Response inhibition at 8 and 9 1/2 years of age in children prenatally exposed to PCBs
304 Mahar Hall, State University of New York at Oswego, Oswego, NY 13126, USA. Neurotoxicology and Teratology
(Impact Factor: 2.76).
11/2005; 27(6):771-80. DOI: 10.1016/j.ntt.2005.07.003
We previously reported a relationship between prenatal PCB exposure and impulsive (excessive) responding on a continuous performance task in children at 4 1/2 years of age [P.W. Stewart, S. Fitzgerald, J. Reihman, B. Gump, E. Lonky, T. Darvill, J. Pagano, P. Hauser, Prenatal PCB exposure, the corpus callosum, and response inhibition, Environmental Health Perspectives 111 (13) (2003b) 1670-1677.]. The current study investigated the stability of this effect at 8 and 9 1/2 years of age. We tested the hypothesis that PCB-related impulsive responding might be a function of impaired response inhibition. Children (n=202) enrolled in the Oswego Children's Study were tested at 8 years of age using the NES2 Continuous Performance Test (CPT). This was followed by a series of Extended Continuous Performance Tests (E-CPT) at 9 1/2 years of age, designed to dissociate response inhibition from sustained attention. After taking into account more than 50 measured covariables, including maternal IQ, maternal sustained attention and maternal response inhibition, results revealed PCB-related associations with impulsive responding at both testing ages. At 8 years of age, prenatal PCB exposure was associated with increased impulsive responding on the CPT. At 9 1/2 years of age, E-CPT testing clearly indicated that the PCB-related impulsive responding was due to impaired response inhibition and not impaired sustained attention. These results were significant after extensive and rigorous control for multiple potential confounders, including several non-PCB contaminants (prenatal MeHg, DDE, HCB, and pre- and postnatal Pb). These data are consistent with, and in fact predicted by, several studies in PCB-exposed animals.
Available from: Dave Saint-Amour
- "These two types of errors were calculated in percentage according to the total number of targets or distractors (omission = number of omissions/number of targets × 100; false alarm = number of false alarms/number of distractors × 100). An index of accuracy was also calculated in percentage, by subtracting the rate of false alarms from the rate of hits, to obtain an indicator of sustained attention (Losier et al., 1996; Stewart et al., 2005). Each child was administered a 22-trial practice with verbal feedback to familiarize him/her with the task. "
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ABSTRACT: Chronic exposure to methylmercury (MeHg), lead (Pb) and polychlorinated biphenyls (PCBs) has been associated with a range of attention deficits in children, but it is not known whether selective spatial attention is also altered. We modified the classic Posner paradigm, which assesses visuospatial attention, to also assess vigilance and impulsivity. This paradigm is based on the well-documented findings that a target will be detected more quickly if a visual cue indicates beforehand where it will appear, and more slowly if the cue indicates a false spatial location. In our task, visual distractors were introduced, in addition to the classic Posner trials, to assess impulsivity, and a central smiley face, whose eye-movement cued the location of the targets, to measure spatial attention. This task was administered to 27 school-age Inuit children (mean age=11.2years) from Nunavik (Arctic Quebec, Canada), in which pre- and postnatal exposures to environmental contaminants had been documented from birth. After controlling for the impact of confounding variables, multivariable regressions revealed that prenatal exposures to PCBs and Pb were significantly associated with greater inattention and impulsivity, respectively, while current exposure to Pb was significantly associated with longer reaction times. Although a significant correlation was observed between cord blood PCB concentration and decreased visuospatial performance, no significant association was found after adjustment for confounders. No effect was found for Hg exposures. These results suggest that our adapted Posner paradigm is sensitive in detecting a range of attention deficits in children exposed to environmental contaminants; implications for future studies are discussed.
Copyright © 2015. Published by Elsevier Inc.
Available from: Monika Kasper-Sonnenberg
- "Alterations in neurotransmitter systems, particularly in dopamine functioning (Sagvolden et al., 2005), are also likely to be involved in the etiology of ADHD (Cortese, 2012). Concerning PCB exposure , different birth cohort studies provide evidence that prenatal exposure impairs neuropsychological functions, such as response inhibition (Stewart et al., 2005), planning (Vreugdenhil et al., 2004) and focused attention (Jacobson and Jacobson, 2003). It could also be associated with increased impulsivity (Jacobson and Jacobson, 2003) and ADHD-associated behavior (Sagiv et al., 2010). "
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Prenatal exposure to polychlorinated biphenyls (PCBs) and lead are thought to be risk factors for attention-deficit hyperactivity disorder (ADHD), whereas the prenatal influence of polychlorinated dibenzo-p-dioxins and -furans (PCDD/Fs) on attention performance has been less studied.
Within the Duisburg Birth Cohort Study, we investigated low-level exposure to these compounds in relation to children's attention.
We measured blood levels of PCDD/Fs, PCBs and lead from pregnant mothers (32nd week of pregnancy) and PCDD/Fs and PCBs in breast milk (2 weeks after delivery). The attention of school-aged children (N = 117) was investigated with a computer-based test battery of attention performance (KITAP) and a parent rating questionnaire of behaviors related to ADHD (FBB-ADHS). Influences of the exposure on attention were analyzed by multiple regression analyses.
Increasing prenatal PCDD/F and PCB concentrations were significantly (p < 0.05) associated with a higher number of omission errors in the subtest Divided Attention (47% and 42%; 95% confidence intervals (95%-CI): 1.08-2.00 and 1.07-1.89, respectively). Prenatal lead concentrations had few significant associations with attention performance (e.g., a 23% higher number of omission errors in the subtest Distractibility; 95%-CI: 1.00-1.51), whereas ADHD-related behavior (questionnaire based) was increased with increasing lead exposure (Overall-ADHD: 9%; 95%-CI: 1.01-1.17). ADHD-related behavior was negatively associated with prenatal PCDD/F or PCB exposures (e.g., for PCB-exposure: -10%; 95%-CI: 0.82-0.99).
Pre- and perinatal PCDD/F and PCB exposure may have subtle influences on attention performance in healthy children at low environmental levels, while behavior changes are negatively associated. Furthermore, we provide additional evidence for the impact of prenatal lead exposure on attention deficits.
Available from: Gina Muckle
- "Most studies of Pb have focused on postnatal exposure, primarily during the toddler period, and there is extensive evidence of long-term effects from postnatal Pb exposure on childhood IQ (e.g., Bellinger et al. 1992; Dietrich et al. 1993) and attention (e.g., Chiodo et al. 2004; Plusquellec et al. 2010). In childhood, prenatal PCB exposure has been linked primarily to reduced IQ and reading achievement (Jacobson and Jacobson 1996; Stewart et al. 2008), with some evidence suggesting vulnerability in response inhibition (Stewart et al. 2005). Effects of prenatal MeHg exposure in childhood have been examined in two large prospective studies—one in the Faroe Islands, where Hg was associated with poorer cognitive performance at 7 and 14 years of age (Debes et al. 2006; Grandjean et al. 1997); and the other, in the Seychelles Islands, where few adverse associations were found (Davidson et al. 2011; Myers et al. 1995, 2003). "
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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.
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