42 Impact Factor
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    ABSTRACT: Prenatal alcohol exposure has been linked to impairment in cerebellar structure and function, including eyeblink conditioning. The deep cerebellar nuclei, which play a critical role in cerebellar-mediated learning, receive extensive inputs from brain stem and cerebellar cortex and provide the point of origin for most of the output fibers to other regions of the brain. We used in vivo (1) H magnetic resonance spectroscopy (MRS) to examine effects of prenatal alcohol exposure on neurochemistry in this important cerebellar region. MRS data from the deep cerebellar nuclei were acquired from 37 children with heavy prenatal alcohol exposure and 17 non- or minimally exposed controls from the Cape Coloured (mixed ancestry) community in Cape Town, South Africa. Increased maternal alcohol consumption around time of conception was associated with lower N-Acetylaspartate (NAA) levels in the deep nuclei (r = -0.33, p < 0.05). Higher levels of alcohol consumption during pregnancy were related to lower levels of the choline-containing metabolites (r = -0.37, p < 0.01), glycerophosphocholine plus phosphocholine (Cho). Alcohol consumption levels both at conception (r = 0.35, p < 0.01) and during pregnancy (r = 0.38, p < 0.01) were related to higher levels of glutamate plus glutamine (Glx). All these effects continued to be significant after controlling for potential confounders. The lower NAA levels seen in relation to prenatal alcohol exposure may reflect impaired neuronal integrity in the deep cerebellar nuclei. Our finding of lower Cho points to disrupted Cho metabolism of membrane phospholipids, reflecting altered neuropil development with potentially reduced content of dendrites and synapses. The alcohol-related alterations in Glx may suggest a disruption of the glutamate-glutamine cycling involved in glutamatergic excitatory neurotransmission.
    Alcoholism Clinical and Experimental Research 03/2014; · 3.42 Impact Factor
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    ABSTRACT: Single voxel spectroscopy (SVS) can generate useful information regarding metabolite concentrations provided that the MR signal can be averaged over several minutes during which the subject remains stationary. This requirement can be particularly challenging for children who cannot otherwise be scanned without sedation. To address this problem we developed an EPI volume navigated (vNav) SVS PRESS sequence, which applies real-time head pose (location and orientation), frequency, and first-order B0 shim adjustments. A water-independent preprocessing algorithm removes residual frequency and phase shifts resulting from within-TR movements. We compare results and performance of the standard and vNav PRESS sequences in a sample of 9- to 10-year-olds from a South African cohort of children with fetal alcohol spectrum disorders (FASD) and healthy controls. Magnetic resonance spectroscopy (MRS) data in the deep cerebellar nuclei were initially acquired with the standard PRESS sequence. The children were re-scanned 1 year later with the vNav PRESS sequence. Good quality data were acquired in 73 % using the vNav PRESS sequence, compared to only 50 % for the standard PRESS sequence. Additionally, tighter linewidths and smaller variances in the measured concentrations were observed. These findings confirm previous reports demonstrating the efficacy of our innovative vNav sequence with healthy volunteers and young children with HIV and expand its application to a school-aged population with FASD-disorders often associated with attention problems and hyperactivity. This study provides the most direct evidence to date regarding degree to which these new methods can improve data quality in research studies employing MRS.
    Metabolic Brain Disease 02/2014; · 2.33 Impact Factor
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    ABSTRACT: Polychlorinated biphenyls (PCBs), methylmercury (MeHg), and lead (Pb) are environmental contaminants known for their adverse effects on cognitive development. This study examined the effects of prenatal exposure to PCBs, MeHg, and Pb on cognitive development in a sample of Inuit infants from Arctic Québec. Mothers were recruited at local prenatal clinics. PCBs, mercury (Hg), Pb, and two seafood nutrients, docosahexaenoic acid (DHA) and selenium (Se), were measured in umbilical cord blood. Infants (N = 94) were assessed at 6.5 and 11 months on the Fagan Test of Infant Intelligence (FTII), A-not-B test, and Bayley Scales of Infant Development-2nd Edition (BSID-II). Multiple regression analyses revealed that higher prenatal PCB exposure was associated with decreased FTII novelty preference, indicating impaired visual recognition memory. Prenatal Hg was associated with poorer performance on A-not-B, which depends on working memory and is believed to be a precursor of executive function. Prenatal Pb was related to longer FTII fixation durations, indicating slower speed of information processing. PCBs, MeHg, and Pb each showed specific and distinct patterns of adverse associations with the outcomes measured during infancy. By contrast, none of these exposures was associated with performance on the BSID-II, a global developmental measure. The more focused, narrow band measures of cognitive function that appeared to be sensitive to these exposures also provide early indications of long-term impairment in specific domains that would otherwise not likely be evident until school age.
    Environmental Health Perspectives 01/2014; · 7.26 Impact Factor
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    ABSTRACT: Prenatal cigarette smoke exposure (PCSE) has been linked to problems in behavioral inhibition and attention deficit hyperactivity disorder in children in several epidemiological studies. We used event-related potentials (ERPs) to examine the effects of PCSE on neural correlates of inhibitory control of behavior. In a prospective longitudinal study on child development in the Canadian Arctic, we assessed 186 Inuit children (mean age = 11.3 years) on a visual Go/No-go response inhibition paradigm. PCSE was assessed through maternal recall. Potential confounders were documented from a maternal interview, and exposure to neurotoxic environmental contaminants was assessed from umbilical cord and child blood samples. PCSE was not related to behavioral performance on this simple response inhibition task. Nevertheless, this exposure was associated with smaller amplitudes of the N2 and P3 components elicited by No-go stimuli, suggesting an impairment in the neural processes underlying response inhibition. Amplitude of the No-go P3 component was also inversely associated with behavioral measures of externalizing problems and hyperactivity/impulsivity in the classroom. This study is the first to report neurophysiological evidence of impaired response inhibition in school-aged children exposed to tobacco smoke in utero. Effects were found on ERP components associated with conflict processing and inhibition of a prepotent response, indicating neurophysiological deficits that may play a critical role in the attention and behavior problems observed in children with PCSE.
    Neurotoxicology and Teratology 01/2014; · 3.18 Impact Factor
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    ABSTRACT: Background Because of their geographical location and traditional lifestyle, Canadian Inuit children are highly exposed to polychlorinated biphenyls (PCBs) and lead (Pb), environmental contaminants that are thought to affect fetal and child growth. We examined the associations of these exposures with the fetal and postnatal growth of Inuit children. Methods We conducted a prospective cohort study among Inuit from Nunavik (Arctic Québec). Mothers were recruited at their first prenatal visit; children (n=290) were evaluated at birth and at 8–14 years of age. Concentrations of PCB 153 and Pb were determined in umbilical cord and child blood. Weight, height and head circumference were measured at birth and during childhood. Results Cord blood PCB 153 concentrations were not associated with anthropometric measurements at birth or school age, but child blood PCB 153 concentrations were associated with reduced weight, height and head circumference during childhood. There was no association between cord Pb levels and anthropometric outcomes at birth, but cord blood Pb was related to smaller height and shows a tendency of a smaller head circumference during childhood. Interpretation Our results suggest that chronic exposure to PCBs during childhood is negatively associated with skeletal growth and weight, while prenatal Pb exposure is related to reduced growth during childhood. This study is the first to link prenatal Pb exposure to poorer growth in school-age children.
    Environmental Research. 01/2014; 134:17–23.
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    ABSTRACT: Reductions in brain volumes represent a neurobiological signature of fetal alcohol spectrum disorders (FASD). Less clear is how regional brain tissue reductions differ after normalizing for brain size differences linked with FASD and whether these profiles can predict the degree of prenatal exposure to alcohol. To examine associations of regional brain tissue excesses/deficits with degree of prenatal alcohol exposure and diagnosis with and without correction for overall brain volume, tensor-based morphometry (TBM) methods were applied to structural imaging data from a well-characterized, demographically homogeneous sample of children diagnosed with FASD (n = 39, 9.6–11.0 years) and controls (n = 16, 9.5–11.0 years). Degree of prenatal alcohol exposure was significantly associated with regionally pervasive brain tissue reductions in: (1) thalamus, midbrain, and ventromedial frontal lobe, (2) superior cerebellum and inferior occipital lobe, (3) dorsolateral frontal cortex, and (4) precuneus and superior parietal lobule. When overall brain size was factored out of the analysis on a subject-by-subject basis, no regions showed significant associations with alcohol exposure. FASD diagnosis was associated with a similar deformation pattern, but few of the regions survived FDR correction. In data-driven independent component analyses (ICA) regional brain tissue deformations successfully distinguished individuals based on extent of prenatal alcohol exposure and to a lesser degree, diagnosis. The greater sensitivity of the continuous measure of alcohol exposure compared with the categorical diagnosis across diverse brain regions, underscores the dose dependence of these effects. The ICA results illustrate that profiles of brain tissue alterations may be a useful indicator of prenatal alcohol exposure when reliable historical data are not available and facial features are not apparent.
    NeuroImage: Clinical. 01/2014;
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    ABSTRACT: Due to their geographic location and traditional diet, rich in seafood and marine mammals, the Inuit living in Arctic Quebec are exposed to high amounts of pollutants, including organochlorine pesticides (OCPs). While the adverse developmental effects of these pesticides on child cognitive functions are well known, the effects of developmental exposure to OP on sensory processes have not been investigated. The aim of this longitudinal study was to assess the effects of prenatal and childhood exposure to 1,1,1-trichloro-2,2-bis(p-chlorophenyl)ethane (p,p′-DDT) and its major metabolite 1,1,-dichloro-2,2-bis(p-chlorophenyl)ethylene (p,p’-DDE), on visual processing in Inuit children in Nunavik (Arctic Québec). p,p′-DDT and p,p′-DDE concentrations were determined from umbilical cord and 5- and 11-year plasma samples. Visual evoked potentials (VEPs) were successfully recorded in 150 children at four contrast levels (95%, 30%, 12%, and 4%). Hierarchical multiple regressions were conducted to determine the association between p,p′-DDT, or p,p′-DDE, exposure and VEPs while controlling for the effects of various confounders, including fish nutrients and other contaminants. p,p′-DDE measured in umbilical cord plasma was significantly related to the amplitude of the N150 response at the lowest contrast (4%). In addition, 5-year p,p′-DDE plasma concentration was significantly associated with decreased N75 amplitude. These findings indicate that p,p′-DDE exposure, both pre- and postnatally, during early childhood is associated with visual processing impairment later in life.
    NeuroToxicology 01/2014; · 2.65 Impact Factor
  • Sandra W. Jacobson, Joseph L. Jacobson
    Clinical Neurophysiology. 01/2014;
  • Sandra W Jacobson, R Colin Carter, Joseph L Jacobson
    The Journal of pediatrics 12/2013; · 4.02 Impact Factor
  • Sandra W Jacobson, Joseph L Jacobson
    Evidence-based medicine 11/2013;
  • Neil C Dodge, Joseph L Jacobson, Sandra W Jacobson
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    ABSTRACT: Alcohol dehydrogenase is a critical enzyme in the metabolism of alcohol. Expression of three alleles at the ADH1B locus results in enzymes that differ in turnover rate and affinity for alcohol. The ADH1B*3 allele, which appears to be unique to individuals of African descent, is associated with more rapid alcohol metabolism than the more prevalent ADH1B*1 allele. It has been previously demonstrated that the presence of at least one maternal ADH1B*3 allele confers a protective effect against alcohol teratogenicity in infants and children. This study was conducted to determine whether the presence of the ADH1B*3 allele in the mother or child continues to be protective in alcohol-exposed individuals during adolescence. 186 adolescents and 167 mothers participating in a 14-year follow-up of the Detroit Longitudinal Cohort were genotyped for ADH1B alleles. Behavioral reports were obtained from classroom teachers. Frequencies of the ADH1B*3 allele were 17.6% in the mothers and 21.0% in the adolescents, which are consistent with the 15-20% expected for African Americans. Prenatal alcohol exposure was associated with increased attention problems and externalizing behaviors in adolescents born to mothers with two ADH1B*1 alleles but not in those whose mothers had at least one ADH1B*3 allele. A similar pattern was seen in relation to the presence or absence of an ADH1B*3 allele in the adolescent, which may have reflected the presence/absence of the maternal variant. This study is the first to demonstrate that the protective effects of the maternal ADH1B*3 allele continue to be evident during adolescence. These persistent individual differences in vulnerability of offspring to the behavioral effects of fetal alcohol exposure are likely attributable to more rapid metabolism of alcohol that the ADH1B*3 variant confers on the mother, leading to a reduction of the peak blood alcohol concentration to which the fetus is exposed during each drinking episode.
    Neurotoxicology and Teratology 11/2013; · 3.18 Impact Factor
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    ABSTRACT: Our aim was to test the hypothesis that emotional withdrawal is an early indicator of affective disorder in infants heavily exposed prenatally to alcohol, which is independent of alcohol-related effects on mother-infant interaction and temperament and discriminated between children later diagnosed with fetal alcohol syndrome (FAS) and partial FAS (PFAS) and predicted cognitive and affective outcomes at 5 and 9 years. The sample consisted of Cape Coloured (mixed ancestry) infants, whose mothers were interviewed during pregnancy regarding their alcohol consumption using a timeline follow-back approach. Infant emotional withdrawal (n = 85) was assessed on the Alarm Distress Baby Scale at 6.5 months. Mother-infant interaction was evaluated from video recordings during free play and infant feeding at 6.5 months (n = 127). Infant temperament was assessed by maternal report on the EAS Temperament Survey at 13 months (n = 119). Sociodemographic and psychological correlates of maternal alcohol use and infant iron deficiency were examined as potential confounders. The children were diagnosed for FAS/PFAS by expert dysmorphologists at 5 years, cognitive and affective function at 5 and 9 years. Prenatal alcohol exposure was associated with increased infant emotional withdrawal and decreased activity, but unrelated to mother-infant interaction or any other temperament measures. Children later diagnosed with FAS and PFAS at 5 years exhibited more emotional withdrawal and less responsivity and activity as infants. Infant withdrawal, responsivity, quality of interaction, and maternal sensitivity also predicted poorer IQ and affective response at 5 and 9 years. When all 4 infant affective measures were examined simultaneously in a regression analysis, only infant emotional withdrawal persisted as a significant predictor of 9-year IQ. This study is the first to document a direct effect of fetal alcohol exposure on emotional withdrawal in infancy. These data link prenatal alcohol to a specific aspect of infant affective function not attributable to mother-infant interaction, infant temperament, or other socioemotional aspects of the infant's environment and identify infant emotional withdrawal as an early indicator of affective disturbance, particularly in children later diagnosed with FAS and PFAS.
    Alcoholism Clinical and Experimental Research 08/2013; · 3.42 Impact Factor
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    ABSTRACT: Prenatal alcohol exposure is responsible for a broad range of brain structural malformations, which can be studied using magnetic resonance imaging (MRI). Advanced MRI methods have emerged to characterize brain abnormalities, but the teratogenic effects of alcohol on cortical morphology have received little attention to date. Twenty-four 9-year-old children with fetal alcohol spectrum disorders (9 with fetal alcohol syndrome, 15 heavy exposed nonsyndromal children) and 16 age-matched controls were studied to assess the effect of alcohol consumption during pregnancy on cortical morphology. An automated method was applied to 3D T1-weighted images to assess cortical gyrification using global and regional sulcal indices and two region-based morphological measurements, mean sulcal depth and fold opening. Increasing levels of alcohol exposure were related to reduced cortical folding complexity, even among children with normal brain size, indicating a reduction of buried cortical surface. Fold opening was the strongest anatomical correlate of prenatal alcohol intake, indicating a widening of sulci in all regions that were examined. These data identify cortical morphology as a suitable marker for further investigation of brain damage associated with prenatal alcohol exposure. Hum Brain Mapp 00:000-000, 2013. © 2013 Wiley Periodicals, Inc.
    Human Brain Mapping 08/2013; · 6.88 Impact Factor
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    ABSTRACT: Smoking during pregnancy is common among Inuit women from the Canadian Arctic. Yet, prenatal cigarette smoke exposure (PCSE) is seen as a major risk factor for childhood behavior problems. Recent data also suggest that co-exposure to neurotoxic environmental contaminants can exacerbate the effects of PCSE on behavior. This study examined the association between PCSE and behavior at school age in a sample of Inuit children from Nunavik, Québec, where co-exposure to environmental contaminants is also an important issue. Interactions with lead (Pb) and mercury (Hg), two contaminants associated with behavioral problems, were also explored. Participants were 271 children (mean age = 11.3 years) involved in a prospective birth-cohort study. PCSE was assessed through maternal recall. Assessment of child behavior was obtained from the child's classroom teacher on the Teacher Report Form (TRF) and the Disruptive Behavior Disorders Rating Scale (DBD). Exposure to contaminants was assessed from umbilical cord and child blood samples. Other confounders were documented by maternal interview. After control for contaminants and confounders, PCSE was associated with increased externalizing behaviors and attention problems on the TRF and higher prevalence of attention deficit hyperactivity disorder (ADHD) assessed on the DBD. No interactions were found with contaminants. This study extends the existing empirical evidence linking PCSE to behavioral problems in school-aged children by reporting these effects in a population where tobacco use is normative rather than marginal. Co-exposure to Pb and Hg do not appear to exacerbate tobacco effects, suggesting that these substances act independently.
    Neurotoxicology and Teratology 08/2013; · 3.18 Impact Factor

Publication Stats

6k Citations
619.70 Total Impact Points

Institutions

  • 2010–2014
    • University of Cape Town
      • Faculty of Health Sciences
      Kaapstad, Western Cape, South Africa
    • University of Rochester
      Rochester, New York, United States
    • University of British Columbia - Vancouver
      • Department of Pediatrics
      Vancouver, British Columbia, Canada
  • 1984–2014
    • Wayne State University
      • • Department of Psychiatry and Behavioral Neurosciences
      • • Department of Psychology
      • • School of Medicine
      Detroit, Michigan, United States
    • Concordia University–Ann Arbor
      Ann Arbor, Michigan, United States
  • 2013
    • Cea Leti
      Grenoble, Rhône-Alpes, France
    • Johns Hopkins University
      • Department of Neurology
      Baltimore, Maryland, United States
    • Université du Québec à Montréal
      Montréal, Quebec, Canada
  • 2011–2013
    • Centre Hospitalier Universitaire de Québec (CHUQ)
      Québec, Quebec, Canada
  • 2012
    • Indiana University-Purdue University Indianapolis
      • Department of Medical and Molecular Genetics
      Indianapolis, IN, United States
  • 2001–2011
    • Laval University
      • • École de Psychologie
      • • Department of Social and Preventive Medicine
      Québec, Quebec, Canada
  • 2007–2010
    • Boston Children's Hospital
      • Division of Emergency Medicine
      Boston, MA, United States